Vendola firma piano
di rientro sanitario
della Regione Puglia
ROMA – E' stato sottoscritto questa sera presso il Ministero per i Rapporti con le Regioni, l’accordo tra il Governo e la Regione Puglia sul Piano di Rientro Sanitario 2010-2012 alla presenza del Ministro Fitto e del Presidente Vendola. Soddisfazione è stata espressa dal Ministro Raffaele Fitto che ha sottolineato come «il Governo, attraverso la verifica svolta in questi mesi con i tecnici dei Ministeri dell’Economia, della Salute e dei Rapporti con le Regioni, ha ottenuto da parte della Regione l’impegno all’avvio di un processo di riqualificazione e di riorganizzazione del proprio servizio sanitario e al riordino della rete ospedaliera nell’interesse della Puglia e dei cittadini pugliesi. L’impegno assunto dalla Regione a rimuovere le cause di illegittimità della recente legislazione regionale in materia, conformemente alle richieste avanzate dal Governo, è stato decisivo per la positiva conclusione dell’accordo che oggi è stato sottoscritto».
L’accordo prevede che sarà possibile assegnare alla Regione Puglia la riattribuzione dei maggiori finanziamenti degli anni passati in sede di verifica del rispetto degli adempimenti regionali. Ciò è reso possibile grazie alla Legge finanziaria 2010 che ha concesso un’ulteriore proroga a quelle Regioni che avrebbero già dovuto sottoscrivere i Piani di rientro entro il 31 dicembre 2009. L'impegno della Regione nella realizzazione del Piano è anche legato all’esecuzione della sentenza della Corte Costituzionale n. 333 del 24 novembre 2010, che ha annullato la legge regionale n. 27/2009, con l’adozione nell’anno 2010, dei provvedimenti necessari nel rispetto dei vincoli di finanza pubblica statale e regionale.
Con la firma dell’Accordo, inoltre, la Regione si è anche impegnata a modificare le leggi regionali n.11 e n.12 del 2010, per adeguarsi ai rilievi di legittimità formulati dal Consiglio dei Ministri il 18 novembre 2010. Infine, qualora gli esiti dei giudizi pendenti alla Corte Costituzionale, in riferimento alle ulteriori leggi impugnate, ivi compresa la legge regionale n. 4 del 2010, dovessero risolversi in senso sfavorevole alla regione, quest’ultima dovrà dare concreta e puntuale esecuzione alle relative sentenze costituzionali, ponendo in essere tutti gli atti e i provvedimenti necessari nel rispetto dei vincoli di finanza pubblica statale e regionale.
«Da oggi – rileva Vendola – parte una grande sfida per la Puglia. Coniugare meno risorse con l’innalzamento della qualità del sistema sanitario». «Il nostro atteggiamento – aggiunge - però non è mai cambiato. Aspettiamo con serenità e fiducia la sentenza della Corte costituzionale in merito alle scelte compiute dalla Regione Puglia. Noi intanto abbiamo bloccato i processi di internalizzazione ma abbiamo messo al riparo chi è già stato contrattualizzato». «Tuttavia oggi – conclude Vendola – bisogna cogliere l'occasione per trasformare il momento dei tagli in un’occasione per rigenerare l’organizzazione del sistema sanitario».
DECARO: ORA LA SFIDA E' RISPONDERE ALLA DOMANDA DI SALUTE
«Ora dobbiamo fare i conti con la domanda di salute delle persone. Abbiamo meno risorse a disposizione e l’esigenza di incrementare sempre di più la qualità del nostro sistema sanitario. E’ a questo che oggi dobbiamo lavorare, coinvolgendo i territori nella riorganizzazione della sanità e limitando al massimo i sacrifici per i cittadini». Lo dichiara il capogruppo Pd alla Regione Puglia, Antonio Decaro, dopo la firma del piano di rientro sanitario regionale da parte del governo.
«Dovremo fare molta attenzione a valutare i tagli di posti letto – sottolinea – analizzando ogni dettaglio, affinchè tutti i pugliesi si sentano sicuri di poter ricevere l’adeguata assistenza nel momento in cui ne avranno bisogno. Non sarà un percorso facile – rileva Decaro – ma la Puglia ha dimostrato in molte occasioni di saper far fronte alle sfide che le si presentano davanti. E il Partito democratico – conclude il capogruppo – è pronto a dare il proprio contributo per dare il via al nuovo corso della sanità pugliese».
29 NOVEMBRE 2010
Medicina e non solo - Dr. Carmine Capasso Otorino Bari
lunedì 29 novembre 2010
domenica 28 novembre 2010
Wikileaks, cresce l'attesa: ora Assange fa paura L'Italia imprevedibile e scomoda che dà fastidio
Wikileaks, cresce l'attesa: ora Assange fa paura L'Italia imprevedibile e scomoda che dà fastidio
di Fausto Biloslavo
Assange fa impazzire il mondo con la crociata di Wikileaks: gli attesi rapporti riservati ottenuti dal sito saranno pubblicati questa sera. In realtà tutte le sue rivelazioni ha sempre colpito l'Occidente
Julian Paul Assange, il pifferaio magico della trasparenza a oltranza, il campione delle rivelazioni scottanti su internet, soprattutto anti-occidentali, è l’uomo meno trasparente del pianeta. Il suo vero motto potrebbe essere: «Pubblico i segreti degli altri, ma non certo i miei».
L’algido visionario fa impazzire il mondo con la crociata di Wikileaks. Il sito che sta inguaiando gli americani dall’Irak all’Afghanistan, in attesa dell’annunciata valanga di documenti che scuoterà più di un alleato degli Stati Uniti compresa l’Italia. Non soltanto: Assange si presenta come paladino anti-cattivoni (Pentagono, Cia, ecc.) ma allo stesso tempo vive e raccoglie informazione come una spia, con la differenza che alla fine le pubblica in rete. Un gioco degli specchi che deve far comodo a qualche servizio segreto, mai sfiorato da una sola rivelazione, come quello russo o cinese.
Capelli bianchi, smilzo, mezzo ascetico e spesso vestito di nero, Assange è nato nel 1971 in Australia. A 17 anni fa il suo esordio nel mondo della pirateria informatica con gli «International subversives», che penetrano i computer della Nasa. Nel 1999 registra il dominio leaks.org, che vuol dire letteralmente «trapelare». Otto anni dopo ci aggiungerà davanti Wiki, per trasformare il suo sito nell’enciclopedia in rete delle rivelazioni planetarie. «I nostri principali bersagli - dichiara al momento del lancio di Wikileaks - sono i regimi oppressivi come la Cina, la Russia, e quelli dell’Asia centrale. Ma ci aspettiamo di essere d’aiuto anche per chi in Occidente vorrebbe che fossero denunciati comportamenti illegali e immorali dei governi e delle grandi società».
In realtà le rivelazioni di Assange si sono concentrate soprattutto contro l’Occidente. Amnesty International lo premia nel 2009 per una fuga di notizie sugli omicidi di stato in Kenya. Tutta robetta, rispetto a oggi, ma il visionario predicatore della trasparenza, a senso unico, comincia a crearsi un’immagine. Vagabonda facendo tappa in Islanda, ma qualcuno giura che ha soggiornato pure in Russia e Georgia. Il sito anti segreti diventa molto famoso quando rende noto un video di elicotteri americani a Bagdad, che uccidono giornalisti locali. Guarda caso Assange conquista il premio Sam Adams, organizzato da ex agenti della Cia, in nome di un’etica nei servizi segreti. I sostenitori del complotto dietro l’11 settembre sono convinti che il guru di internet sia al soldo della Cia. L’unico dato certo è che fino a oggi ha pubblicato migliaia di documenti riservati del Pentagono e sono in arrivo quelli del Dipartimento di Stato, ma dalla sede dell’agenzia a Langley non salta fuori nulla. I colpi grossi arrivano con le rivelazioni sulla guerra in Irak e Afghanistan. La tv americana Fox news chiede a gran voce che Assange sia incriminato per spionaggio. «Queste cosiddette fughe di notizie sono chirurgiche e riguardano sempre l’Occidente. Wikileaks è diventato uno strumento di potere amplificato dai media. Sono tutti sintomi che dimostrano come il sito non sia più in mano a un paladino della verità, ma sotto l’influenza di uno o più apparati di intelligence di grandi potenze», spiega Fabio Ghioni, l’hacker più famoso d’Italia.
Mosca e Pechino, per ora, sono uscite indenni dalle soffiate di Wikileaks, che prima degli scoop mondiali sulle guerre degli americani stava per chiudere i battenti per mancanza di fondi. Proprio sulle finanze del sito anti segreti si addensano i dubbi più pesanti. Assange sostiene di aver incassato nell’ultimo anno un milione di dollari in donazioni via internet. Ufficialmente i collaboratori di Wikileaks lavorano gratis. In realtà mantenere in piedi un’operazione del genere costa molto, a cominciare dai server dispersi per il mondo. Per non parlare dei soldi per tirar fuori le notizie e delle spese di Assange che vive, come dice lui, «in aeroporto, sempre in movimento». Oltre alle parcelle legali per le cause e l’ultima grana sulla presunta violenza sessuale del fondatore in Svezia. Assange ha incaricato della difesa il miglior avvocato del Paese, ma la storia puzza di trappola sessuale, come ai tempi del Kgb. Le due presunte vittime sono strane fan di guru di internet. Lui ha ammesso di esserci andato a letto perché consenzienti. Sull’uomo meno trasparente del mondo è piombato il mandato di cattura di un procuratore svedese. Assange, che voleva chiedere asilo politico in Svizzera, è da pochi giorni un latitante ricercato dall’Interpol. Non si capisce dove sia e chi lo protegga, ma proprio in rete c’è chi ha lanciato un appello alla Cina per concedergli rifugio.
Da "Il Giornale"
di Fausto Biloslavo
Assange fa impazzire il mondo con la crociata di Wikileaks: gli attesi rapporti riservati ottenuti dal sito saranno pubblicati questa sera. In realtà tutte le sue rivelazioni ha sempre colpito l'Occidente
Julian Paul Assange, il pifferaio magico della trasparenza a oltranza, il campione delle rivelazioni scottanti su internet, soprattutto anti-occidentali, è l’uomo meno trasparente del pianeta. Il suo vero motto potrebbe essere: «Pubblico i segreti degli altri, ma non certo i miei».
L’algido visionario fa impazzire il mondo con la crociata di Wikileaks. Il sito che sta inguaiando gli americani dall’Irak all’Afghanistan, in attesa dell’annunciata valanga di documenti che scuoterà più di un alleato degli Stati Uniti compresa l’Italia. Non soltanto: Assange si presenta come paladino anti-cattivoni (Pentagono, Cia, ecc.) ma allo stesso tempo vive e raccoglie informazione come una spia, con la differenza che alla fine le pubblica in rete. Un gioco degli specchi che deve far comodo a qualche servizio segreto, mai sfiorato da una sola rivelazione, come quello russo o cinese.
Capelli bianchi, smilzo, mezzo ascetico e spesso vestito di nero, Assange è nato nel 1971 in Australia. A 17 anni fa il suo esordio nel mondo della pirateria informatica con gli «International subversives», che penetrano i computer della Nasa. Nel 1999 registra il dominio leaks.org, che vuol dire letteralmente «trapelare». Otto anni dopo ci aggiungerà davanti Wiki, per trasformare il suo sito nell’enciclopedia in rete delle rivelazioni planetarie. «I nostri principali bersagli - dichiara al momento del lancio di Wikileaks - sono i regimi oppressivi come la Cina, la Russia, e quelli dell’Asia centrale. Ma ci aspettiamo di essere d’aiuto anche per chi in Occidente vorrebbe che fossero denunciati comportamenti illegali e immorali dei governi e delle grandi società».
In realtà le rivelazioni di Assange si sono concentrate soprattutto contro l’Occidente. Amnesty International lo premia nel 2009 per una fuga di notizie sugli omicidi di stato in Kenya. Tutta robetta, rispetto a oggi, ma il visionario predicatore della trasparenza, a senso unico, comincia a crearsi un’immagine. Vagabonda facendo tappa in Islanda, ma qualcuno giura che ha soggiornato pure in Russia e Georgia. Il sito anti segreti diventa molto famoso quando rende noto un video di elicotteri americani a Bagdad, che uccidono giornalisti locali. Guarda caso Assange conquista il premio Sam Adams, organizzato da ex agenti della Cia, in nome di un’etica nei servizi segreti. I sostenitori del complotto dietro l’11 settembre sono convinti che il guru di internet sia al soldo della Cia. L’unico dato certo è che fino a oggi ha pubblicato migliaia di documenti riservati del Pentagono e sono in arrivo quelli del Dipartimento di Stato, ma dalla sede dell’agenzia a Langley non salta fuori nulla. I colpi grossi arrivano con le rivelazioni sulla guerra in Irak e Afghanistan. La tv americana Fox news chiede a gran voce che Assange sia incriminato per spionaggio. «Queste cosiddette fughe di notizie sono chirurgiche e riguardano sempre l’Occidente. Wikileaks è diventato uno strumento di potere amplificato dai media. Sono tutti sintomi che dimostrano come il sito non sia più in mano a un paladino della verità, ma sotto l’influenza di uno o più apparati di intelligence di grandi potenze», spiega Fabio Ghioni, l’hacker più famoso d’Italia.
Mosca e Pechino, per ora, sono uscite indenni dalle soffiate di Wikileaks, che prima degli scoop mondiali sulle guerre degli americani stava per chiudere i battenti per mancanza di fondi. Proprio sulle finanze del sito anti segreti si addensano i dubbi più pesanti. Assange sostiene di aver incassato nell’ultimo anno un milione di dollari in donazioni via internet. Ufficialmente i collaboratori di Wikileaks lavorano gratis. In realtà mantenere in piedi un’operazione del genere costa molto, a cominciare dai server dispersi per il mondo. Per non parlare dei soldi per tirar fuori le notizie e delle spese di Assange che vive, come dice lui, «in aeroporto, sempre in movimento». Oltre alle parcelle legali per le cause e l’ultima grana sulla presunta violenza sessuale del fondatore in Svezia. Assange ha incaricato della difesa il miglior avvocato del Paese, ma la storia puzza di trappola sessuale, come ai tempi del Kgb. Le due presunte vittime sono strane fan di guru di internet. Lui ha ammesso di esserci andato a letto perché consenzienti. Sull’uomo meno trasparente del mondo è piombato il mandato di cattura di un procuratore svedese. Assange, che voleva chiedere asilo politico in Svizzera, è da pochi giorni un latitante ricercato dall’Interpol. Non si capisce dove sia e chi lo protegga, ma proprio in rete c’è chi ha lanciato un appello alla Cina per concedergli rifugio.
Da "Il Giornale"
sabato 27 novembre 2010
DOLOR DE CABEZA RHINOGENIC: aspectos radiológicos maxilofacial
DOLOR DE CABEZA RHINOGENIC: aspectos radiológicos maxilofacial
Se examinaron 49 pacientes con sordera dolor de cabeza, las patologías relacionadas con ENT, en los pacientes que tuvieron clínicamente, así como frente a la migraña de tipo fronto-orbital, los síntomas fronto-parietal se caracteriza por obstrucción nasal y / o secreción nasal crónica, los síntomas sinusitica por lo menos 6 semanas, se someten ENT médicas y de los hallazgos endoscópicos sinunasales y radiología maxilofacial inició el estudio a través del uso de la tomografía axial computarizada.
Los pacientes fueron examinados entre noviembre de 1998 y diciembre de 1999, la edad de los pacientes oscila desde 16 hasta 70 años, edad media 43 años, 22F y el 27M, con una relación M / F de 1,2.
El estudio se llevó a cabo por la UE. O. de Radiología, Hospital de S. James Monopoli en colaboración con el UO de Otorrinolaringología del mismo hospital. En este estudio, los pacientes reclutados fueron seleccionados sobre la base de los síntomas descritos anteriormente de síntomas relacionados con el dolor de cabeza-y se somete a la terapia antibiótica adecuada con ciprofloxacina 750 mg x 2 v / día x 8 días. y deflazacort 30 mg x 2 v / día x 8 días. y posterior cirugía maxilofacial TC.
La intención de los colegas especialistas del oído fue evaluar la extensión de la patología de la presencia de poliposis naso-sinusal y / o etmoidales, sinusitis maxilar y / o desviaciones del tabique nasal (especialmente la parte posterior y superior) sinusitis y / o frontal y o la bulla etmoidal, con exclusión, por el tratamiento médico previo, la presencia de exudado inflamatorio, con el propósito de cualquier tratamiento quirúrgico, que parece ser un elemento de apoyo para las enfermedades descritas y la presencia de lo que no permite una adecuada definición de las imágenes radiología.
Los pacientes seleccionados se sometieron a CENS (cirugía funcional de la cavidad nasal, sino-por endoscopia) la designación por la endoscopia y la TC.
Los resultados clínicos y radiológicos mostraron una correlación significativa entre el dolor de cabeza y sinusitis etmoidal sordera-maxilar en la presencia de la bulla etmoidal neumatizado también, claramente marcados con el TC coronal análisis realizado en el ostiomeatale nivel de la unidad. La poliposis etmoidal, maxilar-nasal y desviación del tabique nasal posterior, en menor medida estaban relacionados con la sordera cefalea, obstrucción nasal, siendo el primero de los síntomas más frecuentemente referidos por los pacientes.
Adecuada maxilofacial TC, sobre todo en las posibilidades de la corona de exploración sin medio de contraste, puede, después de una visita a la ENT y la endoscopia nasal, senos paranasales, un examen de la eficacia y utilidad para el estudio de la sordera dolor de cabeza, la identificación de la intervención la cirugía y el seguimiento de los pacientes.
La cefalea es la sordera relacionada con las enfermedades que persisten en el nivel de la ostiomeatale. El estudio llevado a cabo con sus colegas de la UE. O. ORL se ha encontrado que en los pacientes sometidos a FESS durante la cirugía se realiza bajo anestesia general se realizó antrotomia promedio etmoidectomía bilaterales anteroposterior y bilaterales (95%) para bullosa turbinoplastica hueco (90%), septoplastia (45%) , el 30% poliposis nasal. En los pacientes sometidos a tomografía computarizada han desaparecido la mayoría de turbinoplastica trastorno debilitante, que es el dolor de cabeza frontal y / o parietal fronto-.
Por lo tanto, una TAC de cavidades paranasales es una prueba importante para el diagnóstico de la sordera en los pacientes con cefalea previamente evaluadas por el especialista en ORL y es una guarnición importante en la evaluación preoperatoria del paciente debe someterse a una cirugía nasal.
CT ayuda a identificar áreas de difícil acceso endoscopia nasal del sino como el ostium del seno maxilar, el etmoidal el'infundibolo receso frontal, y la ubicación y extensión de los procesos de enfermedad, la anatomía de la región y variantes específicas individuales.
La evaluación diagnóstica de pacientes con enfermedad nasal y dolor de cabeza, habría que considerar en una combinación sistemática y óptima de sistemática exploración nasal endoscópica y la TC, por la complementariedad estricto de los dos enfoques en el estudio de la sordera dolor de cabeza.
Dr. Carmine Capasso
Spec ORL
Se examinaron 49 pacientes con sordera dolor de cabeza, las patologías relacionadas con ENT, en los pacientes que tuvieron clínicamente, así como frente a la migraña de tipo fronto-orbital, los síntomas fronto-parietal se caracteriza por obstrucción nasal y / o secreción nasal crónica, los síntomas sinusitica por lo menos 6 semanas, se someten ENT médicas y de los hallazgos endoscópicos sinunasales y radiología maxilofacial inició el estudio a través del uso de la tomografía axial computarizada.
Los pacientes fueron examinados entre noviembre de 1998 y diciembre de 1999, la edad de los pacientes oscila desde 16 hasta 70 años, edad media 43 años, 22F y el 27M, con una relación M / F de 1,2.
El estudio se llevó a cabo por la UE. O. de Radiología, Hospital de S. James Monopoli en colaboración con el UO de Otorrinolaringología del mismo hospital. En este estudio, los pacientes reclutados fueron seleccionados sobre la base de los síntomas descritos anteriormente de síntomas relacionados con el dolor de cabeza-y se somete a la terapia antibiótica adecuada con ciprofloxacina 750 mg x 2 v / día x 8 días. y deflazacort 30 mg x 2 v / día x 8 días. y posterior cirugía maxilofacial TC.
La intención de los colegas especialistas del oído fue evaluar la extensión de la patología de la presencia de poliposis naso-sinusal y / o etmoidales, sinusitis maxilar y / o desviaciones del tabique nasal (especialmente la parte posterior y superior) sinusitis y / o frontal y o la bulla etmoidal, con exclusión, por el tratamiento médico previo, la presencia de exudado inflamatorio, con el propósito de cualquier tratamiento quirúrgico, que parece ser un elemento de apoyo para las enfermedades descritas y la presencia de lo que no permite una adecuada definición de las imágenes radiología.
Los pacientes seleccionados se sometieron a CENS (cirugía funcional de la cavidad nasal, sino-por endoscopia) la designación por la endoscopia y la TC.
Los resultados clínicos y radiológicos mostraron una correlación significativa entre el dolor de cabeza y sinusitis etmoidal sordera-maxilar en la presencia de la bulla etmoidal neumatizado también, claramente marcados con el TC coronal análisis realizado en el ostiomeatale nivel de la unidad. La poliposis etmoidal, maxilar-nasal y desviación del tabique nasal posterior, en menor medida estaban relacionados con la sordera cefalea, obstrucción nasal, siendo el primero de los síntomas más frecuentemente referidos por los pacientes.
Adecuada maxilofacial TC, sobre todo en las posibilidades de la corona de exploración sin medio de contraste, puede, después de una visita a la ENT y la endoscopia nasal, senos paranasales, un examen de la eficacia y utilidad para el estudio de la sordera dolor de cabeza, la identificación de la intervención la cirugía y el seguimiento de los pacientes.
