Effective Solution toward the Issues of Zn-Based Anodes for Advanced Alkaline Ni-Zn Batteries.

Alkaline nickel-zinc (Ni-Zn) batteries, as traditional rechargeable aqueous batteries, possess an obvious advantage in terms of energy density, but their development has been hindered by the anode-concerned problems, Zn dendrites, self-corrosion, passivation, deformation, and hydrogen evolution reaction (HER). Herein, to solve these problems, a dual protective strategy is proposed toward the anode using ZnO as an initial active material, including a C coating on ZnO (ZnO@C) and a thin poly(vinyl alcohol) (PVA) layer coating on the electrode (ZnO@C-PVA). In a three-electrode configuration, the reversible capacity can reach 600 mAh g-1 for the ZnO@C-PVA. Using excessive commercial Ni(OH)2 as the cathode, the alkaline Ni-Zn cells exhibit good electrochemical performance: Discharge capacity can be as high as 640-650 mAh g-1 at 4 A g-1 with a Coulomb efficiency (CE) as high as 97-99% after activity, suggesting low self-corrosion and HER. Capacity retention is 97% after 1200 cycles, indicating rather good durability. The discharge capacity is even slightly increased with the increase of charge/discharge current density (≤8 A g-1), implying good rate performance. Additionally, the discharge voltage can reach 1.8 V (midpoint value) at various current densities, reflecting the fast reaction kinetics of the anode. Most importantly, no Zn dendrites and passivation are observed after long-term cycling. The strategy proposed here can solve the anode-concerned problems effectively, exhibiting a high application prospect.

LncPTSR Triggers Vascular Remodeling in Pulmonary Hypertension by Regulating [Ca2+]i in Pulmonary Arterial Smooth Muscle Cells.

Pulmonary hypertension (PH) is characterized by vascular remodeling and sustained increase in right ventricular systolic pressure. The molecular mechanisms behind PH development remain unclear. Here, a long noncoding RNA (lncRNA) attenuated by platelet-derived growth factor BB (PDGF-BB) was identified, and its functional roles were investigated in vitro and in vivo. Using RNA-sequencing data and rapid amplification of cDNA ends, an lncRNA neighboring the locus of ATPase plasma membrane Ca2+ transporting 4 (PMCA4) was identified and named lncPTSR. It is a highly conserved nuclear lncRNA and was downregulated in pulmonary arterial smooth muscle cells (PASMCs) with PDGF-BB stimulation or hypoxia induction. Gene interruption or overexpression assays revealed that lncPTSR negatively regulates rat PASMC proliferation, apoptosis, and migration. LncPTSR interruption in Sprague Dawley rats using adeno-associated virus type 9-mediated shRNA resulted in a significant increase in right ventricular systolic pressure and vascular remodeling in normoxic condition. LncPTSR knockdown also suppressed PMCA4 expression and attenuated the intracellular Ca2 + efflux of PASMCs in vitro and in vivo. Further studies suggest a complex crosstalk between lncPTSR and mitogen-activated protein kinase pathway: inhibition of mitogen-activated protein kinase kinase and extracellular signal-regulated kinase abolishes the PDGF-BB-mediated lncPTSR downregulation, and lncPTSR plays a feedback regulation for mitogen-activated protein kinase-signaling molecules. The present study suggests that lncPTSR participates in pulmonary artery remodeling via modulating the expression of PMCA4 and intracellular Ca2 + homeostasis downstream of PDGF-BB-driven mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling. These results suggest that lncPTSR may be a promising therapeutic target in PH treatment.

PDGF/MEK/ERK axis represses Ca2+ clearance via decreasing the abundance of plasma membrane Ca2+ pump PMCA4 in pulmonary arterial smooth muscle cells.

Pulmonary arterial hypertension (PAH) is a rare and lethal disease characterized by vascular remodeling and vasoconstriction, which is associated with increased intracellular calcium ion concentration ([Ca2+]i). Platelet-derived growth factor-BB (PDGF-BB) is the most potent mitogen for pulmonary arterial smooth muscle cells (PASMCs) and is involved in vascular remodeling during PAH development. PDGF signaling has been proved to participate in maintaining Ca2+ homeostasis of PASMCs; however, the mechanism needs to be further elucidated. Here, we illuminate that the expression of plasma membrane calcium-transporting ATPase 4 (PMCA4) was downregulated in PASMCs after PDGF-BB stimulation, which could be abolished by restraining the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK). Functionally, suppression of PMCA4 attenuated the [Ca2+]i clearance in PASMCs after Ca2+ entry, promoting cell proliferation and elevating cell locomotion through mediating formation of focal adhesion. Additionally, the expression of PMCA4 was decreased in the pulmonary artery of monocrotaline (MCT)- or hypoxia-induced PAH rats. Moreover, knockdown of PMCA4 could increase the right ventricular systolic pressure (RVSP) and wall thickness (WT) of pulmonary artery in rats raised under normal conditions. Taken together, our findings demonstrate the importance of the PDGF/MEK/ERK/PMCA4 axis in intracellular Ca2+ homeostasis in PASMCs, indicating a functional role of PMCA4 in pulmonary arterial remodeling and PAH development.

