Physiologie

Demling, L

doi:10.1007/978-3-642-65881-5_2

Cited by 4 publications

(3 citation statements)

References 304 publications

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“…Ebenfalls inkonsistent sind die wenigen Studien zur thrombozytären 5-HT-Aufnahme und zum Serotonin-Gehalt in Thrombozyten suizidaler Patienten [47,52]. In einer prospektiven Studie [53] waren erhöhte thrombozytäre 5-HT-Konzentrationen prädiktiv für eine weitere Suizidgefahrdung im Sinne eines "trait"-Markers.…”

Section: Thrombozytäre Parameterunclassified

Neurobiologische Korrelate suizidalen Verhaltens

Brunner

Bronisch

1999

Fortschr Neurol Psychiatr

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Studies in postmortem brain tissue from suicide victims show a presynaptic serotonergic deficit resulting in compensatory upregulation of postsynaptic 5-HT2 receptors in the prefrontal cortex. Reduced levels of cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid, the major serotonin metabolite, are associated with violent suicide attempts independent of psychiatric diagnosis and predict future suicide attempts and suicide completion, consistent with the notion of a biochemical trait. Neuroendocrine challenge tests, platelet studies and a polymorphism in the gene for tryptophan hydroxylase, the rate-limiting enzyme in the biosynthesis of serotonin, suggest that serotonergic activity may be reduced. This serotonergic abnormality might be related to the vulnerability or diathesis for suicidal behaviour by predisposing individuals to impulsive and autoaggressive behaviour. The hypothesis of hyperactivity of the hypothalamic pituitary adrenal axis (HPA) is supported by the postmortem findings of increased CSF corticotropin releasing hormone (CRH) concentrations and reduced CRH receptor binding sites in the frontal cortex of suicide victims (interpreted as downregulation following CRH hypersecretion) and dexamethasone nonsuppression in suicide attempters. Animal studies and in vitro experiments indicate that the HPA system modulates serotonergic activity. It is hypothesized that the serotonergic alterations potentially result from dysregulation of the HPA system. Data from epidemiological and clinical studies demonstrate that low levels of cholesterol are associated with increased suicide risk. In neuronal membranes cholesterol modulates presynaptic and postsynaptic serotonergic neurotransmission. In monkeys dietary cholesterol lowering inhibits central serotonergic activity and predisposes the animals to impulsive and aggressive behaviour. It is speculated that dysregulation of the HPA system and disordered cholesterol metabolism could enhance the serotonergic deficit, thus contributing to a neurobiological vulnerability or diathesis for impulsive and autoaggressive behaviour.

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Section: Thrombozytäre Parameterunclassified

Neurobiologische Korrelate suizidalen Verhaltens

Brunner

Bronisch

1999

Fortschr Neurol Psychiatr

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“…We reported recently that alteration of the GABAergic system by sodium valproate had no significant effect on pulsatile LH secretion by normal women during the late follicular phase (22) and mid-late luteal phase (23). However, the findings in rats that the rise in serum LH concentration following ovariectomy is associated with a fall in hypothalamic GABA levels, and that the fall in serum LH concentration following administration of estradiol is associated with an increase in hypothalamic GABA levels (7,24), suggest that GABAergic regulation of LH secretion may depend on steroid levels (25,26). If so, the absence of any significant change in LH secretion following valproate administration in our study of normal women may have been due to the high estradiol and progesterone levels of our subjects, which may have ensured that their basal GABA levels were already high enough to produce the maximum possible effect of GABA on LH secretion (27).…”

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confidence: 93%

Effects of valproate-induced alteration of the GABAergic system on pulsatile luteinizing hormone secretion in ovariectomized women