La cefalea es la sordera relacionada con las enfermedades que persisten en el nivel de la ostiomeatale. El estudio llevado a cabo con sus colegas de la UE. O. ORL se ha encontrado que en los pacientes sometidos a FESS durante la cirugía se realiza bajo anestesia general se realizó antrotomia promedio etmoidectomía bilaterales anteroposterior y bilaterales (95%) para bullosa turbinoplastica hueco (90%), septoplastia (45%) , el 30% poliposis nasal. En los pacientes sometidos a tomografía computarizada han desaparecido la mayoría de turbinoplastica trastorno debilitante, que es el dolor de cabeza frontal y / o parietal fronto-.
Por lo tanto, una TAC de cavidades paranasales es una prueba importante para el diagnóstico de la sordera en los pacientes con cefalea previamente evaluadas por el especialista en ORL y es una guarnición importante en la evaluación preoperatoria del paciente debe someterse a una cirugía nasal.
CT ayuda a identificar áreas de difícil acceso endoscopia nasal del sino como el ostium del seno maxilar, el etmoidal el'infundibolo receso frontal, y la ubicación y extensión de los procesos de enfermedad, la anatomía de la región y variantes específicas individuales.
La evaluación diagnóstica de pacientes con enfermedad nasal y dolor de cabeza, habría que considerar en una combinación sistemática y óptima de sistemática exploración nasal endoscópica y la TC, por la complementariedad estricto de los dos enfoques en el estudio de la sordera dolor de cabeza.
Dr. Carmine Capasso
Spec ORL
HEADACHE RHINOGENIC: radiological aspects maxillo-facial
HEADACHE RHINOGENIC: radiological aspects maxillo-facial
Were examined 49 patients with headache deafness, ENT-related pathologies, in patients who reported clinically as well as migraine-type front, fronto-orbital, fronto-parietal symptoms characterized by nasal obstruction and / or chronic runny nose, symptoms sinusitica at least 6 weeks, undergo regular medical ENT and sino-nasal endoscopic findings and initiated the study maxillofacial radiology through the use of computerized axial tomography.
Patients were examined between November 1998 and December 1999, the age of patients ranges from 16 to 70 years, mean age 43 years, 22F and 27M, with M / F ratio of 1.2.
The study was conducted by the EU. O. of Radiology, Hospital S. James Monopoli in collaboration with the UO of Otolaryngology of the same hospital. In this study, the patients recruited were selected on the basis of the above-described symptoms of headache-related symptoms and subjected to appropriate antibiotic therapy with ciprofloxacin 750 mg x 2 v / day x 8 days. and deflazacort 30 mg x 2 v / day x 8 days. and subsequent CT maxillofacial surgery.
The intent of the ear specialist colleagues was to evaluate the extent of pathology for the presence of naso-sinus polyposis and / or ethmoid-maxillary sinusitis and / or deviations of the nasal septum (especially the rear and above) and / or frontal sinusitis and or ethmoid bulla, excluding, by prior medical treatment, the presence of inflammatory exudate, for the purpose of any surgical treatment, appears to be a supporting element to the diseases described and the presence of which does not allow a proper definition of the images radiology.
The selected patients underwent FESS (functional surgery of the sino-nasal cavity by endoscopy) designation by endoscopy and CT.
The clinical and radiological results showed a significant correlation between headache and deafness ethmoid-maxillary sinusitis in the presence of ethmoidal bulla pneumatized too, clearly marked with the coronal CT scan conducted at the unit level ostiomeatale. The ethmoid-maxillary-nasal polyposis and nasal septal deviation back to a lesser extent were related to deafness headache, nasal obstruction being the first of the symptom most frequently reported by patients.
Proper CT maxillofacial, especially in the coronal scan without contrast medium, may, after a visit to ENT and nose-sinus endoscopy, an examination of effective and useful for the study of headache deafness, identifying opportunities for intervention surgery and follow-up of patients.
Headache deafness is closely related to diseases which persist in the level of the ostiomeatale. The study conducted with colleagues from the EU. O. ORL has been found that in patients undergoing FESS during surgery performed under general anesthesia was performed antrotomia average bilateral anteroposterior ethmoidectomy and bilateral (95%) for hollow turbinoplastica bullosa (90%), septoplasty (45%) , 30% nasal polyposis. In patients undergoing CT scan have disappeared turbinoplastica most debilitating disorder, which is the frontal headache and / or fronto-parietal.
Therefore, CT of the paranasal cavities is a major test for the diagnosis of deafness in headache patients previously evaluated by the ENT specialist and is an important garrison in the preoperative evaluation of the patient should undergo nasal surgery.
CT helps identify areas not easily accessible nose-sinus endoscopy as the ostium of the maxillary sinus, the frontal recess el'infundibolo ethmoid, and the location and extent of disease processes, anatomy of the region and specific variants individual.
The diagnostic evaluation of patients with nasal disease and headache could also be envisaged in a systematic and optimal combination of systematic nasal endoscopic examination and CT, for the tight complementarity of the two approaches in the study of headache deafness.
Dr. Carmine Capasso
MD ENT
Were examined 49 patients with headache deafness, ENT-related pathologies, in patients who reported clinically as well as migraine-type front, fronto-orbital, fronto-parietal symptoms characterized by nasal obstruction and / or chronic runny nose, symptoms sinusitica at least 6 weeks, undergo regular medical ENT and sino-nasal endoscopic findings and initiated the study maxillofacial radiology through the use of computerized axial tomography.
Patients were examined between November 1998 and December 1999, the age of patients ranges from 16 to 70 years, mean age 43 years, 22F and 27M, with M / F ratio of 1.2.
The study was conducted by the EU. O. of Radiology, Hospital S. James Monopoli in collaboration with the UO of Otolaryngology of the same hospital. In this study, the patients recruited were selected on the basis of the above-described symptoms of headache-related symptoms and subjected to appropriate antibiotic therapy with ciprofloxacin 750 mg x 2 v / day x 8 days. and deflazacort 30 mg x 2 v / day x 8 days. and subsequent CT maxillofacial surgery.
The intent of the ear specialist colleagues was to evaluate the extent of pathology for the presence of naso-sinus polyposis and / or ethmoid-maxillary sinusitis and / or deviations of the nasal septum (especially the rear and above) and / or frontal sinusitis and or ethmoid bulla, excluding, by prior medical treatment, the presence of inflammatory exudate, for the purpose of any surgical treatment, appears to be a supporting element to the diseases described and the presence of which does not allow a proper definition of the images radiology.
The selected patients underwent FESS (functional surgery of the sino-nasal cavity by endoscopy) designation by endoscopy and CT.
The clinical and radiological results showed a significant correlation between headache and deafness ethmoid-maxillary sinusitis in the presence of ethmoidal bulla pneumatized too, clearly marked with the coronal CT scan conducted at the unit level ostiomeatale. The ethmoid-maxillary-nasal polyposis and nasal septal deviation back to a lesser extent were related to deafness headache, nasal obstruction being the first of the symptom most frequently reported by patients.
Proper CT maxillofacial, especially in the coronal scan without contrast medium, may, after a visit to ENT and nose-sinus endoscopy, an examination of effective and useful for the study of headache deafness, identifying opportunities for intervention surgery and follow-up of patients.
Headache deafness is closely related to diseases which persist in the level of the ostiomeatale. The study conducted with colleagues from the EU. O. ORL has been found that in patients undergoing FESS during surgery performed under general anesthesia was performed antrotomia average bilateral anteroposterior ethmoidectomy and bilateral (95%) for hollow turbinoplastica bullosa (90%), septoplasty (45%) , 30% nasal polyposis. In patients undergoing CT scan have disappeared turbinoplastica most debilitating disorder, which is the frontal headache and / or fronto-parietal.
Therefore, CT of the paranasal cavities is a major test for the diagnosis of deafness in headache patients previously evaluated by the ENT specialist and is an important garrison in the preoperative evaluation of the patient should undergo nasal surgery.
CT helps identify areas not easily accessible nose-sinus endoscopy as the ostium of the maxillary sinus, the frontal recess el'infundibolo ethmoid, and the location and extent of disease processes, anatomy of the region and specific variants individual.
The diagnostic evaluation of patients with nasal disease and headache could also be envisaged in a systematic and optimal combination of systematic nasal endoscopic examination and CT, for the tight complementarity of the two approaches in the study of headache deafness.
Dr. Carmine Capasso
MD ENT
CEFALEA RINOGENA: ASPETTI RADIOLOGICI MAXILLO-FACCIALI
CEFALEA RINOGENA: ASPETTI RADIOLOGICI MAXILLO-FACCIALI
Sono stati esaminati 49 pazienti affetti da cefalea rinogena, correlata a patologie di interesse otorinolaringoiatrico, in pazienti che clinicamente riferivano oltre alla cefalea di tipo frontale, fronto-orbitario, fronto-parietale, una sintomatologia caratterizzata da ostruzione nasale e/o rinorrea cronica, sintomatologia sinusitica da almeno 6 settimane, sottoposti a visita ORL e ad accertamenti endoscopici naso-sinusali e avviati allo studio radiologico maxillo-facciale attraverso l’impiego della tomografia assiale computerizzata.
I pazienti sono stati esaminati dal novembre 1998 al dicembre 1999; l’età dei pazienti varia dai 16 ai 70 anni, età media 43 anni, 22F e 27M, con rapporto M/F 1,2.
Lo studio è stato condotto dall’U.O. di Radiologia dell’Ospedale S. Giacomo di Monopoli in collaborazione con l’U.O. di Otorinolaringoiatria dello stesso nosocomio. In tale studio, i pazienti reclutati venivano selezionati sulla base della sintomatologia cefalalgica correlata ai sintomi suddescritti e opportunamente sottoposti ad antibiotico-terapia con ciprofloxacina 750 mg x 2 v/die x 8 gg. e deflazacort 30 mg x 2 v/die x 8 gg. e successiva TC maxillo-facciale.
L’intento dei colleghi otoiatri era quello di valutare l’entità della patologia: evidenziare la presenza della poliposi naso-sinusale e/o sinusite etmoido-mascellare e/o deviazioni del setto nasale (soprattutto posteriore e superiore) e/o sinusite frontale e/o bulla etmoidale, escludendo, attraverso il trattamento medico preventivo, la presenza di essudato infiammatorio che, ai fini di un eventuale trattamento chirurgico, risulta essere un elemento di accompagnamento alle patologie descritte e, la cui presenza, non consente una corretta definizione delle immagini radiologiche.
I pazienti selezionati sono stati sottoposti a FESS (chirurgia funzionale delle cavità naso-sinusali per via endoscopica) sulla scorta delle indicazioni endoscopiche e TC.
I risultati clinico-radiologici hanno mostrato una notevole correlazione tra cefalea rinogena e sinusiti etmoido-mascellari in presenza di bulla etmoidale eccessivamente pneumatizzata, evidenziata con chiarezza con la TC nella scansione coronale condotta al livello dell’unità ostiomeatale. La poliposi nasale-etmoido-mascellare e le deviazioni posteriori del setto nasale risultavano correlate in misura inferiore alla cefalea rinogena, essendo l’ostruzione nasale in primis il sintomo più frequentemente riferito dai pazienti.
Un corretto esame TC maxillo-facciale, soprattutto nella scansione coronale e senza mezzo di contrasto, può costituire, dopo una visita ORL e fibroscopia naso-sinusale, un esame utile ed efficace per lo studio della cefalea rinogena, indicando con precisione le possibilità di intervento chirurgico e nel follow-up dei pazienti.
La cefalea rinogena è strettamente correlata alle patologie che insistono a livello dell’unità ostiomeatale. Dallo studio condotto con i colleghi dell’U.O. ORL è stato rilevato che sui pazienti sottoposti a FESS, nel corso dell’intervento condotto in anestesia generale, è stata effettuata antrotomia media bilaterale ed etmoidectomia anteroposteriore bilaterale (95%), turbinoplastica per conca bullosa (90%), settoplastica (45%), poliposi nasale 30%. Al controllo TC i pazienti sottoposti a turbinoplastica hanno scomparsa del disturbo più invalidante, cioè la cefalea frontale e/o fronto-parietale.
Pertanto la TC delle cavità paranasali costituisce un esame importante sia nella diagnosi delle cefalee rinogene in pazienti già valutati dallo specialista ORL e costituisce un importante presidio nella valutazione pre-operatoria del paziente che deve essere sottoposto a chirurgia endonasale.
La TC consente di identificare aree non facilmente accessibili all’endoscopia naso-sinusale come l’ostio del seno mascellare, il recesso frontale e l’infundibolo etmoidale, nonché la localizzazione e l’estensione dei processi patologici, l’anatomia della regione e le varianti peculiari dell’individuo.
La valutazione diagnostica del paziente con patologia nasale e cefalea si potrebbe avvalere in maniera sistematica ed ottimale della combinazione dell’esame endoscopico nasale sistematico e della TC, per la stretta complementarietà dei due approcci nello studio della cefalea rinogena.
Dr. Carmine Capasso
Spec. ORL
Sono stati esaminati 49 pazienti affetti da cefalea rinogena, correlata a patologie di interesse otorinolaringoiatrico, in pazienti che clinicamente riferivano oltre alla cefalea di tipo frontale, fronto-orbitario, fronto-parietale, una sintomatologia caratterizzata da ostruzione nasale e/o rinorrea cronica, sintomatologia sinusitica da almeno 6 settimane, sottoposti a visita ORL e ad accertamenti endoscopici naso-sinusali e avviati allo studio radiologico maxillo-facciale attraverso l’impiego della tomografia assiale computerizzata.
I pazienti sono stati esaminati dal novembre 1998 al dicembre 1999; l’età dei pazienti varia dai 16 ai 70 anni, età media 43 anni, 22F e 27M, con rapporto M/F 1,2.
Lo studio è stato condotto dall’U.O. di Radiologia dell’Ospedale S. Giacomo di Monopoli in collaborazione con l’U.O. di Otorinolaringoiatria dello stesso nosocomio. In tale studio, i pazienti reclutati venivano selezionati sulla base della sintomatologia cefalalgica correlata ai sintomi suddescritti e opportunamente sottoposti ad antibiotico-terapia con ciprofloxacina 750 mg x 2 v/die x 8 gg. e deflazacort 30 mg x 2 v/die x 8 gg. e successiva TC maxillo-facciale.
L’intento dei colleghi otoiatri era quello di valutare l’entità della patologia: evidenziare la presenza della poliposi naso-sinusale e/o sinusite etmoido-mascellare e/o deviazioni del setto nasale (soprattutto posteriore e superiore) e/o sinusite frontale e/o bulla etmoidale, escludendo, attraverso il trattamento medico preventivo, la presenza di essudato infiammatorio che, ai fini di un eventuale trattamento chirurgico, risulta essere un elemento di accompagnamento alle patologie descritte e, la cui presenza, non consente una corretta definizione delle immagini radiologiche.
I pazienti selezionati sono stati sottoposti a FESS (chirurgia funzionale delle cavità naso-sinusali per via endoscopica) sulla scorta delle indicazioni endoscopiche e TC.
I risultati clinico-radiologici hanno mostrato una notevole correlazione tra cefalea rinogena e sinusiti etmoido-mascellari in presenza di bulla etmoidale eccessivamente pneumatizzata, evidenziata con chiarezza con la TC nella scansione coronale condotta al livello dell’unità ostiomeatale. La poliposi nasale-etmoido-mascellare e le deviazioni posteriori del setto nasale risultavano correlate in misura inferiore alla cefalea rinogena, essendo l’ostruzione nasale in primis il sintomo più frequentemente riferito dai pazienti.
Un corretto esame TC maxillo-facciale, soprattutto nella scansione coronale e senza mezzo di contrasto, può costituire, dopo una visita ORL e fibroscopia naso-sinusale, un esame utile ed efficace per lo studio della cefalea rinogena, indicando con precisione le possibilità di intervento chirurgico e nel follow-up dei pazienti.
La cefalea rinogena è strettamente correlata alle patologie che insistono a livello dell’unità ostiomeatale. Dallo studio condotto con i colleghi dell’U.O. ORL è stato rilevato che sui pazienti sottoposti a FESS, nel corso dell’intervento condotto in anestesia generale, è stata effettuata antrotomia media bilaterale ed etmoidectomia anteroposteriore bilaterale (95%), turbinoplastica per conca bullosa (90%), settoplastica (45%), poliposi nasale 30%. Al controllo TC i pazienti sottoposti a turbinoplastica hanno scomparsa del disturbo più invalidante, cioè la cefalea frontale e/o fronto-parietale.
Pertanto la TC delle cavità paranasali costituisce un esame importante sia nella diagnosi delle cefalee rinogene in pazienti già valutati dallo specialista ORL e costituisce un importante presidio nella valutazione pre-operatoria del paziente che deve essere sottoposto a chirurgia endonasale.
La TC consente di identificare aree non facilmente accessibili all’endoscopia naso-sinusale come l’ostio del seno mascellare, il recesso frontale e l’infundibolo etmoidale, nonché la localizzazione e l’estensione dei processi patologici, l’anatomia della regione e le varianti peculiari dell’individuo.
La valutazione diagnostica del paziente con patologia nasale e cefalea si potrebbe avvalere in maniera sistematica ed ottimale della combinazione dell’esame endoscopico nasale sistematico e della TC, per la stretta complementarietà dei due approcci nello studio della cefalea rinogena.
Dr. Carmine Capasso
Spec. ORL
Comment faire pour grandir
Comment faire pour grandir
Dr Jean Michel PONS
Peut-On Grandir à Tout age?
OUI ! Grandir à tout age est possible
De toutes les discriminations contre lesquelles on fait mine de lutter, il en est une dont on ne parle jamais ou rarement. Celle qui frappe les gens de petite taille. Un livre récemment paru, « l’empire des grands », à la suite d’enquêtes sociologiques poussées établit ce fait : les gens de petite taille occupent des postes moins importants, ont des revenus inférieurs et vivent moins souvent en couple que les autres. Rien n’indique cependant que leurs compétences leurs talents ou leur niveau d’instruction soient moindres. On doit donc les ranger sous l’étiquette de minorités visibles, terme hypocritement utilisés d’ordinaitre pour réintroduire le concept, politiquement incorrect de race.
Il n’est donc pas étonnant qu’ils cherchent des moyens de surmonter ce réel handicap social. Et qu’ils se demandent s’il ne serait pas possible de grandir encore, passé l’âge de la croissance. Eh bien la réponse à cette question est oui.
On peut grandir à tout age, grace à notre programme d'exercices d'étirement et de redressement tout à fait révolutionnaire, qui ne prend que 25 à 30 minutes par jour. Vous allez augmenter sensiblement votre taille et stimuler votre croissance naturelle. Les informations contenues dans ce grand programme de croissance sont absolument sûr, simples et efficaces pour les hommes et les femmes de tous âges.
_________________________________________________________________________
"Comment grandir naturement à tout age" est un livre de 247 pages, il contient toutes les informations nécessaires pour grandir, avec 100 exercices d'étirement et de redressement, ainsi que les conseils sur une meilleur alimentation, le someil,la tenue, la respiration etc....
Vous pouvez commencer votre cours dès reception du livre.
Vous êtes sur le point d'acheter ce programme best-seller, même s'il est 3 heures du matin, votre action vous permettra d'augmenter votre taille de quelques centimètres, même si vous avez cessé de grandir depuis longtemps. Il est également certain que vous ne regretterez pas votre décision.
Pour commencer, il vous suffit de cliquer ici sur "Acheter"
grandir à 25 ans
Prix: 29,99€
Consacrez quelques minutes par jour aux exercices proposés dans cet ouvrage. Ceux-ci, en agissant sur les cartilages situés entre les vertebres, allongeront et assoupliront votre colonne vertébrale et ainsi vous faire gagner de precieux centimetres
________________________________________________________________________
Plus de 65000 exemplaires dejà vendus.
comment grandir vite Quel est le bon régime alimentaire pour grandir.
grandir plus viteQuelle sont les bonnes habitudes de sommeil.
grandir rapidementQuels sont les meilleurs exercices d'étirement que vous devriez pratiquer le plus souvent.
grandir plus viteQuelles sont les meilleures activités quotidiennes pour gagner plus de centimetres.
grandir plus viteComment peut-on équilibrer les trois facteurs les plus importants de la croissance: alimentation, le sommeil, exercice d'étirement.
grandir plus viteQuelles sont les bonnes postures à prendre pour garder une meilleur forme de ses membres
grandir plus viteQuels sont les erreur à éviter pour grandir ?
grandir plus viteEst-ce que l'alcool ou le tabagisme freinent votre croissance ?
grandir plus viteEst-ce que l'haltérophilie ralentie votre croissance ?
grandir plus viteEst-ce que la sexualité précoce et masturbation jouent un role dans la croissance ?
grandir plus viteComment grandir rapidement?
grandir plus viteQuelle est la principale chose que vous devez faire pour grandir et gagner plus de centimetres?
_________________________________________________________________________
commentgrandir rapidement
Sylvie a 20 ans, et a gagné environ 8 cm en seulement dix mois. C'est le cas de gain de taille le plus rapide que nous avons parmi ceux qui suivent notre programme.
Grandir rapidement à tout age est possible, les resultats peuvent etre lents. Il ne faut pas plafonner rapidement au point de vue des performances et des resultats. Pour éviter d'en arriver là, quelques principes de base expliqués dans ce livre sont à appliquer
Grandir est sans doute quelque chose qui vous tente. Gagner quelques centimètres rapidement ou lentement quelque soit votre age, fortifier votre dos, raffermir vos abdominaux, vous assurer une meilleure santé.
Découvrez dans ce livre l’importance de la volonté, de la respiration, du sommeil et d’une saine alimentation dans le processus de la croissance humaine.
A l’aide d’illustrations, vous allez suivre un programme qui s’échelonne sur six mois avec 100 exercices d’étirement et de redressement.