Association of Controlling Nutritional Status Score With 2-Year Clinical Outcomes in Patients With ST Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

BACKGROUND: This study evaluated whether the Controlling Nutritional Status (CONUT) score could predict clinical outcomes in ST elevation myocardial infarction (STEMI) patients. METHODS: We performed a retrospective cohort study of STEMI patients after primary percutaneous coronary intervention (pPCI). The endpoint was major adverse cardiac event (MACE). Information was obtained from medical records and via telephone calls. Patients were divided into three groups: normal (CONUT score 0-1; n=278), mild-moderate (score 2-4; n=418), and severe (score ≥5; n=55) groups. RESULTS: During the 24.6±12 months follow-up, MACEs were observed in 65 (8.7%) patients. The incidence of MACEs was 6.1%, 5.5%, and 45.5% in the normal, mild-moderate, and severe group, respectively (p<0.001). Kaplan-Meier curves revealed that patients with a CONUT score ≥5 had the significantly highest rate of MACE, myocardial re-infarction, and vessel revascularisation. In three Cox proportional hazard models, the CONUT scores were unexceptionally associated with MACE, even after adjusting all other variables (hazard ratio, 12.09; 95% confidence interval [CI], 5.09-28.7; p<0.001). The C-statistic of the CONUT score for the prediction of MACE was 0.692 (95% CI, 0.613-0.771; p<0.001), which is close to that of Global Registry of Acute Coronary Events. CONCLUSIONS: The nutritional status evaluated by the CONUT score can independently predict clinical outcomes in STEMI patients, which suggests that active nutritional management is meaningful for these patients after PCI.

Withdrawal of oral anticoagulants 3 months after successful radiofrequency catheter ablation in patients with atrial fibrillation: A meta-analysis.

BACKGROUND: The best anticoagulation therapy for atrial fibrillation (AF) after radiofrequency catheter ablation (RFCA) remains a challenge. METHODS: A systematic search of PubMed, Ovid, and Cochrane Library was conducted identifying at clinical trials which evaluated the differences between thromboembolism (TE) and hemorrhage in an off-oral anticoagulants (OACs) treatment group (the observation group) and an on-OACs treatment group (the control group), at 3 months after successful RFCA. Meta-analysis was performed using RevMan 5.3 software, and the fixed effect model was used as a relevant statistical model. χ2 test and I2 were used to test for the presence of heterogeneity. Subgroup analysis and sensitivity analysis were also performed. RESULTS: The results showed no significant differences between two groups in TE (relative risk [RR] 0.82, 95% confidence interval [CI], 0.51-1.33, P = 0.42), and only mild heterogeneity (P = 0.22, I2  = 29%). No significant differences in TE between two subgroups were found according to < 3 years and ≥ 3 years follow-up analyses (RR 0.58, 95% CI, 0.26-1.28, P = 0.18; RR 1.00, 95% CI, 0.54-1.85, P = 1.00). Furthermore, there was a lower risk of TE in the observation subgroup (< 60 years) compared to the control group (RR 0.31, 95% CI, 0.12-0.78, P = 0.01). Also, there were no significant differences in TE between two subgroups (≥ 60 years, RR 1.24, 95% CI, 0.67-2.28, P = 0.49). The risk of hemorrhage in the observation group was significantly lower compared to the control group (RR 0.05, 95%CI, 0.02-0.14, P < 0.00001). CONCLUSIONS: The withdrawal of OACs 3 months after successful radiofrequency catheter ablation for patients with AF may be safe and feasible. It needs to be tested by randomized controlled trial.

Enhanced degradation of haloacid by heterologous expression in related Burkholderia species.

Haloacids are environmental pollutant and can be transformed to non-toxic alkanoic acids by microbial dehalogenase. Bacterium Burkholderia species MBA4 was enriched from soil for its ability to bioremediate haloacids such as mono-chloroacetate (MCA), mono-bromoacetate (MBA), 2-mono-chloropropionate, and 2-mono-bromopropionate. MBA4 produces an inducible dehalogenase Deh4a that catalyzes the dehalogenation process. The growth of MBA4 on haloacid also relies on the presence of a haloacid-uptake system. Similar dehalogenase genes can be found in the genome of many related species. However, wildtype Burkholderia caribensis MWAP64, Burkholderia phymatum STM815, and Burkholderia xenovorans LB400 were not able to grow on MCA. When a plasmid containing the regulatory and structural gene of Deh4a was transformed to these species, they were able to grow on haloacid. The specific enzyme activities in these recombinants ranges from 2- to 30-fold that of MBA4 in similar condition. Reverse transcription-quantitative real-time PCR showed that the relative transcript levels in these recombinant strains ranges from 9 to over 1,600 times that of MBA4 in similar condition. A recombinant has produced nearly five times of dehalogenase that MBA4 could ever achieve. While the expressions of Deh4a were more relaxed in these phylogenetically related species, an MCA-uptake activity was found to be inducible. These metabolically engineered strains are better degraders than the haloacid-enriched MBA4.