Erratum: PPAR δ inhibition protects against palmitic acid-LPS induced lipidosis and injury in cultured hepatocyte L02 cell: Erratum.

[This corrects the article DOI: 10.7150/ijms.37677.].

Facile synthesis of L10-PtFe/C intermetallic catalysts with superior catalytic durability for the oxygen reduction reaction.

An o-PtFe/C intermetallic catalyst was prepared by a facile thermal reduction method with the average particle size of only 6.6 nm in the presence of urea. The loss of mass activity is only 25.9% after 50 000 cycles. This work provides guidance on the suppression of grain coarsening for high-temperature synthesis of Pt-based intermetallic catalysts.

Enhanced Oxygen Reduction Reaction Performance by Adsorbed Water on Edge Sites.

Pt-based alloy nanoparticles have broad application prospects as cathode catalyst materials for proton-exchange membrane fuel cells (PEMFCs). Optimization of the oxygen adsorption energy is crucial to boost the performance of oxygen reduction catalysis. We successfully synthesized well-dispersed Pt1.2Ni tetrahedra and obtained the Pt1.2Ni/C catalyst adopting the one-pot synthetic protocol, which exhibits superb activity and good long-term stability for oxygen reduction reaction (ORR), achieving a mass activity of 1.53 A/mgPt at 0.90 VRHE, which is 12 times higher than that of commercial Pt/C. On combining X-ray photoelectron spectroscopy and density functional theory calculations, abundant water is adsorbed stably on the Pt1.2Ni alloy surface. We find that the intense interaction between the adsorbed O atom and adsorbed water can weaken the adsorption of oxygen, contributing to the ORR performance.

SESN2 Could Be a Potential Marker for Diagnosis and Prognosis in Glioma.

(1) Background: Glioma is among the most common brain tumors, and is difficult to eradicate with current therapeutic strategies due to its highly invasive and aggressive characteristics. Sestrin2 (SESN2) is an autophagy inducer. The effect of SESN2 on glioma is controversial and unclear. (2) Methods: We downloaded related RNA-seq data from the TCGA and GTEx databases. Bioinformatic analyses including differential gene expression analysis, KM survival curve analysis, univariate and multivariate Cox regression analyses, nomogram analysis, ROC curve analysis, gene function enrichment analysis, and immune cell infiltration analysis were conducted. In addition, data from the Human Protein Atlas (HPA) database were collected to validate SESN2 expression in glioma. (3) Results: In comparison with normal tissue, expression of SESN2 in glioma tissue was higher, and those with higher expressions had significantly lower overall survival rates. The results of univariate Cox regression analyses showed that SESN2 can be a disadvantageous factor in poor glioma prognosis. Both nomograms and ROC curves confirmed these findings. Meanwhile, according to gene function analysis, SESN2 may be involved in immune responses and the tumor microenvironment (TME). Based on the HPA database results, SESN2 is localized in the cytosol and shows high expression in glioma. (4) Conclusions: The expression of SESN2 in gliomas was positively relevant to a poorer prognosis, suggesting that SESN2 could be used as a prognostic gene.

Obstructive sleep apnea and serum total testosterone: a system review and meta-analysis.

PURPOSE: Testosterone deficiency (TD) negatively affects male sexuality, reproduction, general health, and quality of life. In recent years, decreased serum testosterone levels have been reported to be caused by obstructive sleep apnea (OSA). However, these results are controversial and lack the support of a large number of high-quality studies. Hence, we performed a meta-analysis to assess the association between OSA and serum testosterone levels. METHODS: To identify eligible studies, we conducted a systematic retrieval in the electronic databases (PubMed, Web of Science, the Cochrane Library, EMBASE) from their inception to September 2021. We chose studies with definitive diagnoses of OSA, including effects of OSA on testosterone level. Random effect model was used for analysis. RESULTS: This meta-analysis included 24 case-control studies with 1389 patients (1268 male patients) and 845 controls (745 male control). The serum testosterone levels in the male OSA group were significantly lower than that of control group [SMD = - 0.97, 95% CI (- 1.47, - 0.47)], while there was no difference in female patients with OSA and control [SMD = 0.06, 95% CI (- 0.22, 0.33)]. Subgroup analysis showed that race, age, body mass index (BMI), and detection method were the reason for high heterogeneity (I2 = 94.9%). CONCLUSIONS: The results indicated that OSA is significantly correlated with the decrease in serum testosterone levels in men. Male patients with OSA should be alerted to secondary diseases caused by low testosterone levels.

High expression of MARVELD3 as a potential prognostic biomarker for oral squamous cell carcinoma.

