Carbon-reinforced Ni3S2/Ti3C2Tx MXene composite as an anode for superior-performance lithium-ion capacitors.

Lithium ion capacitors (LICs) are a new generation of energy storage devices that combine the super energy storage capability of lithium ion batteries with the satisfactory power density of supercapacitors. The development of high-performance LICs still faces great challenges due to the unbalanced reaction kinetics at the anode and cathode. Therefore, it is an inevitable need to enhance the electron/ion transfer capability of the anode materials. In this paper, to obtain a superior-rate and high-capacity Ni3S2-based anode, highly conductive Ti3C2Tx MXene sheets were introduced to sever as the carrier of Ni3S2 nanoparticles and simultaneously an amorphous carbon layer which coats onto the surface of Ni3S2 nanoparticles was in-situ generated by the carbonization of dopamine reactant. The as-synthesized Ni3S2/Ti3C2Tx/C composite exhibits a high specific surface area (112.6 m2/g) because of the addition of Ti3C2Tx that can reduce the aggregation of Ni3S2 nanoparticles and the in-situ generated amorphous carbon layer that can suppress the growth of Ni3S2 nanoparticles. The Ni3S2/Ti3C2Tx/C anode possesses a remarkable reversible discharge specific capacity (626.0 mAh/g under 0.2 A/g current density), which increases to 1150.8 mAh/g after 400-cycle charge/discharge measurement at the same measurement condition indicating eminent cyclability, along with superior rate capability. To construct a superior-performance LIC device, a sterculiae lychnophorae derived porous carbon (SLPC) cathode with an average discharge specific capacity of 73.4 mAh/g@0.1A/g was prepared. The Ni3S2/Ti3C2Tx/C//SLPC LIC device with optimal cathode/anode mass ratio has a satisfactory energy density ranging from 32.8 to 119.1 Wh kg-1 at the corresponding power density of 8799.4 to 157.5 W kg-1, together with a prominent capacity retention (95.5 %@1 A/g after 10,000 cycles).

Association of admission hyperglycemia and all-cause mortality in acute myocardial infarction with percutaneous coronary intervention: A dose-response meta-analysis.

Objective: The aim of this study is to evaluate the associations between admission hyperglycemia and the risk of all-cause mortality in patients with acute myocardial infarction (AMI) with or without diabetes, to find optimal admission glucose intervention cut-offs, and to clarify the shape of the dose-response relations. Methods: Medline/PubMed and EMBASE were searched from inception to 1 April 2022. Cohort studies reporting estimates of all-cause mortality risk in patients with admission hyperglycemia with AMI were included. The outcomes of interest include mortality and major adverse cardiac events (MACEs). A random effect dose-response meta-analysis was conducted to access linear trend estimations. A one-stage linear mixed effect meta-analysis was used for estimating dose-response curves. Relative risks and 95% confidence intervals were pooled using a random-effects model. Results: Of 1,222 studies screened, 47 full texts were fully reviewed for eligibility. The final analyses consisted of 23 cohort studies with 47,177 participants. In short-term follow-up, admission hyperglycemia was associated with an increased risk of all-cause mortality (relative risk: 3.12, 95% confidence interval 2.42-4.02) and MACEs (2.34, 1.77-3.09). In long-term follow-up, admission hyperglycemia was associated with an increased risk of all-cause mortality (1.97, 1.61-2.41) and MACEs (1.95, 1.21-3.14). A linear dose-response association was found between admission hyperglycemia and the risk of all-cause mortality in patients with or without diabetes. Conclusion: Admission hyperglycemia was significantly associated with higher all-cause mortality risk and rates of MACEs. However, the association between admission hyperglycemia and long-term mortality risk needs to be determined with caution. Compared with current guidelines recommendations, a lower intervention cut-off and more stringent targets for admission hyperglycemia may be appropriate. Systematic review registration: [https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022317280], identifier [CRD42022317280].

