Postvest0564

Low-temperature synthesis in ionic liquids (ILs) offers an efficient route for the preparation of metal oxide nanomaterials with tailor-made properties in a water-free environment. In this work, we investigated the role of 1-butyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)imide [C4 C1 Pyr][NTf2 ] in the synthesis of cobalt oxide nanoparticles from the molecular precursor Co2 (CO)8 with ozone. We performed a model study in ultra-clean, ultrahigh vacuum (UHV) conditions by infrared reflection absorption spectroscopy (IRAS) using Au(111) as a substrate. Exposure of the pure precursor to ozone at low temperatures results in the oxidation of the first layers, leading to the formation of a disordered Cox Oy passivation layer. Similar protection to ozone is also achieved by deposition of an IL layer onto a precursor film prior to ozone exposure. With increasing temperature, the IL gets permeable for ozone and a cobalt oxide film forms at the IL/precursor interface. We show that the interaction with the IL mediates the oxidation and leads to a more densely packed Cox Oy film compared to a direct oxidation of the precursor.Hepatocellular carcinoma (HCC) inevitably developed oxaliplatin (OXA) resistance after long-term treatment, but the mechanism remains unclear. Here, we found that LncRNA UCA1 was upregulated in most of OXA-resistant HCC tissues and cells (HepG2/OXA and SMMC-7721/OXA). Follow-up analysis and online Kaplan-Meier Plotter revealed that HCC patients with high UCA1 level had a shorter survival compared with those with low expression. Overexpression of UCA1 increased OXA IC50 in HepG2 and SMMC-7721 cells, whereas knockdown of UCA1 decreased OXA IC50 in resistant counterparts. Moreover, dual luciferase reporter assay showed that co-transfection of UCA1-WT plasmid with miR-138-5p mimics enhanced fluorescence signals, whereas co-transfection of UCA1-Mut plasmid and miR-138-5p mimics did not induce any changes. Consistently, UCA1 levels in HepG2/OXA and SMMC-7721/OXA cells were downregulated after transfected with miR-138-5p mimics. UCA1 silencing or transfection of miR-138-5p mmics inhibited the activation of AKT and mTOR in HepG2/OXA and SMMC-7721/OXA cells, whereas UCA1 overexpression increased the phosphorylated AKT and mTOR levels in parental counterparts. Rapamycin or miR-138-5p mimics similarly suppressed the activation of AKT and mTOR, whereas UCA1 overexpression exert opposite roles. Interestingly, administration of rapamycin or miR-138-5p mimics apparently antagonized the effects of UCA1 on AKT and mTOR activation. Besides, depletion of UCA1 triggered more dramatic regression of HepG2 xenografts than that of HepG2/OXA xenografts with OXA treatment and impaired the p-AKT and p-mTOR levels in vivo. In conclusion, our findings provide the evidence that UCA1 may contribute to OXA resistance via miR-138-5p-mediated AK /mTOR activation, suggesting that UCA1 is a potential therapeutic target for HCC.It is unknown whether cholecalciferol supplementation improves allograft outcomes in kidney transplant recipients (KTRs). We conducted a single-center randomized, double-blind, placebo-controlled trial of daily 4000 IU cholecalciferol supplementation in KTRs at 1-month posttransplant. The primary endpoint was the change in eGFR from baseline to 12-month posttransplant. Secondary endpoints included severity of interstitial fibrosis and tubular atrophy (IFTA) at 12-month posttransplant and changes in urinary biomarkers. Of 193 randomized patients, 180 participants completed the study. Changes in eGFR were 1.2 mL/min/1.73 m2 (95% CI; -0.7 to 3.1) in the cholecalciferol group and 1.8 mL/min/1.73 m2 (95% CI, -0.02 to 3.7) in the placebo group, with no significant between-group difference (-0.7 mL/min/1.73 m2 [95% CI; -3.3 to 2.0], p = 0.63). Subgroup analyses showed detrimental effects of cholecalciferol in patients with eGFR less then 45 mL/min/1.73 m2 (Pinteraction less then 0.05, between-group difference; -4.3 mL/min/1.73 m2 [95% CI; -7.3 to -1.3]). The degree of IFTA, changes in urine albumin-to-creatinine ratio, or adverse events including hypercalcemia and infections requiring hospitalization did not differ between groups. In conclusion, cholecalciferol supplementation did not affect eGFR change compared to placebo among incident KTRs. These findings do not support cholecalciferol supplementation for improving allograft function in incident KTRs. Clinical trial registry This study was registered in the University Hospital Medical Information Network Clinical Trials Registry (UMIN-CTR) as UMIN000020597 (please refer to the links below). UMIN-CTR https//upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000023776.The Par-3/Baz family of polarity determinants is highly conserved across metazoans and includes C. elegans PAR-3, Drosophila Bazooka (Baz), human Par-3 (PARD3), and human Par-3-like (PARD3B). The C. elegans PAR-3 protein localises to the anterior pole of asymmetrically dividing zygotes with cell division cycle 42 (CDC42), atypical protein kinase C (aPKC), and PAR-6. The same C. buy Telratolimod elegans 'PAR complex' can also localise in an apical ring in epithelial cells. Drosophila Baz localises to the apical pole of asymmetrically dividing neuroblasts with Cdc42-aPKC-Par6, while in epithelial cells localises both in an apical ring with Cdc42-aPKC-Par6 and with E-cadherin at adherens junctions. These apical and junctional localisations have become separated in human PARD3, which is strictly apical in many epithelia, and human PARD3B, which is strictly junctional in many epithelia. We discuss the molecular basis for this fundamental difference in localisation, as well as the possible