Enhanced metal-free photocatalyst performance by synergistic Coupling of internal magnetic field and piezoelectric field.

Graphitic carbon nitride (g-C3N4) is a promising metal-free photocatalyst; however, its high carrier recombination rate and insufficient redox capacity limit its degradation effect on antibiotics. In order to overcome these shortcomings, the photocatalytic activity is improved by regulating the spin polarization state, constructing the internal electric field, and applying the external piezoelectric field. In this paper, the chlorine-doped and nitrogen-deficient porous carbon nitride composite carbon quantum dots (Nv-Cl/UPCN@CQD) has been synthesized successfully. The doping position of chlorine and spin polarization properties are verified by DFT calculation. The key intermediates *O2- and *OOH for the synthesis of reactive oxygen species were detected by in-situ infrared testing, which promotes the production of •O2- and H2O2. The degradation rate constant of Nv-Cl/UPCN@CQD for removal of tetracycline is 8.45 times higher than that of g-C3N4. The active oxygen production and degradation efficiency of piezoelectric photocatalysis under the synergistic effect of intense stirring and vis-light irradiation are much higher than those of photocatalysis and piezoelectric catalysis, and the conversion of H2O2 to •OH is promoted by piezoelectric field. This paper provides a reliable way to improve the performance of piezoelectric photocatalysts by adjusting their energy band, electronic structure and piezoelectric force.

TeCVP: A Time-Efficient Control Method for a Hexapod Wheel-Legged Robot Based on Velocity Planning.

Addressing the problem that control methods of wheel-legged robots for future Mars exploration missions are too complex, a time-efficient control method based on velocity planning for a hexapod wheel-legged robot is proposed in this paper, which is named time-efficient control based on velocity planning (TeCVP). When the foot end or wheel at knee comes into contact with the ground, the desired velocity of the foot end or knee is transformed according to the velocity transformation of the rigid body from the desired velocity of the torso which is obtained by the deviation of torso position and posture. Furthermore, the torques of joints can be obtained by impedance control. When suspended, the leg is regarded as a system consisting of a virtual spring and a virtual damper to realize control of legs in the swing phase. In addition, leg sequences of switching motion between wheeled configuration and legged configuration are planned. According to a complexity analysis, velocity planning control has lower time complexity and less times of multiplication and addition compared with virtual model control. In addition, simulations show that velocity planning control can realize stable periodic gait motion, wheel-leg switching motion and wheeled motion and the operation time of velocity planning control is about 33.89% less than that of virtual model control, which promises a great prospect for velocity planning control in future planetary exploration missions.

Molecular Dynamics Study on the Diffusion Behavior of Water Molecules and the Dielectric Constant of Vegetable/Mineral Oil Blends.

Insulating oil plays a crucial role in internal insulation of oil-impregnated transformers. It has been demonstrated in a variety of experimental studies that mineral oil (MO) and vegetable oil (VO) can be blended in different ratios to improve insulation properties; however, the mechanisms underlying this phenomenon remain unclear. In this study, a molecular dynamics (MD) simulation approach was used to investigate diffusion of water molecules in VO/MO blends and dielectric constants of a mixture. The results show that the diffusion coefficient of water molecules is negatively correlated with the proportion of VO; thus, addition of VO helps to improve the insulation properties of a mixture. Due to introduction of strong polar functional groups, a decrease in the diffusion behavior of water molecules can be attributed to an increase in the interaction energy and formation of hydrogen bonds between water molecules and the mixed oil system. There is a direct correlation between the dielectric constant of a mixture and VO content; however, it is very sensitive to water content. The presence of strong polar water molecules or functional groups in a mixture leads to an increase in the dielectric constant, which results in a reduction in insulating properties. Accordingly, presence of polar groups plays an important role in determining the insulating properties of a mixture. To increase the insulation performance of a mixture, it is important to consider the diffusion-inhibiting and dielectric effects of the stronger polar groups in vegetable oil compared to those in mineral oil.