Il vous permet enfin, à l’aide de tableaux, de suivre votre progression sur une base hebdomadaire et mensuelle.
Vous allez grandir sans trop d’effort. Seule contrainte consacrer environ 25 à 30 minutes de votre temps par jour. Mais ça vaut le coup.....!
Les gens qui ne comprennent pas l'importance de la taille sont généralement ceux qui sont au-dessus de la taille moyenne... Cela signifie qu'ils ne peuvent tout simplement pas savoir ce que c'est que de perdre confiance en soi, d'etre sujet à des moqueries de ses camarades ou par le sexe opposé, la difficulté à se faire des amis parce qu' on est petit, et la liste est longue.....
Dr Jean Michel PONS
Peut-On Grandir à Tout age?
OUI ! Grandir à tout age est possible
De toutes les discriminations contre lesquelles on fait mine de lutter, il en est une dont on ne parle jamais ou rarement. Celle qui frappe les gens de petite taille. Un livre récemment paru, « l’empire des grands », à la suite d’enquêtes sociologiques poussées établit ce fait : les gens de petite taille occupent des postes moins importants, ont des revenus inférieurs et vivent moins souvent en couple que les autres. Rien n’indique cependant que leurs compétences leurs talents ou leur niveau d’instruction soient moindres. On doit donc les ranger sous l’étiquette de minorités visibles, terme hypocritement utilisés d’ordinaitre pour réintroduire le concept, politiquement incorrect de race.
Il n’est donc pas étonnant qu’ils cherchent des moyens de surmonter ce réel handicap social. Et qu’ils se demandent s’il ne serait pas possible de grandir encore, passé l’âge de la croissance. Eh bien la réponse à cette question est oui.
On peut grandir à tout age, grace à notre programme d'exercices d'étirement et de redressement tout à fait révolutionnaire, qui ne prend que 25 à 30 minutes par jour. Vous allez augmenter sensiblement votre taille et stimuler votre croissance naturelle. Les informations contenues dans ce grand programme de croissance sont absolument sûr, simples et efficaces pour les hommes et les femmes de tous âges.
_________________________________________________________________________
"Comment grandir naturement à tout age" est un livre de 247 pages, il contient toutes les informations nécessaires pour grandir, avec 100 exercices d'étirement et de redressement, ainsi que les conseils sur une meilleur alimentation, le someil,la tenue, la respiration etc....
Vous pouvez commencer votre cours dès reception du livre.
Vous êtes sur le point d'acheter ce programme best-seller, même s'il est 3 heures du matin, votre action vous permettra d'augmenter votre taille de quelques centimètres, même si vous avez cessé de grandir depuis longtemps. Il est également certain que vous ne regretterez pas votre décision.
Pour commencer, il vous suffit de cliquer ici sur "Acheter"
grandir à 25 ans
Prix: 29,99€
Consacrez quelques minutes par jour aux exercices proposés dans cet ouvrage. Ceux-ci, en agissant sur les cartilages situés entre les vertebres, allongeront et assoupliront votre colonne vertébrale et ainsi vous faire gagner de precieux centimetres
________________________________________________________________________
Plus de 65000 exemplaires dejà vendus.
comment grandir vite Quel est le bon régime alimentaire pour grandir.
grandir plus viteQuelle sont les bonnes habitudes de sommeil.
grandir rapidementQuels sont les meilleurs exercices d'étirement que vous devriez pratiquer le plus souvent.
grandir plus viteQuelles sont les meilleures activités quotidiennes pour gagner plus de centimetres.
grandir plus viteComment peut-on équilibrer les trois facteurs les plus importants de la croissance: alimentation, le sommeil, exercice d'étirement.
grandir plus viteQuelles sont les bonnes postures à prendre pour garder une meilleur forme de ses membres
grandir plus viteQuels sont les erreur à éviter pour grandir ?
grandir plus viteEst-ce que l'alcool ou le tabagisme freinent votre croissance ?
grandir plus viteEst-ce que l'haltérophilie ralentie votre croissance ?
grandir plus viteEst-ce que la sexualité précoce et masturbation jouent un role dans la croissance ?
grandir plus viteComment grandir rapidement?
grandir plus viteQuelle est la principale chose que vous devez faire pour grandir et gagner plus de centimetres?
_________________________________________________________________________
commentgrandir rapidement
Sylvie a 20 ans, et a gagné environ 8 cm en seulement dix mois. C'est le cas de gain de taille le plus rapide que nous avons parmi ceux qui suivent notre programme.
Grandir rapidement à tout age est possible, les resultats peuvent etre lents. Il ne faut pas plafonner rapidement au point de vue des performances et des resultats. Pour éviter d'en arriver là, quelques principes de base expliqués dans ce livre sont à appliquer
Grandir est sans doute quelque chose qui vous tente. Gagner quelques centimètres rapidement ou lentement quelque soit votre age, fortifier votre dos, raffermir vos abdominaux, vous assurer une meilleure santé.
Découvrez dans ce livre l’importance de la volonté, de la respiration, du sommeil et d’une saine alimentation dans le processus de la croissance humaine.
A l’aide d’illustrations, vous allez suivre un programme qui s’échelonne sur six mois avec 100 exercices d’étirement et de redressement.
Il vous permet enfin, à l’aide de tableaux, de suivre votre progression sur une base hebdomadaire et mensuelle.
Vous allez grandir sans trop d’effort. Seule contrainte consacrer environ 25 à 30 minutes de votre temps par jour. Mais ça vaut le coup.....!
Les gens qui ne comprennent pas l'importance de la taille sont généralement ceux qui sont au-dessus de la taille moyenne... Cela signifie qu'ils ne peuvent tout simplement pas savoir ce que c'est que de perdre confiance en soi, d'etre sujet à des moqueries de ses camarades ou par le sexe opposé, la difficulté à se faire des amis parce qu' on est petit, et la liste est longue.....
cómo crecer más alto
cómo crecer más alto
No hay mucho que hacer para crecer más alto sin tomar un tratamiento en base a hormonas o algo similar pero estos pasos pueden ayudar. Te has preguntado alguna vez como la gente crece tan rapido? Quieres ser mas alto? Lee y sigue los pasos de aqui debajo.
[editar] Pasos
1. Comer una equilibrada dieta rica en calcio y hierro. Esto ayuda a promover el crecimiento si eres joven.
2. Hacer ejercicios de estiramiento podría ayudarte.
3. Tomar clases de yoga puede ayudar. Algunas personas han reportado que esta clase de estiramiento ha hecho que consigan resultados.
4. Pararte derecho hace que te veas más alto.
5. Primero, consume proteínas y calcio. El calcio ayuda a fortalezer los huesos, mientras que las proteínas ayudan al músculo cercano al hueso.
6. Saltar. Salta, para que tus músculos sean más firmes.
7. Ten buena postura. Ya que tener mala postura hace que te veas más pequeño .
8. Esperar, paciencia.. Las chicas generalmente crecen antes que los chicos, pero solo por un corto período. Los chicos se desarrollan entre los 12 o 14 hasta los 21 o 23.
9. Practica algún deporte. Si te inscribes en un deporte como el baloncesto, la practica puede ayudar mucho.
[editar] Consejos
* Acudir con un médico para que controle tu estado físico durante este proceso.
* Cuando tomes vitaminas, bebidas tales como "Boost" o "Ensure" para ayudarte en tu desarrollo.
* Puedes tomar leche mínimamente dos veces al día
* Al mismo tiempo, el zumo de naranja es una buena bebida que tambien tiene muchas de las vitaminas necesarias.
* Duerme mucho - 8 a 9 hs. como mínimo
* Si quieres crecer tienes que estar motivado.
[editar] Advertencias
* Los ejercicios de estiramiento llevados al extremo pueden causar daños severos. Ten mucho cuidado al hacerlos.
* No hacer las repeticiones muy seguido, demaciado ejercicio suele hacer que los huesos y musculos generen resistencia, lo que frenara el crecimiento.
* NO exagerar ninguno de los pasos sugeridos, hacer mucho o nada de algo suele ser perjudicial y haz ejercicio.
No hay mucho que hacer para crecer más alto sin tomar un tratamiento en base a hormonas o algo similar pero estos pasos pueden ayudar. Te has preguntado alguna vez como la gente crece tan rapido? Quieres ser mas alto? Lee y sigue los pasos de aqui debajo.
[editar] Pasos
1. Comer una equilibrada dieta rica en calcio y hierro. Esto ayuda a promover el crecimiento si eres joven.
2. Hacer ejercicios de estiramiento podría ayudarte.
3. Tomar clases de yoga puede ayudar. Algunas personas han reportado que esta clase de estiramiento ha hecho que consigan resultados.
4. Pararte derecho hace que te veas más alto.
5. Primero, consume proteínas y calcio. El calcio ayuda a fortalezer los huesos, mientras que las proteínas ayudan al músculo cercano al hueso.
6. Saltar. Salta, para que tus músculos sean más firmes.
7. Ten buena postura. Ya que tener mala postura hace que te veas más pequeño .
8. Esperar, paciencia.. Las chicas generalmente crecen antes que los chicos, pero solo por un corto período. Los chicos se desarrollan entre los 12 o 14 hasta los 21 o 23.
9. Practica algún deporte. Si te inscribes en un deporte como el baloncesto, la practica puede ayudar mucho.
[editar] Consejos
* Acudir con un médico para que controle tu estado físico durante este proceso.
* Cuando tomes vitaminas, bebidas tales como "Boost" o "Ensure" para ayudarte en tu desarrollo.
* Puedes tomar leche mínimamente dos veces al día
* Al mismo tiempo, el zumo de naranja es una buena bebida que tambien tiene muchas de las vitaminas necesarias.
* Duerme mucho - 8 a 9 hs. como mínimo
* Si quieres crecer tienes que estar motivado.
[editar] Advertencias
* Los ejercicios de estiramiento llevados al extremo pueden causar daños severos. Ten mucho cuidado al hacerlos.
* No hacer las repeticiones muy seguido, demaciado ejercicio suele hacer que los huesos y musculos generen resistencia, lo que frenara el crecimiento.
* NO exagerar ninguno de los pasos sugeridos, hacer mucho o nada de algo suele ser perjudicial y haz ejercicio.
Gastro-esofágico laringitis por reflujo
Gastro-esofágico laringitis por reflujo
La experiencia diaria, basada en la evidencia, muestra un aumento significativo en la enfermedad de reflujo gastro-esofágico: muchos trastornos relacionados con el ácido, a nivel de la laringe, fueron etiquetados como "mundo histérica" y tratados en consecuencia con los medicamentos contra la ansiedad y espasmolítico! granulomas muchos fueron operados en cuerdas microlaringoscopia atrás varias veces y se repitió con prontitud. La tos con frecuencia, especialmente después de las comidas y por la noche fueron clasificados como alérgica o "nervioso". En la actualidad, la historia médica adecuada, una evaluación completa ENT (examen naso.fibrolaringoscopico) puede "poner de relieve un reflujo gastro-esofágico laringitis dividido en cuatro etapas: a) interaritenoidea inflamación de la mucosa e hiperemia atrás, b) la hiperemia de las cuerdas vocales verdaderas, c ) acorde ab granuloma posterior de 1-2 mm de diámetro d) carácter granuloma interesante abc con la dispneizzante cuerda vocal entera. El tratamiento médico con pantoprazol 40 mg / día o 80 mg (IBP: inhibidores de la bomba de protones), de acuerdo a la gravedad "de la enfermedad, con un mínimo de 60 días de tratamiento, con una media de 6 meses, indefinidamente en la presencia de esófago Barrett. Esencial para la evaluación del gastroenterólogo en la etapa "c" y "d" o el tratamiento con pantoprazol más de 60 días. Gastroenterólogos recomiendan una endoscopia con biopsia después de 40 años y en la presencia de recurrencia de los síntomas después de la interrupción de la terapia. UBT útil (test de aliento). No s muy útil. gastroenterólogos. el pH-metría y la sonda gastroesofágica de retención de doble tradicionales (dos sensores: uno a nivel del CRIC-esofágico y el otro gastro-esofágico) La investigación, considerada muy metódico e incómodo para el paciente.
Para más detalles: "Estudio Multicéntrico: correlación clínica y estadística entre los hallazgos clínicos e instrumentales en el reflujo faringolaríngeo: propuesta de nuevos criterios para la clasificación del reflujo en ORL" CA Leona, F. Moscú - Departamento de ORL del Hospital Monaldi, Nápoles - ACTA Itálica OTORHINOLAYNGOLOGICA 26.264-270, 2006
Dr. Carmine Capasso
Spec ORL
La experiencia diaria, basada en la evidencia, muestra un aumento significativo en la enfermedad de reflujo gastro-esofágico: muchos trastornos relacionados con el ácido, a nivel de la laringe, fueron etiquetados como "mundo histérica" y tratados en consecuencia con los medicamentos contra la ansiedad y espasmolítico! granulomas muchos fueron operados en cuerdas microlaringoscopia atrás varias veces y se repitió con prontitud. La tos con frecuencia, especialmente después de las comidas y por la noche fueron clasificados como alérgica o "nervioso". En la actualidad, la historia médica adecuada, una evaluación completa ENT (examen naso.fibrolaringoscopico) puede "poner de relieve un reflujo gastro-esofágico laringitis dividido en cuatro etapas: a) interaritenoidea inflamación de la mucosa e hiperemia atrás, b) la hiperemia de las cuerdas vocales verdaderas, c ) acorde ab granuloma posterior de 1-2 mm de diámetro d) carácter granuloma interesante abc con la dispneizzante cuerda vocal entera. El tratamiento médico con pantoprazol 40 mg / día o 80 mg (IBP: inhibidores de la bomba de protones), de acuerdo a la gravedad "de la enfermedad, con un mínimo de 60 días de tratamiento, con una media de 6 meses, indefinidamente en la presencia de esófago Barrett. Esencial para la evaluación del gastroenterólogo en la etapa "c" y "d" o el tratamiento con pantoprazol más de 60 días. Gastroenterólogos recomiendan una endoscopia con biopsia después de 40 años y en la presencia de recurrencia de los síntomas después de la interrupción de la terapia. UBT útil (test de aliento). No s muy útil. gastroenterólogos. el pH-metría y la sonda gastroesofágica de retención de doble tradicionales (dos sensores: uno a nivel del CRIC-esofágico y el otro gastro-esofágico) La investigación, considerada muy metódico e incómodo para el paciente.
Para más detalles: "Estudio Multicéntrico: correlación clínica y estadística entre los hallazgos clínicos e instrumentales en el reflujo faringolaríngeo: propuesta de nuevos criterios para la clasificación del reflujo en ORL" CA Leona, F. Moscú - Departamento de ORL del Hospital Monaldi, Nápoles - ACTA Itálica OTORHINOLAYNGOLOGICA 26.264-270, 2006
Dr. Carmine Capasso
Spec ORL
venerdì 26 novembre 2010
Presbyacusis
Presbyacusis
The labyrinth of presbycusis within chapter in the adult, ie in degenerative diseases of the inner ear. For presbycusis is defined as a sensorineural hearing loss frequently observed in both sexes, with greater frequency in males, older, more evident after 60 years of age, but which can already be observed in the early stages after 30 years (Alajmo1995 ).
Man is constantly affected by a progressive weakening of the organ and then the sense of hearing. Diseases such as diabetes mellitus, hypertension, smoking, alcoholism, atherosclerosis, stress, metabolic disorders (hypercholesterolemia) are causes that lead to an aging body. Among these is the significant role played by the NOISE: Significant differences exist between populations living in areas with high rate of industrialization in relation to the populations living in the countryside, as assessed in individuals of the same age. The noise is the cause of occupational disability for many industrial workers (noise of the living or SOCIOACUSIA).
The number of cells present at birth, constituting the organ of Corti, then progressively diminishing (Rossi, 1994). This decrease occurs after the birth of cells in the basal turn of the cochlea and is associated with a reduction of nerve fibers, resulting in a reduction in the audible tonal range after 10 years of age. This particular senescence comes from the fact that it is during waking than during sleep, the organ of Corti is under stress and the functional consequence is called presbycusis, and is the expression of an aging process that affects all sense organs.
The presbycusis is established and progresses slowly and is due to the interest of every sector of the hearing, the eardrum UP BY THE PRIMARY AND SECONDARY cortical areas of the temporal lobe (Brodman AREAS).
The aging process that characterizes the presbycusis involves various processes:
a) thickening of the tympanic membrane and degenerative joints ossiculari that result in increased impedance of the eardrum-ossicular system;
b) loss of elasticity of the basilar membrane of primitive thickening and formation of mineral deposits;
c) degeneration of the cells of the organ of Corti and the ganglion of Corti or associated with atrophy of the industry processes or vascular compression of the nerve fibers to the processes of hyperostosis of the walls of the internal auditory meatus;
d) reducing the number of cell nuclei of the central acoustic pathway;
e) reducing the number of cortical cells of primary and secondary acoustic areas.
The presbycusis is therefore an extremely complex phenomenon that slowly leads to a sensory deficit of quantitative and qualitative: the first related to the quantitative reduction of the structures that carry auditory information to areas of the cortex, the latter linked to the regressive phenomena dependent areas brain, which has the task to decode, analyze, process, interpret the information received. The quantitative deficit makes it difficult to perceive high-pitched sounds, the quality of the difficulty in understanding verbal messages, which can be understood only when the centers are working in optimal conditions, ie when the information is not contaminated by other information presented simultaneously (more people who speak make it difficult to selective hearing, so-called cocktail-party phenomenon: the presbycusis feel better in general, the low frequency, so the old man suffers a greater masking effect of environmental noise) or in the presence of other components (lip-reading ).
In terms of audiometric intentendendo refer to the techniques of tonal liminal audiometry and speech audiometry, the presbycusis may have four different profiles in relation to the prevalence of pathogenic elements that support it.
1) Presbyacusis Neurosensory: is the most common and distinctive and is characterized by regressive changes that affect all structures of the membranous cochlear duct from the base and proceed toward the elicotrema, with the corresponding disappearance of the spiral ganglion neurons (recruitment absent, tone decay test normal).
2) THE MECHANICS presbycusis: involves a stiffening of the basilar membrane or alteration of its mechanical retrogressive changes.
3) THE NEURAL presbycusis: compression of neural atrophy of the auditory nerve fibers to changes of hyperostotic modiolo, resulting in a decrease in the number of cells in the CNS, a process that begins early in youth.
4) THE METABOLIC presbycusis: changes to metabolic processes in the stria vascular load.
The presbycusis is often accompanied by tinnitus, a noise that is pitched with a receptive type of hearing loss on high-pitched sounds and is, in the neurosensory forms, a gradual descent curve, increasing the threshold for the higher frequencies first, and then for the intermediate and serious.
The selective deficits sec. Matshke refer initially to above 2000 Hz, for cell loss and external noise is more evident after 60 years of age, sec. Belal the presbycusis is not an event strongly correlated with age, old age and could exist a picture of normoacusia and it is important to investigate the diagnostic procedures relating to the forms that appear asymmetric sensorineural, could suggest disorders of the inner ear (cochlear otosclerosis, Meniere's disease or tumors of the acoustic nerve.
The healthy lifestyle and food, coupled with the concomitant reduction of the causes of senescence may be an effective way to reduce the aging process and delay the onset of hearing onset of senescence.
The only help the patient presbycusis is the hearing aid, preferably bilateral: the results are usually lower than in young subjects with similar hearing loss and the reason is the central acoustic deficit, which makes it difficult for the intelligibility of the spoken message. But if the denture is well made and correction is binaural and the subject is well trained, the advantages are obvious.
In conclusion we can say with Solomon, that the ability to communicate is fundamental for the autonomy of a person the opportunity to interact with the outside world and be happy.
Dr. Carmine Capasso
MD ENT
The labyrinth of presbycusis within chapter in the adult, ie in degenerative diseases of the inner ear. For presbycusis is defined as a sensorineural hearing loss frequently observed in both sexes, with greater frequency in males, older, more evident after 60 years of age, but which can already be observed in the early stages after 30 years (Alajmo1995 ).
Man is constantly affected by a progressive weakening of the organ and then the sense of hearing. Diseases such as diabetes mellitus, hypertension, smoking, alcoholism, atherosclerosis, stress, metabolic disorders (hypercholesterolemia) are causes that lead to an aging body. Among these is the significant role played by the NOISE: Significant differences exist between populations living in areas with high rate of industrialization in relation to the populations living in the countryside, as assessed in individuals of the same age. The noise is the cause of occupational disability for many industrial workers (noise of the living or SOCIOACUSIA).
The number of cells present at birth, constituting the organ of Corti, then progressively diminishing (Rossi, 1994). This decrease occurs after the birth of cells in the basal turn of the cochlea and is associated with a reduction of nerve fibers, resulting in a reduction in the audible tonal range after 10 years of age. This particular senescence comes from the fact that it is during waking than during sleep, the organ of Corti is under stress and the functional consequence is called presbycusis, and is the expression of an aging process that affects all sense organs.
The presbycusis is established and progresses slowly and is due to the interest of every sector of the hearing, the eardrum UP BY THE PRIMARY AND SECONDARY cortical areas of the temporal lobe (Brodman AREAS).
The aging process that characterizes the presbycusis involves various processes:
a) thickening of the tympanic membrane and degenerative joints ossiculari that result in increased impedance of the eardrum-ossicular system;
b) loss of elasticity of the basilar membrane of primitive thickening and formation of mineral deposits;
c) degeneration of the cells of the organ of Corti and the ganglion of Corti or associated with atrophy of the industry processes or vascular compression of the nerve fibers to the processes of hyperostosis of the walls of the internal auditory meatus;
d) reducing the number of cell nuclei of the central acoustic pathway;
e) reducing the number of cortical cells of primary and secondary acoustic areas.
