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The overexpression of YAP rescued doxorubicin-induced cell loss in hiPSC-CMs by inhibiting apoptosis and inducing proliferation. In contrast, silencing of YAP and TAZ by siRNAs resulted in elevated mitochondrial membrane potential loss in response to doxorubicin. hiPSC-CM calcium transients did not change in response to YAP/TAZ silencing.

Our results suggest that Hippo signalling is involved in clinical anthracycline-induced cardiomyopathy. selleck chemicals Modelling with hiPSC-CMs in vitro showed similar responses to doxorubicin as adult cardiomyocytes and revealed a potential cardioprotective effect of YAP in doxorubicin-induced cardiotoxicity.

Our results suggest that Hippo signalling is involved in clinical anthracycline-induced cardiomyopathy. Modelling with hiPSC-CMs in vitro showed similar responses to doxorubicin as adult cardiomyocytes and revealed a potential cardioprotective effect of YAP in doxorubicin-induced cardiotoxicity.MicroRNAs (miRNAs) are abundant in neurons and play key roles in the function and development of the nervous system. This study focuses on the function of miR-379-5p in neurological function recovery during ischemic stroke. The expression of miR-379-5p in the serum of patients with ischemic stroke was determined. Human cerebral cortical neuron cells (HCN-2) were subjected to oxygen/glucose deprivation (OGD) to mimic an ischemic stroke in vitro, whereas mice subjected to middle cerebral artery occlusion (MCAO) were used as an animal model. The serum of patients with ischemic stroke and OGD-treated HCN-2 cells displayed a poor expression of miR-379-5p. Upregulation of miR-379-5p reduced the OGD-induced cell damage and decreased the expression of the autophagy marker protein Beclin1 in cells. Rapamycin, an autophagy activator, blocked the protective functions of miR-379-5p. Further, miR-379-5p directly bound to MAP3K2. MAP3K2 activated the JNK/c-Jun signaling pathway and suppressed the neuroprotective events mediated by miR-379-5p. The in vitro results were reproduced in vivo, where upregulation of miR-379-5p reduced neurological impairment and infarct size in MCAO-induced mice. This study suggested that miR-379-5p showed a neuroprotective effect on ischemic stroke and reduced autophagy of neurons through the suppression of MAP3K2 and the JNK/c-Jun axis.

Graft-versus-host disease (GVHD) is a rare but serious complication after pediatric liver transplantation (LTx). Early diagnosis is difficult due to nonspecific presenting symptoms and non-pathognomonic skin histopathological features. The aim of this article was to describe a case of pediatric GVHD after LTx and to review available data on pediatric GVHD highlighting the diagnostic difficulty. We also propose a diagnostic algorithm to improve the diagnostic capability and increase clinical awareness about this potentially fatal condition.

We did a comprehensive literatures review on studies on GvHD following pediatric LTx between 1990 and February 2021, chimerism study by short tandem repeat (STR), HLA typing by sequence-specific oligonucleotide (SSO) method, and flowcytometry crossmatch.

Our search yielded 23 case reports. The most common clinical manifestations were fever and rash (91%) followed by diarrhea. Mortality rate was 36.8% mainly due to sepsis and organ failure. Diagnosis was challenging anmatch" and the severe problems imposed by this complication may justify avoidance of HLA homozygous parent's donation.

Sepsis-associated encephalopathy (SAE) always manifests with severe inflammatory symptoms and cognitive impairment. High mobility group box 1 (HMGB1) is a pro-inflammatory cytokine. In this study we investigated the role of HMGB1 in SAE.

An SAE mouse model was established through cecal ligation and puncture surgery and then injected with adenovirus short hairpin RNA (Ad-sh)-HMGB1 or Ad-sh-myeloid differentiation protein (MD-2). The cognitive impairment and pathological injury in mice of different groups were evaluated using the Morris water maze experiment, Y-maze test, tail suspension test, fear conditioning test, and haematoxylin-eosin staining. The expressions of HMGB1 (fully reduced and disulfide (ds)HMGB1), MD-2, and NLRP3 in SAE mice were determined. Then, levels of inflammatory cytokines were measured. The binding relation between HMGB1 and MD-2 was predicted and certified. Additionally, MD-2 was downregulated to verify the role of the binding of HMGB1 and MD-2 in neuroinflammation and cognitive impairment in SAE.

Expressions of HMGB1, MD-2, NLRP3, and inflammatory cytokines were enhanced in the SAE mouse model, which were in parallel with impaired cognitive function. HMGB1 silencing resulted in downregulated NLRP3 expression and alleviated neuroinflammation and cognitive impairment in SAE mice. Mechanically, dsHMGB1 bound to MD-2 to activate NLRP3, thereby exacerbating neuroinflammation and cognitive impairment in SAE mice. The limited binding of HMGB1 and MD-2 downregulated NLRP3 expression to alleviate neuroinflammation and cognitive impairment in SAE mice.

HMGB1 was overexpressed in SAE, and dsHMGB1 bound to MD-2 to activate NLRP3 inflammasome, inducing neuroinflammation and cognitive impairment in SAE.

