Expression of calbindin-D28k and its regulation by estrogen in the human endometrium during the menstrual cycle

Human endometrium resists embryo implantation except during the 'window of receptivity'. A change in endometrial gene expression is required for the development of receptivity. Uterine calbindin-D28k (CaBP-28k) is involved in the regulation of endometrial receptivity by intracellular Ca2+. Currently, this protein is known to be mainly expressed in brain, kidneys, and pancreas, but potential role(s) of CaBP-28k in the human uterus during the menstrual cycle remain to be clarified. Thus, in this study we demonstrated the expression of CaBP-28k in the human endometrium in distinct menstrual phases. During the human menstrual cycle, uterine expression levels of CaBP-28k mRNA and protein increased in the proliferative phase and fluctuated in these tissues, compared with that observed in other phases. We assessed the effects of two sex-steroid hormones, 17beta-estradiol (E2) and progesterone (P4), on the expression of CaBP-28k in Ishikawa cells. A significant increase in the expression of CaBP-28k mRNA was observed at the concentrations of E2 (10(-9 to -7) M). In addition, spatial expression of CaBP-28k protein was detected by immunohistochemistry. CaBP-28k was abundantly localized in the cytoplasm of the luminal and glandular epithelial cells during the proliferative phases (early-, mid-, late-) and early-secretory phase of menstrual cycle. Taken together, these results indicate that CaBP-28k, a uterine calcium binding protein, is abundantly expressed in the human endometrium, suggesting that uterine expression of CaBP-28k may be involved in reproductive function during the human menstrual cycle.     

Glucose lowering effect of transgenic human insulin-like growth factor-I from rice: <Emphasis Type="Italic">in vitro</Emphasis> and <Emphasis Type="Italic">in vivo</Emphasis>studies

Background  

Human insulin-like growth factor-I (hIGF-I) is a growth factor which is highly resemble to insulin. It is essential for cell proliferation and has been proposed for treatment of various endocrine-associated diseases including growth hormone insensitivity syndrome and diabetes mellitus. In the present study, an efficient plant expression system was developed to produce biologically active recombinant hIGF-I (rhIGF-I) in transgenic rice grains.     

Antiproliferative effect of growth hormone-releasing hormone (GHRH) antagonist on ovarian cancer cells through the EGFR-Akt pathway

Background  

Antagonists of growth hormone-releasing hormone (GHRH) are being developed for the treatment of various human cancers.     

Depression of plasma levels of cytokines and ex-vivo cytokine production in relation to the activity of the pituitary-adrenal axis, in patients undergoing major vascular surgery.

The relation between the immune and neuroendocrine response during surgery was studied. In 18 patients undergoing major vascular surgery, circulating interleukin (IL)-1beta and ex-vivo production of IL-1beta and tumour necrosis factor (TNF)-alpha were lower on day 1 after surgery compared to pre-operation values (-14+/-5%, P<0.05; -62+/-9%, P<0.05; and -31+/-54%, P<0.005, respectively). Circulating IL-1 receptor antagonist (IL-1ra) was higher on the 5th day post-operatively compared to pre-operation values (mean +640%+/-400, P<0.05).In a more detailed study in six patients, the ex-vivo production of IL-1beta and TNF-alpha started to decrease at induction of general anaesthesia and dropped to under 10% of initial values at the end of surgery. Circulating IL-1ra and ex-vivo production of IL-1ra started to increase at the end of surgery and remained elevated up to 6 days post-operatively. Plasma antidiuretic hormone (ADH) and adrenocorticotropic hormone (ACTH) increased during surgery, but cortisol remained unchanged.We demonstrate a depression of circulating pro-inflammatory IL-1beta and an increase of circulating anti-inflammatory IL-1ra during surgical stress. The ex-vivo production of IL-1beta and TNF-alpha was suppressed, indicating a downregulation of the production of these cytokines. This parallelled the hormonal reaction with high ADH and ACTH, but not of cortisol, suggesting that glucocorticoid is not the key-factor in downregulation of production and release of pro-inflammatory cytokines.     

Disproportional risk for habitat loss of high‐altitude endemic species under climate change

The expected upward shift of trees due to climate warming is supposed to be a major threat to range‐restricted high‐altitude species by shrinking the area of their suitable habitats. Our projections show that areas of endemism of five taxonomic groups (vascular plants, snails, spiders, butterflies, and beetles) in the Austrian Alps will, on average, experience a 77% habitat loss even under the weakest climate change scenario (+1.8 °C by 2100). The amount of habitat loss is positively related with the pooled endemic species richness (species from all five taxonomic groups) and with the richness of endemic vascular plants, snails, and beetles. Owing to limited postglacial migration, hotspots of high‐altitude endemics are situated in rather low peripheral mountain chains of the Alps, which have not been glaciated during the Pleistocene. There, tree line expansion disproportionally reduces habitats of high‐altitude species. Such legacies of climate history, which may aggravate extinction risks under future climate change have to be expected for many temperate mountain ranges.     

New species of the snakefly genus Mongoloraphidia (Raphidioptera: Raphidiidae) from Japan and Taiwan,with phylogenetic and biogeographical remarks on the Raphidiidae of Eastern Asia

Two species of the snakefly genus Mongoloraphidia Aspöck & Aspöck, 1968 from Japan and Taiwan are described as new to science: Mongoloraphidia (Japanoraphidia) occidentalis sp. nov. and Mongoloraphidia (Formosoraphidia) curvata sp. nov. A key to the species of Mongoloraphidia from Eastern Asia is provided. Phylogenetic and biogeographical aspects on the Raphidiidae from Eastern Asia are discussed.     

Circadian rhythms in rat brain alpha- and beta-adrenergic receptors are modified by chronic imipramine

Circadian rhythms of α- and ß-adrenergic receptor number, with different wave forms, as well as differences in timing of maximal binding, are present in rat brain. Chronic treatment with the tricyclic antidepressant drug imipramine modifies these rhythms: peak binding of both receptors occurs 4–12 hours later than in controls, the 24-hour mean is decreased by 15–30%, and the amplitude is increased by 20–30%. Delaying of the phase position of neurotransmitter receptor rhythms by a tricyclic antidepressant may be relevant to its clinical mode of action, since depressive patients appear to have abnormally phase-advanced circadian rhythms.