Efficient hydrogen evolution reaction (HER) over noble‐metal‐free electrocatalysts provides one of the most promising pathways to face the energy crisis. Herein, facile cobalt‐doping based on Co‐modified MoOx–amine precursors is developed to optimize the electrochemical HER over Mo2C nanowires. The effective Co‐doping into Mo2C crystal structure increases the electron density around Fermi level, resulting in the reduced strength of Mo–H for facilitated HER kinetics. As expected, the Co‐Mo2C nanowires with an optimal Co/Mo ratio of 0.020 display a low overpotential (η10 = 140 and 118 mV for reaching a current density of –10 mA cm−2; η100 = 200 and 195 mV for reaching a current density of –100 mA cm−2), a small Tafel slope (39 and 44 mV dec−1), and a low onset overpotential (40 and 25 mV) in 0.5 m H2SO4 and 1.0 m KOH, respectively. This work highlights a feasible strategy to explore efficient electrocatalysts via engineering on composition and nanostructure.

Insulin resistance, a major characteristic of type 2 diabetes (T2D), is closely associated with adipose tissue macrophages (ATMs) that induce chronic low-grade inflammation. Recently, mesenchymal stem cells (MSCs) have been identified in alleviation of insulin resistance. However, the underlying mechanism still remains elusive. Thus, we aimed to investigate whether the effect of MSCs on insulin resistance was related to macrophages phenotypes in adipose tissues of T2D rats. In this study, human umbilical cord-derived MSCs (UC-MSCs) infusion produced significantly anti-diabetic effects and promoted insulin sensitivity in T2D rats that were induced by a highfat diet combined with streptozotocin and directed ATMs into an alternatively activated phenotype (M2, anti-inflammatory). In vitro, MSC-induced M2 macrophages alleviated insulin resistance caused by classically activated macrophages (M1, pro-inflammatory). Further analysis showed that M1 stimulated UC-MSCs to increase expression of interleukin (IL)-6, a molecule which upregulated IL4R expression, promoted phosphorylation of STAT6 in macrophages, and eventually polarized macrophages into M2 phenotype. Moreover, the UC-MSCs effect on macrophages was largely abrogated by small interfering RNA (siRNA) knockdown of IL-6. Together, our results indicate that UC-MSCs can alleviate insulin resistance in part via production of IL-6 that elicits M2 polarization. Additionally, human obesity and insulin resistance were associated with increased pro-inflammatory ATMs infiltration. Thus, MSCs may be a new treatment for obesityrelated insulin resistance and T2D concerning macrophage polarized effects. STEM CELLS

The exposure of rich active sites is crucial for MoS2 nanocatalysts in efficient hydrogen evolution reaction (HER). However, the active (010) and (100) planes tend to vanish during preparation because of their high surface energy. Employing the protection by thiourea (TU) reactant, a microwave-assisted reactant-protecting strategy is successfully introduced to fabricate active-site-rich MoS2 (AS-rich MoS2). The bifunctionality of TU, as both a reactant and a capping agent, ensures rich interactions for the effective protection and easy exposure of active sites in MoS2, avoiding the complicated control and fussy procedure related to additional surfactants and templates. The as-obtained AS-rich MoS2 presents the superior HER activity characterized by its high current density (j = 68 mA cm(-2) at -300 mV vs RHE), low Tafel slope (53.5 mV dec(-1)) and low onset overpotential (180 mV), which stems from the rich catalytic sites and the promoted conductivity. This work elucidates a feasible way toward high performance catalysts via interface engineering, shedding some light on the development of emerging nanocatalysts.

BACKGROUNDAcute pancreatitis (AP) is a common acute abdominal disease worldwide, and its incidence rate has increased annually. Approximately 20% of AP patients develop into necrotizing pancreatitis (NP), and 40% to 70% of NP patients have infectious complications, which usually indicate a worse prognosis. Infection is an important sign of complications in NP patients.AIMTo investigate the difference in infection time, infection site, and infectious strain in NP patients with infectious complications.METHODSThe clinical data of AP patients visiting the Department of General Surgery of Xuanwu Hospital of Capital Medical University from January 1, 2014 to December 31, 2018 were collected retrospectively. Enhanced computerized tomography or magnetic resonance imaging findings in patients with NP were included in the study. Statistical analysis of infectious bacteria, infection site, and infection time in NP patients with infectious complications was performed, because knowledge about pathogens and their antibiotic susceptibility patterns is essential for selecting an appropriate antibiotic. In addition, the factors that might influence the prognosis of patients were analyzed.RESULTSIn this study, 539 strains of pathogenic bacteria were isolated from 162 patients with NP infection, including 212 strains from pancreatic infections and 327 strains from extrapancreatic infections. Gram-negative bacteria were the main infectious species, the most common of which were Escherichia coli and Pseudomonas aeruginosa. The extrapancreatic infection time (9.1 ± 8.8 d) was earlier than the pancreatic infection time (13.9 ± 12.3 d). Among NP patients with early extrapancreatic infection (< 14 d), bacteremia (25.12%) and respiratory tract infection (21.26%) were predominant. Among NP patients with late extrapancreatic infection (> 14 d), bacteremia (15.94%), respiratory tract infection (7.74%), and urinary tract infection (7.71%) were predominant. Drug sensitivity analysis showed that P. aeruginosa was sensitive to enzymatic penicillins, third- and fourth-generation cephalosporins, and carbapenems. Acinetobacter baumannii and Klebsiella pneumoniae were sensitive only to tigecycline; Staphylococcus epidermidis and Enterococcus faecium were highly sensitive to linezolid, tigecycline, and vancomycin.CONCLUSIONIn this study, we identified the timing, the common species, and site of infection in patients with NP.

BackgroundHepatocellular carcinoma is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. Dysregulation of HomeoboxD10 (HOXD10) was found to suppress or promote cancer progression in different cancer types. The function and regulation of HOXD10 remain unclear in human hepatocellular carcinoma (HCC).MethodsPrimary HCC samples (117), normal liver tissue samples (15), and 13 HCC cell lines (SNU182, SNU449, HBXF344, SMMC7721, Huh7, HepG2, LM3, PLC/PRF/5, BEL7402, SNU387, SNU475, QGY7703, and Huh1) were included in this study. Methylation-specific PCR, flow cytometry, western blot, transwell, siRNA, and chromatin immunoprecipitation assays were employed.ResultsHOXD10 was methylated in 76.9% (90/117) of human primary HCC samples. HOXD10 methylation was significantly associated with vessel cancerous embolus, tumor cell differentiation, and the 3-year overall survival rate (all P < 0.05). The expression of HOXD10 was regulated by promoter region methylation. HOXD10 suppressed colony formation, cell proliferation, cell invasion and migration, and induced G2/M phase arrest and apoptosis in HCC cells. HOXD10 suppressed HCC cell xenograft growth in mice. HOXD10 suppresses HCC growth by inhibiting ERK signaling.ConclusionHOXD10 is frequently methylated in human HCC, and the expression of HOXD10 is regulated by promoter region methylation. HOXD10 suppresses HCC cell growth both in vitro and in vivo. HOXD10 suppresses human HCC by inhibiting ERK signaling.Electronic supplementary materialThe online version of this article (10.1186/s13148-017-0412-9) contains supplementary material, which is available to authorized users.