Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steroid hormones, i.e., corticosteroids, estrogens, androgens and progestogens are formed in the adrenal cortex, male gonads, and the female placenta. Relatively little is known of their influence on behavior and their neuroendocrine function. On the cellular level, the rate of increase of RNA message to produce albumen and avidin is directly proportionate to the presence of steroids and their amount. Corticosteroid receptors are found in the thymus, liver, spleen and heart. The brain has receptors both for the corticosteroids and the sex hormones. These receptors are scattered throughout different regions of the brain, but the synthetic glucocorticoid dexamethasome is found only in the pituitary which accounts for its role in stopping the secretion of ACTH. Testosterone undergoes metabolic changes in the brain, affecting behavior. The A chain undergoes an enzyme reduction to 5aDHT and androstandiol. Following enzyme changes, the A chain of male testosterone can become female estradiol. Laboratory tests prove that sexual behavior in males is affected only by those androgens that can convert to estrogens, while in females it is dependent on the conversion of testosterone to estrogen. Lately psychiatrists have become very interested in the catechol estrogens, fairly new metabolites of estradiol which are produced in the hypothalamus and contain 2 hydroxyl groups (as compared with the 1 hydroxyl in estrogens). Catechol estrogens block estradiol receptors, behaving like antiestrogens. Researchers are investigating the possibility of signaling the desired neural messages without the concomitant effects that estrogen produces, through using catechol estrogens. They are examining this natural derivative of estradiol which may affect among others: sexual behavior, maturity, depression, migraines, and epileptic seizures.
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PMID:[Steroid hormones and the activity of the central nervous system]. 38 16

In young, adult male volunteers Leydig cell function tests were performed consisting of i.m. administration of 1500, 3000 or 4500 IU of HCG on days 1, 2 and 3 and plasma testosterone determination by radioimmunoassay. The stimulatory effect of HCG known from the literature is reconfirmed. However, no difference between the effect of the three dosage levels was found and the first significant effect of HCG was observed 24 h after its first application. Testosterone levels on day 3 and 4 are higher but not different from each other. A depression of plasma testosterone after treatment with an anabolic steroid (1alpha, 17alpha-dimethyl-5alpha-androstan-17-ol-3-one) 20 mg daily for 14 days is described. Reactivity to HCG was sustained in these subjects, but testosterone response to HCG was diminished at all investigated time intervals.
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PMID:Plasma testosterone response to HCG in normal men without and after administration of anabolic drug. 87 Mar 13

Testosterone affects calling in a strange environment in two independent ways. In both sexes, short calls increase in number at the expense of peeps early in the test (when they would in any case be numerous) probably as a result of an increased tendency to repeat the call which has just been given. In males only, peeps are reduced in number during established calling, as a result of the interpolation of brief periods of silence. There is no accompanying depression of escape, but the visual scanning usual during peeps is reduced. The replacement of peeps by silence and immobility may be a consequence of an increase in persistence of attention to particular stimuli.
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PMID:Effects of testosterone on the calling of the domestic chick in a strange environment. 115 14

The permanent epithelial strain EB 33 was initiated from primary cultures of a human prostatic adenocarcinoma in June 1973. To establish androgen dependence of growth EB 33 cells were grown in various media. The effect of androgen withdrawal was studied by the application of media containing sera that had undergone steroid extraction procedures with dichloromethane and activated charcoal. The growth rate of the original EB 33 population was not influenced by withdrawal or addition of androgenic hormones. There were 111 clones developed by single cell plating of EB 33 cells and 23 clonal lines responded to extracted media with a depression of growth of at least 50 per cent. These findings were verified in growth curve experiments. Testosterone and 5-alpha-dihydrotestosterone slightly accelerated growth but did not fully compensate the depression of cell counts seen in extracted media. These findings may be consistent with hormone dependence of growth of clonal lines developed from the human prostatic epithelial strain EB 33.
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PMID:Human prostatic epithelial cells in culture: clonal selection and androgen dependence of cell line EB 33. 124 69