Laparoscopic-assisted endoscopic full-thickness resection of a large gastric schwannoma: A case report.

BACKGROUND: Schwannomas, also known as neurinomas, are benign tumors derived from Schwann cells. Gastrointestinal schwannomas are rare and are most frequently reported in the stomach. They are usually asymptomatic and are difficult to diagnose preoperatively; however, endoscopy and imaging modalities can provide beneficial preliminary diagnostic data. There are various surgical options for management. Here, we present a case of a large gastric schwannoma (GS) managed by combined laparoscopic and endoscopic surgery. CASE SUMMARY: A 28-year-old woman presented with a 2-mo history of epigastric discomfort and a feeling of abdominal fullness. On upper gastrointestinal endoscopy and endoscopic ultrasonography, a hypoechogenic submucosal mass was detected in the gastric antrum: It emerged from the muscularis propria and projected intraluminally. Computed tomography showed a nodular lesion (4 cm × 3.5 cm), which exhibited uniform enhancement, on the gastric antrum wall. Based on these findings, a preliminary diagnosis of gastrointestinal stromal tumor was established, with schwannoma as a differential. Considering the large tumor size, we planned to perform endoscopic resection and to convert to laparoscopic treatment, if necessary. Eventually, the patient underwent combined laparoscopic and gastroscopic surgery. Immunohistochemically, the resected specimen showed positivity for S-100 and negativity for desmin, DOG-1, α-smooth muscle actin, CD34, CD117, and p53. The Ki-67 index was 3%, and a final diagnosis of GS was established. CONCLUSION: Combined laparoscopic and endoscopic surgery is a minimally invasive and effective treatment option for large GSs.

WeChat Public Account Use Improves Clinical Control of Cough-Variant Asthma: A Randomized Controlled Trial.

BACKGROUND WeChat is a convenient and popular social medium, and it seems to be an appropriate platform for education and management of patients. This study sought to identify usefulness in clinical control of cough-variant asthma (CVA). MATERIAL AND METHODS A randomized controlled trial was conducted among 80 CVA patients. After being assigned to either the traditional group (TG) or the WeChat group (WG), they received the same inhalation therapy, but patients in WG received additional education and instruction via our public account on the WeChat application. Questionnaires on asthma and chronic cough, data on pulmonary function, blood-related items, follow-up adherence, and Emergency Department (ED) visits were collected at the initial visit and at 3 months. RESULTS A total of 67 participants completed the trial for analysis. FEV1/predicted and FEV1/FVC were significantly increased in WG (p<0.001; p=0.012) after 3 months. PD20-FEV1 was increased in both groups compared with baseline, but more pronounced in WG (p=0.004). ACQ-7 scores were improved in both groups (p=0.024; p<0.001). Participants allocated to WG experienced a greater improvement in AQLQ and LCQ scores, and between-group differences were significant at 3 months (p=0.040; p=0.001). Furthermore, we observed decreases in blood eosinophil count and FeNO in WG (p=0.048; p=0.014), and WG presented better follow-up compliance (p=0.034). CONCLUSIONS Using WeChat as part of treatment and management of CVA can help patients learn about their disease and medications, as well as improve disease control and therapy outcomes.

[Japanese encephalitis virus with genotype I is predominant in Sichuan Province].

