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Endometrial cancer, a type of primary epithelial malignant tumor in the endometrium, is one of the three most common malignant tumors of the female reproductive system. While the incidence of endometrial cancer has been recently rising, its etiology remains unclear. In this study we found that EM2D9, an independently developed monoclonal antibody, specifically recognized endometrial cancer cells; we further determined that EM2D9 target protein was α5β1. In vitro and in vivo experiments showed that EM2D9 inhibited the migration of endometrial cancer cells. Real-time quantitative PCR results showed that the expression of CD151 mRNA in endometrial carcinoma cells significantly decreased after EM2D9 treatment. We also found that EM2D9 affected the FAK signaling pathway. Collectively, these results shed light on a new mechanism for the development of endometrial carcinoma.

B-site doping is an effective strategy to improve the performance of inorganic perovskite solar cells. Zinc halides (ZnX2, X I, Br, Cl) doped CsPbIBr2 solar cells were prepared by simply introducing ZnX2 salts into the precursor solution for one step spin-coating process. The doped inorganic perovskite films exhibit enhanced crystallinity and improved surface morphology. More over, the photoluminescence and single-carrier device characterizations confirm that the internal defect density of CsPbIBr2 films decreases remarkably after ZnX2 doping and the non-radiative recombination is suppressed. The CsPbIBr2 solar cells based on the ZnI2 doped films achieve a champion efficiency of 8.15%, outperforming that (6.93%) of the pristine counterpart.

The researches on polarized electroluminescence have attracted attention in recent years because of their potential applications in the field of liquid crystal display polarized backlights. The key to producing polarized light is the ordered orientation of anisotropic emission materials. Perovskite nanowires are an anisotropic one-dimensional nanomaterial with excellent optical properties. We used the off-center spin-coating method to fabricate the aligned CsPbBr3 nanowire films and obtained a photoluminescence polarization ratio of 0.46. The light-emitting diodes using the aligned nanowire film as the emission layer was fabricated and the device performance investigated.

Aplastic anemia (AA) is characterized by a reduced number of hematopoietic stem cells and fatty replacement in the bone marrow. Transcriptional factor GATA-2 plays several important roles in both hematopoiesis and adipogenesis. Decreased levels of GATA-2 compromise the proliferation and survival of hematopoietic stem cells. GATA-2 suppresses adipocyte differentiation through direct inhibition of adipogenic factors, including peroxisome proliferator-activated receptor-gamma (PPARgamma). Previous studies have shown that expression of GATA-2 is decreased in marrow CD34-positive cells in AA. To elucidate the mechanisms of fatty marrow replacement, we evaluated the mRNA expression for GATA-2 and PPARgamma in mesenchymal stem cells (MSCs) from patients with AA by quantitative real-time polymerase chain reaction. GATA-2 expression by MSCs from AA patients was significantly lower than in normal subjects. Conversely, expression of PPARgamma was significantly higher in AA patients. Western blot analysis demonstrated that protein levels of GATA-2 were lower in AA patients than those in normal subjects. Moreover, incubation with interferon-gamma induced downregulation of GATA-2 levels in MSCs from normal subjects. These findings indicate that fatty marrow replacement in AA patients can be explained by downregulation of GATA-2 and overexpression of PPARgamma in MSCs. Decreased expression of GATA-2 might be responsible for the pathogenesis and development of the clinical features of the disease.

Peripherally produced corticotrophin-releasing hormone (CRH) is a strong proinflammatory factor involved in many inflammatory diseases. However, to date, there is no evidence about the action of CRH on atherosclerosis, a chronic disease characterized by inflammatory reactions. In this study we observed the effect of CRH on atherosclerosis in low-density lipoprotein receptor-deficient (LDLr-/-) mice. Twelve-week-old, male LDLr-/- mice were subcutaneously injected with CRH (10microg/kg) or vehicle once a day for 8 weeks. The results indicated aortic atherosclerotic lesions were larger (P

As a member of the corticotropin-releasing factor (CRF) family, urocortin (UCN) has been demonstrated to show diverse effects on cardiovascular system. It is commonly considered as a protective agent on vascular function. However, a growing body of evidence suggests that some effects of UCN may lead to endothelial dysfunction (ED) which may be the cause or consequence of vascular disease and a hallmark of known cardiovascular risk factors. The present review is then focused on recent evidence that reveals the beneficial and detrimental effects of UCN on endothelium.

