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Construction of two-dimensional (2D) metal-organic frameworks (MOFs) for energy storage and conversion has attracted great attention due to the synergistic advantages of 2D nanostructures and MOFs. Herein, a Co-MOF material with different 2D morphologies of vertical nanoplate arrays and faveolate nanosheets are in-situ fabricated on Ni foam with and without using polyvinylpyrrolidone (PVP) as a regulator. Toward the application in energy storage, both of two morphologies of the Co-MOF exhibit good electrochemical properties. In particular, the vertical Co-MOF nanoplate arrays deliver a high areal capacity of 8.56 C/cm2 at the current density of 5 mA/cm2, which is much higher than that of faveolate Co-MOF nanosheets (2.39 C/cm2 at 5 mA/cm2). Moreover, a hybrid supercapacitor (HSC) device using the Co-MOF nanoplate arrays positive electrode and activated carbon (AC) negative electrode is assembled, which delivers a volumetric capacitance of 17.9 F/cm3 at 10 mA/cm2, a high energy density of 7.2 mW h cm−3 and a good cyclic stability (retaining over 88.0% of initial capacitance after 3000 cycles). These findings demonstrate that the as-fabricated 2D Co-MOFs possess a huge potential in energy storage.

It is known that chronic stress modulates multiple processes in a complex microenvironment, such as angiogenesis and immune function. However, the role of chronic stress inducing tumor angiogenesis and how it contributes to tumor progression are not quite clear. The following study assess psychological state from numerous ambulatory cancer cases (n=332), and chronic stress-related hormone levels were further measured. Here, we show that chronic stress not only causes behavioral changes in human, most importantly attributed to an elevated level of stress-related hormones. To address this, isoprenaline, the agonist of β2-adrenergic receptor (β2-AR), was utilized for simulating chronic stress and demonstrating the mechanism of stress in tumor angiogenesis at molecular level both in vivo and in vitro. As suggested by this study, isoprenaline promote VEGF autocrine of HUVECs, which can induce plexinA1 and VEGFR2 expression. Moreover, we show that isoprenaline promoted the expression of p-JAK2 and p-STAT3 in vitro. The results reveal that, isoprenaline enhances the autocrine of VEGF in HUVECs and up-regulating plexinA1 and VEGFR2 levels, thus activating the phosphorylation of JAK2-STAT3 pathway, the two essential parts during angiogenesis. The present work indicates that, the mechanism of chronic stress in enhancing angiogenesis is probably achieved through activating the plexinA1/VEGFR2-JAK2-STAT3 signal transduction pathway within HUVECs, and this is probably a candidate target for developing a strategy against angiogenesis in cancer.

BACKGROUND&AIMSInfected pancreatic necrosis (IPN) is a highly morbid complication of acute pancreatitis (AP). Since there is evidence of immunosuppression in the early phase of AP, immune enhancement using Thymosin alpha 1 (Tα1), which stimulates both innate and adaptive immunity, may be a therapeutic strategy to prevent IPN. Our aim was to assess the efficacy of early Tα1 treatment on the development of IPN.METHODSWe conducted a multicenter, randomized, double-blind, placebo-controlled trial in patients with predicted severe acute necrotizing pancreatitis (ANP). ANP patients with an APACHE II score≥8 admitted within seven days of the advent of symptoms were considered eligible. Enrolled patients were assigned to receive a subcutaneous injection of Tα1 1.6 mg, every 12 hours for the first 7 days and 1.6 mg once a day for the subsequent 7 days or matching placebo (normal saline). The primary outcome was the development of IPN during the index admission.RESULTSFrom Mar 2017 through Dec 2020, 508 patients were randomized at 16 hospitals, of whom 254 were assigned to receive Tα1 and 254 placebo. During the index admission, 40/254 (15.7%) patients in the Tα1 group developed IPN compared with 46/254 patients (18.1%) in the placebo group (difference -2.4% [95%CI -7.4% to 5.0%]; p=0.47). The results were similar in four predefined subgroups. There was no difference in other major complications, including new-onset organ failure (10.6% vs. 15.0%; p=0.15), bleeding (6.3% vs. 3.5%; p=0.15), and gastrointestinal fistula (2.0% vs. 2.4%; p=0.75) during the index admission.CONCLUSIONSThe immune-enhancing Tα1 treatment of patients with predicted severe ANP did not reduce the incidence of IPN during the index admission.Trial registrationClinicaltrials.gov registry: NCT02473406.