The presbycusis is therefore an extremely complex phenomenon that slowly leads to a sensory deficit of quantitative and qualitative: the first related to the quantitative reduction of the structures that carry auditory information to areas of the cortex, the latter linked to the regressive phenomena dependent areas brain, which has the task to decode, analyze, process, interpret the information received. The quantitative deficit makes it difficult to perceive high-pitched sounds, the quality of the difficulty in understanding verbal messages, which can be understood only when the centers are working in optimal conditions, ie when the information is not contaminated by other information presented simultaneously (more people who speak make it difficult to selective hearing, so-called cocktail-party phenomenon: the presbycusis feel better in general, the low frequency, so the old man suffers a greater masking effect of environmental noise) or in the presence of other components (lip-reading ).
In terms of audiometric intentendendo refer to the techniques of tonal liminal audiometry and speech audiometry, the presbycusis may have four different profiles in relation to the prevalence of pathogenic elements that support it.
1) Presbyacusis Neurosensory: is the most common and distinctive and is characterized by regressive changes that affect all structures of the membranous cochlear duct from the base and proceed toward the elicotrema, with the corresponding disappearance of the spiral ganglion neurons (recruitment absent, tone decay test normal).
2) THE MECHANICS presbycusis: involves a stiffening of the basilar membrane or alteration of its mechanical retrogressive changes.
3) THE NEURAL presbycusis: compression of neural atrophy of the auditory nerve fibers to changes of hyperostotic modiolo, resulting in a decrease in the number of cells in the CNS, a process that begins early in youth.
4) THE METABOLIC presbycusis: changes to metabolic processes in the stria vascular load.
The presbycusis is often accompanied by tinnitus, a noise that is pitched with a receptive type of hearing loss on high-pitched sounds and is, in the neurosensory forms, a gradual descent curve, increasing the threshold for the higher frequencies first, and then for the intermediate and serious.
The selective deficits sec. Matshke refer initially to above 2000 Hz, for cell loss and external noise is more evident after 60 years of age, sec. Belal the presbycusis is not an event strongly correlated with age, old age and could exist a picture of normoacusia and it is important to investigate the diagnostic procedures relating to the forms that appear asymmetric sensorineural, could suggest disorders of the inner ear (cochlear otosclerosis, Meniere's disease or tumors of the acoustic nerve.
The healthy lifestyle and food, coupled with the concomitant reduction of the causes of senescence may be an effective way to reduce the aging process and delay the onset of hearing onset of senescence.
The only help the patient presbycusis is the hearing aid, preferably bilateral: the results are usually lower than in young subjects with similar hearing loss and the reason is the central acoustic deficit, which makes it difficult for the intelligibility of the spoken message. But if the denture is well made and correction is binaural and the subject is well trained, the advantages are obvious.
In conclusion we can say with Solomon, that the ability to communicate is fundamental for the autonomy of a person the opportunity to interact with the outside world and be happy.
Dr. Carmine Capasso
MD ENT
LA PRESBIACUSIA
LA PRESBIACUSIA
La presbiacusia rientra nel capitolo delle labirintosi nell’adulto, cioè nelle patologie degenerative dell’orecchio interno. Per presbiacusia si intende una ipoacusia neurosensoriale di frequente osservazione in entrambi i sessi, con maggiore frequenza nel sesso maschile, in età avanzata, più evidente dopo il 60° anno di età, ma che può osservarsi nelle fasi iniziali già dopo i 30 anni (Alajmo1995).
L’uomo è costantemente affetto da un indebolimento progressivo dell’organo e quindi del senso dell’udito. Patologie come il diabete mellito, l’ipertensione arteriosa, il tabagismo, l’alcolismo, l’arteriosclerosi, lo stress, le turbe del metabolismo (ipercolesterolemie) sono cause che conducono ad un invecchiamento dell’organismo. Tra queste notevole è il ruolo rivestito dal RUMORE: differenze significative esistono tra le popolazioni che vivono in aree a tasso di industrializzazione elevato rispetto alle popolazioni che vivono in campagna, valutate in soggetti di pari età. Il rumore è la causa d’invalidità professionale per molti lavoratori dell’industria (rumori dell’ambiente di vita o SOCIOACUSIA).
Il numero delle cellule presenti alla nascita, costituenti l’organo di Corti, tende progressivamente a diminuire (Rossi, 1994). Questa diminuzione di cellule avviene dopo la nascita nel giro basale della coclea e si associa ad una riduzione delle fibre nervose, con una conseguente riduzione del campo tonale udibile dopo il 10° anno d’età. Questa particolare senescenza deriva dal fatto che sia durante la veglia che durante il sonno, l’organo del Corti è sottoposto a sollecitazioni e la conseguenza funzionale prende il nome di PRESBIACUSIA, ed è l’espressione di un processo d’invecchiamento che interessa tutti gli organi di senso.
La presbiacusia si instaura e progredisce lentamente ed è dovuta all’interessamento di ogni settore dell’apparato uditivo, DALLA MEMBRANA DEL TIMPANO SINO ALLE AREE CORTICALI PRIMARIE E SECONDARIE DEL LOBO TEMPORALE (AREE DI BRODMAN).
Il processo d’invecchiamento che caratterizza la presbiacusia interessa vari processi:
a) ispessimento della membrana del timpano e fenomeni degenerativi nelle articolazioni ossiculari che si traducono in aumento d’impedenza del sistema timpano-ossiculare;
b) perdita di elasticità della membrana basilare da ispessimenti primitivi e da formazioni di depositi calcarei;
c) degenerazione delle cellule dell’organo di Corti e del ganglio di Corti oppure associata ad una atrofia della stria vascolare o a processi di compressione delle fibre nervose per processi di iperostosi delle pareti del meato acustico interno;
d) riduzione numerica delle cellule dei nuclei della via nervosa acustica centrale;
e) riduzione numerica delle cellule delle aree acustiche corticali primarie e secondarie.
La presbiacusia è quindi un fenomeno estremamente complesso che lentamente conduce ad un deficit sensoriale di tipo quantitativo e di tipo qualitativo: il primo legato alla riduzione quantitativa delle strutture che portano informazioni acustiche alle aree della corteccia, il secondo legato ai fenomeni regressivi a carico delle aree cerebrali, cui spetta il compito di decodificare, analizzare, elaborare, interpretare le informazioni ricevute. Il deficit quantitativo comporta la difficoltà nel percepire i suoni acuti, quello qualitativo la difficoltà nel comprendere i messaggi verbali, che possono essere compresi solo quando i centri lavorano in condizioni ottimali, cioè quando l’informazione non è inquinata da altre informazioni presentate contemporaneamente (più persone che parlano rendono difficile l’ascolto selettivo, cosiddetto fenomeno del cocktail-party: il presbiacusico sente meglio in genere le frequenze gravi, pertanto l’anziano risente maggiormente l’effetto mascherante del rumore ambientale) oppure in presenza di altre componenti (lettura labiale).
Dal punto di vista audiometrico, intentendendo riferirci alle tecniche di audiometria tonale liminare e audiometria vocale, la presbiacusia può presentare quattro diversi profili in rapporto al prevalere degli elementi patogenetici che la sostengono.
1) LA PRESBIACUSIA NEUROSENSORIALE: è la più frequente e caratteristica ed è caratterizzata da alterazioni regressive che interessano tutte le strutture membranose del condotto cocleare e che dalla base procedono verso l’elicotrema, con scomparsa dei corrispondenti neuroni del ganglio spirale (recruitment assente, tone decay test normale).
2) LA PRESBIACUSIA MECCANICA: comporta un irrigidimento della membrana basilare o una alterazione della sua meccanica per alterazioni regressive.
3) LA PRESBIACUSIA NEURALE: atrofia neurale per compressione delle fibre del nervo acustico per alterazioni iperostotiche del modiolo, con conseguente diminuzione del numero delle cellule del Sistema Nervoso Centrale, processo che inizia precocemente in età giovanile.
4) LA PRESBIACUSIA METABOLICA: per modificazioni dei processi metabolici a carico della stria vascolare.
La presbiacusia è spesso accompagnata da ACUFENI , cioè rumori a tonalità acuta con una ipoacusia di tipo recettivo sui suoni acuti ed è, nelle forme neurosensoriali, una curva in graduale discesa, con aumento di soglia inizialmente per le frequenze acute, successivamente per quelle intermedie e gravi.
I deficit selettivi sec. Matshke si riferiscono inizialmente al di sopra dei 2000 Hz, per perdita delle cellule acustiche esterne ed è più evidente dopo i 60 anni d’età; sec. Belal la presbiacusia non è un evento strettamente correlato con l’età, potendo sussistere l’età avanzata e un quadro di normoacusia ed è importante approfondire i procedimenti diagnostici relativi alle forme neurosensoriali che si presentano asimmetriche, potendo ipotizzare patologie a carico dell’orecchio interno (otosclerosi cocleare, malattia di Meniére o tumori del nervo acustico.
L’igiene di vita ed alimentare, associato alla riduzione delle concomitanti cause di senescenza, possono costituire un efficace mezzo per ridurre il processo d’invecchiamento dell’udito e ritardare l’epoca d’insorgenza della senescenza.
L’unico aiuto al paziente presbiacusico è costituito dalla protesi acustica, meglio se bilaterale: i risultati sono di solito inferiori rispetto ai soggetti giovani con analoga perdita uditiva e la ragione è nel deficit acustico centrale, che rende difficile l’intelligibilità del messaggio verbale. Ma, se la correzione protesica è ben fatta ed è binaurale ed il soggetto è ben addestrato, i vantaggi sono evidenti.
Possiamo in conclusione affermare con Solomon, che la possibilità di comunicare riveste un’importanza fondamentale per l’autonomia di una persona, la possibilità di poter interagire con il mondo esterno e di essere felici.
Dr. carmine Capasso
Spec.ORL
La presbiacusia rientra nel capitolo delle labirintosi nell’adulto, cioè nelle patologie degenerative dell’orecchio interno. Per presbiacusia si intende una ipoacusia neurosensoriale di frequente osservazione in entrambi i sessi, con maggiore frequenza nel sesso maschile, in età avanzata, più evidente dopo il 60° anno di età, ma che può osservarsi nelle fasi iniziali già dopo i 30 anni (Alajmo1995).
L’uomo è costantemente affetto da un indebolimento progressivo dell’organo e quindi del senso dell’udito. Patologie come il diabete mellito, l’ipertensione arteriosa, il tabagismo, l’alcolismo, l’arteriosclerosi, lo stress, le turbe del metabolismo (ipercolesterolemie) sono cause che conducono ad un invecchiamento dell’organismo. Tra queste notevole è il ruolo rivestito dal RUMORE: differenze significative esistono tra le popolazioni che vivono in aree a tasso di industrializzazione elevato rispetto alle popolazioni che vivono in campagna, valutate in soggetti di pari età. Il rumore è la causa d’invalidità professionale per molti lavoratori dell’industria (rumori dell’ambiente di vita o SOCIOACUSIA).
Il numero delle cellule presenti alla nascita, costituenti l’organo di Corti, tende progressivamente a diminuire (Rossi, 1994). Questa diminuzione di cellule avviene dopo la nascita nel giro basale della coclea e si associa ad una riduzione delle fibre nervose, con una conseguente riduzione del campo tonale udibile dopo il 10° anno d’età. Questa particolare senescenza deriva dal fatto che sia durante la veglia che durante il sonno, l’organo del Corti è sottoposto a sollecitazioni e la conseguenza funzionale prende il nome di PRESBIACUSIA, ed è l’espressione di un processo d’invecchiamento che interessa tutti gli organi di senso.
La presbiacusia si instaura e progredisce lentamente ed è dovuta all’interessamento di ogni settore dell’apparato uditivo, DALLA MEMBRANA DEL TIMPANO SINO ALLE AREE CORTICALI PRIMARIE E SECONDARIE DEL LOBO TEMPORALE (AREE DI BRODMAN).
Il processo d’invecchiamento che caratterizza la presbiacusia interessa vari processi:
a) ispessimento della membrana del timpano e fenomeni degenerativi nelle articolazioni ossiculari che si traducono in aumento d’impedenza del sistema timpano-ossiculare;
b) perdita di elasticità della membrana basilare da ispessimenti primitivi e da formazioni di depositi calcarei;
c) degenerazione delle cellule dell’organo di Corti e del ganglio di Corti oppure associata ad una atrofia della stria vascolare o a processi di compressione delle fibre nervose per processi di iperostosi delle pareti del meato acustico interno;
d) riduzione numerica delle cellule dei nuclei della via nervosa acustica centrale;
e) riduzione numerica delle cellule delle aree acustiche corticali primarie e secondarie.
La presbiacusia è quindi un fenomeno estremamente complesso che lentamente conduce ad un deficit sensoriale di tipo quantitativo e di tipo qualitativo: il primo legato alla riduzione quantitativa delle strutture che portano informazioni acustiche alle aree della corteccia, il secondo legato ai fenomeni regressivi a carico delle aree cerebrali, cui spetta il compito di decodificare, analizzare, elaborare, interpretare le informazioni ricevute. Il deficit quantitativo comporta la difficoltà nel percepire i suoni acuti, quello qualitativo la difficoltà nel comprendere i messaggi verbali, che possono essere compresi solo quando i centri lavorano in condizioni ottimali, cioè quando l’informazione non è inquinata da altre informazioni presentate contemporaneamente (più persone che parlano rendono difficile l’ascolto selettivo, cosiddetto fenomeno del cocktail-party: il presbiacusico sente meglio in genere le frequenze gravi, pertanto l’anziano risente maggiormente l’effetto mascherante del rumore ambientale) oppure in presenza di altre componenti (lettura labiale).
Dal punto di vista audiometrico, intentendendo riferirci alle tecniche di audiometria tonale liminare e audiometria vocale, la presbiacusia può presentare quattro diversi profili in rapporto al prevalere degli elementi patogenetici che la sostengono.
1) LA PRESBIACUSIA NEUROSENSORIALE: è la più frequente e caratteristica ed è caratterizzata da alterazioni regressive che interessano tutte le strutture membranose del condotto cocleare e che dalla base procedono verso l’elicotrema, con scomparsa dei corrispondenti neuroni del ganglio spirale (recruitment assente, tone decay test normale).
2) LA PRESBIACUSIA MECCANICA: comporta un irrigidimento della membrana basilare o una alterazione della sua meccanica per alterazioni regressive.
3) LA PRESBIACUSIA NEURALE: atrofia neurale per compressione delle fibre del nervo acustico per alterazioni iperostotiche del modiolo, con conseguente diminuzione del numero delle cellule del Sistema Nervoso Centrale, processo che inizia precocemente in età giovanile.
4) LA PRESBIACUSIA METABOLICA: per modificazioni dei processi metabolici a carico della stria vascolare.
La presbiacusia è spesso accompagnata da ACUFENI , cioè rumori a tonalità acuta con una ipoacusia di tipo recettivo sui suoni acuti ed è, nelle forme neurosensoriali, una curva in graduale discesa, con aumento di soglia inizialmente per le frequenze acute, successivamente per quelle intermedie e gravi.
I deficit selettivi sec. Matshke si riferiscono inizialmente al di sopra dei 2000 Hz, per perdita delle cellule acustiche esterne ed è più evidente dopo i 60 anni d’età; sec. Belal la presbiacusia non è un evento strettamente correlato con l’età, potendo sussistere l’età avanzata e un quadro di normoacusia ed è importante approfondire i procedimenti diagnostici relativi alle forme neurosensoriali che si presentano asimmetriche, potendo ipotizzare patologie a carico dell’orecchio interno (otosclerosi cocleare, malattia di Meniére o tumori del nervo acustico.
L’igiene di vita ed alimentare, associato alla riduzione delle concomitanti cause di senescenza, possono costituire un efficace mezzo per ridurre il processo d’invecchiamento dell’udito e ritardare l’epoca d’insorgenza della senescenza.
L’unico aiuto al paziente presbiacusico è costituito dalla protesi acustica, meglio se bilaterale: i risultati sono di solito inferiori rispetto ai soggetti giovani con analoga perdita uditiva e la ragione è nel deficit acustico centrale, che rende difficile l’intelligibilità del messaggio verbale. Ma, se la correzione protesica è ben fatta ed è binaurale ed il soggetto è ben addestrato, i vantaggi sono evidenti.
Possiamo in conclusione affermare con Solomon, che la possibilità di comunicare riveste un’importanza fondamentale per l’autonomia di una persona, la possibilità di poter interagire con il mondo esterno e di essere felici.
Dr. carmine Capasso
Spec.ORL
Gastro-esophageal reflux laryngitis
Gastro-esophageal reflux laryngitis
The daily experience, evidenced based, shows a significant increase in gastro-esophageal reflux disease: many acid-related disorders, laryngeal-level, were labeled as "hysterical world" and treated accordingly with spasmolytic and anti-anxiety drugs! many granulomas were operated in microlaringoscopia chordal back several times and promptly recurred. The cough frequently, especially after meals and at night were classified as allergic or "nervous." Currently, adequate medical history, a complete ENT evaluation (examination naso.fibrolaringoscopico) can 'highlight a gastro-esophageal reflux laryngitis divided into four stages: a) mucosal swelling and hyperemia interaritenoidea back, b) hyperemia of the true vocal cords; c ) ab chord granuloma rear of 1-2 mm in diameter d) abc granuloma interesting character with the entire vocal cord dispneizzante. Medical therapy with pantoprazole 40 mg / day or 80 mg (PPI: proton pump inhibitors) according to the severity 'of disease, with a minimum of 60 days of treatment, mean 6 months, indefinitely in the presence of esophagus Barrett. Essential to the evaluation of the gastroenterologist in stage "c" and "d" or treatment with pantoprazole over 60 days.: Gastroenterologists recommend an endoscopy with biopsy after 40 years and in the presence of recurrence of symptoms after discontinuation of therapy. useful UBT (urea breath test). Not very useful sec. gastroenterologists. the pH-metry and gastroesophageal traditional check dual probe (two sensors: one at CRIC-esophageal level and the other gastro-esophageal), considered very methodical investigation and uncomfortable for the patient.
For further details: "Multicenter study: clinical and statistical correlation between clinical and instrumental findings in reflux Pharyngolaryngeal: proposed new criteria for classification of reflux in ENT" CA Leone, F. Moscow - Department of ENT, Monaldi Hospital, Naples - ACTA OTORHINOLAYNGOLOGICA ITALICA 26.264-270, 2006
Dr. Carmine Capasso
MD ENT
The daily experience, evidenced based, shows a significant increase in gastro-esophageal reflux disease: many acid-related disorders, laryngeal-level, were labeled as "hysterical world" and treated accordingly with spasmolytic and anti-anxiety drugs! many granulomas were operated in microlaringoscopia chordal back several times and promptly recurred. The cough frequently, especially after meals and at night were classified as allergic or "nervous." Currently, adequate medical history, a complete ENT evaluation (examination naso.fibrolaringoscopico) can 'highlight a gastro-esophageal reflux laryngitis divided into four stages: a) mucosal swelling and hyperemia interaritenoidea back, b) hyperemia of the true vocal cords; c ) ab chord granuloma rear of 1-2 mm in diameter d) abc granuloma interesting character with the entire vocal cord dispneizzante. Medical therapy with pantoprazole 40 mg / day or 80 mg (PPI: proton pump inhibitors) according to the severity 'of disease, with a minimum of 60 days of treatment, mean 6 months, indefinitely in the presence of esophagus Barrett. Essential to the evaluation of the gastroenterologist in stage "c" and "d" or treatment with pantoprazole over 60 days.: Gastroenterologists recommend an endoscopy with biopsy after 40 years and in the presence of recurrence of symptoms after discontinuation of therapy. useful UBT (urea breath test). Not very useful sec. gastroenterologists. the pH-metry and gastroesophageal traditional check dual probe (two sensors: one at CRIC-esophageal level and the other gastro-esophageal), considered very methodical investigation and uncomfortable for the patient.
For further details: "Multicenter study: clinical and statistical correlation between clinical and instrumental findings in reflux Pharyngolaryngeal: proposed new criteria for classification of reflux in ENT" CA Leone, F. Moscow - Department of ENT, Monaldi Hospital, Naples - ACTA OTORHINOLAYNGOLOGICA ITALICA 26.264-270, 2006
Dr. Carmine Capasso
MD ENT
Laringite da reflusso gastro-esofageo
Laringite da reflusso gastro-esofageo
L'esperienza giornaliera, evidenced based, mostra un sensibile incremento della patologia da reflusso gastro-esofageo: molti disturbi acido-correlato, a livello laringeo, venivano etichettati come "globo isterico" e trattati di conseguenza con spasmolitici ed ansiolitici! molti granulomi cordali posteriori venivano operati in microlaringoscopia numerose volte e puntualmente recidivavano. La tosse frequente, soprattutto post-prandiale e notturna venivano classificate come allergiche o "nervose". Attualmente, una corretta anamnesi, una valutazione orl completa (esame naso.fibrolaringoscopico) potra' evidenziare una laringite da reflusso gastro-esofagea suddivisa in 4 stadi: a) iperemia e tumefazione mucosa interaritenoidea posteriore; b) a + iperemia delle corde vocali vere; c)a+b+ granuloma cordale posteriore di 1-2 mm di diametro; d) a+b+c+ granuloma interessante l'intera corda vocale con carattere dispneizzante. Terapia medica con pantoprazolo da 40 mg/die o 80 mg/die (PPI: proton pump inhibitors) secondo la gravita' della patologia, con una durata minima del trattamento di 60 gg, media 6 mesi, a tempo indeterminato in presenza di esofago di Barrett. Indispensabile la valutazione del gastroenterologo nello stadio "c" e "d" o per trattamenti con pantoprazolo superiori ai 60 gg.: i gastroenterologi consigliano una egds con biopsia dopo i 40 anni e in presenza di recidive della sintomatologia dopo sospensione della terapia. utile UBT (urea breath test). Poco utile sec. i gastroenterologi. la ph-metria gastroesofagea tradizionale e la check dual probe (due sensori: uno a livello crico-esofageo e l'altro a livello gastro-esofageo), considerata metodica indaginosa e oltremodo scomoda per il paziente.