OBJECTIVE: To understand molecular characteristics of Japanese encephalitis virus (JEV) isolated from the major Japanese encephalitis epidemic areas in Sichuan Province, and to provide the foundation for JEV prevention. METHODS: 13 JEV strains were isolated from mosquitoes in Sichuan during 2007-2010, E genes and preM genes were sequenced and phylogenetic analyses were performed using MEGA5 molecular software. RESULTS: Phylogenetic analysis indicated that all 13 JEV strains from Sichuan belonged to genotype I, homologies at nucleotide level and deduced amino acid level in PreM gene were 97%-100% and 98.7%-100%, and 97.8%-99.9% and 99.6%-100% in E gene, respectively. Homologies at nucleotide level and deduced amino acid level in PreM gene between 13 JEV strains and JEV isolated in 2004 in Sichuan were 96.2%-99.1% and 97.5%-98.7%, and were 97.7%-99.6% and 98. 6%-100% in E gene, respectively. By comparison with vaacine strains P3 and SA14-14-2, homologies at nucleotide level and deduced amino acid level were 84.1%-85.8% and 93.7%-96.2% in PreM gene, and were 87.6%-88.3% and 97%-97.8% in E gene, respectively. The neurovirulence-related 8 amino acid sites encode by E gene remained unchanged in 13 JEV strains. CONCLUSION: JEV with genotype I predominated in Sichuan, nucleotide sequences and deduced amino acid sequences in PreM gene and E gene were highly conserved, key neurovirulence-rerlated sites remained unchanged. It suggested currently used vaccine is still capable of preventing JEV infection.

Involvement of an alternatively spliced mitochondrial oxodicarboxylate carrier in adipogenesis in 3T3-L1 cells.

BACKGROUND: Adipogenesis is a complex process that involves many genes/proteins at different stages of differentiation. In order to identify genes critical for adipogenesis, we took a novel approach based on phenotype change of individual cell, to search for genes with regulatory roles in adipogenesis genome-wide in 3T3-L1 cells. METHODS: Lentivirus-based inducible random homologous knockdown was used for the screening of functional gene that altered lipid formation in the adipocyte during differentiation. RESULTS: In the present study, we reported the identification of an alternatively spliced mitochondrial oxodicarboxylate carrier (ODC), so named ODC-AS. ODC-AS is different from ODC by replacing 22 amino acids with 29 amino acids at the N-terminal. ODC was widely expressed in most tissues in mouse as determined by multi-tissue cDNA panel polymerase chain reaction. However, ODC-AS was only detected in adipose tissue and in iris and sclera-choroid complex of the eye. The expression of ODC-AS in 3T3-L1 was detected after the induction of differentiation, and reached a peak at day 4 and then reduced thereafter, whereas no ODC transcript detected in the cells neither before nor after differentiation. Knocking down of ODC-AS expression by RNA interference led to significant reduction in lipid accumulation as determined by triglyceride measurement and Nile Red staining, as well as adipogenic marker CEBPalpha, PPARgamma, aP2 and CD36. Although both ODC and ODC-AS are expressed in white and brown adipose tissues, only the expression of ODC-AS was down-regulated in brown adipose tissue by cold exposure. CONCLUSION: These results implicate that ODC-AS may promote lipid accumulation during adipocyte differentiation and play an important role in the regulation of lipid metabolism in adipose tissues.

The sirtuin inhibitor nicotinamide enhances neuronal cell survival during acute anoxic injury through AKT, BAD, PARP, and mitochondrial associated "anti-apoptotic" pathways.

Understanding the role of nicotinamide (NIC) in different cell systems represents a significant challenge in several respects. Recently, NIC has been reported to have diverse roles during cell biology. In the absence of NIC, sirtuin protein activity is enhanced and pyrazinamidase/nicotinamidase 1 (PNC1) expression, an enzyme that deaminates NIC to convert NIC into nicotinic acid, is increased to lead to lifespan extension during calorie restriction, at least in yeast. Yet, NIC may be critical for cell survival as well as the modulation of inflammatory injury during both experimental models as well as in clinical studies. We therefore investigated some of the underlying signal transduction pathways that could be critical for the determination of the neuroprotective properties of NIC. We examined neuronal injury by trypan blue exclusion, DNA fragmentation, phosphatidylserine (PS) exposure, Akt1 phosphorylation, Bad phosphorylation, mitochondrial membrane potential, caspase activity, cleavage of poly(ADP-ribose) polymerase (PARP), and mitogen-activated protein kinases (MAPKs) phosphorylation. Application of NIC (12.5 mM) significantly increased neuronal survival from 38 -/+ 3% of anoxia treated alone to 68 +/- 3%, decreased DNA fragmentation and membrane PS exposure from 67 -/+ 4% and 61 -/+ 5% of anoxia treated alone to 30 +/- 4% and 26 +/- 4% respectively. We further demonstrate that NIC functions through Akt1 activation, Bad phosphorylation, and the downstream modulation of mitochrondrial membrane potential, cytochrome c release, caspase 1, 3, and 8 - like activities, and PARP integrity to prevent genomic DNA degradation and PS externalization during anoxia. Yet, NIC does not alter the activity of either the MAPKs p38 or JNK, suggesting that protection by NIC during anoxia is independent of the p38 and JNK pathways. Additional investigations targeted to elucidate the cellular pathways responsible for the ability of NIC to modulate both lifespan extension and cytoprotection may offer critical insight for the development of new therapies for nervous system disorders.

