Preparation, Characterization and NO-CO Redox Reaction Studies over Palladium and Rhodium Oxides Supported on Manganese Dioxide

The catalytic activity of PdO/MnO2 and Rh2O3/MnO2 is investigated for NO-CO redox reaction. Supported catalysts are prepared by wet impregnation method. Among the tested catalysts, PdO/MnO2 shows higher activity for this reaction. Active metal dispersion on MnO2 enhances the selectivity for N2 over N2O in this reaction. The XRD substantiate the formation of MnO2 monophasic phase. SEM images show the formation of elongated particles. TEM images indicate nano-size rod-like morphologies. An increase in the catalytic activity is observed on supported Pd and Rh oxides on MnO2. Temperature programed desorption studies with NO and CO are undertaken to investigate the catalytic surface studies. © 2015 BCREC UNDIP. All rights reserve

Photoluminescence and photocatalytic degradation studies on some metallophthalocyanines

This paper deals with the up-conversion intrinsic photoluminescence by exciting the Metallo-Phthalocyanine (MPc) prepared by melt method. MPcs were further characterized using UV visible spectrophotometer, FT-IR, and thermal analysis. The magnetic susceptibility, optical absorption and photoluminescence behavior of these compounds were studied. Photocatalytic degradation of amido black 10B dye using different MPcs at varing pH was done to see the efficiency of these compounds. High emission intensity and easy preparation makes these systems potential candidates for application as luminescent material

Partial Oxidation of Propylene over as Prepared and Acid Enriched Bi2Mo1-xWxO6 System

The compounds Bi2Mo1-xWxO6 (x = 0.0, 0.2, and 0.4) were obtained through a Citrate sol-gel process. Thermogravimetric differential thermal analysis (TG-DTA), X-ray diffraction (XRD), Scanning electron microscopy (SEM) and X-ray photoelectron spectroscopy (XPS) techniques were used for characterization. Reitveld refinement of the XRD data confirmed the crystal structure of all the compositions to be orthorhombic, having Pca21 space group. XPS studies indicated the presence of +6 as well as +4 oxidation state for Mo. Surface acid enrichment of all the catalysts was done and monitored by NH3-TPD studies. Partial oxidation of propylene was studied over all the compounds. The W doping was found to increase the catalytic activity. Moreover, as-prepared catalysts and acid enriched catalysts were compared for their catalytic activity wherein, acid-enriched catalysts showed the improved conversion of propylene without hampering the product selectivity profile.

Characterization of the Endometrium of Women with Reproductive Failure

Differentiation of human endometrial stromal cells (HESCs) into decidual cells represents a highly coordinated process essential for embryo implantation. Following the post-ovulatory rise in progesterone levels HESCs undergo biochemical and morphological transformation in a process known as decidualization. It heralds the end of the mid-secretory phase implantation window, defined as the limited period during which progesterone-driven changes in the luminal epithelium allow apposition, attachment and invasion of a developmentally competent blastocyst. Failure of the endometrium to acquire a receptive phenotype is widely viewed as a major cause of infertility and IVF treatment failure. Conversely, recurrent pregnancy loss (RPL) is associated with impaired decidualization. Firstly, analysis of mid-secretory endometrial biopsies from RPL patients demonstrated that there is a decreased expression of the decidual marker, Prolactin but increased levels of pro-inflammatory cytokine, Prokineticin-1. Secondly, HESCs were then identified to mount a highly coordinated but transient inflammatory response that renders the endometrium receptive, by rapidly releasing Interleukin-33, up-regulating its cognate transmembrane receptor-ST2L and other pro-inflammatory mediators before mounting an anti-inflammatory response that includes down-regulation of ST2L and increased secretion of the soluble decoy receptor sST2. In agreement, only during the transient pro-inflammatory phase of the decidual process did HESCs secrete factors conducive to implantation in mice. Failure of HESCs to constrain this pro-inflammatory response appeared to prolong the implantation window and was associated with RPL. Furthermore, deregulated Serum and Glucocorticoid Kinase 1 (SGK1) activity in the endometrium during the window of implantation either interfered with embryo implantation, leading to infertility, or compromised the integrity of the decidual-placental interface, resulting in pregnancy loss. A constitutively active SGK1 mutant was expressed in luminal epithelial cells of the mouse uterus; perturbing uterine fluid handling and abolished embryo implantation. However, implantation was not impaired in Sgk1-deficient mice, although there was evidence of fetal demise. RPL was also associated with lower SGK1 induction in decidualizing HESCs and impaired expression of oxidative stress defence genes. In summary, impaired decidualization or unfettered endometrial receptivity carries an obvious risk of implantation of developmentally delayed or compromised embryos thus triggering a spectrum of pathological events, leading to miscarriage or predisposing for obstetrical complications. Together, these findings provide fundamental insights of uterine receptivity and describe a novel paradigm of reproductive failure with potentially far-reaching clinical implications

Role of Dicer Enzyme in the Regulation of Store Operated Calcium Entry (SOCE) in CD4+ T Cells