Per approfondimenti: “Studio multicentrico: correlazione clinico-statistica tra dati clinici e rilievi strumentali nel reflusso laringofaringeo: proposta di un nuovo criterio di classificazione del reflusso in ORL” C.A. Leone, F. Mosca – Dipartimento di ORL, Ospedale Monaldi, Napoli – ACTA OTORHINOLAYNGOLOGICA ITALICA 26,264-270, 2006
Dr. Carmine Capasso
Spec. ORL
L'esperienza giornaliera, evidenced based, mostra un sensibile incremento della patologia da reflusso gastro-esofageo: molti disturbi acido-correlato, a livello laringeo, venivano etichettati come "globo isterico" e trattati di conseguenza con spasmolitici ed ansiolitici! molti granulomi cordali posteriori venivano operati in microlaringoscopia numerose volte e puntualmente recidivavano. La tosse frequente, soprattutto post-prandiale e notturna venivano classificate come allergiche o "nervose". Attualmente, una corretta anamnesi, una valutazione orl completa (esame naso.fibrolaringoscopico) potra' evidenziare una laringite da reflusso gastro-esofagea suddivisa in 4 stadi: a) iperemia e tumefazione mucosa interaritenoidea posteriore; b) a + iperemia delle corde vocali vere; c)a+b+ granuloma cordale posteriore di 1-2 mm di diametro; d) a+b+c+ granuloma interessante l'intera corda vocale con carattere dispneizzante. Terapia medica con pantoprazolo da 40 mg/die o 80 mg/die (PPI: proton pump inhibitors) secondo la gravita' della patologia, con una durata minima del trattamento di 60 gg, media 6 mesi, a tempo indeterminato in presenza di esofago di Barrett. Indispensabile la valutazione del gastroenterologo nello stadio "c" e "d" o per trattamenti con pantoprazolo superiori ai 60 gg.: i gastroenterologi consigliano una egds con biopsia dopo i 40 anni e in presenza di recidive della sintomatologia dopo sospensione della terapia. utile UBT (urea breath test). Poco utile sec. i gastroenterologi. la ph-metria gastroesofagea tradizionale e la check dual probe (due sensori: uno a livello crico-esofageo e l'altro a livello gastro-esofageo), considerata metodica indaginosa e oltremodo scomoda per il paziente.
Per approfondimenti: “Studio multicentrico: correlazione clinico-statistica tra dati clinici e rilievi strumentali nel reflusso laringofaringeo: proposta di un nuovo criterio di classificazione del reflusso in ORL” C.A. Leone, F. Mosca – Dipartimento di ORL, Ospedale Monaldi, Napoli – ACTA OTORHINOLAYNGOLOGICA ITALICA 26,264-270, 2006
Dr. Carmine Capasso
Spec. ORL
giovedì 25 novembre 2010
I pesci: la visione
I pesci: la visione
La visione consente ai pesci di ottenere informazioni da oggetti posti nelle vicinanze mentre la sua utilità si riduce all'aumentare della distanza, ciò a causa del contrasto visivo che decresce rapidamente nell'acqua. In acque molto trasparenti la capacità visiva di un pesce non oltrepassa generalmente i 40 mt.
La vista è sicuramente importante in ambienti costieri, come dimostra la diffusione di colorazioni appariscenti in molte specie di teleostei, spesso legate al loro comportamento sociale e riproduttivo. I pesci sono in grado di distinguere pattern di colorazioni differenti e forme diverse. La vista però nei pesci funziona in maniera diversa rispetto a quella degli esseri umani. Gli occhi sono in posizione distanziata ai lati del capo e da ciò risulta che ciascun occhio ha un suo campo di visione separato, ad eccezione di una piccola area posta davanti al muso del pesce dove questi due campi di visione si sovrappongono. Quindi solo in questa piccola area i pesci riescono a percepire la prospettiva. Rispetto all'occhio umano, inoltre, l'occhio si adatta più lentamente ai cambiamenti dell'intensità luminosa. La messa a fuoco avviene muovendo il cristallino avanti e indietro (non possono dilatare le pupille).
campo visivo dei pesci
Il problema della visione subacquea è legato sostanzialmente alla bassa intensità di luce e al cambiamento dello spettro luminoso che avviene all'aumentare della profondità. In relazione a queste due caratteristiche ambientali i pesci hanno evoluto fotorecettori particolarmente sensibili e capaci di catturare fotoni a basse intensità luminose. Inoltre i pigmenti visivi predominanti nelle cellule fotorecettrici dell'occhio variano da specie a specie in relazione con l'habitat in cui queste vivono. In generale esiste, infatti, una corrispondenza tra distribuzione spettrale della luce ambientale e la capacità di assorbimento luminoso dei pigmenti presenti nell'occhio.
I pesci che conducono vita pelagica in acque oceaniche e che vivono in acque profonde hanno pigmenti visivi (rodopsina) con il massimo di assorbimento in uno intervallo dello spettro luminoso tra 450-550 µm, che corrisponde al verde e al blu. I pesci che vivono in acque superficiali costiere tendono ad avere fotorecettori il cui massimo di assorbimento varia da 450 µm (blu) a 650 µm (arancione - rosso). I pesci che effettuano migrazioni verticali e che quindi si spostano tra ambienti con caratteristiche luminose differenti, hanno un complesso di pigmenti per poter vedere in condizioni luminose differenti.
In altre specie e stato però evidenziato che questa corrispondenza tra pigmenti visivi e luce ambientale non si verifica ma che, anzi, la capacita massima di assorbimento della luce dell'occhio avviene ad una lunghezza d'onda piu o meno distante da quella predominante nell'ambiente. Questo fenomeno e stato spiegato con la necessità da parte di queste specie di poter accentuare il contrasto visivo degli oggetti rispetto allo spazio circostante. In questa situazione, infatti, aumenta la capacità di distinguere oggetti che hanno un'elevata capacità di assorbimento luminoso. I pesci abissali sono in grado di produrre luce (bioluminescenza) che viene emessa da speciali organelli (fotofori), distribuiti sul corpo e in alcune specie sul capo. In genere il fenomeno è prodotto da batteri simbionti bioluminescenti. Il sistema coinvolto e quello della luciferina-luciferasi. Gli occhi di questi pesci hanno fotorecettori in grado di recepire la luce nella banda luminosa prodotta dai fotofori.
La visione consente ai pesci di ottenere informazioni da oggetti posti nelle vicinanze mentre la sua utilità si riduce all'aumentare della distanza, ciò a causa del contrasto visivo che decresce rapidamente nell'acqua. In acque molto trasparenti la capacità visiva di un pesce non oltrepassa generalmente i 40 mt.
La vista è sicuramente importante in ambienti costieri, come dimostra la diffusione di colorazioni appariscenti in molte specie di teleostei, spesso legate al loro comportamento sociale e riproduttivo. I pesci sono in grado di distinguere pattern di colorazioni differenti e forme diverse. La vista però nei pesci funziona in maniera diversa rispetto a quella degli esseri umani. Gli occhi sono in posizione distanziata ai lati del capo e da ciò risulta che ciascun occhio ha un suo campo di visione separato, ad eccezione di una piccola area posta davanti al muso del pesce dove questi due campi di visione si sovrappongono. Quindi solo in questa piccola area i pesci riescono a percepire la prospettiva. Rispetto all'occhio umano, inoltre, l'occhio si adatta più lentamente ai cambiamenti dell'intensità luminosa. La messa a fuoco avviene muovendo il cristallino avanti e indietro (non possono dilatare le pupille).
campo visivo dei pesci
Il problema della visione subacquea è legato sostanzialmente alla bassa intensità di luce e al cambiamento dello spettro luminoso che avviene all'aumentare della profondità. In relazione a queste due caratteristiche ambientali i pesci hanno evoluto fotorecettori particolarmente sensibili e capaci di catturare fotoni a basse intensità luminose. Inoltre i pigmenti visivi predominanti nelle cellule fotorecettrici dell'occhio variano da specie a specie in relazione con l'habitat in cui queste vivono. In generale esiste, infatti, una corrispondenza tra distribuzione spettrale della luce ambientale e la capacità di assorbimento luminoso dei pigmenti presenti nell'occhio.
I pesci che conducono vita pelagica in acque oceaniche e che vivono in acque profonde hanno pigmenti visivi (rodopsina) con il massimo di assorbimento in uno intervallo dello spettro luminoso tra 450-550 µm, che corrisponde al verde e al blu. I pesci che vivono in acque superficiali costiere tendono ad avere fotorecettori il cui massimo di assorbimento varia da 450 µm (blu) a 650 µm (arancione - rosso). I pesci che effettuano migrazioni verticali e che quindi si spostano tra ambienti con caratteristiche luminose differenti, hanno un complesso di pigmenti per poter vedere in condizioni luminose differenti.
In altre specie e stato però evidenziato che questa corrispondenza tra pigmenti visivi e luce ambientale non si verifica ma che, anzi, la capacita massima di assorbimento della luce dell'occhio avviene ad una lunghezza d'onda piu o meno distante da quella predominante nell'ambiente. Questo fenomeno e stato spiegato con la necessità da parte di queste specie di poter accentuare il contrasto visivo degli oggetti rispetto allo spazio circostante. In questa situazione, infatti, aumenta la capacità di distinguere oggetti che hanno un'elevata capacità di assorbimento luminoso. I pesci abissali sono in grado di produrre luce (bioluminescenza) che viene emessa da speciali organelli (fotofori), distribuiti sul corpo e in alcune specie sul capo. In genere il fenomeno è prodotto da batteri simbionti bioluminescenti. Il sistema coinvolto e quello della luciferina-luciferasi. Gli occhi di questi pesci hanno fotorecettori in grado di recepire la luce nella banda luminosa prodotta dai fotofori.
I SEGRETI DEL MARE
http://www.isegretidelmare.it/pesci.asp
* L'ambiente marino
* La barriera corallina
* Caratteristiche
* Fisico-chimiche
* Composizione
* La luce
* Gli abitanti
* I pesci
* I cetacei
* Il Plancton
*
* Invertebrati
* Superiori
* Inferiori
*
* Le alghe
* Le alghe
* Le zooxantelle
* Categorie
*
* Articoli
*
* Dizionario
* Immagini
*
* Necton
I segreti del Mare
"La lingua non è sufficiente a dire e nemmeno la mano riesce a scrivere tutte le meraviglie del mare"
E con questa frase di uno dei più grandi navigatori di tutti i tempi, Cristoforo Colombo, che voglio iniziare questo sito amatoriale dedicato al Mare ed a tutto quello che esso contiene.
Un sentito ringraziamento a tutti i visitatori ed a tutti quelli che mi contatteranno per eventuali critiche e/o consigli (entrambi graditi) per il miglioramento di questo sito. Buona navigazione!
Fabrizio
Con una superficie più che doppia rispetto alle terre emerse (310 milioni di chilometri quadrati, otto volte quella della Luna!) il mare è un vero e proprio mondo nascosto agli occhi degli uomini.
Quattro quinti della flora e della fauna del mondo intero vivono nei mari costieri poco profondi che limitano i continenti e solo con cifre di smisurata grandezza si può definire la densità di popolazione di queste acque.
Una piccolissima parte di questa vita è qui rappresentata, pesci, poriferi, conchiglie, coralli e alghe dove la natura sembra aver giocato con le forme e i colori per stupire ogni volta noi uomini, ultimi arrivati a scoprire questo fantastico pianeta blu.
In queste pagine potrete trovare le descrizioni dei maggiori rappresentanti, sia in termini di fauna che di flora, dei più importanti colonizzatori delle acque marine e corredate da oltre 500 immagini. Avviso ai naviganti:
rinecanthusPer identificare i pesci si è generalmente utilizzato l'" Atlas of marine aquarium fishes" del Dr.Burgess e "L'enciclopedia dei pesci marini tropicali" di Frank De Graaf. Per molte foto però l'identificazione del pesce è dubbia, o per una difficile "visione" dell'animale o per delle incongruenze tassonomiche. Per una più facile ricerca di un termine nel caso si conosca il nome comune ma non quello scientifico si può consultare la pagina Dizionario
Opera, the fastest and most secure web browser
@ webmaster © 2008 I Segreti del Mare
*
I pesci
Le origini
Biodiversità
Forma del corpo
Le branchie
La visione
L'olfatto
La linea laterale
L'elettrorecezione
*
I Cetacei
Osservazione
Tutela
Sottordini
*
Invertebrati superiori
i Cefalopodi
I Molluschi
Gli Echinoidi
Le stelle marine
Le conchiglie
Le Gorgonie
*
Invertebrati inferiori
I Poriferi
I Cnidari
*
Il budego
La bavosa occhiuta
La stella gorgona
La mazzancolla
Una lepre
extracomunitaria
* L'ambiente marino
* La barriera corallina
* Caratteristiche
* Fisico-chimiche
* Composizione
* La luce
* Gli abitanti
* I pesci
* I cetacei
* Il Plancton
*
* Invertebrati
* Superiori
* Inferiori
*
* Le alghe
* Le alghe
* Le zooxantelle
* Categorie
*
* Articoli
*
* Dizionario
* Immagini
*
* Necton
I segreti del Mare
"La lingua non è sufficiente a dire e nemmeno la mano riesce a scrivere tutte le meraviglie del mare"
E con questa frase di uno dei più grandi navigatori di tutti i tempi, Cristoforo Colombo, che voglio iniziare questo sito amatoriale dedicato al Mare ed a tutto quello che esso contiene.
Un sentito ringraziamento a tutti i visitatori ed a tutti quelli che mi contatteranno per eventuali critiche e/o consigli (entrambi graditi) per il miglioramento di questo sito. Buona navigazione!
Fabrizio
Con una superficie più che doppia rispetto alle terre emerse (310 milioni di chilometri quadrati, otto volte quella della Luna!) il mare è un vero e proprio mondo nascosto agli occhi degli uomini.
Quattro quinti della flora e della fauna del mondo intero vivono nei mari costieri poco profondi che limitano i continenti e solo con cifre di smisurata grandezza si può definire la densità di popolazione di queste acque.
Una piccolissima parte di questa vita è qui rappresentata, pesci, poriferi, conchiglie, coralli e alghe dove la natura sembra aver giocato con le forme e i colori per stupire ogni volta noi uomini, ultimi arrivati a scoprire questo fantastico pianeta blu.
In queste pagine potrete trovare le descrizioni dei maggiori rappresentanti, sia in termini di fauna che di flora, dei più importanti colonizzatori delle acque marine e corredate da oltre 500 immagini. Avviso ai naviganti:
rinecanthusPer identificare i pesci si è generalmente utilizzato l'" Atlas of marine aquarium fishes" del Dr.Burgess e "L'enciclopedia dei pesci marini tropicali" di Frank De Graaf. Per molte foto però l'identificazione del pesce è dubbia, o per una difficile "visione" dell'animale o per delle incongruenze tassonomiche. Per una più facile ricerca di un termine nel caso si conosca il nome comune ma non quello scientifico si può consultare la pagina Dizionario
Opera, the fastest and most secure web browser
@ webmaster © 2008 I Segreti del Mare
*
I pesci
Le origini
Biodiversità
Forma del corpo
Le branchie
La visione
L'olfatto
La linea laterale
L'elettrorecezione
*
I Cetacei
Osservazione
Tutela
Sottordini
*
Invertebrati superiori
i Cefalopodi
I Molluschi
Gli Echinoidi
Le stelle marine
Le conchiglie
Le Gorgonie
*
Invertebrati inferiori
I Poriferi
I Cnidari
*
Il budego
La bavosa occhiuta
La stella gorgona
La mazzancolla
Una lepre
extracomunitaria
OSAS
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What Is Sleep Apnea?
Sleep apnea (AP-ne-ah) is a common disorder in which you have one or more pauses in breathing or shallow breaths while you sleep.
Breathing pauses can last from a few seconds to minutes. They often occur 5 to 30 times or more an hour. Typically, normal breathing then starts again, sometimes with a loud snort or choking sound.
Sleep apnea usually is a chronic (ongoing) condition that disrupts your sleep. You often move out of deep sleep and into light sleep when your breathing pauses or becomes shallow.
This results in poor sleep quality that makes you tired during the day. Sleep apnea is one of the leading causes of excessive daytime sleepiness.
Overview
Sleep apnea often goes undiagnosed. Doctors usually can't detect the condition during routine office visits. Also, there are no blood tests for the condition.
Most people who have sleep apnea don't know they have it because it only occurs during sleep. A family member and/or bed partner may first notice the signs of sleep apnea.
The most common type of sleep apnea is obstructive sleep apnea. This most often means that the airway has collapsed or is blocked during sleep. The blockage may cause shallow breathing or breathing pauses.
When you try to breathe, any air that squeezes past the blockage can cause loud snoring. Obstructive sleep apnea is more common in people who are overweight, but it can affect anyone. For example, small children may have enlarged tonsil tissues in their throats, which can lead to obstructive sleep apnea.
The animation below shows how obstructive sleep apnea occurs. Click the "start" button to play the animation. Written and spoken explanations are provided with each frame. Use the buttons in the lower right corner to pause, restart, or replay the animation, or use the scroll bar below the buttons to move through the frames.
The animation shows how air flow to the lungs can be blocked, causing sleep apnea.
The animation shows how air flow to the lungs can be blocked, causing sleep apnea.
Central sleep apnea is a less common type of sleep apnea. This disorder happens if the area of your brain that controls your breathing doesn't send the correct signals to your breathing muscles. As a result, you'll make no effort to breathe for brief periods.
Central sleep apnea can occur in anyone. However, it's more common in people who have certain medical conditions or use certain medicines.
Central sleep apnea often occurs with obstructive sleep apnea, but it can occur alone. Snoring doesn't typically happen with central sleep apnea.
This article mainly focuses on obstructive sleep apnea.
Outlook
Untreated sleep apnea can:
* Increase the risk of high blood pressure, heart attack, stroke, obesity, and diabetes
* Increase the risk of, or worsen, heart failure
* Make arrhythmias (ah-RITH-me-ahs), or irregular heartbeats, more likely
* Increase the chance of having work-related or driving accidents
Sleep apnea is a chronic condition that requires long-term management. Lifestyle changes, mouthpieces, surgery, and/or breathing devices can successfully treat sleep apnea in many people.
Revised August 2010
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National Heart, Lung, and Blood Institute: Diseases and Conditions Index
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DCI Home: Sleep Disorders: Sleep Apnea: What Is ...
Sleep Apnea
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What Is ...
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What Is Sleep Apnea?
Sleep apnea (AP-ne-ah) is a common disorder in which you have one or more pauses in breathing or shallow breaths while you sleep.
Breathing pauses can last from a few seconds to minutes. They often occur 5 to 30 times or more an hour. Typically, normal breathing then starts again, sometimes with a loud snort or choking sound.
Sleep apnea usually is a chronic (ongoing) condition that disrupts your sleep. You often move out of deep sleep and into light sleep when your breathing pauses or becomes shallow.
This results in poor sleep quality that makes you tired during the day. Sleep apnea is one of the leading causes of excessive daytime sleepiness.
Overview
Sleep apnea often goes undiagnosed. Doctors usually can't detect the condition during routine office visits. Also, there are no blood tests for the condition.
Most people who have sleep apnea don't know they have it because it only occurs during sleep. A family member and/or bed partner may first notice the signs of sleep apnea.
The most common type of sleep apnea is obstructive sleep apnea. This most often means that the airway has collapsed or is blocked during sleep. The blockage may cause shallow breathing or breathing pauses.
When you try to breathe, any air that squeezes past the blockage can cause loud snoring. Obstructive sleep apnea is more common in people who are overweight, but it can affect anyone. For example, small children may have enlarged tonsil tissues in their throats, which can lead to obstructive sleep apnea.
The animation below shows how obstructive sleep apnea occurs. Click the "start" button to play the animation. Written and spoken explanations are provided with each frame. Use the buttons in the lower right corner to pause, restart, or replay the animation, or use the scroll bar below the buttons to move through the frames.
The animation shows how air flow to the lungs can be blocked, causing sleep apnea.
The animation shows how air flow to the lungs can be blocked, causing sleep apnea.
Central sleep apnea is a less common type of sleep apnea. This disorder happens if the area of your brain that controls your breathing doesn't send the correct signals to your breathing muscles. As a result, you'll make no effort to breathe for brief periods.
Central sleep apnea can occur in anyone. However, it's more common in people who have certain medical conditions or use certain medicines.
Central sleep apnea often occurs with obstructive sleep apnea, but it can occur alone. Snoring doesn't typically happen with central sleep apnea.
This article mainly focuses on obstructive sleep apnea.
Outlook
Untreated sleep apnea can:
* Increase the risk of high blood pressure, heart attack, stroke, obesity, and diabetes
* Increase the risk of, or worsen, heart failure
* Make arrhythmias (ah-RITH-me-ahs), or irregular heartbeats, more likely
* Increase the chance of having work-related or driving accidents
Sleep apnea is a chronic condition that requires long-term management. Lifestyle changes, mouthpieces, surgery, and/or breathing devices can successfully treat sleep apnea in many people.
Revised August 2010
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growth hormone
Dictionary: growth hormone
Home > Library > Literature & Language > Dictionary
n. (Abbr. GH)
1. A polypeptide hormone secreted by the anterior lobe of the pituitary gland that promotes growth of the body, especially by stimulating release of somatomedin, and that influences the metabolism of proteins, carbohydrates, and lipids. Also called human growth hormone, somatotropic hormone, Also called somatotropin.
2. Any of various natural or synthetic substances that regulate the growth of animals or plants, such as pituitary growth hormone in vertebrates and auxins in plants.
