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)

The influence of two different premedication regimens (diazepam versus pethidine/promethazine with fentanyl substitution before induction) on the endocrine stress-response during halothane anaesthesia was investigated in twenty orthopedic surgery patients. After premedication, the levels of plasma catecholamines, ADH, ACTH and cortisol were lower in the pethidine/promethazine-than in the diazepam-group. The levels of adrenaline remained significantly lower during the whole observation period. Thirty minutes after extubation all endocrine parameters except noradrenaline were lower in the pethidine/promethazine-group than in the diazepam-group.
 ...
PMID:[Effect of premedication and fentanyl administration on the endocrine stress reaction during halothane anesthesia]. 363 65

The in vitro carboxyl methylation-demethylation of exogenous and endogenous proteins was investigated in rapidly proliferating thymocytes. Of all the cell fractions tested protein carboxyl methyltransferase activity was highest in the nucleoplasmic fraction (3.2 pmol/mg per minute with ACTH and 0.8 pmol/mg per minute with endogenous substrates). The only other fraction with significant activity was the cytosol (1.2 pmol/mg per minute with ACTH). The nuclei from thymocytes are extremely large; consequently some 70-80% of protein carboxyl methyltransferase in these cells is of nuclear origin. The cellular concentration of protein carboxyl methyltransferase and methyl acceptor proteins paralleled the development of the thymus. Mature lymphocytes contained about 25% of the activity of immature thymocytes. Failure to accumulate protein methyl esters, either in vitro in in vivo, was most likely due to the presence of a very active protein methylesterase. This rapid turnover of protein methyl esters was manifest by the continuous production of [3H]methanol when soluble fractions were incubated with S-adenosyl-L-[methyl-3H]methionine ([methyl-3H]AdoMet). [3H]Methanol production was enhanced upon the further addition of the particulate fractions, particularly chromatin. The turnover of protein methyl esters was primarily enzymatic, since no [3H]methanol was formed when ACTH was incubated with AdoMet and purified protein carboxyl methyltransferase. Utilizing [3H]methanol formation as an index of the rate of protein methylation-demethylation would yield minimal values, since this compound was oxidized via alcohol dehydrogenase or oxidase in these cells. The majority of the methyl acceptor proteins were located in the nuclei. The rapid methylation-demethylation of these proteins may play some role in development and (or) differentiation.
 ...
PMID:Protein carboxyl methylation-demethylation in rat thymocytes. 407 25

We measured basal and dexamethasone-suppressed plasma ACTH in 246 patients with bronchogenic carcinoma (105 with small-cell carcinoma); in 138 of these patients (67 with small-cell carcinoma) basal and pentagastrin-stimulated serum calcitonin was also determined. In addition, in a subgroup of 120 patients (58 with small-cell carcinoma) plasma ADH with reference to plasma osmolality was also assayed. Non-suppressible plasma ACTH was found in 45% of patients with small-cell carcinoma but only in isolated cases of large-cell carcinoma, adenocarcinoma, and squamous-cell carcinoma. Serum calcitonin was increased in 28% of patients with small-cell carcinoma but only in few patients with other tumor types. Stimulation of calcitonin by pentagastrin was ineffective. Plasma ADH was inappropriately high in 47% of patients with small-cell carcinoma. Strikingly high also was the incidence of increased ADH concentrations in patients with large-cell (40%), adenocarcinoma (46%), and squamous-cell carcinoma (29%). By measuring plasma ACTH after dexamethasone suppression and ADH with reference to osmolality, the sensitivity of these tumor markers in detecting pathological hormone secretion is markedly increased. In small-cell carcinoma the simultaneous measurement of ACTH, ADH, and calcitonin gives a high yield of positive results (74%), indicating that this set of tumor markers is a promising aid in diagnosis and therapy control.
 ...
PMID:Adrenocorticotropin, calcitonin, and antidiuretic hormone as tumor markers in patients with bronchogenic carcinoma of various histological types. 609 27

This report concerns a review of the neuroendocrine effects of narcotic analgesics and endorphins. Acute administration of narcotic analgesics to rats increases the blood levels of ACTH, GH and prolactin, and decreases levels of LH and TSH, however, there is no general consensus regarding changes in serum FSH, ADH and oxytocin as induced by narcotics in rats. In humans, the narcotic analgesic increases in serum prolactin, decreases in serum LH and has no effect on the release of other known pituitary hormones. Endorphins mimic morphine regarding hormonal effects. Effects of naloxone on the basal levels of prolactin, LH or GH were inverse to the effects seen with narcotics and endorphins, therefore endorphins may play a role in regulating the basal levels of these hormones. Narcotics analgesics depress the increased blood levels of prolactin, gonadotropins or TSH elicited by specific measures. While chronic administration of morphine results in tolerance to the stimulant effect of ACTH, and possibly of prolactin secretion, tolerance does not develop to the stimulant effect on GH secretion. The analgesic potency of narcotic analgesics correlates with their suppressive effect on the pituitary-gonadal system and the potency with which endorphins bind to the opiate receptors correlates with their prolactin releasing activity. It is assumed that narcotic analgesics and endorphins exert their hormonal effects by altering the release of neurotransmitters in the CNS. Thus, a release of hypothalamic releasing hormones is involved rather than a direct action on the pituitary. The central neurotransmitter systems involved in the hormonal effects of narcotics are now being intensively investigated by various groups of workers.
 ...
PMID:[Narcotic analgesics and endorphins and the release of pituitary hormones (author's transl)]. 611 Jun 21