Objectives: Tight junction-associated marvel proteins (TAMP) is a transmembrane protein whose members are associated with tight junctions between cells and epithelial remodeling. MARVEL domain containing 3 (MARVELD3) is one of the members of the TAMP. MARVELD3, as a novel tight junction protein involved in bicellular tight junction assembly, has attracted growing attention in the field of oncology. This study aimed to investigate the prognostic role of MARVELD3 and to determine how it functions in tumorigenesis in oral squamous cell carcinoma (OSCC), thus providing additional data to help the guidance of clinical practice. Materials and Methods: RNA-seq data and relevant clinical information were obtained from TCGA. Bioinformatics means used in this study included differential gene expression analysis, KM survival curve analysis, univariate and multivariate Cox regression analyses, nomogram analysis, ROC curve analysis, methylation level analysis, gene function enrichment analysis, and immune cell infiltration analysis. Results: MARVELD3 was significantly higher expressed in OSCC tissue than in normal tissue, and the overall survival of the high expression group was significantly lower than that of the normal group. Univariate and multivariate Cox regression analyses showed that MARVELD3 could serve as an independent contributing factor to poor OSCC prognosis. The nomograms and ROC curves supported the results above. Its expression was negatively correlated with DNA methylation sites. Analysis of PPI networking and gene functional enrichment showed that MARVELD3 was involved in the functional activities of DNA and RNA and was associated with immune cell infiltration. Conclusion: The high expression of MARVELD3 is associated with poor prognosis in OSCC, and MARVELD3 could be recognized as a novel independent prognostic factor for OSCC.

Differences in Supragingival Microbiome in Patients with and without Full-Crown Prostheses.

Objectives: To characterize the microflora profile of supragingival biofilm in patients with and without full-crown prostheses. Methods: Plaque samples of full-crown prostheses and teeth in patients with porcelain-fused-to-metal crowns, all-ceramic crowns, and no prostheses were collected (three patients per group), using 16S rRNA high-throughput sequencing technology to conduct DNA sequencing on the samples and using Qiime, R, and PICRUSt2 software to perform bioinformatics analyses and functional analyses on sequencing data. Results: In total, 110,209 valid sequences were obtained in the experiment, corresponding to 11 phyla and 120 genera. The predominant species shared by the three groups were phyla Actinobacteria, Bacteroidetes, Firmicutes, Fusobacteria, and Proteobacteria and genera Rothia, Porphyromonas, Prevotella, Streptococcus, Veillonella, Leptotrichia, Neisseria, Citrobacter, and Pseudomonas. The species-difference analysis showed that genus Hameophilus significantly increased after the patient wore the dental prosthesis. Compared with the no-prosthesis samples, the functional analysis showed that cell motility increased in the samples from full-crown prostheses, while replication and repair, and translation decreased. Conclusions: This study reveals the changes in the oral microbial community of patients with full-crown prostheses, which could provide insights regarding the safety of materials for long-term use in the oral cavity.

A meta-analysis of based radiomics for predicting lymph node metastasis in patients with biliary tract cancers.

Background: To assess the predictive value of radiomics for preoperative lymph node metastasis (LMN) in patients with biliary tract cancers (BTCs). Methods: PubMed, Embase, Web of Science, Cochrane Library databases, and four Chinese databases [VIP, CNKI, Wanfang, and China Biomedical Literature Database (CBM)] were searched to identify relevant studies published up to February 10, 2022. Two authors independently screened all publications for eligibility. We included studies that used histopathology as a gold standard and radiomics to evaluate the diagnostic efficacy of LNM in BTCs patients. The quality of the literature was evaluated using the Radiomics Quality Score (RQS) and the Quality Assessment of Diagnostic Accuracy Studies 2 (QUADAS-2). The diagnostic odds ratio (DOR), sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), and area under the receiver operating characteristic curve (AUC) were calculated to assess the predictive validity of radiomics for lymph node status in patients with BTCs. Spearman correlation coefficients were calculated, and Meta-regression and subgroup analyses were performed to assess the causes of heterogeneity. Results: Seven studies were included, with 977 patients. The pooled sensitivity, specificity and AUC were 83% [95% confidence interval (CI): 77%, 88%], 78% (95% CI: 71, 84) and 0.88 (95% CI: 0.85, 0.90), respectively. The substantive heterogeneity was observed among the included studies (I 2 = 80%, 95%CI: 58,100). There was no threshold effect seen. Meta-regression showed that tumor site contributed to the heterogeneity of specificity analysis (P < 0.05). Imaging methods, number of patients, combined clinical factors, tumor site, model, population, and published year all played a role in the heterogeneity of the sensitivity analysis (P < 0.05). Subgroup analysis revealed that magnetic resonance imaging (MRI) based radiomics had a higher pooled sensitivity than contrast-computed tomography (CT), whereas the result for pooled specificity was the opposite. Conclusion: Our meta-analysis showed that radiomics provided a high level of prognostic value for preoperative LMN in BTCs patients.

