A one-dimensional cadmium(II) complex supported by a sulfur–nitro­gen mixed-donor ligand

In the title compound, catena-poly[cadmium(II)-bis­(μ-5-am­ino-1,3,4-thia­diazole-2-thiol­ato)-κ2 N 3:S 2;κ2 S 2:N 3], [Cd(C2H2N3S2)2]n, the CdII ion is coordinated by two N atoms of the 1,3,4-thia­diazole rings from two ligands and two S atoms of sulfhydryl from two other ligands in a slightly distorted tetra­hedral geometry. The ligands bridge CdII ions, forming one-dimensional chains along [001], which are connected by N—H⋯N and N—H⋯S hydrogen bonds into a three-dimensional network

Tunable interfacial chemisorption with atomic-level precision in a graphene WSe2 heterostructure

It has long been an ultimate goal to introduce chemical doping at the atomic level to precisely tune properties of materials. Two-dimensional materials have natural advantage because of its highly-exposed surface atoms, however, it is still a grand challenge to achieve this goal experimentally. Here, we demonstrate the ability to introduce chemical doping in graphene with atomic-level precision by controlling chemical adsorption of individual Se atoms, which are extracted from the underneath WSe2, at the interface of graphene-WSe2 heterostructures. Our scanning tunneling microscopy (STM) measurements, combined with first-principles calculations, reveal that individual Se atoms can chemisorbed on three possible positions in graphene, which generate distinct pseudospin-mediated atomic-scale vortices in graphene. We demonstrate that the chemisorbed positions of individual Se atoms can be manipulated by STM tip, which enables us to achieve atomic-scale controlling quantum interference of the pseudospin-mediated vortices in graphene. This result offers the promise of controlling properties of materials through chemical doping with atomic-level precision

(Arg) 9 -SH2 superbinder: A novel promising anticancer therapy to melanoma by blocking phosphotyrosine signaling

Background: Melanoma is a malignant tumor with high misdiagnosis rate and poor prognosis. The bio-targeted therapy is a prevailing method in the treatment of melanoma; however, the accompanying drug resistance is inevitable. SH2 superbinder, a triple-mutant of the Src Homology 2 (SH2) domain, shows potent antitumor ability by replacing natural SH2-containing proteins and blocking multiple pY-based signaling pathways. Polyarginine (Arg) 9 , a powerful vector for intracellular delivery of large molecules, could transport therapeutic agents across cell membrane. The purpose of this study is to construct (Arg) 9 -SH2 superbinder and investigate its effects on melanoma cells, expecting to provide potential new approaches for anti-cancer therapy and overcoming the unavoidable drug resistance of single-targeted antitumor agents. Methods: (Arg) 9 and SH2 superbinder were fused to form (Arg) 9 -SH2 superbinder via genetic engineering. Pull down assay was performed to identify that (Arg) 9 -SH2 superbinder could capture a wide variety of pY proteins. Immunofluorescence was used to detect the efficiency of (Arg) 9 -SH2 superbinder entering cells. The proliferation ability was assessed by MTT and colony formation assay. In addition, wound healing and transwell assay were performed to evaluate migration of B16F10, A375 and A375/DDP cells. Moreover, apoptosis caused by (Arg) 9 -SH2 superbinder was analyzed by flow cytometry-based Annexin V/PI. Furthermore, western blot revealed that (Arg) 9 -SH2 superbinder influenced some pY-related signaling pathways. Finally, B16F10 xenograft model was established to confirm whether (Arg) 9 -SH2 superbinder could restrain the growth of tumor. Results: Our data showed that (Arg) 9 -SH2 superbinder had the ability to enter melanoma cells effectively and displayed strong affinities for various pY proteins. Furthermore, (Arg) 9 -SH2 superbinder could repress proliferation, migration and induce apoptosis of melanoma cells by regulating PI3K/AKT, MAPK/ERK and JAK/STAT signaling pathways. Importantly, (Arg) 9 -SH2 superbinder could significantly inhibit the growth of tumor in mice. Conclusions: (Arg) 9 -SH2 superbinder exhibited high affinities for pY proteins, which showed effective anticancer ability by replacing SH2-containing proteins and blocking diverse pY-based pathways. The remarkable ability of (Arg) 9 -SH2 superbinder to inhibit cancer cell proliferation and tumor growth might open the door to explore the SH2 superbinder as a therapeutic agent for cancer treatment