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Britannica Concise Encyclopedia:
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Peptide hormone secreted by the anterior lobe of the pituitary gland. It promotes growth of bone and other body tissues by stimulating protein synthesis and fat breakdown (for energy). Excessive production causes gigantism, acromegaly, or other malformations; deficient production results in dwarfism, dramatically relieved if GH is given before puberty. Genetic engineering techniques now permit large-scale production of adequate amounts of GH for that purpose.
For more information on growth hormone, visit Britannica.com.
World of the Body:
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Growth hormone also called somatotrophin, is secreted from the anterior part of the pituitary gland. It is a major product of the gland, which contains 5 mg of the hormone (about 10% of its dry weight). As the name implies, growth hormone is important in controlling linear growth and, together with the thyroid hormones and the sex hormones, is important in determining the final height and development of an individual. It also has a role in controlling metabolism of foodstuffs, so that lack of the hormone in children results in short stature with the whole body in proportion, whereas deficiency in the adult results in weakness and depression.
Growth stops when the epiphyses (ends) of the bones fuse to the main shaft between them. Oversecretion before this occurs results in gigantism, whereas oversecretion afterwards results in acromegaly, a condition characterized by coarsening of the facial features and enlargement of the hands and feet. Interest in dwarfism, gigantism, and acromegaly has spanned the centuries; literature, especially for children, is filled with stories about dwarfs and giants, while Old Testament writings have several descriptions of giants. A study of paintings can also reveal subjects with disturbances of growth hormone secretion. A portrait from about 1365 bc of Tutankhamun's father-in-law illustrates some of the chacterisitics of acromegaly, but it was not until the late eighteenth century that Saucerette, a French surgeon, described a subject with features suggestive of this condition. During the nineteenth century a number of reports appeared and the term ‘acromegaly’ was coined in 1886 by Pierre Marie. In the following year, Minkowski (who also performed some of the early experiments important in the discovery of insulin) noted that acromegaly was associated with a pituitary tumour. Such tumours are now known to be the cause of gigantism and acromegaly. Once this was established, surgical treatment of the condition began to be attempted in the 1890s. In 1912 Cushing, a famous American neurosurgeon who also made major contributions to endocrinology, pioneered the technique of operating on pituitary tumours via the nasal route.
The nasal approach to the pituitary is possible because the gland itself lies in the midline at the base of the brain. Part of the visual pathway, the ‘optic chiasma’, lies in front of the pituitary, so a spreading tumour may lead to visual defects. This could explain why Goliath of Gath failed to see the pebble launched by David.
Growth hormone is a large peptide of 191 amino acids and is relatively species-specific, so only primate growth hormone is effective in man. This meant that until 1985, when it became possible to synthesize it, treatment of short stature employed growth hormone extracted from human pituitaries. As with some preparations of human gonadotrophins previously used in fertility treatment, some of the preparations were contaminated, leading to 1 in 1000 patients developing Creuzfeld Jacob disease, resulting in dementia and death. Currently biosynthetic growth hormone is employed.
Growth hormone is always detectable in the plasma of healthy individuals throughout life; it is not secreted continuously over the 24 hours, but in bursts. The most marked increase follows the onset of sleep, so there may be a basis for the old wives' tale that you will not grow if you do not get a good night's sleep. The hormone is present in the fetus, but does not appear to be necessary for growth until soon after birth. Its release is increased in puberty, at an earlier stage in girls than in boys. Secretion of growth hormone is controlled by the hypothalamus, a region of the brain which is important in regulating many functions including a major role in the response to stress: growth hormone is released in response to a number of stresses such as exercise, anaesthesia, and surgery. Prolonged stress may however suppress growth hormone release, so that children with marked emotional deprivation can show secondary growth failure. One such case is said to be Sir James Barrie who was short of stature and may have had some affinity with his creation, Peter Pan.
Release is stimulated in response to a rapid fall in blood glucose, which can be produced by an injection of insulin in a clinical test for growth hormone secretion. The hypothalamus controls growth hormone secretion by means of its own secretion of two peptides; somatostatin, which inhibits secretion, and growth hormone releasing hormone, which is stimulatory; these hormones reach the nearby anterior pituitary through local blood vessels.
Growth hormone stimulates the growth of the long bones, not directly but through the action of somatomedins, which are insulin-like growth factors made in the liver, and which also inhibit release of the hormone. It has a direct effect on metabolic processes throughout the body, supporting growth through enhanced formation of protein and nucleic acids (anabolic action) and of other constituents of lean body mass. By contrast its effects promote breakdown of carbohydrate and fat, with the energy released supporting growth. Because of the anabolic effects and because detection is difficult, growth hormone has been used by athletes to improve performance, although studies have shown it to be of little value.
— Mary L. Forsling
See also development and growth; hypothalamus; peptides; pituitary gland.
Food and Nutrition:
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Somatotrophin, a peptide hormone secreted by the pituitary gland that promotes growth of bone and soft tissues. It also reduces the utilization of glucose, and increases breakdown of fats to fatty acids; because of this it has been promoted as an aid to weight reduction, with little evidence of efficacy. Sometimes abbreviated to HGH (human growth hormone); growth hormone from other mammals differs in structure and activity. See also bovine somatotrophin.
Food and Fitness:
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Body growth is greatly influenced by a protein hormone secreted by the anterior pituitary gland. This growth hormone (also known as human growth hormone, GH, or hGH) can now be manufactured by a genetic engineering technique called recombinant DNA technology. The growth hormone gene is cut out of human DNA and spliced into bacterial DNA. The bacteria are fermented and secrete growth hormone (sometimes called recombinant GH) identical to that produced in human cells. Growth hormone is used clinically to treat people with stunted growth. Until recombinant GH became available, the only source of growth hormone was human pituitary glands. This source is extremely expensive and was used almost exclusively for treating people of severely restricted growth (those with severe undersecretion of GH). Growth hormone from pituitary glands was also associated with a number of cases of Creutzfeldt-Jakob disease. The production of recombinant GH has meant treatment is safer and easier to obtain, so that those with less severe growth restriction can be treated. Unfortunately, its wider availability has been abused. It is used by body-builders and participants in power sports to accelerate muscle growth. Other sports people use it to accelerate the healing of musculoskeletal injuries. People concerned about their looks use it to decrease body fat. However, although growth hormone may increase the muscle bulk of inactive individuals, it probably has no significant effect on the muscle growth of young individuals who are engaged in an intense weight-training programme. Intense exercise combined with an adequate diet is sufficient to stimulate maximum protein synthesis in most individuals. In addition, excessive use of growth hormone may cause gigantism in prepubertal individuals and acromegaly (increase in size of the bones in hands, feet, and face) in adults. Other potential adverse effects include muscular weakness, arthritis, impotence, diabetes, and heart disorders. Use of growth hormone supplements is banned by the International Olympic Committee and some other sports federations, but it is very difficult to detect it.
Dental Dictionary:
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(GH) a single-chain peptide secreted by the anterior pituitary gland in response to growth hormone releasing factor (GHRF) from the hypothalamus. Growth hormone promotes protein synthesis in all cells, increased fat mobilization and use of fatty acids for energy, and decreased use of carbohydrates.
Nutrition Encyclopedia:
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Human growth hormone (HGH) stimulates the growth of bones and affects the metabolism of carbohydrate, protein, and fat. It is secreted by the pituitary gland, which is located in the brain. Whereas HGH is produced in the body, genetic engineering has resulted in the development of recombinant human growth hormone (rHGH), which is used to treat stunted growth in children. Bovine somatotropin (BST) is a naturally occurring protein hormone in cows that increases milk production when administered as a supplement. BST is not biologically active in humans and is broken down into inactive amino acids and peptides when consumed. Therefore, milk from cows treated with BST is believed to be as safe and nutritious as milk from untreated cows.
Supplemental HGH is used by athletes, particularly body builders and power lifters, to increase muscle mass and decrease body fat. Individuals who are HGH-deficient and take supplemental HGH will see an increase in muscle mass and decreased body fat, whereas those with normal HGH levels will see an increase in lean body mass from an increase in the size of heart, liver, and kidneys, and from fluid retention, but there will be no increase in muscle mass. Excessive use can cause acromegaly (an increase in the size of the bones of the hand, feet, and jaw), as well as muscle weakness, arthritis, impotence, and diabetes. Since HGH increases the size of the liver, kidneys, and heart, its use can predispose the individual to chronic diseases. HGH is classified as an anabolic hormone, and its ability to increase muscle and decrease fat confers an unfair athletic advantage on the user. The use of HGH is thus banned by the International Olympic Committee (IOC), the National Collegiate Athletic Association (NCAA), and many professional sporting organizations.
See also Ergogenic acids; Sports nutrition.
Bibliography
Rosenbloom, Christine, ed. (2000). Sports Nutrition: A Guide for the Professional Working with Active People, 3rd edition. Chicago: American Dietetic Association.
Williams, M. (1998). The Ergogenics Edge. Champaign, IL: Human Kinetics.
Columbia Encyclopedia:
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growth hormone or somatotropin (sōmăt'ətrō'pən), glycoprotein hormone released by the anterior pituitary gland that is necessary for normal skeletal growth in humans (see protein). Evidence suggests that the secretion of human growth hormone (HGH) is regulated by the release of certain peptides by the hypothalamus of the brain. One such substance, called somatostatin, has been shown to inhibit the secretion of HGH. HGH is known to act upon many aspects of cellular metabolism, but its most obvious effect is the stimulation of the growth of cartilage and bone in children.
See also auxins (plant growth hormones).
Role in Dwarfism and Gigantism
A deficiency of growth hormone secretion before puberty (by the end of which the synthesis of new bone tissue is complete) results in pituitary dwarfism. Pituitary dwarfs, who can be as little as 3 to 4 ft (91-122 cm) tall, are generally well proportioned except for the head, which may be relatively large when compared to the body (this relationship of head to body is similar to that of normal children). Unlike cretins, whose dwarfism is caused by a deficiency of thyroxine, pituitary dwarfs are not mentally retarded; they are often sexually immature. They can be treated by injections of synthetic growth hormone, either somatrem or somatropin, which are produced by genetically engineered bacteria.
An excess of growth hormone in children results in gigantism; these children grow to be over 7 ft (213 cm) in height and have disproportionately long limbs. Excess growth hormone produced after puberty has little effect on the growth of the skeleton, but it results in a disease affecting terminal skeletal structures known as acromegaly.
Other Medical Uses
HGH has been used with some success to combat the weight loss and general wasting characteristic of AIDS and cancer. It is used illegally by bodybuilders and athletes to increase muscle mass. Controversy surrounds its use in normal children who simply want to be taller. In addition, a 1990 medical study that reported the reversal of many of the physiological effects of aging with regular injections of HGH has created a lucrative black market for it and has prompted funding of further trials. There has been no conclusive evidence, however, to support the use of HGH as an anti-aging treatment, and it can cause serious side effects, including diabetes, in older adults.
Veterinary Dictionary:
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Growth hormone.
Wikipedia:
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"HGH" redirects here. For other uses, see HGH (disambiguation).
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Growth hormone 1
Somatotropine.GIF
Growth hormone
Identifiers
Symbol GH1
Entrez 2688
HUGO 4261
OMIM 139250
RefSeq NM_022562
UniProt P01241
Other data
Locus Chr. 17 q22-q24
Growth hormone 2
Identifiers
Symbol GH2
Entrez 2689
HUGO 4262
OMIM 139240
RefSeq NM_002059
UniProt P01242
Other data
Locus Chr. 17 q22-q24
Growth hormone (GH) is a protein-based peptide hormone. It stimulates growth, cell reproduction and regeneration in humans and other animals. Growth hormone is a 191-amino acid, single-chain polypeptide that is synthesized, stored, and secreted by the somatotroph cells within the lateral wings of the anterior pituitary gland. Somatotropin refers to the growth hormone 1 produced naturally in animals, whereas the term somatropin refers to growth hormone produced by recombinant DNA technology,[1] and is abbreviated "HGH" in humans.
Growth hormone is used in medicine to treat children's growth disorders and adult growth hormone deficiency. In recent years, growth hormone replacement therapies have become popular in the battle against ageing and obesity. Reported effects on GH-deficient patients (but not on healthy people) include decreased body fat, increased muscle mass, increased bone density, increased energy levels, improved skin tone and texture, increased sexual function, and improved immune system function. At this time, hGH is still considered a very complex hormone, and many of its functions are still unknown.[2]
In its role as an anabolic agent, HGH has been used by competitors in sports since the 1970s, and it has been banned by the IOC and NCAA. Traditional urine analysis could not detect doping with HGH, so the ban was unenforceable until the early 2000s when blood tests that could distinguish between natural and artificial hGH were starting to be developed. Blood tests conducted by WADA at the 2004 Olympic Games in Athens, Greece primarily targeted HGH.[2]
Contents [hide]
* 1 Gene locus
* 2 Structure
o 2.1 Regulation
o 2.2 Secretion patterns
* 3 Functions of GH
o 3.1 Excesses
o 3.2 Deficiencies
* 4 Therapeutic use
o 4.1 Treatments unrelated to deficiency
o 4.2 Anti-aging agent
o 4.3 Athletic enhancement
o 4.4 Side-effects
* 5 History
* 6 References
* 7 External links
Gene locus
Main articles: Growth hormone 1 and Growth hormone 2
Genes for human growth hormone, known as growth hormone 1 (somatotropin) and growth hormone 2, are localized in the q22-24 region of chromosome 17 and are closely related to human chorionic somatomammotropin (also known as placental lactogen) genes. GH, human chorionic somatomammotropin, and prolactin belong to a group of homologous hormones with growth-promoting and lactogenic activity.
Structure
Mind map showing a Summary of Growth Hormone Physiology
The major isoform of the human growth hormone is a protein of 191 amino acids and a molecular weight of 22,124 daltons. The structure includes four helices necessary for functional interaction with the GH receptor. It appears that, in structure, GH is evolutionarily homologous to prolactin and chorionic somatomammotropin. Despite marked structural similarities between growth hormone from different species, only human and primate growth hormones have significant effects in humans.
Several molecular isoforms of GH exist in the pituitary gland and are released to blood. In particular, a ~ 20 kDa variant originated by an alternative splicing is present in a rather constant 1:9 ratio,[3] while recently an additional variant of ~ 23-24 kDa has also been reported in post-exercise states at higher proportions.[4] This variant has not been identified, but it has been suggested to coincide with a 22 kDa glycosilated variant of 23 kDa identified in the pituitary gland.[5] Furthermore, these variants circulate partially bound to a protein (growth hormone-binding protein, GHBP), which is the truncated part of the growth hormone receptor, and an acid-labile subunit (ALS).
Regulation
Peptides released by neurosecretory nuclei of the hypothalamus (Growth hormone-releasing hormone/somatocrinin and Growth hormone-inhibiting hormone/somatostatin) into the hypophyseal portal venous blood surrounding the pituitary are the major controllers of GH secretion by the somatotropes. However, although the balance of these stimulating and inhibiting peptides determines GH release, this balance is affected by many physiological stimulators (e.g., exercise, nutrition, sleep) and inhibitors of GH secretion (e.g., Free fatty acids)[6] Stimulators of HGH secretion include:
* peptide hormones
o Growth hormone-releasing hormone (GHRH) through binding to the growth hormone-releasing hormone receptor (GHRHR)[7]
o ghrelin through binding to growth hormone secretagogue receptors (GHSR)[8]
* sex hormones[9]
o increased androgen secretion during puberty (in males from testis and in females from adrenal cortex)
o estrogen
* clonidine and L-DOPA by stimulating GHRH release[10]
* hypoglycemia, arginine[11] and propranolol by inhibiting somatostatin release[10]
* deep sleep[12]
* fasting[13]
* vigorous exercise [14]
Inhibitors of GH secretion include:
* somatostatin from the periventricular nucleus [15]
* circulating concentrations of GH and IGF-1 (negative feedback on the pituitary and hypothalamus)[2]
* hyperglycemia[10]
* glucocorticoids[16]
* dihydrotestosterone
In addition to control by endogenous and stimulus processes, a number of foreign compounds (xenobiotics such as drugs and endocrine disruptors) are known to influence GH secretion and function.[17]
Secretion patterns
HGH is synthesized and secreted from the anterior pituitary gland in a pulsatile manner throughout the day; surges of secretion occur at 3- to 5-hour intervals.[2] The plasma concentration of GH during these peaks may range from 5 to even 45 ng/mL.[18] The largest and most predictable of these GH peaks occurs about an hour after onset of sleep.[19] Otherwise there is wide variation between days and individuals. Nearly fifty percent of HGH secretion occurs during the third and fourth REM sleep stages.[20] Between the peaks, basal GH levels are low, usually less than 5 ng/mL for most of the day and night.[19] Additional analysis of the pulsatile profile of GH described in all cases less than 1 ng/ml for basal levels while maximum peaks were situated around 10-20 ng/mL.[21][22]
A number of factors are known to affect HGH secretion, such as age, gender, diet, exercise, stress, and other hormones.[2] Young adolescents secrete HGH at the rate of about 700 μg/day, while healthy adults secrete HGH at the rate of about 400 μg/day.[23]
Functions of GH
Main pathways in endocrine regulation of growth.
Effects of growth hormone on the tissues of the body can generally be described as anabolic (building up). Like most other protein hormones, GH acts by interacting with a specific receptor on the surface of cells.
Increased height during childhood is the most widely known effect of GH. Height appears to be stimulated by at least two mechanisms:
1. Because polypeptide hormones are not fat-soluble, they cannot penetrate sarcolemma. Thus, GH exerts some of its effects by binding to receptors on target cells, where it activates the MAPK/ERK pathway.[24] Through this mechanism GH directly stimulates division and multiplication of chondrocytes of cartilage.
2. GH also stimulates, through the JAK-STAT signaling pathway,[24] the production of insulin-like growth factor 1 (IGF-1, formerly known as somatomedin C), a hormone homologous to proinsulin.[25] The liver is a major target organ of GH for this process and is the principal site of IGF-1 production. IGF-1 has growth-stimulating effects on a wide variety of tissues. Additional IGF-1 is generated within target tissues, making it what appears to be both an endocrine and an autocrine/paracrine hormone. IGF-1 also has stimulatory effects on osteoblast and chondrocyte activity to promote bone growth.
In addition to increasing height in children and adolescents, growth hormone has many other effects on the body:
* Increases calcium retention, and strengthens and increases the mineralization of bone
* Increases muscle mass through sarcomere hyperplasia
* Promotes lipolysis
* Increases protein synthesis
* Stimulates the growth of all internal organs excluding the brain
* Plays a role in fuel homeostasis
* Reduces liver uptake of glucose
* Promotes gluconeogenesis in the liver[26]
* Contributes to the maintenance and function of pancreatic islets
* Stimulates the immune system
Excesses
The most common disease of GH excess is a pituitary tumor composed of somatotroph cells of the anterior pituitary. These somatotroph adenomas are benign and grow slowly, gradually producing more and more GH. For years, the principal clinical problems are those of GH excess. Eventually, the adenoma may become large enough to cause headaches, impair vision by pressure on the optic nerves, or cause deficiency of other pituitary hormones by displacement.
Prolonged GH excess thickens the bones of the jaw, fingers and toes. Resulting heaviness of the jaw and increased size of digits is referred to as acromegaly. Accompanying problems can include sweating, pressure on nerves (e.g., carpal tunnel syndrome), muscle weakness, excess sex hormone-binding globulin (SHBG), insulin resistance or even a rare form of type 2 diabetes, and reduced sexual function.
GH-secreting tumors are typically recognized in the fifth decade of life. It is extremely rare for such a tumor to occur in childhood, but, when it does, the excessive GH can cause excessive growth, traditionally referred to as pituitary gigantism.
Surgical removal is the usual treatment for GH-producing tumors. In some circumstances, focused radiation or a GH antagonist such as pegvisomant may be employed to shrink the tumor or block function. Other drugs like octreotide (somatostatin agonist) and bromocriptine (dopamine agonist) can be used to block GH secretion because both somatostatin and dopamine negatively inhibit GHRH-mediated GH release from the anterior pituitary.
Deficiencies
Main article: Growth hormone deficiency
The effects of growth hormone deficiency vary depending on the age at which they occur. In children, growth failure and short stature are the major manifestations of GH deficiency, with common causes including genetic conditions and congenital malformations. It can also cause delayed sexual maturity. In adults, deficiency is rare,[27] with the most common cause a pituitary adenoma, and others including a continuation of a childhood problem, other structural lesions or trauma, and very rarely idiopathic GHD.
Adults with GHD present with non-specific problems including truncal obesity with a relative decrease in muscle mass and, in many instances, decreased energy and quality of life.[27]
Diagnosis of GH deficiency involves a multiple-step diagnostic process, usually culminating in GH stimulation tests to see if the patient's pituitary gland will release a pulse of GH when provoked by various stimuli.
Treatment with exogenous GH is indicated only in limited circumstances,[27] and needs regular monitoring due to the frequency and severity of side-effects. GH is used as replacement therapy in adults with GH deficiency of either childhood-onset (after completing growth phase) or adult-onset (usually as a result of an acquired pituitary tumor). In these patients, benefits have variably included reduced fat mass, increased lean mass, increased bone density, improved lipid profile, reduced cardiovascular risk factors, and improved psychosocial well-being.
Therapeutic use
Main article: Growth hormone treatment
Treatments unrelated to deficiency
GH can be used to treat conditions that produce short stature but are not related to deficiencies in GH. However, results are not as dramatic when compared to short stature that is solely attributable to deficiency of GH. Examples of other causes of shortness often treated with GH are Turner syndrome, chronic renal failure, Prader–Willi syndrome, intrauterine growth retardation, and severe idiopathic short stature. Higher ("pharmacologic") doses are required to produce significant acceleration of growth in these conditions, producing blood levels well above normal ("physiologic"). Despite the higher doses, side-effects during treatment are rare, and vary little according to the condition being treated.