functions of Par-3/Baz family proteins as oligomeric clustering agents at the apical domain or at adherens junctions in epithelial stem cells. The evolution of Par-3 family proteins into distinct apical PARD3 and junctional PARD3B orthologs coincides with the emergence of stratified squamous epithelia in vertebrates, where PARD3B, but not PARD3, is strongly expressed in basal layer stem cells - which lack a typical apical domain. We speculate that PARD3B may contribute to clustering of E-cadherin, signalling from adherens junctions via Src family kinases or mitotic spindle orientation by adherens junctions in response to mechanical forces.Invited for this month's cover is the group of Michael Ruck at the Technische Universität Dresden (Germany). The cover picture shows the spiro-dicubane Bi7 S85+ in the center, accompanied by two Bi4 S44+ hetero-cubanes on both sides, which are shown along their threefold axis. These sulfidobismuth polycations were isolated in salts with [AlCl4 ]- and [S(AlCl3 )3 ]2- anions. The starting material was Bi2 S3 , which is generally hard to dissolve but can easily be activated under ionothermal conditions. Moreover, the presence of noble metal ions, such as Ag+ , Au+ or Pt2+ , played a crucial role for the formation of those compounds. This research was performed in the framework of the Priority Program SPP 1708 "Material Synthesis Near Room Temperature" of the German Research Council (DFG). Read the full text of their Full Paper at 10.1002/open.202000246.Due to a shortage of donation after brain death (DBD) organs, donation after circulatory death (DCD) is increasingly performed. In the field of islet transplantation, there is uncertainty regarding the suitability of DCD pancreas in terms of islet yield and function after islet isolation. The aim of this study was to investigate the potential use of DCD pancreas for islet transplantation. Islet isolation procedures from 126 category 3 DCD and 258 DBD pancreas were performed in a 9-year period. Islet yield after isolation was significantly lower for DCD compared to DBD pancreas (395 515 islet equivalents [IEQ] and 480 017 IEQ, respectively; p = .003). The decrease in IEQ during 2 days of culture was not different between the two groups. Warm ischemia time was not related to DCD islet yield. In vitro insulin secretion after a glucose challenge was similar between DCD and DBD islets. After islet transplantation, DCD islet graft recipients had similar graft function (AUC C-peptide) during mixed meal tolerance tests and Igls score compared to DBD graft recipients. In conclusion, DCD islets can be considered for clinical islet transplantation.Lung transplant recipients are at high risk for herpes zoster and preventive measures are a significant unmet need. We investigated the safety and immunogenicity of two doses of a recombinant zoster vaccine (RZV) in lung transplant recipients (≥50 years). We enrolled 50 patients of which 49 received at least one vaccine dose. Anti-glycoprotein E (gE) antibody levels (n = 43) increased significantly compared to baseline (median optical density [OD] 1.96; interquartile range [IQR] 1.17-2.89) after the first (median OD 3.41, IQR 2.54-3.81, p less then .0001) and second vaccine dose (median OD 3.63, IQR 3.39-3.86, p less then .0001). gE-specific polyfunctional CD4+ T cell frequencies (n = 38) also increased from baseline (median 85 per 106 CD4+ T cells; IQR 46-180) to the first (median 128 per 106 CD4+ T cells; IQR 82-353; p = .023) and after the second dose (median 361 per 106 CD4+ T cells; IQR 146-848; p less then .0001). Tenderness (83.0%; 95%CI 69.2-92.4%) and redness (31.9%; 95%CI 19.1-47.1%) at injection site were common. One rejection episode within 3 weeks of vaccination was observed. This is the first study demonstrating that RZV was safe and elicited significant humoral and cell-mediated immunity in lung transplant recipients. RZV is a new option for the prevention of shingles in this population.Nutrition is recognized as one of the leading factors influencing the growing incidence of noncommunicable diseases. Despite society experiencing a global rise in obesity, specific populations remain at risk of nutrient deficiencies. The food industry can use health claims to inform consumers about the health benefits of foods through labeling and the broader promotion of specific food products. As health claims are carefully regulated in many countries, their use is limited due to considerable investments required to fulfill the regulatory requirement. Although health claims represent a driving force for innovation in the food industry, the risk of misleading of consumers need to be avoided. The health claim scientific substantiation process must be efficient and transparent in order to meet the needs of companies in the global market, but should be based on strong scientific evidence and plausible mechanisms of actions, to ensure highest level of consumer protection. The objective of this review is to compare the possibilities for using health claims on foods in the European Union, the USA, Canada, and Australia and New Zealand. In particular, we focused on differences in the classification of claims, on the scientific substantiation processes and requirements for health claims use on foods in the selected regions. Reduction of disease risk (RDR) claims are associated with relatively similar procedures and conditions for use, whereas several notable differences were identified for other types of claims. In all cases, RDR claims must be approved prior their introduction to the market, and only a few such claims have been authorized. Much greater differences were observed concerning other types of claims.