The NAD+ precursor nicotinamide governs neuronal survival during oxidative stress through protein kinase B coupled to FOXO3a and mitochondrial membrane potential.

Nicotinamide, a beta-nicotinamide adenine dinucleotide (NAD) precursor and an essential nutrient for cell growth and function, may offer critical insights into the specific cellular mechanisms that determine neuronal survival, since this agent significantly impacts upon both neuronal and vascular integrity in the central nervous system. The authors show that nicotinamide provides broad, but concentration-specific, protection against apoptotic genomic DNA fragmentation and membrane phosphatidylserine exposure during oxidative stress to secure cellular integrity and prevent phagocytic cellular demise. Activation of the protein kinase B (Akt1) pathway is a necessary requirement for nicotinamide protection, because transfection of primary hippocampal neurons with a plasmid encoding a kinase-deficient dominant-negative Akt1 as well as pharmacologic inhibition of phosphatidylinositol-3-kinase phosphorylation of Akt1 eliminates cytoprotection by nicotinamide. Nicotinamide fosters neuronal survival through a series of intimately associated pathways. At one level, nicotinamide directly modulates mitochondrial membrane potential and pore formation to prevent cytochrome c release and caspase-3-and 9-like activities through mechanisms that are independent of the apoptotic protease activating factor-1. At a second level, nicotinamide maintains an inhibitory phosphorylation of the forkhead transcription factor FOXO3a at the regulatory sites of Thr and Ser and governs a unique regulatory loop that prevents the degradation of phosphorylated FOXO3a by caspase-3. Their work elucidates some of the unique neuro-protective pathways used by the essential cellular nutrient nicotinamide that may direct future therapeutic approaches for neurodegenerative disorders.

The tyrosine phosphatase SHP2 modulates MAP kinase p38 and caspase 1 and 3 to foster neuronal survival.

1. The Src homology protein tyrosine phosphatase SHP2 is associated with cytoskeletal maintenance, cell division, and cell differentiation, but the role of SHP2 during central nervous system injury requires further definition. We therefore characterized the role of SHP2 during nitric oxide (NO)-induced programmed cell death (PCD). 2. Employing primary hippocampal neurons from mice with a dominant negative SHP2 mutant to render the phosphatase site of the SHP2 protein biologically inactive, but functionally capable of binding substrate, neuronal injury was evaluated by trypan blue, DNA fragmentation, membrane phosphatidyl serine (PS) exposure, mitogen-activated protein (MAP) kinase phosphorylation, and cysteine protease activity. NO was administered through the NO generators SIN-1 (300 microM) or NOC-9 (300 microM). 3. Following NO exposure, neuronal survival decreased from 89 +/- 3% in untreated controls to 37 +/- 2% in wild-type neurons and to 21 +/- 4% in SHP2 mutant neurons. In sister cultures following NO exposure, this increased susceptibility to neuronal injury paralleled enhanced genomic DNA degradation and membrane PS exposure with PCD induction increasing in SHP2 mutant neurons by approximately 42% during specified time periods when compared to wild-type neurons. Interestingly, modulation of the MAP kinase p38 appears to represent an initial level of neuronal protection employed by SHP2. In addition, both the rate and degree of caspase 1- and caspase 3-like activities in SHP2 mutant neurons were significantly increased over a 24-h course when compared to wild-type neurons. Inhibition of caspase 1- and caspase 3-like activities reversed the progression of neuronal PCD, suggesting that inhibition of cysteine protease activity is a downstream mechanism for SHP2 to afford neuronal protection. 4. Our work supports the premise that the tyrosine phosphatase SHP2 plays a dominant role during NO-induced PCD and may offer a potential molecular "checkpoint" against neurodegenerative disease.

