PubMed · 906509
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K B Prutis. 1977-09-15. [Gynecomastia in hyperthyroidism].. https://pubmed.ncbi.nlm.nih.gov/906509/
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In all organisms, mild heat pretreatments induce tolerance to high temperatures. In the yeast Saccharomyces cerevisiae, such pretreatments strongly induce heat-shock protein (Hsp) 104, and hsp104 mutations greatly reduce high-temperature survival, indicating Hsp1O4 plays a critical role in induced thermotolerance. Surprisingly, however, a heat-shock transcription factor mutation (hsf1-m3) that blocks the induction of Hsps does not block induced thermotolerance. To resolve these apparent contradictions, we reexamined Hsp expression in hsf1-m3 cells. HsplO4 was expressed at a higher basal level in this strain than in other S. cerevisiae strains. Moreover, whereas the hsf1-m3 mutation completely blocked the induction of Hsp26 by heat, it did not block the induction of Hsp1O4. HSP104 could not be deleted in hsf1-m3 cells because the expression of heat-shock factor (and the viability of the strain) requires nonsense suppression mediated by the yeast prion [PSI+], which in turn depends upon Hsp1O4. To determine whether the level of Hsp1O4 expressed in hsf1-m3 cells is sufficient for thermotolerance, we used heterologous promoters to regulate Hsp1O4 expression in other strains. In the presence of other inducible factors (with a conditioning pretreatment), low levels of Hsp1O4 are sufficient to provide full thermotolerance. More remarkably, in the absence of other inducible factors (without a pretreatment), high levels of Hsp1O4 are sufficient. We conclude that Hsp1O4 plays a central role in ameliorating heat toxicity. Because Hsp1O4 is nontoxic and highly conserved, manipulating the expression of Hsp1OO proteins provides an excellent prospect for manipulating thermotolerance in other species.
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Twenty-two perimenopausal patients (aged 47-56 years) admitted for elective abdominal hysterectomy and salpingo-oophorectomy were selected to understand better the clinical significance of increasing gonadotropin levels as an indicator of target organ responsiveness. Prior to anesthesia, blood was drawn from the patients for subsequent analyses of serum follicle-stimulating hormone (FSH), luteinizing hormone (LH) and 17beta-estradiol (E2) levels. Ovarian tissue was obtained during surgery and frozen at -70 degrees C for subsequent analyses for FSH and LH receptor content. The phase of the menstrual cycle of the patients or postmenopause was determined by serum gonadotropin and E2 levels and histological evaluation of the endometrium. Patients with no detectable FSH receptors showed significantly higher serum FSH and LH levels (4.7- and 4.3-fold, respectively) when compared to patients with detectable FSH receptors; FSH receptors were present in 27% of the patients, LH receptors were present in 68% of the patients and a negative correlation was found between serum LH levels and ovarian LH receptors. In postmenopausal patients, neither FSH receptors nor LH receptors were detectable. High serum gonadotropin levels in perimenopausal patients thus suggest the existence of low or undetectable ovarian gonadotropin receptor levels.