GH treatment improves muscle strength and slightly reduces body fat in Prader-Willi syndrome, which are significant concerns beyond the need to increase height. GH is also useful in maintaining muscle mass in wasting due to AIDS. GH can also be used in patients with short bowel syndrome to lessen the requirement for intravenous total parenteral nutrition.
GH can also be used for conditions that do not cause short stature. Typically, growth hormone treatment for conditions unrelated to stature is controversial and experimental. GH has been used for remission of multiple sclerosis, to reverse the effects of aging in older adults (see below), to enhance weight loss in obesity, as well as fibromyalgia, heart failure, Crohn's disease and ulcerative colitis, burns and bodybuilding or athletic enhancement.
Anti-aging agent
Claims for GH as an anti-aging treatment date back to 1990 when the New England Journal of Medicine published a study wherein GH was used to treat 12 men over 60.[28] At the conclusion of the study, all the men showed statistically significant increases in lean body mass and bone mineral, while the control group did not. The authors of the study noted that these improvements were the opposite of the changes that would normally occur over a 10- to 20-year aging period. Despite the fact the authors at no time claimed that GH had reversed the aging process itself, their results were misinterpreted as indicating that GH is an effective anti-aging agent.[29][30][31] This has led to organizations such as the controversial American Academy of Anti-Aging Medicine promoting the use of this hormone as an "anti-aging agent".[32]
A Stanford University School of Medicine survey of clinical studies on the subject published in early 2007 showed that the application of GH on healthy elderly patients increased muscle by about 2 kg and decreased body fat by the same amount.[29] However, these were the only positive effects from taking GH. No other critical factors were affected, such as bone density, cholesterol levels, lipid measurements, maximal oxygen consumption, or any other factor that would indicate increased fitness.[29] Researchers also did not discover any gain in muscle strength, which led them to believe that GH merely let the body store more water in the muscles rather than increase muscle growth. This would explain the increase in lean body mass.
Athletic enhancement
Main article: HGH treatment for athletic enhancement
Athletes in many sports use human growth hormone to enhance their athletic performance. Some recent studies have not been able to support claims that human growth hormone can improve the athletic performance of professional male athletes.[33][34]
Side-effects
Main article: HGH controversies
There is theoretical concern that HGH treatment may increase the risks of diabetes, especially in those with other predispositions treated with higher doses. If used for training, growth at a young age (25 or less) can cause severe symptoms. One survey of adults that had been treated with replacement cadaver GH (which has not been used anywhere in the world since 1985) during childhood showed a mildly increased incidence of colon cancer and prostate cancer, but linkage with the GH treatment was not established.[35]
Regular application of extra GH may show several negative side-effects such as joint swelling, joint pain, carpal tunnel syndrome, and an increased risk of diabetes.[29] Other side effects can include less sleep needed after dosing. This is common initially and decreases in effect after habitual use of GH.
History
Main article: Growth hormone treatment#History
The identification, purification and later synthesis of growth hormone is associated with Choh Hao Li. Genentech pioneered the first use of recombinant human growth hormone for human therapy in 1981.
Prior to its production by recombinant DNA technology, growth hormone used to treat deficiencies was extracted from the pituitary glands of cadavers. Attempts to create a wholly synthetic HGH failed. Limited supplies of HGH resulted in the restriction of HGH therapy to the treatment of idiopathic short stature.[36] Furthermore, growth hormone from other primates was found to be inactive in humans.[37]
In 1985, unusual cases of Creutzfeldt-Jacob disease were found in individuals that had received cadaver-derived HGH ten to fifteen years previously. Based on the assumption that infectious prions causing the disease were transferred along with the cadaver-derived HGH, cadaver-derived HGH was removed from the market.[23]
In 1985, biosynthetic human growth hormone replaced pituitary-derived human growth hormone for therapeutic use in the U.S. and elsewhere.
As of 2005, recombinant growth hormones available in the United States (and their manufacturers) included Nutropin (Genentech), Humatrope (Lilly), Genotropin (Pfizer), Norditropin (Novo), and Saizen (Merck Serono). In 2006, the U.S. Food and Drug Administration (FDA) approved a version of rhGH called Omnitrope (Sandoz). A sustained-release form of growth hormone, Nutropin Depot (Genentech and Alkermes) was approved by the FDA in 1999, allowing for fewer injections (every 2 or 4 weeks instead of daily); however, the product was discontinued by Genentech/Alkermes in 2004 for financial reasons (Nutropin Depot required significantly more resources to produce than the rest of the Nutropin line[38]).
References
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2. ^ a b c d e Powers M (2005). "Performance-Enhancing Drugs". In Deidre Leaver-Dunn; Joel Houglum; Harrelson, Gary L.. Principles of Pharmacology for Athletic Trainers. Slack Incorporated. pp. 331–332. ISBN 1-55642-594-5.
3. ^ Leung KC, Howe C, Gui LY, Trout G, Veldhuis JD, Ho KK (October 2002). "Physiological and pharmacological regulation of 20-kDa growth hormone". Am. J. Physiol. Endocrinol. Metab. 283 (4): E836–43. doi:10.1152/ajpendo.00122.2002. PMID 12217902.
4. ^ Kohler M, Püschel K, Sakharov D, Tonevitskiy A, Schänzer W, Thevis M (November 2008). "Detection of recombinant growth hormone in human plasma by a 2-D PAGE method". Electrophoresis 29 (22): 4495–502. doi:10.1002/elps.200800221. PMID 19003817.
5. ^ Bustamante JJ, Gonzalez L, Carroll CA, Weintraub ST, Aguilar RM, Muñoz J, Martinez AO, Haro LS (July 2009). "O-Glycosylated 24 kDa human growth hormone has a mucin-like biantennary disialylated tetrasaccharide attached at Thr-60". Proteomics 9 (13): 3474–88. doi:10.1002/pmic.200800989. PMID 19579232.
6. ^ Bartholomew, Edwin F.; Martini, Frederic; Judi Lindsley Nath (2009). Fundamentals of anatomy & physiology. Upper Saddle River, NJ: Pearson Education Inc. pp. 616–617. ISBN 0-321-53910-9.
7. ^ Lin-Su K, Wajnrajch MP (December 2002). "Growth Hormone Releasing Hormone (GHRH) and the GHRH Receptor". Rev Endocr Metab Disord 3 (4): 313–23. doi:10.1023/A:1020949507265. PMID 12424433.
8. ^ Wren AM, Small CJ, Ward HL, Murphy KG, Dakin CL, Taheri S, Kennedy AR, Roberts GH, Morgan DG, Ghatei MA, Bloom SR (November 2000). "The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion". Endocrinology 141 (11): 4325–8. doi:10.1210/en.141.11.4325. PMID 11089570.
9. ^ Meinhardt UJ, Ho KK (October 2006). "Modulation of growth hormone action by sex steroids". Clin. Endocrinol. (Oxf) 65 (4): 413–22. doi:10.1111/j.1365-2265.2006.02676.x. PMID 16984231.
10. ^ a b c Low LC (1991). "Growth hormone-releasing hormone: clinical studies and therapeutic aspects". Neuroendocrinology 53 Suppl 1: 37–40. PMID 1901390.
11. ^ Alba-Roth J, Müller OA, Schopohl J, von Werder K (December 1988). "Arginine stimulates growth hormone secretion by suppressing endogenous somatostatin secretion". J. Clin. Endocrinol. Metab. 67 (6): 1186–9. doi:10.1126/science.2237411. PMID 2903866.
12. ^ Van Cauter E, Latta F, Nedeltcheva A, Spiegel K, Leproult R, Vandenbril C, Weiss R, Mockel J, Legros JJ, Copinschi G (June 2004). "Reciprocal interactions between the GH axis and sleep". Growth Horm. IGF Res. 14 Suppl A: S10–7. doi:10.1016/j.ghir.2004.03.006. PMID 15135771.
13. ^ Nørrelund H (April 2005). "The metabolic role of growth hormone in humans with particular reference to fasting". Growth Horm. IGF Res. 15 (2): 95–122. doi:10.1016/j.ghir.2005.02.005. PMID 15809014.
14. ^ Kanaley JA, Weltman JY, Veldhuis JD, Rogol AD, Hartman ML, Weltman A (November 1997). "Human growth hormone response to repeated bouts of aerobic exercise". J. Appl. Physiol. 83 (5): 1756–61. PMID 9375348. http://jap.physiology.org/cgi/content/full/83/5/1756.
15. ^ Guillemin R, Gerich JE (1976). "Somatostatin: physiological and clinical significance". Annu. Rev. Med. 27: 379–88. doi:10.1146/annurev.me.27.020176.002115. PMID 779605.
16. ^ Allen DB (September 1996). "Growth suppression by glucocorticoid therapy". Endocrinol. Metab. Clin. North Am. 25 (3): 699–717. doi:10.1016/S0889-8529(05)70348-0. PMID 8879994.
17. ^ Scarth JP (2006). "Modulation of the growth hormone-insulin-like growth factor (GH-IGF) axis by pharmaceutical, nutraceutical and environmental xenobiotics: an emerging role for xenobiotic-metabolizing enzymes and the transcription factors regulating their expression. A review". Xenobiotica 36 (2-3): 119–218. doi:10.1080/00498250600621627. PMID 16702112.
18. ^ Natelson BH, Holaday J, Meyerhoff J, Stokes PE (August 1975). "Temporal changes in growth hormone, cortisol, and glucose: relation to light onset and behavior". Am. J. Physiol. 229 (2): 409–15. PMID 808970. http://ajplegacy.physiology.org/cgi/content/abstract/229/2/409.
19. ^ a b Takahashi Y, Kipnis D, Daughaday W (1968). "Growth hormone secretion during sleep". J Clin Invest 47 (9): 2079–90. doi:10.1172/JCI105893. PMID 5675428.
20. ^ Mehta, Ameeta and Hindmarsh, Peter. 2002. The use of somatropin (recombinant growth hormone) in children of short stature. Pediatric Drugs. 4: 37-47.
21. ^ Nindl BC, Hymer WC, Deaver DR, Kraemer WJ (1 July 2001). "Growth hormone pulsatility profile characteristics following acute heavy resistance exercise". J. Appl. Physiol. 91 (1): 163–72. PMID 11408427. http://jap.physiology.org/cgi/content/abstract/91/1/163.
22. ^ Juul A, Jørgensen JO, Christiansen JS, Müller J, Skakkeboek NE (1995). "Metabolic effects of GH: a rationale for continued GH treatment of GH-deficient adults after cessation of linear growth". Horm. Res. 44 Suppl 3: 64–72. doi:10.1159/000184676. PMID 8719443.
23. ^ a b Gardner, David G., Shoback, Dolores (2007). Greenspan's Basic and Clinical Endocrinology (8th ed.). New York: McGraw-Hill Medical. pp. 193–201. ISBN 0-07-144011-9.
24. ^ a b Binder G, Wittekindt N, Ranke MB (February 2007). "Noonan Syndrome: Genetics and Responsiveness to Growth Hormone Therapy". Horm Res 67 (Supplement 1): 45–49. doi:10.1159/000097552. ISBN 9783805582551. http://books.google.com/?id=nQ9ilbixQEgC&pg=PA46&lpg=PA46&dq=gh+growth+hormone+ras&q=gh%20growth%20hormone%20ras.
25. ^ "Actions of Anterior Pituitary Hormones: Physiologic Actions of GH". Medical College of Georgia. 2007. http://www.lib.mcg.edu/edu/eshuphysio/program/section5/5ch2/s5ch2_19.htm. Retrieved 2008-01-16.
26. ^ King, MW (2006). "Structure and Function of Hormones: Growth Hormone". Indiana State University. http://web.indstate.edu/thcme/mwking/peptide-hormones.html#gh. Retrieved 2008-01-16.
27. ^ a b c Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Shalet SM, Vance ML; Endocrine Society's Clinical Guidelines Subcommittee, Stephens PA (May 2006). "Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society Clinical Practice Guideline". J. Clin. Endocrino. Metab. 91 (5): 1621–34. doi:10.1210/jc.2005-2227. PMID 16636129.
28. ^ Rudman D, Feller AG, Nagraj HS, Gergans GA, Lalitha PY, Goldberg AF, Schlenker RA, Cohn L, Rudman IW, Mattson DE (July 1990). "Effects of human growth hormone in men over 60 years old". N. Engl. J. Med. 323 (1): 1–6. doi:10.1056/NEJM199007053230101. PMID 2355952.
29. ^ a b c d Liu H, Bravata DM, Olkin I, Nayak S, Roberts B, Garber AM, Hoffman AR (January 2007). "Systematic review: the safety and efficacy of growth hormone in the healthy elderly". Ann. Intern. Med. 146 (2): 104–15. PMID 17227934.
30. ^ "No proof that growth hormone therapy makes you live longer, study finds". PhysOrg.com. 2007-01-16. http://www.physorg.com/news88140162.html. Retrieved 2009-03-16.
31. ^ Gordon, Mark L. M.D. Human Growth Hormone (HGH) as an Anti-Aging Agent
32. ^ Kuczynski, Alex (12 April, 1998). "Anti-Aging Potion or Poison?". New York Times. http://www.nytimes.com/1998/04/12/style/anti-aging-potion-or-poison.html.
33. ^ http://www.bloomberg.com/apps/news?pid=20601124&sid=awlswGxIiU5c&refer=home
34. ^ http://grg51.typepad.com/steroid_nation/2008/03/review-from-sta.html
35. ^ Swerdlow AJ, Higgins CD, Adlard P, Preece MA (July 2002). "Risk of cancer in patients treated with human pituitary growth hormone in the UK, 1959-85: a cohort study". Lancet 360 (9329): 273–7. doi:10.1016/S0140-6736(02)09519-3. PMID 12147369.
36. ^ Maybe, Nancy G (1984). "Direct expression of human growth in Escherichia coli with the lipoprotein promoter". In Arthur P. Bollon. Recombinant DNA products: insulin, interferon, and growth hormone. Boca Raton: CRC Press. ISBN 0-8493-5542-7.
37. ^ Hintz, Raymond L. (1984). "Biological actions in humans of recombinant DNA synthesized human growth hormone". In Arthur P. Bollon. Recombinant DNA products: insulin, interferon, and growth hormone. Boca Raton: CRC Press. ISBN 0-8493-5542-7.
38. ^ Genentech and Alkermes Announce Decision to Discontinue Commercialization of Nutropin Depot. http://findarticles.com/p/articles/mi_m0EIN/is_2004_June_1/ai_n6050768/
External links
* Magic Foundation, Support for adults and children affected with growth hormone deficiency.
* Central Precocious Puberty Treatment, SupprelinLA is a central precocious puberty treatment for children with growth hormone disorders.
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growth hormone
Dictionary: growth hormone
Home > Library > Literature & Language > Dictionary
n. (Abbr. GH)
1. A polypeptide hormone secreted by the anterior lobe of the pituitary gland that promotes growth of the body, especially by stimulating release of somatomedin, and that influences the metabolism of proteins, carbohydrates, and lipids. Also called human growth hormone, somatotropic hormone, Also called somatotropin.
2. Any of various natural or synthetic substances that regulate the growth of animals or plants, such as pituitary growth hormone in vertebrates and auxins in plants.
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Britannica Concise Encyclopedia:
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Peptide hormone secreted by the anterior lobe of the pituitary gland. It promotes growth of bone and other body tissues by stimulating protein synthesis and fat breakdown (for energy). Excessive production causes gigantism, acromegaly, or other malformations; deficient production results in dwarfism, dramatically relieved if GH is given before puberty. Genetic engineering techniques now permit large-scale production of adequate amounts of GH for that purpose.
For more information on growth hormone, visit Britannica.com.
World of the Body:
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Growth hormone also called somatotrophin, is secreted from the anterior part of the pituitary gland. It is a major product of the gland, which contains 5 mg of the hormone (about 10% of its dry weight). As the name implies, growth hormone is important in controlling linear growth and, together with the thyroid hormones and the sex hormones, is important in determining the final height and development of an individual. It also has a role in controlling metabolism of foodstuffs, so that lack of the hormone in children results in short stature with the whole body in proportion, whereas deficiency in the adult results in weakness and depression.
Growth stops when the epiphyses (ends) of the bones fuse to the main shaft between them. Oversecretion before this occurs results in gigantism, whereas oversecretion afterwards results in acromegaly, a condition characterized by coarsening of the facial features and enlargement of the hands and feet. Interest in dwarfism, gigantism, and acromegaly has spanned the centuries; literature, especially for children, is filled with stories about dwarfs and giants, while Old Testament writings have several descriptions of giants. A study of paintings can also reveal subjects with disturbances of growth hormone secretion. A portrait from about 1365 bc of Tutankhamun's father-in-law illustrates some of the chacterisitics of acromegaly, but it was not until the late eighteenth century that Saucerette, a French surgeon, described a subject with features suggestive of this condition. During the nineteenth century a number of reports appeared and the term ‘acromegaly’ was coined in 1886 by Pierre Marie. In the following year, Minkowski (who also performed some of the early experiments important in the discovery of insulin) noted that acromegaly was associated with a pituitary tumour. Such tumours are now known to be the cause of gigantism and acromegaly. Once this was established, surgical treatment of the condition began to be attempted in the 1890s. In 1912 Cushing, a famous American neurosurgeon who also made major contributions to endocrinology, pioneered the technique of operating on pituitary tumours via the nasal route.
The nasal approach to the pituitary is possible because the gland itself lies in the midline at the base of the brain. Part of the visual pathway, the ‘optic chiasma’, lies in front of the pituitary, so a spreading tumour may lead to visual defects. This could explain why Goliath of Gath failed to see the pebble launched by David.
Growth hormone is a large peptide of 191 amino acids and is relatively species-specific, so only primate growth hormone is effective in man. This meant that until 1985, when it became possible to synthesize it, treatment of short stature employed growth hormone extracted from human pituitaries. As with some preparations of human gonadotrophins previously used in fertility treatment, some of the preparations were contaminated, leading to 1 in 1000 patients developing Creuzfeld Jacob disease, resulting in dementia and death. Currently biosynthetic growth hormone is employed.
Growth hormone is always detectable in the plasma of healthy individuals throughout life; it is not secreted continuously over the 24 hours, but in bursts. The most marked increase follows the onset of sleep, so there may be a basis for the old wives' tale that you will not grow if you do not get a good night's sleep. The hormone is present in the fetus, but does not appear to be necessary for growth until soon after birth. Its release is increased in puberty, at an earlier stage in girls than in boys. Secretion of growth hormone is controlled by the hypothalamus, a region of the brain which is important in regulating many functions including a major role in the response to stress: growth hormone is released in response to a number of stresses such as exercise, anaesthesia, and surgery. Prolonged stress may however suppress growth hormone release, so that children with marked emotional deprivation can show secondary growth failure. One such case is said to be Sir James Barrie who was short of stature and may have had some affinity with his creation, Peter Pan.
Release is stimulated in response to a rapid fall in blood glucose, which can be produced by an injection of insulin in a clinical test for growth hormone secretion. The hypothalamus controls growth hormone secretion by means of its own secretion of two peptides; somatostatin, which inhibits secretion, and growth hormone releasing hormone, which is stimulatory; these hormones reach the nearby anterior pituitary through local blood vessels.
Growth hormone stimulates the growth of the long bones, not directly but through the action of somatomedins, which are insulin-like growth factors made in the liver, and which also inhibit release of the hormone. It has a direct effect on metabolic processes throughout the body, supporting growth through enhanced formation of protein and nucleic acids (anabolic action) and of other constituents of lean body mass. By contrast its effects promote breakdown of carbohydrate and fat, with the energy released supporting growth. Because of the anabolic effects and because detection is difficult, growth hormone has been used by athletes to improve performance, although studies have shown it to be of little value.
— Mary L. Forsling
See also development and growth; hypothalamus; peptides; pituitary gland.
Food and Nutrition:
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Somatotrophin, a peptide hormone secreted by the pituitary gland that promotes growth of bone and soft tissues. It also reduces the utilization of glucose, and increases breakdown of fats to fatty acids; because of this it has been promoted as an aid to weight reduction, with little evidence of efficacy. Sometimes abbreviated to HGH (human growth hormone); growth hormone from other mammals differs in structure and activity. See also bovine somatotrophin.
Food and Fitness:
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Body growth is greatly influenced by a protein hormone secreted by the anterior pituitary gland. This growth hormone (also known as human growth hormone, GH, or hGH) can now be manufactured by a genetic engineering technique called recombinant DNA technology. The growth hormone gene is cut out of human DNA and spliced into bacterial DNA. The bacteria are fermented and secrete growth hormone (sometimes called recombinant GH) identical to that produced in human cells. Growth hormone is used clinically to treat people with stunted growth. Until recombinant GH became available, the only source of growth hormone was human pituitary glands. This source is extremely expensive and was used almost exclusively for treating people of severely restricted growth (those with severe undersecretion of GH). Growth hormone from pituitary glands was also associated with a number of cases of Creutzfeldt-Jakob disease. The production of recombinant GH has meant treatment is safer and easier to obtain, so that those with less severe growth restriction can be treated. Unfortunately, its wider availability has been abused. It is used by body-builders and participants in power sports to accelerate muscle growth. Other sports people use it to accelerate the healing of musculoskeletal injuries. People concerned about their looks use it to decrease body fat. However, although growth hormone may increase the muscle bulk of inactive individuals, it probably has no significant effect on the muscle growth of young individuals who are engaged in an intense weight-training programme. Intense exercise combined with an adequate diet is sufficient to stimulate maximum protein synthesis in most individuals. In addition, excessive use of growth hormone may cause gigantism in prepubertal individuals and acromegaly (increase in size of the bones in hands, feet, and face) in adults. Other potential adverse effects include muscular weakness, arthritis, impotence, diabetes, and heart disorders. Use of growth hormone supplements is banned by the International Olympic Committee and some other sports federations, but it is very difficult to detect it.