Protectin D1 (PD1), a DHA-derived lipid mediator, has recently been shown to possess anti-inflammatory and pro-resolving properties. To date, little is known about the effect of PD1 on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The aim of the present study was to investigate the therapeutic effects of PD1 on LPS-induced ALI and its potential mechanisms of action. ALI was induced via an intraperitoneal injection of LPS, where PD1 (2 ng/mouse) was administered intravenously 30 min after LPS challenge. Mice were sacrificed 24 h after modeling. Lung histopathological changes were assessed using hematoxylin and eosin staining and myeloperoxidase (MPO) activity was tested using immunohistochemistry. Tumor necrosis-α and interleukin-6 levels in the bronchoalveolar lavage fluid (BALF) and serum were measured using ELISA. To detect neutrophil extracellular traps produced by infiltrated neutrophils in the lung tissue, immunofluorescence staining was performed using anti-MPO and anti-histone H3 antibodies. The results indicated that PD1 significantly attenuated histological damage and neutrophil infiltration in lung tissue, reduced the lung wet/dry weight ratio, protein concentration and proinflammatory cytokine levels in BALF and decreased proinflammatory cytokine levels in serum. Moreover, neutrophil citrullinated histone H3 (CitH3) expression was also reduced after PD1 administration. In conclusion, PD1 attenuated LPS-induced ALI in mice via inhibition of neutrophil extracellular trap formation in lung tissue. Therefore, PD1 administration may serve to be a new strategy for treating ALI.

Background. Both long-term proton pump inhibitor use and surgical fundoplication have potential drawbacks as treatments for chronic gastroesophageal reflux disease (GERD). Our aim was to investigate the potential efficacy of antireflux mucosectomy (ARMS) in porcine and determine the optimal circumference of resection in relation to gastroesophageal junction (GEJ). Methods. Nine pigs were allocated into the following 3 groups by computerized randomization: group A: control, group B: 1/3 circumference of the esophagus, and group C: 2/3 circumference of the esophagus. We performed mucosectomy with a crescentic mucosal resection at 3 cm above the GEJ and 1 cm below the GEJ. The animals were kept on a liquid diet for 24 h prior to endoscopy. At 6 weeks, animals underwent esophagoscopy, barium radiography, gastric yield pressure (GYP), and gastric yield volume (GYV) determination. Results. The weight of swines has no significant difference, and all pigs had maintained their weight after the procedure. We both found scar formation at the GEJ in group B and C. Compared with group A and B, group C produced significantly higher GYP (24.23±3.42 mmHg, p=0.004) and significantly smaller GYV (2200.0±238.96 mL, p=0.028) after 6 weeks. Barium radiography showed that the width of the cardia was narrower (13.73±1.19 mm, p=0.032) in group C after 6-week postprocedure. Conclusion. Our study demonstrated the potential antireflux effect of ARMS. We also recommend the 2/3 circumference resection of mucosa at 3 cm distance from the GEJ.

IntroductionInfected pancreatic necrosis (IPN) and its related septic complications are the major causes of death in patients with acute necrotising pancreatitis (ANP). Therefore, the prevention of IPN is of great clinical value, and immunomodulatory therapy with thymosin alpha 1 may be beneficial. This study was designed to test the hypothesis that the administration of thymosin alpha 1 during the acute phase of ANP will result in a reduced incidence of IPN.Methods and analysisThis is a randomised, multicentre, double-blind, placebo-controlled study. 520 eligible patients with ANP will be randomised in a 1:1 ratio to receive either the thymosin alpha 1 or the placebo using the same mode of administration. The primary endpoint is the incidence of IPN during the index admission. Most of the secondary endpoints will be registered within the index admission including in-hospital mortality, the incidence of new-onset organ failure and new-onset persistent organ failure (respiration, cardiovascular and renal), receipt of new organ support therapy, requirement for drainage or necrosectomy, bleeding requiring intervention, human leucocyte antigens-DR(HLA-DR) on day 0, day 7, day 14, and so on and adverse events. Considering the possibility of readmission, an additional follow-up will be arranged 90 days after enrolment, and IPN and death at day 90 will also be served as secondary outcomes.Ethics and disseminationThis study was approved by the ethics committee of Jinling Hospital, Nanjing University (Number 2015NZKY-004-02). The thymosin alpha 1 in the prevention of infected pancreatic necrosis following acute necrotising pancreatitis(TRACE) trial was designed to test the effect of a new therapy focusing on the immune system in preventing secondary infection following ANP. The results of this trial will be disseminated in peer-reviewed journals and at scientific conferences.Trial registration numberClinicalTrials.gov Registry (NCT02473406).

