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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Biophys J. 1979 Sep;27(3):371-92.
Transepithelial current-voltage relationships of toad urinary bladder and colon. Estimates of ENaA and shunt resistance.

Macchia DD, Helman SI.

Studies were done to investigate the transepithelial current-voltage (IT-VT) relationships of urinary bladder and colon of the toad Bufo marinus. Like several other Na transporting epithelia, the IT-VT plots characteristically showed a break at voltage E1, averaging near 124 mV for urinary bladder and 110 mV for colon. With bladders treated with antidiuretic hormone, estimates of ENa and shunt resistance, Rs, were obtained according to a method outlined by Yonath and Civan, 1971 (J Membr. Biol. 5:336-385). Our results not only confirmed their observations, but were consistent with the notion that the values of E1 (IT-VT plots) were the same as those of ENa. In addition, the values of Rs were found to be the same as those estimated from the quotient E1/I1 obtained from the voltage and current coordinates at the break of the IT-VT plot of bladders studied in both stretched and unstretched states. Amiloride at concentrations up to 10(-5) M caused a small decrease of both E1 and E1/I1 of urinary bladder. Similarly, amiloride caused small but significant changes of ENa and RNa of the colon. For both epithelia, the values of E1 and E1/I1 of the IT-VT plots were the same as those of ENa and Rs estimated by an independent method. In general, these findings are similar to those of several other epithelia where the ENa and Rs can be estimated directly from their IT-VT relationships.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=122255&dopt=Abstract

J Clin Endocrinol Metab. 1978 May;46(5):715-20.
Acute effects of alcohol on anterior pituitary secretion of the tropic hormones.

Ylikahri RH, Huttunen MO, Harkonen M, Leino T, Helenius T, Liewendahl K, Karonen SL.

The plasma or serum concentrations of GH, TSH, LH, PRL, testosterone, cortisol, T4, and T3, and the values of the T3 uptake test were monitored in 12 healthy male volunteers for a period of 20 h after administration of one large dose of ethanol (1.5 g/kg BW). The effects of TRH and LRH on the secretion of TSH, PRL, and LH were studied in these subjects once during the period of acute alcohol intoxication (4 h after the start of drinking) and once during the hangover period (14 h after the start of drinking). Each subject served as his own control by drinking water only during another experimental session. Alcohol had no significant effect on basal concentrations of GH, TSH, LH, T4, T3, or testosterone. The concentration of cortisol in plasma was elevated during the whole 20-h period after ingestion of alcohol, as compared with the control values. Alcohol also did not significantly alter the effects of TRH and LRH on plasma TSH and LH levels at 4 and 14 h. During the hangover period, the PRL response to TRH was totally blocked, but during alcohol intoxication, there was a slight increase in the PRL response to TRH. The lack of response of PRL to TRH during the hangover suggests that withdrawal symptoms are associated with increased dopaminergic activity in the hypothalamus.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=122287&dopt=Abstract

J Clin Endocrinol Metab. 1978 May;46(5):816-23.
Impaired estrogen-induced luteinizing hormone release in young women with anovulatory dysfunctional uterine bleeding.

Van Look PF, Hunter WM, Fraser IS, Baird DT.

Spontaneous ovarian activity, as reflected by the urinary excretion of total estrogen and pregnanediol measured serially (thrice weekly) over a period of 3-4 months, was studied in nine young women (15-27 yr old) with a history of dysfunctional uterine bleeding of at least 2-yr duration. Results were compared to those obtained in sex regularly menstruating women, aged 23-45 yr. All control women had ovulatory cycles, but seven of the nine patients with DUB failed to ovulate during at least three consecutive cycles. The profiles of urinary total estrogen excretion in these seven subjects were consistent with regular follicular development, but the follicular phase was prolonged and the amount of estrogen excretion increased, as compared to controls. In four of these seven patients, the endometrium had previously shown cystic glandular hyperplasia. Although the release of LH and FSH after injection of 50 micrograms synthetic LRH was normal, the surge of LH induced in response to exogenous estrogen (200 micrograms ethinylestradiol/day for 3 days) was significantly (P less than 0.005) lower in the patients (16.2 +/- 3.7 mU/ml) than that of control women )35.0 +/- 5.5 mU/ml). It is concluded that the failure to ovulate in young women with anovulatory dysfunctional uterine bleeding is due to inadequate release of LH in response to estrogen. The results support the hypothesis that the basic defect in these women may be a decrease of hypothalamic sensitivity to positive feedback.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=122291&dopt=Abstract

