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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

Mol Cell Endocrinol. 2003 Mar 28;201(1-2):97-108.
Maintenance of glucocorticoid receptor function following severe heat-shock of heat-conditioned cells.

Mitsiou DJ, Siriani D, Katsanou ES, Florentin I, Georgakopoulos A, Alexis MN.

Molecular Endocrinology Programme, Institute of Biological Research and Biotechnology, The National Hellenic Research Foundation, 48 Vas. Constantinou Avenue, 11635, Athens, Greece

The competence of the glucocorticoid receptor to regulate gene expression is thought to depend on Hsp70-driven continuous reactivation following spontaneous inactivation of its hormone-binding state. We show here that the glucocorticoid-binding capacity of HeLa cells fell with increasing temperature in the range 43-45 degrees C in a manner that closely paralleled the loss of soluble receptor protein. Receptor activity was maintained during moderate (43 degrees C) but not severe (45 degrees C) heat shock. Hsp70 was rapidly rendered insoluble and was replenished by soluble chaperone at 43 but not 45 degrees C. In heat-conditioned cells expressing different levels of Hsp70, we observed a positive correlation between the concentration of active receptor and the amount of Hsp70 rendered insoluble by heat shock. Much higher amounts of Hsp70 were rendered insoluble and receptor competence to regulate gene expression was preserved after severe heat shock of appropriately heat-conditioned cells. An excess of Hsp90 was found associated with resolubilized heat-inactivated receptor from severely heat-shocked cells. The data indicate that GR activity is maintained, provided that denaturation and/or aggregation of the receptor is prevented by Hsp70; and that the concentration of the chaperone is the limiting determinant of receptor activity in heat-shocked HeLa cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12706298&dopt=Abstract [PubMed - in process]

J Clin Endocrinol Metab. 1978 Jan;46(1):77-82.
Hyperthyroidism without triiodothyronine excess: an effect of severe non-thyroidal illness.

Engler D, Donaldson EB, Stockigt JR, Taft P.

Serial changes in thyroid hormone levels are described in two patients in whom hyperthyroidism was associated with transient non-thyroidal illness. In a 74-year-old woman with mild hyperthyroidism, two episodes of cholecystitis were associated with subnormal concentrations of serum T3 and increased concentrations of serum rT3; T3 became elevated during recovery, associated with a simultaneous fall in rT3. The TSH response to TRH was undetectable on three occasions. A cholecystectomy was performed after preparation with Lugol's iodine and subsequent tests showed evolution through T3 toxicosis to classical hyperthyroidism. In the second case, symptoms and signs of classical hyperthyroidism were noted during an undiagnosed illness characterized by severe abdominal pain and fever. Six days after the onset of this illness, an elevated level of serum T4 was associated with a normal total T3 concentration and increased concentration of rT3. After resolution of abdominal symptoms, serum T3 was markedly increased, associated with persistent T4 and rT3 excess. These findings indicate that the changes in T3 and reverse T3 described in non-thyroidal illness also occur in hyperthyroid patients, and suggest that the fall in T3 may be of sufficient magnitude to make T3 measurement diagnostically unreliable in the presence of non-thyroidal illness.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=109456&dopt=Abstract

J Clin Endocrinol Metab. 1978 Mar;46(3):369-73.
Biphasic change in pituitary capacity induced by estrogen in hypogonadal women.

Lachelin GC, Yen SS.

PIP: 5 healthy postmenopausal women aged 52-59 years with elevated gonadotropin levels and low estradiol (E2) (10+ or -1.5 pg/mol) concentrations volunteered for this study which measured changes in responses to pulses of luteinizing hormone-releasing factor (LHF) (10 mcg at 2-hour intervals 3 times) and thyroid-releasing factor (TRF) (200 mcg at 2-hour intervals 3 times) for luteinizing hormone (LH), follicle stimulating hormone (FSH), and prolactin (PL) before and during administration of a large dose of ethinyl estradiol (EE) (400 mcg/day) for 5 days. Responses to LRF and TRF stimulation on the 2nd and 5th days of EE treatment were studied in 2 experimental periods in the same individual at an interval of at least 10 weeks between treatments. During 5 days of EE treatment, LH 1st declined (50%) and then returned to the original level, forming a previously observed U-shaped curve. The initial fall in basal FSH level was not followed by a return to pretreatment level. These changes were accompanied by an exponential increase of more than 3-fold in the PL levels. The bidirectional pattern of LH release was associated with parallel changes in pituitary sensitivity to a 10-mcg pulse of LRF. Pituitary reserve, defined as the response to the 2nd and 3rd pulses of LRF, exhibited unidirectional augmentation. This progression in PL release upwards was unaccompanied by changes in pituitary PL sensitivity and reserve. The contribution of hypothalamic LRF and dopamine in the participation of these functional changes of LH, FSH, and PL are discussed.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=109457&dopt=Abstract

