Dipole Coupling Accelerated H2 O Dissociation by Magnesium-Based Intermetallic Catalysts.

The water (H2 O) dissociation is critical for various H2 O-associated reactions, including water gas shift, hydrogen evolution reaction and hydrolysis corrosion. While the d-band center concept offers a catalyst design guideline for H2 O activation, it cannot be applied to intermetallic or main group elements-based systems because Coulomb interaction was not considered. Herein, using hydrolysis corrosion of Mg as an example, we illustrate the critical role of the dipole of the intermetallic catalysts for H2 O dissociation. The H2 O dissociation kinetics can be enhanced using Mgx Mey (Me=Co, Ni, Cu, Si and Al) as catalysts, and the hydrogen generation rate of Mg2 Ni-loaded Mg reached 80 times as high as Ni-loaded Mg. The adsorbed H2 O molecules strongly couple with the Mg-Me dipole of Mgx Mey , lowering the H2 O dissociation barrier. The dipole-based H2 O dissociation mechanism is applicable to non-transition metal-based systems, such as Mg2 Si and Mg17 Al12 , offering a flexible catalyst design strategy for controllable H2 O dissociation.

USP29 activation mediated by FUBP1 promotes AURKB stability and oncogenic functions in gastric cancer.

BACKGROUND: Gastric cancer is a highly prevalent cancer type and the underlying molecular mechanisms are not fully understood. Ubiquitin-specific peptidase (USP) 29 has been suggested to regulate cell fate in several types of cancer, but its potential role in gastric carcinogenesis remains unclear. METHODS: The expression of USP29 in normal and gastric cancer tissues was analyzed by bioinformatics analysis, immunohistochemistry and immunoblot. Gene overexpression, CRISPR-Cas9 technology, RNAi, and Usp29 knockout mice were used to investigate the roles of USP29 in cell culture, xenograft, and benzo[a]pyrene (BaP)-induced gastric carcinogenesis models. We then delineated the underlying mechanisms using mass spectrometry, co-immunoprecipitation (Co-IP), immunoblot, ubiquitination assay, chromatin immunoprecipitation (ChIP), quantitative real-time PCR (qRT-PCR), and luciferase assays. RESULTS: In this study, we found that USP29 expression was significantly upregulated in gastric cancers and associated with poor patient survival. Ectopic expression of USP29 promoted, while depletion suppressed the tumor growth in vitro and in vivo mouse model. Mechanistically, transcription factor far upstream element binding protein 1 (FUBP1) directly activates USP29 gene transcription, which then interacts with and stabilizes aurora kinase B (AURKB) by suppressing K48-linked polyubiquitination, constituting a FUBP1-USP29-AURKB regulatory axis that medicates the oncogenic role of USP29. Importantly, systemic knockout of Usp29 in mice not only significantly decreased the BaP-induced carcinogenesis but also suppressed the Aurkb level in forestomach tissues. CONCLUSIONS: These findings uncovered a novel FUBP1-USP29-AURKB regulatory axis that may play important roles in gastric carcinogenesis and tumor progression, and suggested that USP29 may become a promising drug target for cancer therapy.

Association of thyroid hormone sensitivity index with stroke in patients with coronary artery disease.

BACKGROUND AND AIMS: Thyroid hormones (THs) will affect the occurrence and prognosis of stroke, and the research on THs sensitivity index and stroke in patients with coronary heart disease (CHD) is scarce. The goal of this study is to look into the relationship between central and peripheral THs sensitivity index and stroke in patients with CHD. METHODS: Between January 1, 2014, and September 30, 2020, 30,160 patients with CHD were enrolled in this study. By computing the thyroid feedback quantile index (TFQI), thyroid stimulating hormone index (TSHI), and thyrotropin thyroxine resistance index (TT4RI), the central sensitivity indexes to THs was assessed, and the ratio of serum free triiodothyronine (FT3) to serum free thyroxine (FT4) was used to assess peripheral THs sensitivity. The relationship between central and peripheral THs sensitivity index and stroke was investigated using logistic regression, especially in different types of stroke, ages, sexes, and blood glucose levels. RESULTS: Stroke risk is positive associated with TSHI, TFQI, and PTFQI. In subgroup analysis, the OR values of these relationships are higher in people younger than 65 years old, male, and diagnosed with diabetes. In addition, stroke risk was negatively associated with FT3/FT4, and the OR values of these relationships were lower in people older than 65 years, female, and diagnosed with prediabetes. CONCLUSIONS: This study demonstrates that the increase in the central THs sensitivity index and the decrease in the peripheral THs sensitivity index are associated with a higher risk of stroke in CHD patients, and provides new ideas for the assessment of stroke in patients with CHD.