[Effect of orthodontic traction on the microstructure of dental enamel].

OBJECTIVE: To investigate the effect of orthodontic traction on the microstructure of dental enamel. METHODS: Forty-eight isolated premolars were randomly divided into 6 groups (n=8), including Group A (blank control group), in which the teeth were bonded with the orthodontic brackets without any loading force; Groups B1, B2, and B3 where the teeth were bonded with the orthodontic brackets using clinical adhesives and loaded with 50 g force for 6 months, 200 g force for 6 months, and 200 g force for 1 month, respectively; and Groups C1 and C2, where the teeth were bonded with straight wire brackets using light curing bonding and chemical curing bonding techniques, respectively. All the teeth were embedded with non-decalcified epoxy resin. Scanning electron microscope (SEM), atomic force microscope (AFM), and energy spectrometer (EDS) were used to analyze interface morphology and elemental composition of the teeth sliced with a hard tissue microtome. RESULTS: Compared with those in Group A, the teeth in the other 5 groups showed increased adhesive residue index with microcracks and void structures on the enamel surface under SEM; AFM revealed microcracks on the enamel surface with angles to the grinding direction. A larger loading force on the bracket resulted in more microcracks on the enamel interface. The interface roughness differed significantly between Groups A and C2, and the peak-to-valley distance differed significantly between Groups A, C, and C2. CONCLUSIONS: Orthodontic traction can cause changes in the microstructure of normal dental enamel.

PPAR δ inhibition protects against palmitic acid-LPS induced lipidosis and injury in cultured hepatocyte L02 cell.

Background: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and its pathogenesis and mechanism are intricate. In the present study, we aimed to evaluate the role of PPAR δ in LPS associated NAFLD and to investigate the signal transduction pathways underlying PPAR δ treatment in vitro. Material and Methods: L02 cells were exposed to palmitic acid (PA) and/or LPS in the absence or presence of PPAR δ inhibition and/or activation. Results: LPS treatment markedly increased lipid deposition, FFA contents, IL-6 and TNF-α levels, and cell apoptosis in PA treatment (NAFLD model). PPAR δ inhibition protects L02 cells against LPS-induced lipidosis and injury. Conversely, the result of PPAR δ activation showed the reverse trend. LPS+PA treatment group significantly decreases the relative expression level of IRS-1, PI3K, AKT, phosphorylation of AKT, TLR-4, MyD88, phosphorylation of IKKα, NF-κB, Bcl-2 and increases the relative expression level of Bax, cleaved caspase 3 and cleaved caspase 8, compared with the cells treated with NAFLD model. PPAR δ inhibition upregulated the related proteins' expression level in insulin resistance and inflammation pathway and downregulated apoptotic relevant proteins. Instead, PPAR δ agonist showed the reverse trend. Conclusion: Our data show that PPAR δ inhibition reduces steatosis, inflammation and apoptosis in LPS-related NAFLD damage, in vitro. PPAR δ may be a potential therapeutic implication for NAFLD.

[Involvement of heme oxygenase in PM2.5-toxicity in human umbilical vein endothelial cells].

OBJECTIVE: To investigate the involvement of heme oxygenase (HO-1) in PM2.5 induced toxic responses in human umbilical vein endothelial cells (HUVECs). METHODS: The experiment groups are as follows: (1) control group; (2) PM2.5 groups: the cells were cultured with various concentrations of PM2.5 (200, 400, 800 µg/ml) for 24 h and 400 µg/ml was chosen for the main study; (3) PM2.5+Trion group: the cells were pre-treated by 10 µmol/L Trion [a scavenger of reactive oxygen species(ROS)] for 1 h before PM2.5 (400 µg/ml) treatment for 24 h; (4) PM2.5+ZnPP group: the cells were pretreated by HO-1 inhibitor ZnPP (10 µmol/L) for 1 h before treatment with PM2.5 (400 µg/ml) for 24 h. MTT assay was used to detect cell viability. Reverse transcription polymerase chain reaction (RT-PCR) and indirect immunofluorescence assay were used to determine the mRNA and protein expressions of HO-1. Fluorescence labeling probe method was used to measure intracellular ROS level and flow cytometry was used for cell apoptosis. Colorimetric assay was used to detect intracellular caspase-3 activity. RESULTS: Compared with control, PM2.5 significantly decreased cell viability, increased intracellular ROS, cell apoptosis and caspase-3 activity (all P < 0.05), these effects were significantly attenuated in PM2.5+Tiron group while enhanced in PM2.5+ZnPP group (all P < 0.05 vs. PM2.5 group). PM2.5 upregulated HO-1 mRNA and protein expressions in HUVECs which was downregulated in both PM2.5+Tiron group and PM2.5+ZnPP group. CONCLUSION: PM2.5 could induce oxidative injury through increasing ROS production via modulating HO-1 mRNA and protein expressions, the injury could be aggravated with inhibition of the activity of HO-1 suggesting a potential protective role of HO-1 against PM2.5 induced oxidative stress in HUVECs.