Thymic secretory peptides thymosin beta 4 and alpha 1 have possible endocrine roles in both immune and reproductive systems; thus, they should respond to endocrine feedback control mechanisms consistent with gonadal function. In an initial experiment, male pigs (boars; n = 90; 10/time) were bled at 1, 3, 6, 12, 18, 24, 30, 36, and 96 wk of age before and 24 h after hCG stimulation. Thymosin beta 4 concentrations were significantly depressed 24 h after hCG challenge. Testosterone concentrations increased with age up to 36 wk and were further increased with hCG stimulation (p less than 0.01). In a subsequent experiment, boars (n = 12) and barrows (males castrated shortly after birth; n = 12) were blood-sampled, administered hCG, and sampled again 24 h later at 1, 3, 6, 12, 18, and 24 wk of age. Barrows (n = 12) were administered testosterone with the same protocol. Testosterone concentrations increased in boars with maturity and were further increased from the hCG stimulation (p less than 0.01). Thymosin beta 4 concentrations decreased with age in boars and barrows (p less than 0.01), and hCG challenge depressed thymosin alpha 1 and beta 4 concentrations in boars and thymosin beta 4 in barrows (p less than 0.01). Testosterone treatment of barrows also depressed thymosin beta 4 and alpha 1 in barrows (p less than 0.01). The depression of thymosins by hCG treatment points to a role for gonadotropins in altering circulating thymosin concentrations independent of, but in conjunction with, the effect of gonadal steroids.
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PMID:Developmental changes of serum thymosin alpha 1 and beta 4 in male and male castrated pigs: modulation by testosterone and human chorionic gonadotropin. 159 44

The consequences of sleep deprivation and stress in residency training have not been quantified. In the course of assembling a control group for other studies, we unexpectedly observed a significant (P less than 0.005) and marked depression of serum testosterone levels in healthy male internal medicine residents (means = 11.8 +/- 1.1 nmol/L, n = 7) compared with other hospital personnel (means = 20.6 +/- 5.3 nmol/L, n = 18). Testosterone concentrations in the two groups were entirely nonoverlapping, while luteinizing hormone levels were not significantly different. We conclude that the stress of residency training leads to a quantifiable depression of gonadal function, and that gonadal steroid concentrations may be useful in evaluating measures intended to reduce that stress.
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PMID:Subnormal serum testosterone levels in male internal medicine residents. 162 Dec 62

Sleep EEG and the nocturnal secretion of cortisol and testosterone in 12 male patients (mean age 46.4 +/- 11.26 years) with major endogenous depression were investigated concomitantly during acute depression, before treatment and after recovery and drug cessation. Testosterone concentration increased after remission, while cortisol secretion decreased. Sleep EEG disturbances remained unchanged in remitted patients. The data suggest that a blunted testosterone and an elevated cortisol secretion are state markers of acute depression, which normalize independently from sleep structure. An interaction between the hypothalamic-pituitary-gonadal axis and the limbic-hypothalamic-pituitary-adrenocortical axis appears likely.
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PMID:Sleep EEG and nocturnal secretion of testosterone and cortisol in patients with major endogenous depression during acute phase and after remission. 177 14

The influence of testosterone on the development of the pressor response to common carotid occlusion was investigated in control and median eminence-lesioned male rats. In control rats (N = 9), gonadectomy performed 21 days before the experiments reduced by 22% (from 51 +/- 2 to 40 +/- 2 mmHg) and treatment with testosterone (300 micrograms for 4 days before the measurements) increased the initial peak pressor response (from 51 +/- 2 to 57 +/- 2 mmHg) which depends on carotid innervation. The maintained response which is of central origin (probably ischemic) was less affected. In nongonadectomized rats (N = 6), lesions of median eminence (6 days) decreased the initial peak by 19% (from 52 +/- 2 to 42 +/- 3 mmHg) and the maintained response by 56% (from 32 +/- 2 to 14 +/- 1 mmHg). Sham-operated rats served as controls. In gonadectomized animals (N = 6) the lesion reduced only the maintained response (from 23 +/- 2 to 11 +/- 1 mmHg). Testosterone supplementation restored the maintained response but did not alter the initial peak. These results indicate that the pressor response to common carotid occlusion in male rats is modulated by testosterone and that the depression in the maintained response caused by median eminence lesion can be reversed by steroid supplementation.
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PMID:Effect of testosterone on the pressor response to common carotid occlusion in gonadectomized conscious male rats with lesion of the median eminence. 179 93