To elucidate the ectopic hormonal pattern in patients with small cell carcinoma of the lung, plasma ACTH, serum calcitonin, serum gastrin, plasma glucagon, serum insulin, plasma secretin, plasma VIP, serum growth hormone, serum hCG/LH, the total of serum hCG and hCG-beta-subunit,serum alpha-subunit, serum human placental lactogen, urine ADH, urine 5-HIAA, urine VMA, urine HVA, and urine hCG-LH were measured prior to therapy in 75 patients. Twenty-two patients (29%) had elevated plasma ACTH, and 18 of these had concomitant increased values of corticosteroid in a 24-hour urine sample. Forty-eight patients (64%) were found to have elevated serum calcitonin, and one-third of the patients were diagnosed as having the ectopic ADH syndrome. Serum gastrin concentrations were increased in 20% of the patients, but the elevations were marginal in almost all cases. None of the remaining substances was found to be significantly elevated. Concentrations of plasma ACTH, serum calcitonin, and urine ADH were not found to be correlated with the stage of the disease, and no correlation of these substances with the histological subtypes of small cell carcinoma was disclosed.
 ...
PMID:Hormonal polypeptides and amine metabolites in small cell carcinoma of the lung, with special reference to stage and subtypes. 624 82

A woman with oat cell carcinoma of the lung showed the typical findings of the syndrome of inappropriate secretion of ADH initially during her hospital course. Ectopic production of ADH was indicated. The presence of ectopic production of ACTH was then suggested after the appearance of the elevation of plasma cortisol and ACTH which was not suppressed by dexamethasone administration. The laboratory findings of metabolic alkalosis and hypokalemia were also consistent with hyperadrenocorticism. In tumor tissue obtained by biopsy, ACTH and ADH were proven to be present by radioimmunoassay as well as nicotine-stimulated-neurophysin and estrogen-stimulated-neurophysin. This was a rare case in which the simultaneous production of ADH and ACTH was clinically diagnosed. It is suggested that the elevation of neurophysins in plasma is of value in the diagnosis of ectopic production of ADH.
 ...
PMID:A case of oat cell carcinoma of the lung associated with ectopic production of ADH, neurophysin and ACTH. 625 Aug 6

The ectopically produced polypeptide hormones ACTH, ADH, and calcitonin were investigated as tumor markers in patients with small-cell carcinoma of the lung (SCC). Plasma ADH concentrations were evaluated separately as well as in relation to concomitantly obtained plasma osmolality levels. No significant nor consistent changes of marker concentrations caused by lysis of tumor cells were found immediately after administration of cytotoxic drugs. After tumor regression, plasma ACTH and serum calcitonin concentrations and inappropriate ADH secretion (plasma ADH levels inappropriately high compared with plasma osmolality) became normal in most cases; however, progressive disease was not followed consistently by changes in plasma ACTH concentrations and occurrence of inappropriate ADH secretion. Contrary to this, among 12 patients with disease progression, serum calcitonin levels increased in ten patients and plasma ADH levels increased in 11 patients. In most cases, however, these changes were only moderate, and serum calcitonin concentrations were found to be increased after tumor regression in patients who had normal pretreatment levels. It is concluded that decisions on treatment of patients with SCC cannot exclusively be based on changes in the concentrations of the polypeptide hormones that might be of ectopic origin.
 ...
PMID:ACTH, ADH, and calcitonin concentrations as markers of response and relapse in small-cell carcinoma of the lung. 625 49

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.
 ...
PMID:Angiotensin II mediated ACTH release in rat pituitary cell culture. 628 87

Opioid peptides are found throughout the central nervous system, and have profound effects on neuroendocrine function. In man, exogenous opiates and opioids elevate circulating prolactin, GH and TSH, and suppress the release of the gonadotrophins and pro-opiocortin-related peptides. However, unlike in other species, there is substantial evidence for a physiological role of endogenous opioids only in the case of the gonadotrophins and ACTH/LPH. Most evidence suggests that LH and FSH are modulated via the hypothalamus or amygdala, where concentrations of opioids and opioid receptors are very high. Endogenous opioids appear to be principally concerned with the frequency-modulated release of GnRH, and this may be important clinically in patients presenting with amenorrhoea. ACTH/LPH are under tonic inhibition by endogenous opioids acting at hypothalamic and/or pituitary levels, and changes in this inhibition may be responsible for the release of these peptides in response to certain forms of stress. It has been reported that the opiate antagonist, naloxone, is clinically useful in paradoxically inhibiting the release of ACTH in patients with Nelson's syndrome, but this requires adequate confirmation. Vasopressin is under biphasic opiate control, but the principal effect is probably opiate-mediated inhibition of vasopressin release. The endogenous ligand for this response is likely to be dynorphin. Suppression of vasopressin release by opiates may become a useful therapy in the treatment of the 'Syndrome of inappropriate ADH'.
 ...
PMID:Brain opiates and neuroendocrine function. 632 67

The authors have studied on 25 cases of hypercorticism, one of the mechanisms of producing arterial hypertension, the renin-angiotensin system. The study showed that in only 20% of the cases plasma renin activity was high whereas in the remaining 80% other mechanisms were responsible for the hypertension. In the cases in which the plasma activity of renin was high, by studying the changes in the value of electrolytes we were able to derive some understanding of the mechanism of action of the RA2A system. Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism.
 ...
PMID:The role of the renin-angiotensin system in arterial hypertension in hypercorticism. 634 18


<< Previous 1 2 3 4 5 6 7 8 Next >>