[Effect of ginsenoside on fine particulate matter induced oxidative injury in human endothelial cells].

OBJECTIVE: To explore the mechanism of fine particulate matter (PM(2.5)) induced endothelial injury and the efficacy and mechanism of ginsenoside Rg1 on the inhibition of endothelium injuries in human endothelial cells exposure to PM(2.5). METHODS: Human umbilical vein endothelial cells (HUVECs) were stimulated with various concentrations PM(2.5) (0.1, 0.2, 0.4, 0.8 mg/ml) and PM(2.5) at concentration 0.8 mg/ml induced significant endothelial injury and was chosen for the main study in the presence or absence of Rg1 (0.04 mg/ml). After 24 h treatment, cell growth A value was detected through MTT, intracellular reactive oxygen species (ROS) level through fluorescence labeling probe method and HO-1, Nrf2 mRNA expression was detected by RT-PCR. RESULTS: The cell A value was significantly lower while the ROS fluorescence gray value and the average optical density ratio of HO-1 were significantly higher in PM(2.5) group than in the control group (all P < 0.05). The average optical density ratio of Nrf2 was similar between PM(2.5) group and control group (P > 0.05). The A value and the average optical density ratio of HO-1 were significantly higher while the ROS fluorescence gray value was significantly lower in co-treated PM(2.5) (0.8 mg/ml) + Rg1 (0.04 mg/ml) group than in the PM(2.5) (0.8 mg/ml) group (all P < 0.05). CONCLUSION: PM(2.5) could induce human endothelial cells injury by increasing oxidative stress which could be attenuated by ginsenoside Rg1.

[The comparison study on effects of water-soluble components of fine particulate matter on vasomotor functions in aortas from rats after exposure in different time].

OBJECTIVE: To compare the difference of vasomotor functions in aortas segments from Wistar rats between 1-hour and 6-hours after exposure of water-soluble components of fine particulate matter (PM2.5). METHODS: All 30 Wistar rats were assigned to five groups (n=6 for each group) at random: the blank control group, control group for 1-hour and 6-hours, exposure group for 1-hour and 6-hours. The rats were sacrificed 1-hour or 6-hours later and aorta ring segments were mounted on wire myographs. RESULTS: (1) There was no significant difference in vasomotor functions among three control groups (P>0.05). (2) 1-hour or 6-hours after exposure there was a decrease of contraction elicited by 60 mmol/L KCl in contrast to the control group (P<0.05), whereas no significant change between the exposure group for 1-hour and 6-hours (P>0.05). (3) On the level of 10(-5) or 10(-7) mol/L, 1-hour after exposure there was a decrease in endothelium-dependent acetylcholine (ACh) elicited relaxation precontracted by 10(-6) mol/L NE compared with the control group (P<0.01 or P<0.05), on the level from 10(-5) to 10(-7) mol/L there was a decrease compared with the exposure group for 6-hours (P<0.05), whereas no difference between the exposure group for 6-hours and the control group (P>0.05). On the level from 10(-5) to 10(-9) mol/L, 1-hour after exposure there was a decrease in endothelium-independent sodium nitroprusside (SNP) elicited relaxation precontracted by 10(-6) mol/L NE as compared with the control group (P<0.01 or P<0.05) and a decrease on the level of 10(-6) or 10(-9) mol/L compared with the exposure group for 6-hours (P<0.05), 6-hours after exposure a decrease was caused as compared with the control group on the level from 10(-5) to 10(-7) mol/L (P<0.01 or P<0.05). CONCLUSIONS: Inhibition of contraction and impairment of relaxation in aortas should be caused 1-hour after exposure to water-soluble components of PM2.5 in the air, which is weaken 6-hours after exposure.

[Study of effects of drugs on myocardial hypertrophy due to overload].

