Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We examined the renal function in 18 brain dead patients 2-0 h before removing the kidneys and 72 h after their transplantation to the recipient. The kidneys were preserved by simple hypothermia. In brain dead patients we found no demonstrable relationships between PCr and CCr or between Purea and CCr. At this time the Purea and PCr values are not a sufficiently accurate indicator of renal function. We also examined the plasma and urinary concentrations of Na, K, urea and osmotically active substances and calculated their excretion fractions. We found that, prior to removal, the kidneys were in a state of combined osmotic and water diuresis. The osmotic diuresis was chiefly of a non-sodium type and was produced by a mannitol load. Water diuresis was evidently caused by inhibition of ADH output consequent to brain hypoxia. We also investigated the relationship between the CCr values before nephrectomy and in the early posttransplantation phase. We found that there was a relationship between the recipient's CCr values in the early posttransplantation period and donor's CCr/total ischaemic time index. Calculation of this index can be valuable, especially in high risk transplantations.
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PMID:Renal function in brain dead patients with respect to transplantation. 621 7

As follows from the experiments on the genotypic related populations of Drosophila melanogaster with different frequency of ADH allozymes selection for postponement of ageing and resistance to hypothermia lead to saturation of population with S-allozyme ADH, and genotypic adaptation to ethanol-to increasing of frequency of F-allozyme. It is supposed that genotypic adaptation is realized by selection of specimens with the most favourable alleles of genes. At the same time ontogenetic adaptation is accompanied by biochemical modification of existing allozymes.
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PMID:[Gene-enzyme alcohol dehydrogenase system and adaptability in Drosophila melanogaster]. 927 30

Patients with multiple sclerosis sometimes show subthalamic lesions presenting syndrome of inappropriate secretion of ADH (SIADH), hypothermia, hyperprolactinemia, weight loss, and cachexia. Hyperprolactinemia also has been found in the patients with active systemic lupus erythematosus, because prolactin can be produced from human activated lymphocytes. We described a case of multiple sclerosis showing galactorrhea-amenorrhea syndrome with hyperprolactinemia. A 31-year-old woman showed a high level of prolactin in the serum (79.6 ng/ml) during remission stage 5 months after the onset of multiple sclerosis. She showed galactorrhea-amenorrhea syndrome 3 years later. She showed dysesthesia in her limbs, relapsing monoparesis, visual disturbance and Gd-enhanced plaques in Brain MRI for 6 years. She was admitted to our hospital on November 24, 1995. A neurological examination showed hyporeflexia of the upper extremities, hyperreflexia of the lower extremities, bilateral ankle clonus, truncal ataxia, and neurogenic bladder. Laboratory tests revealed increased level of serum prolactin, exaggerated secretion of serum prolactin after intravenous injection of 500 micrograms TRH, and marked suppression after oral administration of 2.5 mg bromocriptine. Brain MRI showed demyelinating lesions near the lateral ventricle, and cervical MRI (T2 image) showed high signal intensity lesions in the spinal cord from C2 to C5. In the previous case, galactorrhea-amenorrhea syndrome was found during the exacerbation stage of multiple sclerosis. Hyperprolactinemia may be caused from subthalamic lesions or by activated lymphocytes in multiple sclerosis. We considered that hyperprolactinemia and galactorrhea-amenorrhea syndrome in our patient might be caused from subthalamic lesions because lymphocytes were not activated during the remission stage of multiple sclerosis.
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PMID:[A case of multiple sclerosis with galactorrhea-amenorrhea syndrome]. 936 74