LncRNA SOX2OT facilitates LPS-induced inflammatory injury by regulating intercellular adhesion molecule 1 (ICAM1) via sponging miR-215-5p.

AIM: Long non-coding RNA SOX2 overlapping transcript (SOX2OT) is closely related to heart failure and myocardial damage. We attempted to investigate its role in endotoxin lipopolysaccharide (LPS) injury in cardiomyocytes. MATERIALS & METHODS: Cell viability, apoptosis rate, and levels of pro-inflammatory cytokines and apoptosis- and oxidative stress-related proteins were measured by MTS assay kit, flow cytometry, western blotting, and commercial kits. Physical interactions were confirmed by dual-luciferase report assay and RNA immunoprecipitation assay. RESULTS: Silencing SOX2OT and reinforcing miRNA (miR)-215-5p protected human AC16 cardiomyocytes from LPS-induced oxidative and inflammatory injuries by inhibiting intercellular adhesion molecule 1 (ICAM1). SOX2OT directly interacted with miR-215-5p, and miR-215-5p could target ICAM1. CONCLUSION: Inhibiting SOX2OT/miR-215-5p/ICAM1 axis might be a possible approach to treat myocardial damage. LAY ABSTRACT: Lipopolysaccharide (LPS) is an endotoxin from some bacteria including Escherichia coli, and it can cause inflammation in different tissues/cells including myocardia/cardiomyocytes, resulting in diseases such as myocarditis, cardiomyopathy, and cardiac hypertrophy. The underlying mechanism was not completely clarified, but known to include the dysregulation of non-coding RNAs. Herein, we demonstrated the biological role of long non-coding RNA SOX2 overlapping transcript (SOX2OT) in LPS-infected cardiomyocytes. Eventually, we found that inhibiting the expression of SOX2OT could mitigate LPS-induced a series of injuries in human cardiomyocytes, and SOX2OT interacts with a microRNA named as miR-215-5p. Besides, restoring miR-215-5p elicited similar effects to SOX2OT knockdown. Collectively, we concluded that SOX2OT binding to miR-215-5p might protect cardiomyocytes from LPS infection through regulating an important protein named ICAM1. This study suggested SOX2OT/miR-215-5p might be novel potential treatment targets in bacterial infection-related myocardial damages.

Folate deficiency enhances the in vitro genotoxicity of bile acids in human colon and liver cells.

Obese subjects have a high baseline of genotoxic stress, but the underlying mechanism is poorly understood. Given that obesity is associated with high bile acids (BA) and low folate, we aimed to determine the interactive effect of folate deficient or supplementation to the genotoxicity and cytotoxicity of BA in human colon and liver cells. NCM460 and L-02 cells were cultured in folate-deficient (22.6 nM) and replete (2260 nM) Roswell Park Memorial Institute (RPMI)-1640 medium with or without 50 µM deoxycholic acid (DCA) or lithocholic acid (LCA) for 7 days. Moreover, these cells were cultured in folate supplemented (5.65, 11.3 and 22.6 µM) and standard (2.26 µM) medium with 200 µM DCA or LCA for 7 days. Genotoxicity and cytotoxicity were measured using the cytokinesis-block micronucleus cytome assay. Our results showed that under folate-replete condition, 50 µM DCA or LCA significantly increased the rate of micronuclei (MN) in NCM460 and L-02 cells. Significantly, the MN-inducing effect of 50 µM DCA or LCA was further enhanced by folate deficiency. Interestingly, folate supplementation exerted a dose-dependent manner to significantly decrease the rates of MN, nucleoplasmic bridges, nuclear buds, apoptosis, and necrosis induced by 200 µM DCA or LCA in NCM460 and L-02 cells. In conclusion, the genotoxicity of moderate BA (50 µM) was exacerbated by folate deficiency and folate supplementation could efficiently protect cells against the genotoxicity and cytotoxicity of high BA (200 µM).

New Ultrasound-Controlled Paclitaxel Releasing Balloon vs. Asymmetric Drug-Eluting Stent in Primary ST-Segment Elevation Myocardial Infarction　- A Prospective Randomized Trial.