Background/Aims: Activation of T cell receptors (TCRs) in CD4+ T cells leads to a cascade of signalling reactions including increase of intracellular calcium (Ca2+) levels with subsequent Ca2+ dependent stimulation of gene expression, proliferation, cell motility and cytokine release. The increase of cytosolic Ca2+ results from intracellular Ca2+ release with subsequent activation of store-operated Ca2+ entry (SOCE). Previous studies suggested miRNAs are required for the development and functions of CD4+ T cells. An enzyme called Dicer is required during the process of manufacturing mature miRNAs from the precursor miRNAs. In this study, we explored whether loss of Dicer in CD4+ T cells affects SOCE and thus Ca2+ dependent regulation of cellular functions. Methods: We tested the expression of Orai1 by q-RT-PCR and flow cytometry. Further, we measured SOCE by an inverted phase-contrast microscope with the Incident-light fluorescence illumination system using Fura-2. Intracellular Ca2+ was also measured by flow cytometry using Ca2+ sensitive dye Fluo-4. Results: We found that in Dicer deficient (DicerΔ/Δ) mice Orai1 was downregulated at mRNA and protein level in CD4+ T cells. Further, SOCE was significantly smaller in DicerΔ/Δ CD4+ T cells than in CD4+ T cells isolated from wild-type (Dicerfl/fl) mice. Conclusion: Our data suggest that miRNAs are required for adequate Ca2+ entry into CD4+ T cells and thus triggering of Ca2+ sensitive immune functions

Uterine selection of human embryos at implantation

Human embryos frequently harbor large-scale complex chromosomal errors that impede normal development. Affected embryos may fail to implant although many first breach the endometrial epithelium and embed in the decidualizing stroma before being rejected via mechanisms that are poorly understood. Here we show that developmentally impaired human embryos elicit an endoplasmic stress response in human decidual cells. A stress response was also evident upon in vivo exposure of mouse uteri to culture medium conditioned by low-quality human embryos. By contrast, signals emanating from developmentally competent embryos activated a focused gene network enriched in metabolic enzymes and implantation factors. We further show that trypsin, a serine protease released by pre-implantation embryos, elicits Ca2+ signaling in endometrial epithelial cells. Competent human embryos triggered short-lived oscillatory Ca2+ fluxes whereas low-quality embryos caused a heightened and prolonged Ca2+ response. Thus, distinct positive and negative mechanisms contribute to active selection of human embryos at implantation

Activation of SGK1 in endometrial epithelial cells in response to PI3K/AKT inhibition impairs embryo implantation

Background: Serum & Glucocorticoid Regulated Kinase 1 (SGK1) plays a fundamental role in ion and solute transport processes in epithelia. In the endometrium, down-regulation of SGK1 during the window of receptivity facilitates embryo implantation whereas expression of a constitutively active mutant in the murine uterus blocks implantation. Methods/Results: Here, we report that treatment of endometrial epithelial cells with specific inhibitors of the phosphoinositide 3-kinase (PI3K)/AKT activity pathway results in reciprocal activation of SGK1. Flushing of the uterine lumen of mice with a cell permeable, substrate competitive phosphatidylinositol analogue that inhibits AKT activation (AKT inhibitor III) resulted in Sgk1 phosphorylation, down-regulation of the E3 ubiquitin-protein ligase Nedd4-2, and increased expression of epithelial Na+ channels (ENaC). Furthermore, exposure of the uterine lumen to AKT inhibitor III prior to embryo transfer induced a spectrum of early pregnancy defects, ranging from implantation failure to aberrant spacing of implantation sites. Conclusion: Taken together, our data indicate that the balanced activities of two related serine/threonine kinases, AKT and SGK1, critically govern the implantation process

LEFTY2 inhibits endometrial receptivity by downregulating Orai1 expression and store-operated Ca²+ entry

Early embryo development and endometrial differentiation are initially independent processes, and synchronization, imposed by a limited window of implantation, is critical for reproductive success. A putative negative regulator of endometrial receptivity is LEFTY2, a member of the transforming growth factor (TGF)-β family. LEFTY2 is highly expressed in decidualizing human endometrial stromal cells (HESCs) during the late luteal phase of the menstrual cycle, coinciding with the closure of the window of implantation. Here, we show that flushing of the uterine lumen in mice with recombinant LEFTY2 inhibits the expression of key receptivity genes, including Cox2, Bmp2, and Wnt4, and blocks embryo implantation. In Ishikawa cells, a human endometrial epithelial cell line, LEFTY2 downregulated the expression of calcium release-activated calcium channel protein 1, encoded by ORAI1, and inhibited store-operated Ca2+ entry (SOCE). Furthermore, LEFTY2 and the Orai1 blockers 2-APB, MRS-1845, as well as YM-58483, inhibited, whereas the Ca2+ ionophore, ionomycin, strongly upregulated COX2, BMP2 and WNT4 expression in decidualizing HESCs. These findings suggest that LEFTY2 closes the implantation window, at least in part, by downregulating Orai1, which in turn limits SOCE and antagonizes expression of Ca2+-sensitive receptivity genes