OBJECTIVE: To study the relation of expression change of tumor necrosis factor-alpha (TNF-alpha), angiotensin II (Ang II), and endothelin-1 (ET-1), and the effect of imidapril on myocardial hypertrophy due to overload. METHODS: Sixty-three rats were randomly divided into four groups: sham operation (n=15), overload group (n=16), imidapril group (n=16), and Caweidiluo group (n=16). Hypertrophic myocardium was reproduced in rats by constricting abdominal aorta. Blood samples and heart were harvested 12 weeks after aorta constriction, and myocardial hypertrophy index, the contents of Ang II, ET-1 in the myocardium and plasma were determined by radioimmunoassay and TNF-alpha in the myocardium and plasma were determined by enzyme linked immunoadsorbent assay. RESULTS: Left ventricle showed obvious hypertrophy 12 weeks after operation. The contents of TNF-alpha, Ang II and ET-1 in the myocardium, and the content of TNF-alpha in serum, Ang II and ET-1 in plasma were increased compared with those of controls (all P<0.01). The treatment of imidapril and Caweidiluo could restrain the development of left ventricle hypertrophy after operation, and imidapril decreased the contents of TNF-alpha, Ang II and ET-1 in myocardium compared with overload group (all P<0.01). Imidapril lowered the contents of TNF-alpha in serum, Ang II and ET-1 in plasma, compared with overload group (all P<0.01), but not ET-1. Caweidiluo lowered the contents of TNF-alpha, Ang II and ET-1 in myocardium, the contents of TNF-alpha in serum, Ang II and ET-1 in plasma (all P<0.01) compared with overload group (both P<0.01). CONCLUSION: The activation of rennin-angiotensin system (RAS) by over load results to an elevation of TNF-alpha contents in plasma and myocardium, and it is probably one of the major regulatory pathways of myocardial hypertrophy.

Inotropic effects of MCI-154 on rat cardiac myocytes.

Calcium sensitizers exert positive inotropic effects without increasing intracellular Ca(2+). Thus, they avoid the undesired effects of Ca(2+) overload such as arrhythmias and cell injury, but most of them may impair myocyte relaxation. However, MCI-154, also a calcium sensitizer, has no impairment to cardiomyocyte relaxation. To clarify the underlying mechanisms, we examined the effects of MCI-154 on Ca(2+) transient and cell contraction using ion imaging system, and its influence on L-type Ca(2+) current and Na(+)/ Ca(2+) exchange current with patch clamp technique in rat ventricular myocytes as well. The results showed that: (1) MCI-154 (1-100 micromol/L) had no effect on L-type Ca(2+) current; (2) MCI-154 concentration-dependently increased cell shortening from 5.00+/-1.6 microm of control to 6.2+/-1.6 microm at 1 micromol/L, 8.7+/-1.6 microm at 10 micromol/L and 14.0+/-1.4 microm at 100 micromol/L, respectively, with a slight increase in Ca(2+) transient amplitude and an abbreviation of Ca(2+) transient restore kinetics assessed by time to 50% restore (TR(50)) and time to 90% restore (TR(90)); (3) MCI-154 dose-dependently increased the electrogenic Na(+)/ Ca(2+) exchange current both in the inward and the outward directions in rat ventricular myocytes. These results indicate that MCI-154 exerted a positive inotropic action without impairing myocyte relaxation. The stimulation of inward Na(+)/ Ca(2+) exchange current may accelerate the Ca(2+) efflux, leading to abbreviations of TR(50) and TR(90) in rat myocytes. The findings suggest that the improvement by MCI-154 of myocyte relaxation is attributed to the forward mode of Na(+)/ Ca(2+) exchange.

Inhibition of Na+/Ca2+ exchange by hexapeptide FRCRSFa in rat ventricular myocytes.

AIM: To study the effect of Phe-Arg-Cys-Arg-Ser-Phe-CONH2 (FRCRSFa) on Na+/Ca2+ exchange and its specificity in rat ventricular myocytes. METHODS: Na+/Ca2+ exchange current (INa+/Ca2+) and other currents were measured using whole-cell voltage clamp technique. RESULTS: A concentration-dependent inhibition of hexapeptide FRCRSFa on Na +/Ca2+ exchange was observed in rat ventricular myocytes. IC50 of inward and outward INa+/Ca2+ were 2 and 4 micromol/L, respectively. FRCRSFa 5 micromol/L did not affect L-type Ca2+ current, voltage-gated Na+ current, transient outward K+ current, and inward rectifier K+ current. CONCLUSION: These data indicate that FRCRSFa is an available inhibitor of Na+/Ca2+ exchange with relative selectivity and m ay be valuable for studies of the Na+/Ca2+ exchange in cardiac myocytes.