Testosterone and cortisol in male marathon runners (n = 11) were determined in saliva samples (n = 28) collected during the three rest days preceding a competitive marathon and in the samples collected at 08.00h on the race day. An Eysenck Personality Inventory was completed on the first rest day and psychological state was assessed on rest days and on the morning of the marathon by completion of visual analogue scales for anxiety, depression, hostility and libido at four times each day. Anxiety, depression and hostility were positively inter-correlated. Extraversion and depression were negatively correlated. At 08.00h on the day of the marathon, anxiety and hostility scores were significantly higher than those on rest days, but depression and libido scores were unchanged. No relationship was found between depression or libido and any hormonal parameter. Race day cortisol correlated negatively with hostility, and changes in cortisol (09.00h) between the race day and the mean rest-day levels correlated with the corresponding changes in anxiety.
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PMID:Salivary steroids and psychometric parameters in male marathon runners. 260 48

Excess body fat has been clearly associated with an increased risk of oligo-ovulation and endometrial/breast carcinoma. The connection has been assumed to lie within derangements of the metabolic/endocrine compartments, particularly of estrogens and androgens. To differentiate the effect of obesity from its related disease process, an attempt has been made to define the reproductive-endocrinologic alterations encountered in otherwise asymptomatic obese women. Androgen metabolism is accelerated in obesity. It is not clear whether the increased clearance precedes or follows the accelerated production of androgens. A servocontrol mechanism appears to be operative in these asymptomatic individuals, maintaining plasma steroid levels normal. The unbound fraction of T may be somewhat increased in overweight women with predominantly upper body fat deposition. The increased clearance of androgen may arise from an obesity-related depression in SHBG concentration (e.g., for T, E2, delta 5-diol, etc.). Adipose tissue, by virtue of the lipid solubility of most of these steroids, concentrates androgens, estrogens, and progesterone. This steroid sequestration not only contributes to the obesity-related increase in androgen clearance but also leads to an extremely enlarged total body steroid pool. Fat tissue sequestration also increases the concentration of androgens in the vicinity of adipose stromal cells, possibly encouraging their aromatization. Adipose tissue also has a moderate degree of 17-hydroxysteroid dehydrogenase activity, which appears to stimulate the conversion of A to T. Finally, alterations in peripheral and hepatic conjugation and an accelerated urinary excretion may contribute to the elevated clearance of androgens. The accelerated PR of androgens may simply result as compensation for the elevated MCR in obesity. Nonetheless, evidence of alteration(s) in adrenocortical steroidogenesis has been presented suggesting a selective obesity-related enhancement in adrenal androgen secretion. These remain to be confirmed. Nonetheless, adrenocortical abnormalities may arise secondary to the influence of other circulating and intra-adrenal factors, including insulin, prolactin, estrogens, and androgens. It is not known whether the accelerated androgen metabolism or the aberrant adrenal steroidogenesis improve with weight reduction. Excess body fat increases androgen aromatization which, together with an obesity-related decrease in SHBG, is associated with mildly elevated levels of E1 and free E2 in postmenopausal women. Although premenopausal obese individuals have the same tendency, the far greater ovarian estrogen secretion overshadows any differences. The bulk of aromatization activity in fat lies in the stromal comportment. The major substrate for peripheral estrogen production is A. Testosterone also contributes to the estrogen pool via its conversion to E2.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reproductive endocrinologic alterations in female asymptomatic obesity. 268 Jun 25


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