BACKGROUND: Application of drug-coated balloons (DCBs) is popular for the treatment of percutaneous coronary intervention (PCI). A new DCB has been designed as ultrasound-controlled paclitaxel releasing. This study was conducted to determine whether a DCB-only strategy has a similar safety profile and equal angiographic and clinical outcomes to DES implantation in primary ST-elevation myocardial infarction (STEMI) patients, as well as determine the efficiency and safety of this new DCB.Methods and Results:Overall, 184 pretreated STEMI patients were randomized into DCB and DES groups with a 1:1 allocation. The main study end-point was late lumen loss (LLL) during the 9 months after PCI. Late lumen loss was reported to be 0.24±0.39 mm in the DCB group and 0.31±0.38 mm in the DES group (P=0.215). Diameter stenosis was 28.27±15.35% in the DCB group and 25.73±15.41% in the DES group (P=0.312). Major adverse cardiovascular events (MACEs) were reported in 3 patients (3.4%) in the DCB group and 4 patients (4.7%) in the DES group (P=0.718). TLR and TVR in the DCB group was 2.3%, 3.4% and 2.4%, 3.5% in the DES group (P=1.000), respectively. No cardiac death and stent thrombosis (ST) was found in the DCB group at 12 months clinical follow up. CONCLUSIONS: The DCB-only strategy showed good angiographic and clinical outcomes in the 9- and 12-month follow-up periods, respectively. The VasoguardTM DCB is safe and feasible to treat STEMI patients.

Circ_0000064 knockdown attenuates high glucose-induced proliferation, inflammation and extracellular matrix deposition of mesangial cells through miR-424-5p-mediated WNT2B inhibition in cell models of diabetic nephropathy.

BACKGROUND: Circular RNA (circRNA) is widely shown to be associated with the development of diabetic nephropathy (DN). Our study aimed to further explore the role of circ_0000064 and provide a new mechanism for its action in DN. METHODS: Cell models of DN in vitro were constructed by treating human renal mesangial cells (HRMCs) with high glucose (HG). The expression of circ_0000064, microRNA-424-5p (miR-424-5p) and Wnt family member 2B (WNT2B) mRNA was detected by quantitative real-time PCR (qPCR). Cell proliferation was assessed by CCK-8 assay and EdU assay. Cell cycle was characterized by DNA content using flow cytometry. The releases of pro-inflammatory factors were checked using commercial ELISA kits. The expression of cell cycle- and fibrosis-associated proteins was detected by western blot. The interplays between miR-424-5p and circ_0000064 or WNT2B were verified by dual-luciferase reporter assay and RIP assay. RESULTS: Circ_0000064 and WNT2B were upregulated, while miR-424-5p was downregulated in HG-treated HRMCs. Circ_0000064 knockdown largely attenuated HG-induced proliferation, inflammatory responses and extracellular matrix (ECM) accumulation in HRMCs, and miR-424-5p deficiency reversed the role of circ_0000064 knockdown. MiR-424-5p was a target of circ_0000064, and miR-424-5p directly bound to WNT2B. MiR-424-5p restoration alleviated HG-induced proliferation, inflammatory responses and ECM accumulation in HRMCs, and WNT2B overexpression partially abolished the effects of miR-424-5p. CONCLUSION: Circ_0000064 knockdown ameliorated HG-induced HRMC dysfunctions through miR-424-5p enrichment-mediated WNT2B inhibition, hinting that circ_0000064 contributed to DN development.

Generation and Identification of the Number of Copies of Exogenous Genes and the T-DNA Insertion Site in SCN-Resistance Transformation Event ZHs1-2.

