Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothalamic hormones as well as anterior pituitary hormones were detected in the peripheral plasma after the diagnosis of brain death. It is possible that residual hypothalamic tissue was functioning after satisfying the usual criteria of total brain death. To examine this possibility, endocrinological and morphological alterations of the hypothalamic-pituitary system was evaluated in 28 brain dead patients. Intrinsic ADH was depleted in the plasma shortly after the diagnosis of brain death. Anterior pituitary hormones were initially detected in all patients, but gradually disappeared. The direct TRH (thyrotropin releasing hormone) stimulation to the anterior lobe was responded to well. Morphological studies showed a partial necrosis of the anterior lobe and the preservation of the posterior lobe for as long as a week. These data prove that the pituitary is partially preserved after brain death. LH-RH (luteinizing hormone releasing hormone) was detected in the peripheral plasma of all patients and GRF (growth hormone releasing factor) was detected in half of the patients for as long as 15 days, but autopsy revealed the fact that the brain tissue including the hypothalamus became extensively necrotic after the sixth day of brain death. In order to solve this controversy it is proposed that these hormones originate from extracranial tissues such as pancreas. The detection of hypothalamic hormones after the diagnosis of brain death therefore is not contradictory to the concept of total brain death.
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PMID:Morphological and functional alterations of the hypothalamic-pituitary system in brain death with long-term bodily living. 131 58

We reported an 11-year-old boy who suffered from transient hypernatremia, hypothermia, and circadian rhythm disturbances of sleep-wakefulness and body temperature from the age of 4 years, as sequelae of acute subdural hematoma. T1-weighted magnetic resonance imaging (MRI) of the brain revealed low intensity consistent with necrotic change in the whole left cerebral hemisphere, hypothalamic region, and the right-sided brain stem including tegmentum, while the pituitary structure was well preserved. Anterior pituitary function was almost normal. ADH (antidiuretic hormone) was neither stimulated by hyperosmolality nor suppressed by hyposmolality but continued to be secreted at almost constant level approximating the normal basal state. This pattern seemed to be due to complete destruction of the osmoreceptor located in the anterior hypothalamus. He exhibited a dispersed-type sleep with differentiated stages of NREM (non-rapid eye movement), although the percentage of sleep was higher at night than in the daytime. It is suggested that circadian rhythm of sleep-wakefulness and differentiation of NREM sleep stages are regulated by different neuromechanisms. Brain stem lesion on MRI may be connected with the pathogenesis of the dispersed-type sleep with special respect to amplitude reduction of sleep-waking circadian rhythm. Circadian rhythm of body temperature (BT) was irregular in amplitude, phase, and period without synchronization with sleep-wakefulness rhythm. Hypothermia was also demonstrated at the basal state, while BT increased when he suffered from respiratory infection. It is likely that hypothermia in our case is caused by the BT shift to the lower side due to malfunction of BT integrating system including preoptic area and anterior hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sodium regulation disorder, hypothermia, and circadian rhythm disturbances of the body temperature and sleep-wakefulness as sequelae of acute subdural hematoma]. 205 28

Anterior pituitaries from normal rats were enzymatically dispersed and placed into monolayer cell culture in order to determine if and how angiotensin II (Ang II) mediates the in vitro release of ACTH and other pituitary hormones. Ang II stimulated ACTH secretion in a time dependent fashion. This release occurred at physiologic concentrations of Ang II and was linearly correlated with the log dose of Ang II. One hour pretreatment of the cells with cycloheximide, a inhibitor of protein synthesis, significantly decreased the cellular ACTH secretory response to Ang II. Ang 11 did not mediate the release of LH nor of ADH, a proposed stimulator of ACTH secretion.
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PMID:Angiotensin II mediated ACTH release in rat pituitary cell culture. 628 87