Maternal behavior: activation of the central oxytocin receptor system in parturient rats?

Parturition plays a critical role in the full expression of maternal behavior in postpartum females, yet the precise mechanism remains unclear. Here we examined the role of parturition in the activation of Fos and FosB in the central oxytocin receptor (OTR) system in rats. Although expression of FosB, not Fos, was seen in the piriform cortex (Pir) and caudate putamen of virgin and pregnant females, activation of Fos and FosB with extensive co-localization was found in the medial preoptic area, the bed nucleus of the stria terminalis and Pir of parturient brain. This parturition induced activation of Fos and FosB was identified in the central OTR-expressing cells as well as in oxytocinergic neurons. Our data provide direct evidence, for the first time, that parturition activates Fos and FosB in the central OTR system. We propose that Fos and FosB may have comparable functions on initiating maternal behavior at parturition.

Erythropoietin prevents early and late neuronal demise through modulation of Akt1 and induction of caspase 1, 3, and 8.

Erythropoietin (EPO) modulates primarily the proliferation of immature erythroid precursors, but little is known of the potential protective mechanisms of EPO in the central nervous system. We therefore examined the ability of EPO to modulate a series of death-related cellular pathways during anoxia and free radical induced neuronal degeneration. Neuronal injury was evaluated by trypan blue, DNA fragmentation, membrane phosphatidylserine exposure, protein kinase B phosphorylation, cysteine protease activity, mitochondrial membrane potential, and mitogen-activated protein (MAP) kinase phosphorylation. We demonstrate that constitutive neuronal EPO is insufficient to prevent cellular injury, but that signaling through the EPO receptor remains biologically responsive to exogenous EPO administration. Exogenous EPO is both necessary and sufficient to prevent acute genomic DNA destruction and subsequent phagocytosis through membrane PS exposure, because neuronal protection by EPO is completely abolished by co-treatment with an anti-EPO neutralizing antibody. Through pathways that involve the initial activation of protein kinase B, EPO maintains mitochondrial membrane potential. Subsequently, EPO inhibits caspase 8-, caspase 1-, and caspase 3-like activities linked to cytochrome c release through mechanisms that are independent from the MAP kinase systems of p38 and JNK. Elucidating some of the novel neuroprotective pathways employed by EPO may further the development of new therapeutic strategies for neurodegenerative disorders.

Possible role of Marcks in the cellular modulation of monocytic tissue factor-initiated hypercoagulation.