Soybean cyst nematode (SCN, Heterodera glycines Ichinohe) causes an estimated economic loss of about USD 3 billion each year in soybean (Glycine max L.) production worldwide. Overexpression of resistance genes against SCN provides a powerful approach to develop SCN resistance cultivars in soybean. The clarification of molecular characterization in transformation events is a prerequisite for ecological risk assessment, food safety, and commercial release of genetically modified crops. Here, we generated transgenic events harboring the BCN (beet cyst nematode) resistance Hs1pro-1 gene using the Agrobacterium-mediated method in soybean, evaluated their resistance to SCN infection, and clarified the molecular characterization of one of the transformation events. Five independent and stable inheritable transformation events were generated by an Agrobacterium-mediated transformation method. SCN resistance tests showed the average number of developed females per plant and female index (FI) in T4 ZHs1-1, ZHs1-2, ZHs1-3, ZHs1-4, and ZHs1-5 transformation events were significantly lower than that in the nontransgenic control. Among these, the ZHs1-2 transformation event had the lowest number of developed females per plant and FI. Southern hybridization showed the exogenous target Hs1pro-1 gene was inserted in one copy and the Bar gene was inserted two copies in the ZHs1-2 transformation event. The exogenous T-DNA fragment was integrated in the reverse position of Chr02: 5351566-5231578 (mainly the Bar gene expression cassette) and in the forward position of Chr03: 17083358-17083400 (intact T-DNA, including Hs1pro-1 and Bar gene expression cassette) using a whole genome sequencing method (WGS). The results of WGS method and Southern hybridization were consistent. All the functional elements of exogenous T-DNA fragments were verified by PCR using specific primer pairs in the T5 and T6 ZHs1-2 transformation events. These results demonstrated that the overexpression of Hs1pro-1 gene enhanced SCN resistance, and provide an important reference for the biosafety assessment and the labeling detection in transformation event ZHs1-2.

Causal effect between total cholesterol and HDL cholesterol as risk factors for chronic kidney disease: a mendelian randomization study.

BACKGROUND: While observational studies show an association between serum lipid levels and cardiovascular disease (CVD), intervention studies that examine the preventive effects of serum lipid levels on the development of CKD are lacking. METHODS: To estimate the role of serum lipid levels in the etiology of CKD, we conducted a two-sample mendelian randomization (MR) study on serum lipid levels. Single nucleotide polymorphisms (SNPs), which were significantly associated genome-wide with serum lipid levels from the GLGC and CKDGen consortium genome-wide association study (GWAS), including total cholesterol (TC, n = 187,365), triglyceride (TG, n = 177,861), HDL cholesterol (HDL-C, n = 187,167), LDL cholesterol (LDL-C, n = 173,082), apolipoprotein A1 (ApoA1, n = 20,687), apolipoprotein B (ApoB, n = 20,690) and CKD (n = 117,165), were used as instrumental variables. None of the lipid-related SNPs was associated with CKD (all P > 0.05). RESULTS: MR analysis genetically predicted the causal effect between TC/HDL-C and CKD. The odds ratio (OR) and 95% confidence interval (CI) of TC within CKD was 0.756 (0.579 to 0.933) (P = 0.002), and HDL-C was 0.85 (0.687 to 1.012) (P = 0.049). No causal effects between TG, LDL-C- ApoA1, ApoB and CKD were observed. Sensitivity analyses confirmed that TC and HDL-C were significantly associated with CKD. CONCLUSIONS: The findings from this MR study indicate causal effects between TC, HDL-C and CKD. Decreased TC and elevated HDL-C may reduce the incidence of CKD but need to be further confirmed by using a genetic and environmental approach.

Short-term in vitro glutamine restriction differentially impacts the chromosomal stability of transformed and non-transformed cells.

