63 research outputs found
IL-7 and IL-8 inhibit gamete interaction in the zona-free hamster egg sperm penetration assay
Mapping of the dark exciton landscape in transition metal dichalcogenides
Transition metal dichalcogenides (TMDs) exhibit a remarkable exciton physics including bright and optically forbidden dark excitonic states. Here, we show how dark excitons can be experimentally revealed by probing the intraexcitonic 1s-2p transition. Distinguishing the optical response shortly after the excitation and after the exciton thermalization allows us to reveal the relative position of bright and dark excitons. We find both in theory and experiment a clear blueshift in the optical response demonstrating the transition of bright exciton populations into lower-lying dark excitonic states
EPA-0502 - A systematic analysis of all studies that ambiguously prove copycat suicides after media coverage of suicide [Abstract]
IL-7 and IL-8 inhibit gamete interaction in the zona-free hamster egg sperm penetration assay
Current thought in reproductive endocrinology suggests hat endometriosis-associated subfertility may be the result of an adverse influence of activated immunocompetent cells on fertilization and embryo development. Inflammatory ediators such as interleukin-1 and tumour necrosis actor have been implicated in the pathophysiology of this process. The purpose of this study was to assess the effect of two recently characterized cytokines, interleukin-7 (IL-7 ) and interleukin-8 (IL-8), on gamete interaction in the perm penetration assay (SPA). Donor sperm were preincubated or 4 h with 0.5, 5, 50, or 500 ng ml-1 of human ecombinant IL-7 or IL-8. Sperm penetration was determined by an experienced gametologist by the presence of decondensed sperm heads or pronuclei formation. A dose-dependent inhibition of gamete interaction was observed following coincubation with either IL-7 or IL-8. These data offer the possibility that IL-7 and IL-8 may play a role in the pathogenesis of immunocompetent cell-associated subfertility
Mg(2+) Deprivation Elicits Rapid Ca(2+) Uptake and Activates Ca(2+)/Calcineurin Signaling in Saccharomyces cerevisiae
To learn about the cellular processes involved in Mg(2+) homeostasis and the mechanisms allowing cells to cope with low Mg(2+) availability, we performed RNA expression-profiling experiments and followed changes in gene activity upon Mg(2+) depletion on a genome-wide scale. A striking portion of genes up-regulated under Mg(2+) depletion are also induced by high Ca(2+) and/or alkalinization. Among the genes significantly up-regulated by Mg(2+) starvation, Ca(2+) stress, and alkalinization are ENA1 (encoding a P-type ATPase sodium pump) and PHO89 (encoding a sodium/phosphate cotransporter). We show that up-regulation of these genes is dependent on the calcineurin/Crz1p (calcineurin-responsive zinc finger protein) signaling pathway. Similarly to Ca(2+) stress, Mg(2+) starvation induces translocation of the transcription factor Crz1p from the cytoplasm into the nucleus. The up-regulation of ENA1 and PHO89 upon Mg(2+) starvation depends on extracellular Ca(2+). Using fluorescence resonance energy transfer microscopy, we demonstrate that removal of Mg(2+) results in an immediate increase in free cytoplasmic Ca(2+). This effect is dependent on external Ca(2+). The results presented indicate that Mg(2+) depletion in yeast cells leads to enhanced cellular Ca(2+) concentrations, which activate the Crz1p/calcineurin pathway. We provide evidence that calcineurin/Crz1p signaling is crucial for yeast cells to cope with Mg(2+) depletion stress
- …