The enhanced extrinsic tissue factor (TF)-initiated coagulation, often resulting from sepsis, could lead to disseminated intravascular coagulation presenting cardiovascular complications. Using model human leukaemia THP-1 monocytes, we studied monocytic TF (mTF) hypercoagulation and its regulation. After an 8 h exposure to bacterial endotoxin [lipopolysaccharide (LPS); 100 ng/ml], mTF activity was significantly upregulated as the result of the enhanced mTF synthesis. Thereafter, LPS induction declined, exhibiting a "quiescent-desensitizing' phenomenon. Such diminished LPS induction was,however,associated with sustained LPS-enhanced mTF synthesis, revealing the possible occurrence of a post-translational downregulation. It was noted that LPS desensitization was accompanied by the increased expression of myristoylated alanine-rich C kinase substrate (Marcks). In contrast, A23187 (20 micromol/l) or Quin-2AM (20 micromol/l) drastically activated mTF activity without detectable effect on mTF synthesis; both of which showed that sustained functional upregulation during 24 h culture did not enhance Marcks expression. These inverse correlations between mTF activity upregulation and Marcks expression suggested that Marcks could be inhibitory. Marcks phosphorylation site domain (151-175) (Marcks PSD) readily inhibited mTF-dependent FVII activation and diminished FVIIa formation in LPS-challenged cells. As a result, Marcks PSD offset LPS-induced mTF hypercoagulation upon inclusion in the single-stage clotting assays. The anticoagulant activity was confirmed by showing that Marcks PSD significantly blocked rabbit brain thromboplastin (rbTF) procoagulation and inhibited rbTF-dependent FVII activation as well as FVIIa formation. Our study suggests that Marcks expression plays a role in a novel cellular modulation to downregulate mTF hypercoagulation.

Nicotinamide modulates mitochondrial membrane potential and cysteine protease activity during cerebral vascular endothelial cell injury.

Microvascular endothelial cell (EC) apoptosis or programmed cell death (PCD) during free radical injury may be involved in the development of cerebral ischemic and degenerative diseases. Yet, the cellular mechanisms that mediate cerebral EC injury require further definition. We therefore used the agent nicotinamide as an investigative tool in EC cultures to examine the role of free radical nitric oxide (NO)-induced PCD. EC injury was evaluated by the trypan blue dye exclusion method, DNA fragmentation, membrane phosphatidylserine (PS) exposure, cysteine protease activity, mitochondrial membrane potential, and mitogen-activated protein kinase phosphorylation. We demonstrate that cerebrovascular PCD consists of two distinct pathways that involve the degradation of genomic DNA and the exposure of membrane PS residues. Each of these pathways is reversible in nature and is controlled independently by caspase 8, caspase 1, and caspase 3. As a cytoprotectant, nicotinamide is novel in the vascular system and functions at two levels. Nicotinamide not only maintains the mitochondrial membrane potential and the prevention of cytochrome c release, but also prevents the induction of caspase-8-, caspase-1- and caspase-3-like activities linked to the DNA repair enzyme poly(ADP-ribose) polymerase through mechanisms that are independent from the MAP kinase systems of p38 and JNK. The work begins to identify therapeutic strategies for the protection of the cerebral vasculature during both acute and chronic degenerative disorders.

Nicotinamide: A Nutritional Supplement that Provides Protection Against Neuronal and Vascular Injury.

In addition to functioning as an essential nutrient for cellular growth and maintenance, nicotinamide also may be an attractive therapeutic agent with efficacy demonstrated against free radical ischemic programmed cell death (PCD). Yet, the cellular mechanisms that mediate cellular PCD, as well as protection by nicotinamide, are considered to require further definition. In primary rat hippocampal neurons and rat cerebrovascular endothelial cells (ECs), cellular injury was determined through trypan blue dye exclusion, externalization of membrane phosphatidylserine (PS) residues, and activation of the mitogen-activated protein kinase p38 through Western blot analysis. Nicotinamide was without cellular toxicity at concentrations lower than 50 mM in both neuronal and EC populations. Exposure to either anoxia or the nitric oxide (NO) donors sodium nitroprusside and NOC-9 significantly decreased neuronal and EC survival from approximately 85% to 38% and increased membrane PS exposure from approximately 10% to 80% over a 24-hour period. Pretreatment with nicotinamide (12.5 mM) prevented anoxic and NO cytodegeneration by significantly increasing survival and decreasing membrane PS expression. Protection by nicotinamide in both neurons and ECs appeared to be independent and downstream from p38 activation. Further investigations that define the cellular and molecular mechanisms employed by the nutrient nicotinamide may provide greater insight into the potential therapeutic targets that determine neuronal and vascular injury.