Glutamine (Gln) is a non-essential amino acid central for generating building blocks and cellular energy in tumours and rapidly proliferating non-transformed cells. However, the influence of Gln on regulating chromosomal stability of transformed and non-transformed cells remain poorly understand. We hypothesised that Gln is required for maintaining a homeostatic level of chromosomal stability. To this end, transformed cells HeLa and A375 and non-transformed cells NCM460 and HUVEC cells were intervened with varying concentrations of Gln (10, 1, 0.1 and 0.01 mM), with or without cisplatin (0.1 µg/ml), for 24 h. The cytokinesis-block micronucleus (MN) assay was used to determine chromosomal instability (CIN), the extent of which is reflected by the frequency of MN, nucleoplasmic bridge (NPB) and nuclear bud (NB). We demonstrated an unexpected decrease in the spontaneous rate of MN, but not NPB and NB, after Gln restriction in HeLa and A375 cells. Gln restriction reduced cisplatin-induced MN, but not NPB and NB, in HeLa and A375 cells. We further revealed that Gln restriction suppressed the proliferation of HeLa cells with high CIN induced by nocodazole, partially explaining why Gln restriction decreased the frequency of spontaneous and cisplatin-induced MN in transformed cells. In contrast, Gln restriction increased MN and NB, but not NPB, in NCM460 cells. In HUVEC cells, Gln restriction increased MN, NPB and NB. Meanwhile, Gln restriction sensitised NCM460 cells to cisplatin-induced genotoxicity. A similar but more pronounced pattern was observed in HUVEC cells. Collectively, these results suggest that the in vitro influences of Gln metabolism on CIN depend on cellular contexts: Transformed cells require high Gln to fine tune their CIN in an optimal rate to maximise genomic heterogeneity and fitness, whereas non-transformed cells need high Gln to prevent CIN.

Systematic identification and analysis of dysregulated miRNA and transcription factor feed-forward loops in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiovascular disease. Although some genes and miRNAs related with HCM have been studied, the molecular regulatory mechanisms between miRNAs and transcription factors (TFs) in HCM have not been systematically elucidated. In this study, we proposed a novel method for identifying dysregulated miRNA-TF feed-forward loops (FFLs) by integrating sample matched miRNA and gene expression profiles and experimentally verified interactions of TF-target gene and miRNA-target gene. We identified 316 dysregulated miRNA-TF FFLs in HCM, which were confirmed to be closely related with HCM from various perspectives. Subpathway enrichment analysis demonstrated that the method was outperformed by the existing method. Furthermore, we systematically analysed the global architecture and feature of gene regulation by miRNAs and TFs in HCM, and the FFL composed of hsa-miR-17-5p, FASN and STAT3 was inferred to play critical roles in HCM. Additionally, we identified two panels of biomarkers defined by three TFs (CEBPB, HIF1A, and STAT3) and four miRNAs (hsa-miR-155-5p, hsa-miR-17-5p, hsa-miR-20a-5p, and hsa-miR-181a-5p) in a discovery cohort of 126 samples, which could differentiate HCM patients from healthy controls with better performance. Our work provides HCM-related dysregulated miRNA-TF FFLs for further experimental study, and provides candidate biomarkers for HCM diagnosis and treatment.

"W-shaped" injection current dependence of electroluminescence linewidth in green InGaN/GaN-based LED grown on silicon substrate.

Injection current, and temperature, dependences of the electroluminescence (EL) spectrum from green InGaN/GaN multiple quantum well (MQW)-based light-emitting diodes (LED) grown on a Si substrate, are investigated over a wide range of injection currents (0.5 µA-350 mA) and temperatures (6-350 K). The results show that an increasing temperature can result in the change of injection current-dependent behavior of the EL spectrum in initial current range. That is, with increasing the injection current in the low current range, the emission process of the MQWs is dominated by filling effect of low-energetic localized states at the low temperature range of around 6 K, and by Coulomb screening of the quantum confinement Stark effect followed by a filling effect of the higher levels of the low-energetic localized states at the intermediate temperature range of around 160 K. However, when the temperature is further raised to the higher temperature range of around 350 K, the emission process of the MQWs in the low current range is dominated by carrier-scattering effect followed by non-radiative recombination process. The aforementioned current-dependent behaviors of the EL spectrum are mainly attributed to the strong localized effect of the green LED, as confirmed by the anomalous temperature dependence of the EL spectrum measured at the low injection current of 5 µA. In addition, the injection current dependence of external quantum efficiency at different temperatures shows that, with increasing temperature from 6 to 350 K, in addition to the enhanced non-radiative recombination, electron overflow becomes more significant, especially in the higher temperature range above 300 K.