HMGB1 was overexpressed in SAE, and dsHMGB1 bound to MD-2 to activate NLRP3 inflammasome, inducing neuroinflammation and cognitive impairment in SAE.A single-electron transfer mode coupled with the shuttle behavior of organic iodine batteries results in insufficient capacity, a low redox potential, and poor cycle durability. Sluggish kinetics are well known in conventional lithium-iodine (Li-I) batteries, inferior to other conversion congeners. Herein, we demonstrate new two-electron redox chemistry of I- /I+ with inter-halogen cooperation based on a developed haloid cathode. The new iodide-ion conversion battery exhibits a state-of-art capacity of 408 mAh gI-1 with fast redox kinetics and superior cycle stability. Equipped with a newly emerged 3.42 V discharge voltage plateau, a recorded high energy density of 1324 Wh kgI-1 is achieved. Such robust redox chemistry is temperature-insensitive and operates efficiently at -30 °C. With systematic theoretical calculations and experimental characterizations, the formation of Cl-I+ species and their functions are clarified.Stem cell transplantation is expected to be an effective treatment for intractable skin ulcers by promoting angiogenesis; however, it is challenging to quickly realize a sufficient bloodstream for the ulcers. For this treatment, sheet-like materials with monolayer cells such as cell sheets have been investigated. However, they have a limitation of cell number that can be transplanted at one time due to the two-dimensional, monolayer cell structure, and sufficient secretion of growth factors cannot be expected. In this regard, cellular aggregates, such as spheroids, can reproduce three-dimensional cell-cell interactions that cause biological functions of living tissues more representative than monolayer cells, which is important to achieving efficient secretion of growth factors. In this study, we focused on free-standing porous polymer ultrathin films ("porous nanosheets") comprising poly(d,l-lactic acid) (PDLLA) and succeeded in developing a spheroid-covered nanosheet, on which more than 1000 spheroids from adipose-tissue derived stem cells (ASCs) were loaded. The porous structure with an average pore diameter of 4 μm allowed for facile filtration and carrying spheroids on the nanosheet, as well as sufficient oxygen and nutrients inflow to the cells. The spheroid-covered nanosheet achieved homogeneous transference of spheroids to a whole skin defect in diabetic model mice. Given the continuous release of vascular endothelial growth factor (VEGF) from the spheroids, the transplanted spheroids promoted healing with more accelerated angiogenesis than a nanosheet with a monolayer of cells. The spheroid-covered nanosheet may be a new regenerative material for promoting intractable skin ulcer healing.

Acute chest syndrome (ACS) is a leading cause of morbidity and mortality in sickle cell patients, and it is often challenging to establish its diagnosis.

This was a prospective observational study conducted in a pediatric emergency (PEM) department. We aimed to investigate the performance characteristics of point-of-care lung ultrasound (LUS) for diagnosing ACS in sickle cell children. LUS by trained PEM physicians was performed and interpreted as either positive or negative for consolidation. LUS results were compared to chest X-ray (CXR) and discharge diagnosis as reference standards.

Four PEM physicians performed the LUS studies in 79 suspected ACS cases. The median age was 8years (range 1-17years). Fourteen cases (18%) received a diagnosis of ACS based on CXR and 21 (26.5%) had ACS discharge diagnosis. Comparing to CXR interpretation as the reference standard, LUS had a sensitivity of 100% (95% CI 77%-100%), specificity of 68% (95% CI 56%-79%), positive predictive value of 40% (95% CI 24%-56%), and negative predictive value of 100% (95% CI 92%-100%). Overall LUS accuracy was 73.42% (95% CI 62%-83%). Using discharge diagnosis as the endpoint for both CXR and LUS, LUS had significantly higher sensitivity (100% vs. 62%, p=.0047) and lower specificity (76% vs.100%, p=.0002). LUS also had lower positive (60% vs.100%, p<.0001) and higher negative (100% vs.77%, p=.0025) predictive values. The overall accuracy was similar for both tests (82% vs. 88%, p=.2593).

The high negative predictive value, with narrow CIs, makes LUS an excellent ruling-out tool for ACS.

The high negative predictive value, with narrow CIs, makes LUS an excellent ruling-out tool for ACS.

The aim of this study was to evaluate the efficacy and safety of berberine as an adjuvant in treating antipsychotic-associated weight gain and metabolic syndrome.

One hundred thirteen participants with schizophrenia spectrum disorders who had developed metabolic syndrome were recruited. They were randomly assigned to berberine (600 mg/d, n=58) or placebo (n=55) groups for 12 weeks. The primary outcome was the change from baseline to week 12 in net weight. Secondary outcomes included body mass index, waist circumference, serum glucose and lipid profiles, and the severity of psychotic symptoms.

Compared with the placebo group, the berberine group showed a significantly greater reduction in weight gain at 9 weeks (mean difference [MD], -0.75; 95% CI, -1.42 to -0.07 [P=0.031, d=0.41]) and 12 weeks (MD,-1.08; 95% CI, -1.76 to -0.40 [P=0.002, d=0.59]). Patients who received berberine also showed statistically significant improvements in end point in body mass index (MD,-0.41; 95% CI, -0.65 to -0.17 [P=0.001, d=0.64]), total cholesterol (MD,-0.58; 95% CI, -0.74 to -0.41 [P < 0.001, d=1.31]), low-density lipoprotein (MD,-0.52; 95% CI, -0.68 to -0.35 [P < 0.001, d=1.19]), and glycated hemoglobin (MD,-0.09; 95% CI, -0.18 to 0 [P=0.05, d=0.37]). Berberine was well tolerated without serious adverse events and aggravation of psychotic symptoms compared with placebo.

The findings suggest that berberine is effective in attenuating antipsychotic-associated weight gain and metabolic syndrome.

The findings suggest that berberine is effective in attenuating antipsychotic-associated weight gain and metabolic syndrome.