Spinal cord injury (SCI) causes sensory dysfunctions such as paresthesia, dysesthesia, and chronic neuropathic pain. MiR-20a facilitates the axonal outgrowth of the cortical neurons. However, the role of miR-20a in the axonal outgrowth of primary sensory neurons and spinal cord dorsal column lesion (SDCL) is yet unknown. Therefore, the role of miR-20a post-SDCL was investigated in rat. The NF-200 immunofluorescence staining was applied to observe whether axonal outgrowth of dorsal root ganglion (DRG) neurons could be altered by miR-20a or PDZ-RhoGEF modulation in vitro. The expression of miR-20a was quantized with RT-PCR. Western blotting analyzed the expression of PDZ-RhoGEF/RhoA/GAP43 axis after miR-20a or PDZ-RhoGEF was modulated. The spinal cord sensory conduction function was assessed by somatosensory-evoked potentials and tape removal test. The results demonstrated that the expression of miR-20a decreased in a time-dependent manner post-SDCL. The regulation of miR-20a modulated the axonal growth and the expression of PDZ-RhoGEF/RhoA/GAP43 axis in vitro. The in vivo regulation of miR-20a altered the expression of miR-20a-PDZ-RhoGEF/RhoA/GAP43 axis and promoted the recovery of ascending sensory function post-SDCL. The results indicated that miR-20a/PDZ-RhoGEF/RhoA/GAP43 axis is associated with the pathophysiological process of SDCL. Thus, targeting the miR-20a/PDZ-RhoGEF /RhoA/GAP43 axis served as a novel strategy in promoting the sensory function recovery post-SCI.

Background Human parechovirus (HPeV) is a genus of virus in the family Picornaviridae, having two species A and B. HPeVs are common infectious agents, usually causing mild diarrhea and respiratory disease in young children. Results Here, we collected and sequenced the near complete genome sequences of 17 novel HPeVs from children with diarrhea in eastern China, which showed significant nucleotide sequence divergence. Phylogenetic analysis based on the complete genomes of these HPeV strains revealed that they belonged to seven different genotypes (including three putative novel genotypes), suggesting that HPeVs showed genotype diversity in this area. Recombination analysis indicated that one of the HPeVs, belonging to HPeV-1 with strain name 146Chzj02, was a recombinant generated by inter-genotype recombination among three HPeV strains belonging to three different genotypes, respectively. Conclusion Our data revealed the property of the genotype diversity of HPeVs prevalent in children with diarrhea in eastern China, which will be helpful in the future study of the viral evolution of HPeVs and the identification and typing of HPeVs in the clinical laboratory.

This manuscript reports the application of the selective-withdrawal coating technique to the microencapsulation of insulin-producing pancreatic islets within thin poly(ethylene glycol) coatings. These polymer coatings permit the islets to respond to changes in glucose concentration by producing insulin with a dose-response profile that is substantially similar to that of unencapsulated islets. Furthermore, the hydrogel capsules exclude the large molecules of the immune system. These results suggest that the microencapsulation technique-which combines droplet formation from a flow of two immiscible fluids with polymerization chemistries-has the characteristics required for the transplantation of islets for the treatment of Type I diabetes.

This manuscript reports the application of the selective-withdrawal coating technique to the microencapsulation of insulin-producing pancreatic islets within thin poly(ethylene glycol) coatings. These polymer coatings permit the islets to respond to changes in glucose concentration by producing insulin with a dose-response profile that is substantially similar to that of unencapsulated islets. Furthermore, the hydrogel capsules exclude the large molecules of the immune system. These results suggest that the microencapsulation technique-which combines droplet formation from a flow of two immiscible fluids with polymerization chemistries-has the characteristics required for the transplantation of islets for the treatment of Type I diabetes.