Cigarette smoking might weaken the prognostic significance of cytochrome P450 2C19*2 polymorphism in acute myocardial infarction patients.

Prognostic significance of cytochrome P450 2C19*2 polymorphism in acute myocardial infarction is still not well investigated. The aim of the study was to determine the relationship between the genetic polymorphism and the outcome of the acute myocardial infarction patients, and to further clarify the impact of smoking on such relationship. Six hundred acute myocardial infarction patients were enrolled. All of them provided blood samples and underwent clopidogrel treatment. The genetic polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism analysis, and the platelet function was assessed using conventional aggregometry. Of the included patients, 287 carried GG wild-type genotypes, 225 carried GA genotypes and 88 carried AA genotypes. The platelet aggregation rate was significantly elevated in the AA genotype patients, mainly in the non-smoking patients (P < 0.001) and the former-smoking patients (P < 0.001). During 5-year follow-up period, after adjusted for multiple confounding factors, AA genotypes were associated with the increase in 5-year mortalities in the non-smoking patients [OR: 7.06, 95% confidence interval (CI): 2.16-11.49] and the former-smoking patients (OR: 4.38, 95% CI: 1.05-9.40), but not in the current-smoking patients (OR: 1.12, 95% CI: 0.60-2.31). In conclusion, the study suggested a potential role of P450 2C19*2 polymorphism as a prognostic indicator in acute myocardial infarction patients. We had also obtained some evidence that current smoking might weaken the prognostic significance of the genetic polymorphism in patients.

MKL1 is an epigenetic modulator of TGF-ß induced fibrogenesis.

Transforming growth factor (TGF-ß) induced activation of portal fibroblast cells serves as a primary cause for liver fibrosis following cholestatic injury. The underlying epigenetic mechanism is not clear. We studied the role of a transcriptional modulator, megakaryoblastic leukemia 1 (MKL1) in this process. We report here that MKL1 deficiency ameliorated BDL-induced liver fibrosis in mice as assessed by histological stainings and expression levels of pro-fibrogenic genes. MKL1 silencing by small interfering RNA (siRNA) abrogated TGF-ß induced transactivation of pro-fibrogenic genes in portal fibroblast cells. TGF-ß stimulated the binding of MKL1 on the promoters of pro-fibrogenic genes and promoted the interaction between MKL1 and SMAD3. While SMAD3 was necessary for MKL1 occupancy on the gene promoters, MKL1 depletion impaired SMAD3 binding reciprocally. TGF-ß treatment induced the accumulation of trimethylated histone H3K4 on the gene promoters by recruiting a methyltransferase complex. Knockdown of individual members of this complex significantly weakened the binding of SMAD3 and down-regulated the activation of portal fibroblast cells. In conclusion, we have identified an epigenetic pathway that dictates TGF-ß induced pro-fibrogenic transcription in portal fibroblast thereby providing novel insights for the development of therapeutic solutions to treat liver fibrosis.

Histone Methyltransferase SET1 Mediates Angiotensin II-Induced Endothelin-1 Transcription and Cardiac Hypertrophy in Mice.

OBJECTIVE: Endothelin-1 is a potent vasoconstrictor derived from vascular endothelium. Elevated endothelin-1 levels are observed in a host of cardiovascular pathologies including cardiomyopathy. The epigenetic mechanism responsible for endothelin-1 induction in these pathological processes remains elusive. APPROACH AND RESULTS: We report here that induction of endothelin-1 expression in endothelial cells by angiotensin II (Ang II) was accompanied by the accumulation of histone H3K4 trimethylation, a preeminent histone modification for transcriptional activation, on the endothelin-1 promoter. In the meantime, Ang II stimulated the expression and the occupancy of Suv, Ez, and Trithorax domain 1 (SET1), a mammalian histone H3K4 trimethyltransferase, on the endothelin-1 promoter, both in vitro and in vivo. SET1 was recruited to the endothelin-1 promoter by activating protein 1 (c-Jun/c-Fos) and synergized with activating protein 1 to activate endothelin-1 transcription in response to Ang II treatment. Knockdown of SET1 in endothelial cells blocked Ang II-induced endothelin-1 synthesis and abrogated hypertrophy of cultured cardiomyocyte. Finally, endothelial-specific depletion of SET1 in mice attenuated Ang II-induced pathological hypertrophy and cardiac fibrosis. CONCLUSIONS: Our data suggest that SET1 epigenetically activates endothelin-1 transcription in endothelial cells, thereby contributing to Ang II-induced cardiac hypertrophy. As such, screening of small-molecule compound that inhibits SET1 activity will likely offer a new therapeutic solution to the treatment of cardiomyopathy.