Relationship Between Serum Uric Acid and Carotid Plaque in Patients With Coronary Artery Disease by Sex and Blood Pressure Status.

The purpose of this study was to explore the sex difference and effects of blood pressure (BP) on the relationship between serum uric acid (SUA) and carotid plaque in patients with coronary heart disease (CHD). This large multicenter retrospective study included 12099 patients with CHD (aged 35-75 years) between January 1, 2014 and September 30, 2020. Patients were divided into three groups according to systolic BP (SBP) and diastolic BP (DBP), and the SUA levels in males and females were converted into three groups. Logistic regression was used to analyze the influence of sex and BP on the relationship between SUA levels and carotid plaque in patients with CHD. In the model of male BP subgroups, using the BP of group A (normal with SBP <120 mmHg and DBP <80 mmHg) as a reference, SUA levels were significantly correlated with the occurrence of carotid plaque under different BP states (P < .001). In contrast, in the model of female BP subgroups, most of these correlations were not statistically significant. Our study showed that SUA levels were significantly associated with carotid plaque occurrence in males with CHD, which remained significant across different BP states.

Association Between Anemia Status and the Risk of Different Types of Heart Failure: A RCSCD-TCM Study in China.

We investigated the association between anemia status and the risk of heart failure (HF) in patients with coronary heart disease (CHD) based on a multi-center, large-sample and retrospective cross-sectional study including 89,207 patients. Heart failure was categorized as HF with reduced ejection fraction (HFrEF), HF with preserved ejection fraction (HFpEF), and HF with mid-range ejection fraction (HFmrEF). In multi-adjusted models, compared with patients without anemia, mild anemia (odds ratio [OR] 1.71; 95% confidence interval [CI] 1.53-1.91; P < .001), moderate anemia (OR 3.68; 95% CI, 3.25-4.17; P < .001), and severe anemia (OR 8.02; 95% CI, 6.50-9.88; P < .001) were associated with the risk of HF among CHD patients. Men aged <65 years were more likely to develop HF. In subgroup analyses, the multi-adjusted ORs and 95% CI of HFpEF, HFrEF, and HFmrEF related to anemia were 3.24 (95% CI 1.43-7.33), 2.22 (95% CI 1.28-3.84), and 2.55 (95% CI 2.24-2.89), respectively. These findings suggest that anemia might be associated with increased risk of different types of HF, especially HFpEF.

Integrin αvß1 facilitates ACE2-mediated entry of SARS-CoV-2.

Integrins have been suggested to be involved in SARS-CoV-2 infection, but the underlying mechanisms remain largely unclear. This study aimed to investigate how integrins facilitate the ACE2-mediated cellular entry of SARS-CoV-2. We first tested the susceptibility of a panel of human cell lines to SARS-CoV-2 infection using the spike protein pseudotyped virus assay and examined the expression levels of integrins in these cell lines by qPCR, western blot and flow cytometry. We found that integrin αvß1 was highly enriched in the SARS-CoV-2 susceptible cell lines. Additional studies demonstrated that RGD (403-405)→AAA mutant was defective in binding to integrin αvß1 compared to its wild type counterpart, and anti-αvß1 integrin antibodies significantly inhibited the entry of SARS-CoV-2 into the cells. Further studies using mouse NIH3T3 cells expressing human ACE2, integrin αv, integrin ß1, and/or integrin αvß1 suggest that integrin αvß1 was unable to function as an independent receptor but could significantly facilitate the cellular entry of SASR-CoV-2. Finally, we observed that the Omicron exhibited a significant increase in the ACE2-mediated viral entry. Our findings may enhance our understanding of the pathogenesis of SARS-CoV-2 infection and offer potential therapeutic target for COVID-19.