J Clin Endocrinol Metab. 1978 May;46(5):830-3.
Influence of methyl-TRH-induced prolactin increase on serum testosterone levels in normal adult men.

Rubin RT, Poland RE, Sowers JR, Hershman JM.

Our previous studies suggest that increased serum PRL, secondary to haloperidol-induced dopamine blockade, augments serum testosterone (T) levels in normal men. To rule out a direct effect of haloperidol on the testis, serum samples from a methyl-TRH study in normal men, in whom serum PRL levels were increased by a stimulus other than dopamine blockade, were analyzed for T. Fourteen subjects received both a low dose (6.25-12.5 micrograms) and a high dose (100-500 micrograms) of methyl-TRH on separate days; blood sampling was done for 15 min before and for 4 h after drug infusion. Compared to a saline control group of 14 normal men, who showed a diurnal decline of serum T levels, the methyl-TRH treated subjects had statistically significant increases in serum T after both low and high doses. These data provide further support for the concept that PRL is a pituitary hormone capable of augmenting serum T levels in normal adult men.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=122292&dopt=Abstract

J Clin Endocrinol Metab. 1978 Jul;47(1):119-25.
Progesterone effects on gonadotropin release in women pretreated with estradiol.

Chang RJ, Jaffe RB.

This study was designed to investigate whether the amounts of progesterone (P) normally present at midcycle, when administered to normal women pretreated with estradiol benzoate (E2B), alter the release of LH and FSH. Twelve subjects (four groups of three) were studied during two menstrual cycles. On day 1 of both the initial (E2 control) and a subsequent (study) cycle, each subject received E2B im (2.5 micrograms/kg/12 h) for a total of seven injections. Twelve hours after the final injection, gonadotropin-releasing hormone (GnRH) was given. In the study cycle, P in oil was added to each of the last three injections of E2B in doses of 1.25 (group I), 2.5 (group II), or 5.0 (group III) mg/12 h, and in one group (IV) in graded doses of 1.25 2.5, and 5.0 mg/12 h. Estradiol levels were similar in both cycles, with a mean (+/- SE) of 271 +/- 3 pg/ml. During the interval of P administration, mean P levels rose gradually from 0.3 +/- 0.02 to 1.3 +/-0.12 ng/ml (mean +/- SE of all groups). In the study cycle, an FSH rise occurred in 8 of 12 subjects, while an LH surge greater than that in the E2 control cycle occurred in all but one subject. Peak levels of these surges usually occurred within 24 h of the initial P injection, which is similar to the relationship between the initial rise of P and the occurrence of peak gonadotropin levels at midcycle in normal women. The mean delta max of FSH and LH in subjects exhibiting gonadotropin rises approximated the magnitude of the gonadotropin increases observed normally at midcycle. In response to GnRH during the study cycle, the magnitude of the FSH rise was augmented in 6 of 12 subjects and of LH in 9 of 12, when compared to the E2 control cycles. These data suggest that P, in the presence of late follicular phase levels of E2, 1) augments the release of LH, 2) may induce the release of FSH, and 3) further modulates pituitary responsiveness to GnRH. The data are consistent with the hypothesis that the rising concentrations of E2 to which the hypothalamic-pituitary system is exposed for an appropriate duration serve to initiate the surge of LH at midcycle. This increased LH in turn, stimulates the production of P, which not only further augments the LH surge but, when coupled with E2, also can effect the midcycle FSH surge.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=122395&dopt=Abstract

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