Probucol via inhibition of NHE1 attenuates LPS-accelerated atherosclerosis and promotes plaque stability in vivo.

Activation of Na(+)/H(+) exchanger 1 (NHE1) by lipopolysaccharide (LPS) via Ca(2+)/calpain is responsible in vascular smooth muscle cell (VSMC) apoptosis and to the process of atherosclerosis. Probucol is a lipid-lowering drug which has an anti-atherosclerosis effect. The mechanism remains poorly understood. Here we hypothesized that probucol via inhibition of NHE1 in VSMCs attenuates LPS-accelerated atherosclerosis and promotes plaque stability. Our results revealed that treatment of VSMCs with LPS increased the NHE1 activity in a time-dependent manner, associated with the increased Ca(2+)i. Probucol inhibited the LPS-induced increase of NHE1 activity in a dose-dependent manner in VSMCs for 24-hour co-incubation, as well as the change of Ca(2+)i. In addition, LPS enhanced the calpain activity. Both probucol and calcium chelation of Ca(2+) abolished the LPS-induced increase of calpain activity. Treatment of VSMCs with LPS reduced the expression of Bcl-2 without altering the mRNA level. Probucol inhibited the LPS-reduced expression of Bcl-2 protein in VSMCs. Animal studies indicated administration of probucol suppressed LPS-accelerated apoptosis, atherosclerosis and plaque instability in Apoe(-/-) mice. In conclusion, probucol via inhibition of NHE1 attenuates atherosclerosis lesion growth and promotes plaque stability.

Functional and structural alterations of peritoneum and secretion of fibrotic cytokines in rats caused by high glucose peritoneal dialysis solutions.

OBJECTIVE: To determine functional and structural alterations of peritoneum and fibrotic cytokines expression in peritoneal dialysis (PD) rats. METHODS: 28 Sprague-Dawley (S-D) rats were randomly divided into four groups and dialyzed with various solutions daily for four weeks: (1) no solution (CON group), (2) 0.9% Saline solution (NS group), (3) 1.5% Dianeal (LG group), (4) 4.25% Dianeal (HG group). Peritoneal equilibration tests, ultrafiltration function and effluent protein quantification were measured. Peritoneum morphology was studied and immunohistochemistry were performed for detection of transforming growth factor ß1 (TGF-ß1), connective tissue growth factor (CTGF), and fibronectin (FN) proteins. Reverse transcriptional-polymerase chain reaction was used to analyze the expression of TGF-ß1, CTGF mRNA. RESULTS: Administration of 4.25% Dianeal caused functional and structural changes of peritoneum, including protein loss through the transport process, decrease of peritoneal solute transport rate and ultrafiltration capacity. The collagen of peritoneum in the HG group was thicker than the other groups. The levels of CTGF, TGF-ß1, and FN proteins were significantly the highest in the HG group, followed by the LG group. The liner correlation analysis showed positive correlations between the levels of CTGF, TGF-ß1, and FN proteins and the collagen thickness. The expression of TGF-ß1 and CTGF mRNA in the HG group were significantly higher than those in the other groups and were indicated positive correlation. CONCLUSION: Using high glucose peritoneal dialysis solutions in rats may not only lead to processing of peritoneal fibrosis, which is promoted by ectopic expression of TGF-ß1, but also increase the expression of CTGF. CTGF is an important fibrotic media of peritoneal fibrosis in PD rats.

Permutation Equivariant Graph Framelets for Heterophilous Graph Learning.