PTPN11, the gene which encodes protein tyrosine phosphatase SHP-2, plays an important role in regulating intracellular signaling. Germline mutations in PTPN11 were first observed in Noonan syndrome, while somatic mutations were identified in hematological myeloid malignancies. Recently, PTPN11 mutations have been reported in children with acute lymphoblastic leukemia (ALL). In the present study, we investigated the prevalence of mutations in PTPN11, RAS and FLT3 in samples from 95 Japanese children with ALL. We observed exon 3 and 8 missense mutations of PTPN11 in 6 children with B precursor ALL. One patient with Down syndrome and ALL had PTPN11 mutation. We also identified RAS mutations in ten patients and FLT3 internal tandem duplication (FLT3/ITD) in one patient. None of the patients had simultaneous mutations in PTPN11 and RAS, while one patient had both PTPN11 and FLT3 mutations. These data suggest that PTPN11 mutation may play an important role for leukemogenesis in a proportion of children with ALL, particularly B precursor ALL.

Genistein (4,5,7-trihydroxyisoflavone), a phytoestrogen with selective estrogen receptor modulator properties, has received a great deal of attention over the last few years because of its potentially preventive roles against cardiovascular diseases. However, the precise molecular mechanisms for this modulation are not fully elucidated. In this study, we investigated (both in vivo and in vitro) the relationship between genistein and the changes of angiotensin-converting enzyme (ACE) in rat aortic endothelial cells (RAECs), serum and tissue (aorta). ACE expression was assessed by the immunofluorescence and the reverse transcriptase-polymerase chain reaction (RT-PCR) assay. Serum and tissue ACE activity was detected with a commercial kit. Genistein exhibited a concentration-dependent inhibitory effect on the expression of ACE, particularly at higher concentrations (24.70+/-1.20 at 100microM, P0.01, and 18.22+/-0.92 at 200microM, P0.01 compared with the control group 50.49+/-5.19). The estrogen receptor blocker tamoxifen at 100microM attenuated this effect of genistein. The extracellular signal-regulated kinase 1/2 (ERK1/2) blocker PD98059 also markedly inhibited this effect. The observations in vivo were highly consistent with the data in RAECs. These results indicate that genistein inhibits the expression of ACE via estrogen receptor and subsequently ERK1/2 signaling pathway in RAECs. Our results suggest that the down-regulation of ACE with a consequent change in the circulating levels of angiotensin II (Ang II), vasorelaxant angiotensin-(1-7) [Ang-(1-7)] and bradykinin plays an important role in cardiovascular effects of genistein through the ERK1/2 pathway.

Bronchial asthma is defined as a chronic airway inflammatory disease characterized by sustained activation of many inflammatory cells including mast cells. Urocortin (UCN) is synthesized and secreted by human mast cells and activated mast cells release more UCN. On the other hand, UCN can induce mast cell degranulation and generation of many proinflammatory factors. The purpose of this study was to examine the expression profile of UCN in rat lung with allergic asthma. Twenty-four male Sprague-Dawley rats were allocated to normal control, asthma model, and dexamethasone group, respectively. Animals were actively sensitized by subcutaneous injection of ovalbumin (OVA) and challenged by an aerosol of 1% OVA 2 weeks after sensitization. Both UCN mRNA and peptide were expressed in normal rat lungs. Rats in asthma model group developed severe infiltration of inflammatory cells and inflammation in airway, together with a significantly up-regulated expression of urocortin mRNA detected by semi-quantitative reverse transcriptase-polymerase chain reaction and peptide measured both by immunohistochemistry and Western blot analysis. In contrast, treatment with dexamethasone resulted in markedly ameliorated airway inflammation and alleviated airway inflammatory cell infiltration, coupled with a significantly decreased urocortin expression. Regression analysis revealed a positive correlation between urocortin expression and the number of inflammatory cells in bronchoalveolar lavage fluid (P