Transcriptomic characterization of interactions between sodium selenite and coenzyme Q10 on preventing cadmium-induced testicular defects.

The effect of heavy metal cadmium (Cd) on testicular function is recognized. However, the mechanism involved is not well-established. In the present study, we analyzed the testicular transcriptomic changes induced by acute Cd exposure of adult rats with and without supplementation of antioxidants selenium (Se) and/or coenzyme Q10 (CoQ). Cd significantly decreased serum testosterone and two steroidogenic proteins SCARB1 and STAR. RNA-Seq analyses of testicular RNAs revealed specific activation of oxidative stress-, inflammation-, MAPK- and NF-κB-related signaling molecules. In addition, Cd treatment down-regulated gene for I, III and IV complexes of mitochondrial electron transport chain and up-regulated genes for NADPH-oxidase, major cascade in ROS production. The decrease in steroidogenesis and increase in inflammation may result from oxidative stress since supplementation of Se and CoQ, but not with either alone, almost completely prevented these changes, including overall alterations in transcriptome. Cd exposure induced total of 1192 differentially expressed genes (DEGs), which was reduced to 29 without considering confounding factors associated with Se/CoQ, a 97.6% protection rate. In conclusion, Cd exposure inhibited Leydig cell steroidogenesis by down-regulating SCARB1 and STAR through increasing oxidative stress and inflammation, but Se plus CoQ synergistically prevented all the changes induced by the Cd exposure.

Pyroptosis Induction with Nanosonosensitizer-Augmented Sonodynamic Therapy Combined with PD-L1 Blockade Boosts Efficacy against Liver Cancer.

Induction of pyroptosis can promote anti-PD-L1 therapeutic efficacy due to the release of pro-inflammatory cytokines, but current approaches can cause off target toxicity. Herein, a phthalocyanine-conjugated mesoporous silicate nanoparticle (PMSN) is designed for amplifying sonodynamic therapy (SDT) to augment oxidative stress and induce robust pyroptosis in tumors. The sub-10 nm diameter structure and c(RGDyC)-PEGylated modification enhance tumor targeting and renal clearance. The unique porous architecture of PMSN doubles ROS yield and enhances pyroptotic cell populations in tumors (25.0%) via a cavitation effect. PMSN-mediated SDT treatment efficiently reduces tumor mass and suppressed residual tumors in treated and distant sites by synergizing with PD-L1 blockade (85.93% and 77.09%, respectively). Furthermore, loading the chemotherapeutic, doxorubicin, into PMSN intensifies SDT-pyroptotic effects and increased efficacy. This is the first report of the use of SDT regimens to induce pyroptosis in liver cancer. This noninvasive and effective strategy has potential for clinical translation.

Fibrinogen/albumin ratio and carotid artery plaques in coronary heart disease patients with different glucose metabolic states: a RCSCD-TCM study.

AIM: The relationship between fibrinogen/albumin ratio (FAR) and carotid artery plaques (CAPs) was investigated in patients with coronary heart disease (CHD). METHODS: A total of 11,624 patients with CHD were enrolled and divided into quartiles based on the FAR (Q1: FAR index ≤ 0.0663; Q2: 0.0664 ≤ FAR index ≤ 0.0790; Q3: 0.0791 ≤ FAR index ≤ 0.0944; Q4: FAR index > 0.0944). Patients were classified into three groups according to their blood glucose levels: normal glucose regulation (NGR), prediabetes mellitus (pre-DM), and diabetes mellitus (DM) groups. Carotid ultrasonography was performed to detect CAPs. The relationship between FAR and CAPs was evaluated using logistic and subgroup analyses. RESULTS: Among 11,624 participants, 8738 (75.14%) had CAPs. Compared with Q1, the odds ratio (OR) of Q4 in patients with CHD was 2.00 (95% confidence interval [CI]: 1.71-2.34) after multivariate adjustment. Taking Q1 as a reference, a higher OR was observed in Q4 of FAR for CAPs in men [OR: 2.26; 95% CI: 1.73-2.95] in the multi-adjusted models. Moreover, multivariate adjustment indicated that the highest OR was observed in patients with CHD and DM (OR: 2.36; 95% CI: 1.80-3.10). CONCLUSIONS: A significant association between FAR and CAPs was observed in patients with CHD, regardless of sex or blood glucose levels. Therefore, FAR may be used as an effective indicator to identify patients at a high risk of CAPs among patients with CHD.