Lado-Abeal¹,

Liz²,

Rey

et al. 1996

European Journal of Endocrinology

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It is well established that valproate increases hypothalamic concentrations of gamma-aminobutyric acid (GABA). Although little research has been done on the role of GABA in the control of pulsatile luteinizing hormone (LH) secretion in humans, our group recently found that administration of valproate had no significant effect on pulsatile LH secretion in late follicular and mid-late luteal phase normal women. However, the results of several studies of rats suggest that GABAergic regulation of LH secretion may depend on steroid levels. The objective of this work was to determine whether regular administration of sodium valproate inhibits pulsatile LH secretion in ovariectomized women. Twelve women who had undergone ovariectomy for causes other than malignant tumors were each studied in two 8 h sessions, in each of which blood samples were taken every 5 min. The first session was the control; for the second. 400 mg of sodium valproate was administered every 8 h during the seven preceding days and at 08.00 h and 14.00 h on the day of the study session. Serum valproate was determined by repolarization fluorescence spectrophotometry, and LH, estradiol and progesterone by radioimmunoassay. The serum LH series were subjected to a deconvolution procedure to reconstruct the pattern of pituitary LH secretion. Luteinizing hormone pulses were identified by the authors' non-parametric method. Control and post-valproate results were compared with regard to number of pulses, pulse duration, the quantity of LH secreted in each pulse, interpulse interval and mean serum LH level. There was no statistically significant difference between control and post-valproate results for any of the variables considered. It is concluded that sustained serum valproate levels do not alter pulsatile secretion of LH in ovariectomized women. This implies that, in humans, GABA is probably not a decisive factor in the regulation of the GnRH pulse generator.

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“…Zazwyczaj ma to miejsce w około trzeciej dobie po urazie. W następstwie procesu zapalnego dochodzi do nasilenia niewydolności oddechowej [9][10][11][12]. Zmiany powstałe w układzie oddechowym mogą mieć charakter przemijający, jednak często prowadzą do rozwoju ARDS, który charakteryzuje się wysoką śmiertelnością [4,6].…”

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Oparzenia dróg oddechowych

Wróblewski¹,

Knefel²,

Trzaska³

et al. 2011

Advances in Respiratory Medicine

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Oparzenia inhalacyjne są głębokimi urazami obarczonymi znaczną śmiertelnością, które w istotny sposób pogarszają rokowanie chorych z ciężkimi oparzeniami ciała. Zmiany zachodzące pod wpływem urazu inhalacyjnego obejmują: obrzęk i martwicę błony śluzowej oskrzeli, zwiększenie przepływu krwi przez naczynia płucne i wzrost ich przepuszczalności, gromadzenie się w świetle oskrzeli wałeczków zbudowanych ze śluzu, obumarłych komórek, włóknika i neutrofili oraz uogólnioną reakcję zapalną mediowaną przez cytokiny. W wyniku opisanych procesów dochodzi do zaburzeń wymiany gazowej w płucach i w konsekwencji do niedotlenienia tkanek. Wprowadzenie standaryzowanych procedur diagnostyki endoskopowej u chorych z podejrzeniem oparzenia dróg oddechowych pozwoliło na szybkie rozpoznanie tego urazu i wdrożenie specjalistycznego leczenia, skutkującego zmniejszeniem liczby zgonów z powodu oparzeń. Stosowane metody terapeutyczne nie zawsze są skuteczne, a przy tym obarczone powikłaniami wynikającymi z instrumentacji dróg oddechowych. Istnieje więc konieczność stałej modyfikacji postępowania i poszukiwania nowych metod leczenia. Obserwowane korzystne efekty wczesnych zabiegów tlenoterapii hiperbarycznej dają nadzieję na szybkie wprowadzenie tej metody do standardów leczenia oparzeń inhalacyjnych.

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Physiologie

Cited by 4 publications

References 304 publications

Neurobiologische Korrelate suizidalen Verhaltens

Neurobiologische Korrelate suizidalen Verhaltens

Effects of valproate-induced alteration of the GABAergic system on pulsatile luteinizing hormone secretion in ovariectomized women

Oparzenia dróg oddechowych

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