The nature of heterophilous graphs is significantly different from that of homophilous graphs, which causes difficulties in early graph neural network (GNN) models and suggests aggregations beyond the one-hop neighborhood. In this article, we develop a new way to implement multiscale extraction via constructing Haar-type graph framelets with desired properties of permutation equivariance, efficiency, and sparsity, for deep learning tasks on graphs. We further design a graph framelet neural network model permutation equivariant graph framelet augmented network (PEGFAN) based on our constructed graph framelets. The experiments are conducted on a synthetic dataset and nine benchmark datasets to compare the performance with other state-of-the-art models. The result shows that our model can achieve the best performance on certain datasets of heterophilous graphs (including the majority of heterophilous datasets with relatively larger sizes and denser connections) and competitive performance on the remaining.

Physicochemical, functional, and antioxidant properties of black soldier fly larvae protein.

This study explores the multifaceted attributes of black soldier fly larvae protein (BSFLP), focusing on its physicochemical, functional, and antioxidant properties. BSFLP is characterized by 16 amino acids, with a predominant random coil secondary structure revealed by circular dichroism spectra. Differential scanning calorimetry indicates a substantial thermal denaturation temperature of 97.63°C. The protein exhibits commendable solubility, emulsification, and foaming properties in alkaline and low-salt environments, albeit with reduced water-holding capacity and foam stability under elevated alkaline and high-temperature conditions. In vitro assessments demonstrate that BSFLP displays robust scavenging proficiency against 2,2-diphenyl-1-picrylhydrazyl, 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid), and hydroxyl radicals, with calculated EC50 values of 1.90 ± 0.57, 0.55 ± 0.01, and 1.14 ± 0.02 mg/mL, respectively, along with notable reducing capabilities. Results from in vivo antioxidant experiments reveal that BSFLP, administered at doses of 300 and 500 mg/kg, significantly enhances the activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) (p < 0.05) while simultaneously reducing malondialdehyde levels in both serum and tissues of d-galactose-induced oxidative stress in mice. Moreover, the protein effectively attenuates oxidative damage in liver and hippocampal tissues. These findings underscore the potential utility of BSFLP as a natural antioxidant source, with applications spanning the food, pharmaceutical, and cosmetic industries. PRACTICAL APPLICATION: Black soldier fly larvae protein emerges as an environmentally sustainable reservoir of natural antioxidants, holding significant promise for the food, pharmaceutical, and cosmetic sectors. Its advantageous amino acid composition, robust thermal resilience, and impressive functional attributes position it as a compelling subject for continued investigation and advancement in various applications.

Tuning the electronic metal-carbon interactions in Lignin-based carbon-supported ruthenium-based electrocatalysts for enhanced hydrogen evolution reactions.

Ruthenium (Ru) nanoparticles dispersed on carbon support are promising electrocatalysts for hydrogen evolution reaction (HER) due to strong electronic metal-carbon interactions (EMCIs). Defects engineering in carbon supports is an effective strategy to adjust EMCIs. We prepared nitrogen/sulfur co-doped carbon supported Ru nanoparticles (Ru@N/S-LC) using sodium lignosulfonate and urea as feedstocks. Intrinsic S dopants from sodium lignosulfonate create rich S defects, thus enhancing the EMCIs within Ru@N/S-LC, leading a faster electron transfer between Ru nanoparticles and N/S-LC compared with N-doped carbon supported Ru nanoparticles (Ru@N-CC). The resulting Ru@N/S-LC exhibits an enhanced work function and a down-shifted d-band center, inducing stronger electron capturing ability and weaker hydrogen desorption energy than Ru@N-CC. Ru@N/S-LC requires only 7 and 94 mV overpotential in acidic medium and alkaline medium to achieve a current density of 10 mA cm-2. Density Functional Theory (DFT) calculations were utilized to clarify the impact of sulfur (S) doping and the mechanism underlying the notable catalytic activity of Ru@N/S-LC. This study offers a perspective for utilizing the natural dopants of biomass to adjust the EMCIs for electrocatalysts.