Thymosin α1 modulated the immune landscape of COVID-19 patients revealed by single-cell RNA and TCR sequencing.

BACKGROUND: The Coronavirus disease-19 (COVID-19) pandemic has posed a serious threat to global health. Thymosin α1 (Tα1) was considered to be applied in COVID-19 therapy. However, the data remains limited. METHODS: Participants with or without Tα1 treatment were recruited. Single cell RNA-sequencing (scRNA-seq) and T cell receptor-sequencing (TCR-seq) of the peripheral blood mononuclear cell (PBMC) samples were done to analyze immune features. The differential expression analysis and functional enrichment analysis were performed to explore the mechanism of Tα1 therapy. RESULTS: 33 symptomatic SARS-CoV-2-infected individuals (COV) and 11 healthy controls (HC) were enrolled in this study. The proportion of CD3+ KLRD1+ NKT, TBX21+ CD8+ NKT was observed to increase in COVID-19 patients with Tα1 treatment (COVT) than those without Tα1 (COV) (p = 0.024; p = 0.010). These two clusters were also significantly higher in Health controls with Tα1 treatment (HCT) than those without Tα1 (HC) (p = 0.016; p = 0.031). Besides, a series of genes and pathways related to immune responses were significantly higher enriched in Tα1 groups TBX21+ CD8+ NKT, such as KLRB1, PRF1, natural killer cell-mediated cytotoxicity pathway, chemokine signaling pathway, JAK-STAT signaling pathway. The increased TRBV9-TRBJ1-1 pair existed in both HCs and COVID-19 patients after Tα1 treatment. 1389 common complementarity determining region 3 nucleotides (CDR 3 nt) were found in COV and HC, while 0 CDR 3 nt was common in COVT and HCT. CONCLUSIONS: Tα1 increased CD3+ KLRD1+ NKT, TBX21+ CD8+ NKT cell proportion and stimulated the diversity of TCR clones in COVT and HCT. And Tα1 could regulate the expression of genes associated with NKT activation or cytotoxicity to promote NKT cells. These data support the use of Tα1 in COVID-19 patients.

Engineering of a NIR fluorescent probe for high-fidelity tracking of lipid droplets in living cells and nonalcoholic fatty liver tissues.

LDs (Lipid droplets) are key organelles for lipid metabolism and storage, which are closely related to ferroptosis and fatty liver. Due to its small size and highly dynamic nature, developing high-fidelity fluorescent probes for imaging of LDs is crucial for observing the dynamic physiological processes of LDs and investigating LDs-associated diseases. Herein, we synthesized three dicyanoisophorone-based fluorescent probes (DCIMe, DCIJ, and DCIQ) with different electron-donating groups and studied their imaging performance for LDs. The results show that DCIQ is highly polarity sensitive and can perform high-fidelity imaging for LDs, with significantly better performance than DCIMe, DCIJ, and commercial LD probe BODIPY 493/503. Based on this, DCIQ was successfully applied to real-time observe the interplays between LDs and other organelles (mitochondria, lysosomes, and endoplasmic reticulum), and to image the dynamics of LDs with fast scanning mode (0.44 s/frame) and the generation of oleic acid-induced LDs with high-fidelity. Finally, DCIQ was used to study the changes of LDs in the ferroptosis process and nonalcoholic fatty liver disease tissues. Overall, this study provided a powerful tool for high-fidelity imaging of LDs in cells and tissues.