Dental Dictionary:
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n
(GH) a single-chain peptide secreted by the anterior pituitary gland in response to growth hormone releasing factor (GHRF) from the hypothalamus. Growth hormone promotes protein synthesis in all cells, increased fat mobilization and use of fatty acids for energy, and decreased use of carbohydrates.
Nutrition Encyclopedia:
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Human growth hormone (HGH) stimulates the growth of bones and affects the metabolism of carbohydrate, protein, and fat. It is secreted by the pituitary gland, which is located in the brain. Whereas HGH is produced in the body, genetic engineering has resulted in the development of recombinant human growth hormone (rHGH), which is used to treat stunted growth in children. Bovine somatotropin (BST) is a naturally occurring protein hormone in cows that increases milk production when administered as a supplement. BST is not biologically active in humans and is broken down into inactive amino acids and peptides when consumed. Therefore, milk from cows treated with BST is believed to be as safe and nutritious as milk from untreated cows.
Supplemental HGH is used by athletes, particularly body builders and power lifters, to increase muscle mass and decrease body fat. Individuals who are HGH-deficient and take supplemental HGH will see an increase in muscle mass and decreased body fat, whereas those with normal HGH levels will see an increase in lean body mass from an increase in the size of heart, liver, and kidneys, and from fluid retention, but there will be no increase in muscle mass. Excessive use can cause acromegaly (an increase in the size of the bones of the hand, feet, and jaw), as well as muscle weakness, arthritis, impotence, and diabetes. Since HGH increases the size of the liver, kidneys, and heart, its use can predispose the individual to chronic diseases. HGH is classified as an anabolic hormone, and its ability to increase muscle and decrease fat confers an unfair athletic advantage on the user. The use of HGH is thus banned by the International Olympic Committee (IOC), the National Collegiate Athletic Association (NCAA), and many professional sporting organizations.
See also Ergogenic acids; Sports nutrition.
Bibliography
Rosenbloom, Christine, ed. (2000). Sports Nutrition: A Guide for the Professional Working with Active People, 3rd edition. Chicago: American Dietetic Association.
Williams, M. (1998). The Ergogenics Edge. Champaign, IL: Human Kinetics.
Columbia Encyclopedia:
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growth hormone or somatotropin (sōmăt'ətrō'pən), glycoprotein hormone released by the anterior pituitary gland that is necessary for normal skeletal growth in humans (see protein). Evidence suggests that the secretion of human growth hormone (HGH) is regulated by the release of certain peptides by the hypothalamus of the brain. One such substance, called somatostatin, has been shown to inhibit the secretion of HGH. HGH is known to act upon many aspects of cellular metabolism, but its most obvious effect is the stimulation of the growth of cartilage and bone in children.
See also auxins (plant growth hormones).
Role in Dwarfism and Gigantism
A deficiency of growth hormone secretion before puberty (by the end of which the synthesis of new bone tissue is complete) results in pituitary dwarfism. Pituitary dwarfs, who can be as little as 3 to 4 ft (91-122 cm) tall, are generally well proportioned except for the head, which may be relatively large when compared to the body (this relationship of head to body is similar to that of normal children). Unlike cretins, whose dwarfism is caused by a deficiency of thyroxine, pituitary dwarfs are not mentally retarded; they are often sexually immature. They can be treated by injections of synthetic growth hormone, either somatrem or somatropin, which are produced by genetically engineered bacteria.
An excess of growth hormone in children results in gigantism; these children grow to be over 7 ft (213 cm) in height and have disproportionately long limbs. Excess growth hormone produced after puberty has little effect on the growth of the skeleton, but it results in a disease affecting terminal skeletal structures known as acromegaly.
Other Medical Uses
HGH has been used with some success to combat the weight loss and general wasting characteristic of AIDS and cancer. It is used illegally by bodybuilders and athletes to increase muscle mass. Controversy surrounds its use in normal children who simply want to be taller. In addition, a 1990 medical study that reported the reversal of many of the physiological effects of aging with regular injections of HGH has created a lucrative black market for it and has prompted funding of further trials. There has been no conclusive evidence, however, to support the use of HGH as an anti-aging treatment, and it can cause serious side effects, including diabetes, in older adults.
Veterinary Dictionary:
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Growth hormone.
Wikipedia:
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"HGH" redirects here. For other uses, see HGH (disambiguation).
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Growth hormone 1
Somatotropine.GIF
Growth hormone
Identifiers
Symbol GH1
Entrez 2688
HUGO 4261
OMIM 139250
RefSeq NM_022562
UniProt P01241
Other data
Locus Chr. 17 q22-q24
Growth hormone 2
Identifiers
Symbol GH2
Entrez 2689
HUGO 4262
OMIM 139240
RefSeq NM_002059
UniProt P01242
Other data
Locus Chr. 17 q22-q24
Growth hormone (GH) is a protein-based peptide hormone. It stimulates growth, cell reproduction and regeneration in humans and other animals. Growth hormone is a 191-amino acid, single-chain polypeptide that is synthesized, stored, and secreted by the somatotroph cells within the lateral wings of the anterior pituitary gland. Somatotropin refers to the growth hormone 1 produced naturally in animals, whereas the term somatropin refers to growth hormone produced by recombinant DNA technology,[1] and is abbreviated "HGH" in humans.
Growth hormone is used in medicine to treat children's growth disorders and adult growth hormone deficiency. In recent years, growth hormone replacement therapies have become popular in the battle against ageing and obesity. Reported effects on GH-deficient patients (but not on healthy people) include decreased body fat, increased muscle mass, increased bone density, increased energy levels, improved skin tone and texture, increased sexual function, and improved immune system function. At this time, hGH is still considered a very complex hormone, and many of its functions are still unknown.[2]
In its role as an anabolic agent, HGH has been used by competitors in sports since the 1970s, and it has been banned by the IOC and NCAA. Traditional urine analysis could not detect doping with HGH, so the ban was unenforceable until the early 2000s when blood tests that could distinguish between natural and artificial hGH were starting to be developed. Blood tests conducted by WADA at the 2004 Olympic Games in Athens, Greece primarily targeted HGH.[2]
Contents [hide]
* 1 Gene locus
* 2 Structure
o 2.1 Regulation
o 2.2 Secretion patterns
* 3 Functions of GH
o 3.1 Excesses
o 3.2 Deficiencies
* 4 Therapeutic use
o 4.1 Treatments unrelated to deficiency
o 4.2 Anti-aging agent
o 4.3 Athletic enhancement
o 4.4 Side-effects
* 5 History
* 6 References
* 7 External links
Gene locus
Main articles: Growth hormone 1 and Growth hormone 2
Genes for human growth hormone, known as growth hormone 1 (somatotropin) and growth hormone 2, are localized in the q22-24 region of chromosome 17 and are closely related to human chorionic somatomammotropin (also known as placental lactogen) genes. GH, human chorionic somatomammotropin, and prolactin belong to a group of homologous hormones with growth-promoting and lactogenic activity.
Structure
Mind map showing a Summary of Growth Hormone Physiology
The major isoform of the human growth hormone is a protein of 191 amino acids and a molecular weight of 22,124 daltons. The structure includes four helices necessary for functional interaction with the GH receptor. It appears that, in structure, GH is evolutionarily homologous to prolactin and chorionic somatomammotropin. Despite marked structural similarities between growth hormone from different species, only human and primate growth hormones have significant effects in humans.
Several molecular isoforms of GH exist in the pituitary gland and are released to blood. In particular, a ~ 20 kDa variant originated by an alternative splicing is present in a rather constant 1:9 ratio,[3] while recently an additional variant of ~ 23-24 kDa has also been reported in post-exercise states at higher proportions.[4] This variant has not been identified, but it has been suggested to coincide with a 22 kDa glycosilated variant of 23 kDa identified in the pituitary gland.[5] Furthermore, these variants circulate partially bound to a protein (growth hormone-binding protein, GHBP), which is the truncated part of the growth hormone receptor, and an acid-labile subunit (ALS).
Regulation
Peptides released by neurosecretory nuclei of the hypothalamus (Growth hormone-releasing hormone/somatocrinin and Growth hormone-inhibiting hormone/somatostatin) into the hypophyseal portal venous blood surrounding the pituitary are the major controllers of GH secretion by the somatotropes. However, although the balance of these stimulating and inhibiting peptides determines GH release, this balance is affected by many physiological stimulators (e.g., exercise, nutrition, sleep) and inhibitors of GH secretion (e.g., Free fatty acids)[6] Stimulators of HGH secretion include:
* peptide hormones
o Growth hormone-releasing hormone (GHRH) through binding to the growth hormone-releasing hormone receptor (GHRHR)[7]
o ghrelin through binding to growth hormone secretagogue receptors (GHSR)[8]
* sex hormones[9]
o increased androgen secretion during puberty (in males from testis and in females from adrenal cortex)
o estrogen
* clonidine and L-DOPA by stimulating GHRH release[10]
* hypoglycemia, arginine[11] and propranolol by inhibiting somatostatin release[10]
* deep sleep[12]
* fasting[13]
* vigorous exercise [14]
Inhibitors of GH secretion include:
* somatostatin from the periventricular nucleus [15]
* circulating concentrations of GH and IGF-1 (negative feedback on the pituitary and hypothalamus)[2]
* hyperglycemia[10]
* glucocorticoids[16]
* dihydrotestosterone
In addition to control by endogenous and stimulus processes, a number of foreign compounds (xenobiotics such as drugs and endocrine disruptors) are known to influence GH secretion and function.[17]
Secretion patterns
HGH is synthesized and secreted from the anterior pituitary gland in a pulsatile manner throughout the day; surges of secretion occur at 3- to 5-hour intervals.[2] The plasma concentration of GH during these peaks may range from 5 to even 45 ng/mL.[18] The largest and most predictable of these GH peaks occurs about an hour after onset of sleep.[19] Otherwise there is wide variation between days and individuals. Nearly fifty percent of HGH secretion occurs during the third and fourth REM sleep stages.[20] Between the peaks, basal GH levels are low, usually less than 5 ng/mL for most of the day and night.[19] Additional analysis of the pulsatile profile of GH described in all cases less than 1 ng/ml for basal levels while maximum peaks were situated around 10-20 ng/mL.[21][22]
A number of factors are known to affect HGH secretion, such as age, gender, diet, exercise, stress, and other hormones.[2] Young adolescents secrete HGH at the rate of about 700 μg/day, while healthy adults secrete HGH at the rate of about 400 μg/day.[23]
Functions of GH
Main pathways in endocrine regulation of growth.
Effects of growth hormone on the tissues of the body can generally be described as anabolic (building up). Like most other protein hormones, GH acts by interacting with a specific receptor on the surface of cells.
Increased height during childhood is the most widely known effect of GH. Height appears to be stimulated by at least two mechanisms:
1. Because polypeptide hormones are not fat-soluble, they cannot penetrate sarcolemma. Thus, GH exerts some of its effects by binding to receptors on target cells, where it activates the MAPK/ERK pathway.[24] Through this mechanism GH directly stimulates division and multiplication of chondrocytes of cartilage.
2. GH also stimulates, through the JAK-STAT signaling pathway,[24] the production of insulin-like growth factor 1 (IGF-1, formerly known as somatomedin C), a hormone homologous to proinsulin.[25] The liver is a major target organ of GH for this process and is the principal site of IGF-1 production. IGF-1 has growth-stimulating effects on a wide variety of tissues. Additional IGF-1 is generated within target tissues, making it what appears to be both an endocrine and an autocrine/paracrine hormone. IGF-1 also has stimulatory effects on osteoblast and chondrocyte activity to promote bone growth.
In addition to increasing height in children and adolescents, growth hormone has many other effects on the body:
* Increases calcium retention, and strengthens and increases the mineralization of bone
* Increases muscle mass through sarcomere hyperplasia
* Promotes lipolysis
* Increases protein synthesis
* Stimulates the growth of all internal organs excluding the brain
* Plays a role in fuel homeostasis
* Reduces liver uptake of glucose
* Promotes gluconeogenesis in the liver[26]
* Contributes to the maintenance and function of pancreatic islets
* Stimulates the immune system
Excesses
The most common disease of GH excess is a pituitary tumor composed of somatotroph cells of the anterior pituitary. These somatotroph adenomas are benign and grow slowly, gradually producing more and more GH. For years, the principal clinical problems are those of GH excess. Eventually, the adenoma may become large enough to cause headaches, impair vision by pressure on the optic nerves, or cause deficiency of other pituitary hormones by displacement.
Prolonged GH excess thickens the bones of the jaw, fingers and toes. Resulting heaviness of the jaw and increased size of digits is referred to as acromegaly. Accompanying problems can include sweating, pressure on nerves (e.g., carpal tunnel syndrome), muscle weakness, excess sex hormone-binding globulin (SHBG), insulin resistance or even a rare form of type 2 diabetes, and reduced sexual function.
GH-secreting tumors are typically recognized in the fifth decade of life. It is extremely rare for such a tumor to occur in childhood, but, when it does, the excessive GH can cause excessive growth, traditionally referred to as pituitary gigantism.
Surgical removal is the usual treatment for GH-producing tumors. In some circumstances, focused radiation or a GH antagonist such as pegvisomant may be employed to shrink the tumor or block function. Other drugs like octreotide (somatostatin agonist) and bromocriptine (dopamine agonist) can be used to block GH secretion because both somatostatin and dopamine negatively inhibit GHRH-mediated GH release from the anterior pituitary.
Deficiencies
Main article: Growth hormone deficiency
The effects of growth hormone deficiency vary depending on the age at which they occur. In children, growth failure and short stature are the major manifestations of GH deficiency, with common causes including genetic conditions and congenital malformations. It can also cause delayed sexual maturity. In adults, deficiency is rare,[27] with the most common cause a pituitary adenoma, and others including a continuation of a childhood problem, other structural lesions or trauma, and very rarely idiopathic GHD.
Adults with GHD present with non-specific problems including truncal obesity with a relative decrease in muscle mass and, in many instances, decreased energy and quality of life.[27]
Diagnosis of GH deficiency involves a multiple-step diagnostic process, usually culminating in GH stimulation tests to see if the patient's pituitary gland will release a pulse of GH when provoked by various stimuli.
Treatment with exogenous GH is indicated only in limited circumstances,[27] and needs regular monitoring due to the frequency and severity of side-effects. GH is used as replacement therapy in adults with GH deficiency of either childhood-onset (after completing growth phase) or adult-onset (usually as a result of an acquired pituitary tumor). In these patients, benefits have variably included reduced fat mass, increased lean mass, increased bone density, improved lipid profile, reduced cardiovascular risk factors, and improved psychosocial well-being.
Therapeutic use
Main article: Growth hormone treatment
Treatments unrelated to deficiency
GH can be used to treat conditions that produce short stature but are not related to deficiencies in GH. However, results are not as dramatic when compared to short stature that is solely attributable to deficiency of GH. Examples of other causes of shortness often treated with GH are Turner syndrome, chronic renal failure, Prader–Willi syndrome, intrauterine growth retardation, and severe idiopathic short stature. Higher ("pharmacologic") doses are required to produce significant acceleration of growth in these conditions, producing blood levels well above normal ("physiologic"). Despite the higher doses, side-effects during treatment are rare, and vary little according to the condition being treated.
GH treatment improves muscle strength and slightly reduces body fat in Prader-Willi syndrome, which are significant concerns beyond the need to increase height. GH is also useful in maintaining muscle mass in wasting due to AIDS. GH can also be used in patients with short bowel syndrome to lessen the requirement for intravenous total parenteral nutrition.
GH can also be used for conditions that do not cause short stature. Typically, growth hormone treatment for conditions unrelated to stature is controversial and experimental. GH has been used for remission of multiple sclerosis, to reverse the effects of aging in older adults (see below), to enhance weight loss in obesity, as well as fibromyalgia, heart failure, Crohn's disease and ulcerative colitis, burns and bodybuilding or athletic enhancement.
Anti-aging agent
Claims for GH as an anti-aging treatment date back to 1990 when the New England Journal of Medicine published a study wherein GH was used to treat 12 men over 60.[28] At the conclusion of the study, all the men showed statistically significant increases in lean body mass and bone mineral, while the control group did not. The authors of the study noted that these improvements were the opposite of the changes that would normally occur over a 10- to 20-year aging period. Despite the fact the authors at no time claimed that GH had reversed the aging process itself, their results were misinterpreted as indicating that GH is an effective anti-aging agent.[29][30][31] This has led to organizations such as the controversial American Academy of Anti-Aging Medicine promoting the use of this hormone as an "anti-aging agent".[32]
A Stanford University School of Medicine survey of clinical studies on the subject published in early 2007 showed that the application of GH on healthy elderly patients increased muscle by about 2 kg and decreased body fat by the same amount.[29] However, these were the only positive effects from taking GH. No other critical factors were affected, such as bone density, cholesterol levels, lipid measurements, maximal oxygen consumption, or any other factor that would indicate increased fitness.[29] Researchers also did not discover any gain in muscle strength, which led them to believe that GH merely let the body store more water in the muscles rather than increase muscle growth. This would explain the increase in lean body mass.
Athletic enhancement
Main article: HGH treatment for athletic enhancement
Athletes in many sports use human growth hormone to enhance their athletic performance. Some recent studies have not been able to support claims that human growth hormone can improve the athletic performance of professional male athletes.[33][34]
Side-effects
Main article: HGH controversies
There is theoretical concern that HGH treatment may increase the risks of diabetes, especially in those with other predispositions treated with higher doses. If used for training, growth at a young age (25 or less) can cause severe symptoms. One survey of adults that had been treated with replacement cadaver GH (which has not been used anywhere in the world since 1985) during childhood showed a mildly increased incidence of colon cancer and prostate cancer, but linkage with the GH treatment was not established.[35]
Regular application of extra GH may show several negative side-effects such as joint swelling, joint pain, carpal tunnel syndrome, and an increased risk of diabetes.[29] Other side effects can include less sleep needed after dosing. This is common initially and decreases in effect after habitual use of GH.
History
Main article: Growth hormone treatment#History
The identification, purification and later synthesis of growth hormone is associated with Choh Hao Li. Genentech pioneered the first use of recombinant human growth hormone for human therapy in 1981.
Prior to its production by recombinant DNA technology, growth hormone used to treat deficiencies was extracted from the pituitary glands of cadavers. Attempts to create a wholly synthetic HGH failed. Limited supplies of HGH resulted in the restriction of HGH therapy to the treatment of idiopathic short stature.[36] Furthermore, growth hormone from other primates was found to be inactive in humans.[37]
In 1985, unusual cases of Creutzfeldt-Jacob disease were found in individuals that had received cadaver-derived HGH ten to fifteen years previously. Based on the assumption that infectious prions causing the disease were transferred along with the cadaver-derived HGH, cadaver-derived HGH was removed from the market.[23]
In 1985, biosynthetic human growth hormone replaced pituitary-derived human growth hormone for therapeutic use in the U.S. and elsewhere.
As of 2005, recombinant growth hormones available in the United States (and their manufacturers) included Nutropin (Genentech), Humatrope (Lilly), Genotropin (Pfizer), Norditropin (Novo), and Saizen (Merck Serono). In 2006, the U.S. Food and Drug Administration (FDA) approved a version of rhGH called Omnitrope (Sandoz). A sustained-release form of growth hormone, Nutropin Depot (Genentech and Alkermes) was approved by the FDA in 1999, allowing for fewer injections (every 2 or 4 weeks instead of daily); however, the product was discontinued by Genentech/Alkermes in 2004 for financial reasons (Nutropin Depot required significantly more resources to produce than the rest of the Nutropin line[38]).
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17. ^ Scarth JP (2006). "Modulation of the growth hormone-insulin-like growth factor (GH-IGF) axis by pharmaceutical, nutraceutical and environmental xenobiotics: an emerging role for xenobiotic-metabolizing enzymes and the transcription factors regulating their expression. A review". Xenobiotica 36 (2-3): 119–218. doi:10.1080/00498250600621627. PMID 16702112.
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23. ^ a b Gardner, David G., Shoback, Dolores (2007). Greenspan's Basic and Clinical Endocrinology (8th ed.). New York: McGraw-Hill Medical. pp. 193–201. ISBN 0-07-144011-9.
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25. ^ "Actions of Anterior Pituitary Hormones: Physiologic Actions of GH". Medical College of Georgia. 2007. http://www.lib.mcg.edu/edu/eshuphysio/program/section5/5ch2/s5ch2_19.htm. Retrieved 2008-01-16.
26. ^ King, MW (2006). "Structure and Function of Hormones: Growth Hormone". Indiana State University. http://web.indstate.edu/thcme/mwking/peptide-hormones.html#gh. Retrieved 2008-01-16.
27. ^ a b c Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Shalet SM, Vance ML; Endocrine Society's Clinical Guidelines Subcommittee, Stephens PA (May 2006). "Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society Clinical Practice Guideline". J. Clin. Endocrino. Metab. 91 (5): 1621–34. doi:10.1210/jc.2005-2227. PMID 16636129.
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36. ^ Maybe, Nancy G (1984). "Direct expression of human growth in Escherichia coli with the lipoprotein promoter". In Arthur P. Bollon. Recombinant DNA products: insulin, interferon, and growth hormone. Boca Raton: CRC Press. ISBN 0-8493-5542-7.
37. ^ Hintz, Raymond L. (1984). "Biological actions in humans of recombinant DNA synthesized human growth hormone". In Arthur P. Bollon. Recombinant DNA products: insulin, interferon, and growth hormone. Boca Raton: CRC Press. ISBN 0-8493-5542-7.
38. ^ Genentech and Alkermes Announce Decision to Discontinue Commercialization of Nutropin Depot. http://findarticles.com/p/articles/mi_m0EIN/is_2004_June_1/ai_n6050768/
External links
* Magic Foundation, Support for adults and children affected with growth hormone deficiency.
* Central Precocious Puberty Treatment, SupprelinLA is a central precocious puberty treatment for children with growth hormone disorders.
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