J Clin Endocrinol Metab. 1979 Jul;49(1):138-40.
Lack of evidence for thyrotropin-releasing hormone deamidation in normal and hyperthyroid human sera.

Emerson CH, Mishal A, Mahabeer HL, Currie BL.

Two-hour incubations of human serum with 50 ng TRH or pyroglutamyl-histidyl-proline (TRH-OH) were performed under substrate conditions of 0.2 microgram substrate/ml serum. During incubations with normal serum, 46.3 +/- 1.3 (SEM) ng TRH were degraded while only 14.2 +/- 5.1 ng TRH-OH were degraded (P less than 0.001). During incubations with serum from patients with hyperthyroidism, 42.7 +/- 2.6 ng TRH were degraded compared to only 19.6 +/- 2.0 ng TRH-OH (P less than 0.001). Despite the fact that TRH degradation was significantly greater than TRH-OH degradation in both normal and hyperthyroid serum, no formation of TRH-OH (less than 3.1 ng/incubation tube) from TRH was detected. Formation of TRH-OH from TRH was also not noted when normal or hyperthyroid serum was incubated with TRH at substrate concentrations of 62.5 microgram/ml serum. These data confirm other reports that TRH deamidation does not occur in normal serum and extends this observation to hyperthyroid serum.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=109463&dopt=Abstract

J Clin Invest. 1979 Jul;64(1):206-17.
Regulation of the metabolism of 25-hydroxyvitamin D3 in primary cultures of chick kidney cells.

Trechsel U, Bonjour JP, Fleisch H.

A primary chick kidney cell culture is described, capable of forming 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], and 1,24,25-trihydroxyvitamin D3 [1,24,25(OH)3D3] over several days. The apparent Km values were 0.125 microM for the 1-hydroxylase and 2.1 microM for the 24-hydroxylase. Exogenous 1,25(OH)2D3 decreased 1-hydroxylase and increased 24-hydroxylase within 4 h. 24,25(OH)2D3 produced similar effects, but only in the absence of fetal calf serum. R and S isomers of 1,24,25(OH)3D3 were about fives times less active than 1,25(OH)2D3. Bovine parathyroid hormone stimulated the 1- and reduced the 24-hydroxylase in 6 h, but this only occurred in cultures either previously treated with 1,25(OH)2D3 and EGTA to lower Ca to 0.8 mM or in cultures grown in the presence of 25-hydroxyvitamin D3 (25(OH)D3). Under the latter condition, the sensitivity to bovine parathyroid hormone was enhanced, 0.04 U/ml producing a maximum response. Synthetic aminoterminal tetratriacontapeptide (1-34) human parathyroid hormone was equally effective. In the absence of D metabolites, estradiol for 6 h produced a dose-dependent inhibition of the 1-hydroxylase, but no change in the 24-hydroxylase. Progesterone, testosterone, and corticosterone had no significant effect. In cultures grown in the presence of 25(OH)D3 no reproducible effects were obtained with either 1 microM estradiol or 1 microM testosterone, alone or in combination, but 5 microM corticosterone decreased the 1- and increased the 24-hydroxylase. Changes in Ca and P concentrations of the medium as well as addition of ethane-l-hydroxy-1, 1-diphosphate for 48 h did not affect any of the hydroxylase activities. The modulation of the hydroxylase activities by vitamin D3 metabolites and parathyroid hormone suggests that these factors regulate the renal hydroxylase by direct actions, whereas it would appear that ethane-1-hydroxy-1,1-diphosphate, Ca, P, and steroid may exert their influence indirectly.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=109470&dopt=Abstract

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