Transmission Characteristics of Barley Yellow Striate Mosaic Virus in Its Planthopper Vector Laodelphax striatellus

The most economically important plant viruses are specifically transmitted by phytophagous insects that significantly affect viral epidemiology. Barley yellow striate mosaic virus (BYSMV), a member of the genus Cytorhabdovirus, is transmitted by the small brown planthopper (SBPH, Laodelphax striatellus) in a persistent-propagative manner. However, the infection route of BYSMV in SBPHs is poorly understood. In this study, immunofluorescence confocal laser scanning microscopy (iCLSM) was performed to investigate the route of BYSMV in SBPHs. We unexpectedly found that BYSMV initially infected the hindgut epithelium of SBPHs, instead of the midgut epithelium initially infected by other persistent-propagative viruses. Subsequently, BYSMV disseminated to the hindgut visceral muscles and spread to other parts of alimentary canals, hemolymph, and salivary glands. Comparative analysis of gene expression on viral mRNAs and the BYSMV nucleoprotein by using different molecular detection and immunohistochemistry further demonstrated that BYSMV initially infected and replicated in the hindgut epithelial cells of SBPHs. Collectively, our study provides the first insight into that hindgut is initial infection site of BYSMV that represents a new dissemination route of persistent-propagative viruses

Increased CD4+CD25+ regulatory T cells correlate with poor short-term outcomes in hepatitis B virus-related acute-on-chronic liver failure patients

BackgroundThe roles of CD4+CD25+ regulatory T cells (Treg) in chronicity of hepatitis B virus (HBV) infection have been confirmed. We aimed to explore alteration of Treg in patients with HBV-related acute-on-chronic liver failure (ACLF).MethodsThirty-two HBV-related ACLF patients, 44 chronic hepatitis B patients, and 41 healthy controls were recruited. We detected frequencies of peripheral Treg and intrahepatic forkhead winged helix transcription factor (Foxp3)+ cells. Inhibitory activity of Treg was assessed by functional suppression assays. Serum interferon-γ and interleukin-10 were also determined.ResultsPeripheral Treg and intrahepatic Foxp3+ cells were more markedly increased in ACLF than chronic hepatitis B and controls (all p < 0.001), and the Foxp3+ cells located predominantly in the portal areas. The Treg frequency was positively correlated with HBV DNA load, international normalized ratio, model of end stage liver disease score, and serum interleukin-10 level in ACLF patients. Functional assays in vitro demonstrated that ACLF patients exhibited higher suppressive effects of Treg on proliferations of autologous CD4+CD25− T cells than controls. On logistic regression, prolonged international normalized ratio and higher peripheral Treg frequency predicted 30-day survival of ACLF.ConclusionThe patients with HBV-related ACLF exhibit increased amounts of Treg, of which redistribution from periphery to liver seems to modulate liver inflammation. Higher Treg amounts are associated with more severe liver disease in ACLF, and its level in combination with international normalized ratio may assist prediction of short-term outcomes of HBV-related ACLF

A cytomegalovirus peptide-specific antibody alters natural killer cell homeostasis and ss shared in several autoimmune diseases

Human cytomegalovirus (hCMV), a ubiquitous beta-herpesvirus, has been associated with several autoimmune diseases. However, the direct role of hCMV in inducing autoimmune disorders remains unclear. Here we report the identification of an autoantibody that recognizes a group of peptides with a conserved motif matching the Pp150 protein of hCMV (anti-Pp150) and is shared among patients with various autoimmune diseases. Anti-Pp150 also recognizes the single-pass membrane protein CIP2A and induces the death of CD56bright NK cells, a natural killer cell subset whose expansion is correlated with autoimmune disease. Consistent with this finding, the percentage of circulating CD56bright NK cells is reduced in patients with several autoimmune diseases and negatively correlates with anti-Pp150 concentration. CD56bright NK cell death occurs via both antibody- and complement-dependent cytotoxicity. Our findings reveal that a shared hCMV-induced autoantibody is involved in the decrease of CD56bright NK cells and may thus contribute to the onset of autoimmune disorders