Associations Between GGT/ALT Ratio and Carotid Plaque in Inpatients With Coronary Artery Disease: A RCSCD-TCM Study.

This study investigated the relationship between gamma-glutamyltransferase/alanine aminotransferase (GGT/ALT) ratio and carotid plaques in patients with coronary artery disease (CAD). This multicenter retrospective study included 8,255 patients with CAD who were divided according to GGT/ALT quartiles: Q1 (GGT/ALT ≤ 1.00), Q2 (1.00 < GGT/ALT ≤ 1.41), Q3 (1.41 < GGT/ALT ≤ 2.05), and Q4 (GGT/ALT > 2.05). Logistic regression was used to analyze the relationship between GGT/ALT, carotid plaques, and carotid plaque echogenicity. GGT/ALT ratio (odds ratio [OR]: 1.16; 95% confidence interval [CI]: 1.11-1.21; P < .001) was significantly associated with carotid plaque risk. The degree of relevance was higher in men (OR: 1.71; 95% CI: 1.35-2.15; P < .001) than in women (OR: 1.56; 95% CI: 1.28-1.91; P < .001). The ORs value of carotid plaque risk was higher in middle-aged patients (OR: 2.23; 95% CI: 1.78-2.80; P < .001) than in older patients (OR: 1.77; 95% CI: 1.44-2.18; P < .001). The GGT/ALT ratio was significantly associated with different carotid plaque echogenicity, and the highest OR values were for isoechoic plaques (OR: 1.18; 95% CI: 1.12-1.24; P < .001). These findings suggest that the GGT/ALT ratio might be associated with a high risk of developing carotid plaques and different types of plaque echoes and was more significantly associated with isoechoic plaques.

The Association Between Hemoglobin Glycation Index and Carotid Artery Plaque in Patients With Coronary Heart Disease.

This study aimed to examine the association between the hemoglobin glycation index (HGI) and carotid artery plaque (CAP) in patients with coronary heart disease (CHD). We conducted a cross-sectional analysis of 10,778 patients with CHD. The participants were divided into three groups by HGI tertiles (T1 HGI<-0.44, T2 -0.44 ≤ HGI ≤ 0.15, T3 HGI>0.15). The presence of CAP was used to diagnose by carotid ultrasonography. Logistic regression analysis was used to analyze the association between the HGI and CAP. The association between HGI and CAP was also assessed according to sex, age, smoking status, and drinking status. We further assessed the association between HGI and the ultrasound characteristics of CAP. The baseline analysis showed substantial differences in relevant parameters between the three groups of patients with CHD according to the tertiles of the HGI. Multivariate logistic regression analysis showed that HGI was significantly associated with CAP (odds ratio [OR] 1.32; 95% confidence interval [CI] 1.26-1.39). The association between HGI and CAP exists among different sex, age, smoking, and drinking status. Furthermore, there was a significant and positive association between HGI and all four different echogenicities of the CAP.

Associations Between Atherosclerosis and Elevated Serum Alkaline Phosphatase in Patients With Coronary Artery Disease in an Inflammatory State.

BACKGROUND AND AIM: Serum alkaline phosphatase (ALP) has been shown to be associated with cardiovascular disease (CVD) risk. Inflammation is the initiator of atherosclerosis, throughout the life of atherosclerosis. This study investigated the relationship between serum ALP and atherosclerosis in patients with coronary artery disease (CAD) in an inflammatory state. METHODS: This was a multicentre retrospective study including 22,989 patients with CAD. Serum alkaline phosphatase was converted into the quartiles. C-reactive protein (CRP) was assayed as a marker of systemic inflammation. The atherosclerosis index (AI) was used to assess the degree of atherosclerosis. Binary logistic regression was used to analyse the relationship between ALP and AI. Stratified analysis was performed according to sex and age. RESULTS: Elevated serum ALP was associated with the risk of atherosclerosis in patients with CAD, and after quartiling ALP, the OR for Q4 was 1.17 (95% CI 1.08-1.26; p<0.001) when using Q1 as reference. The odds ratio (OR) for ALP and risk of atherosclerosis was higher in patients aged ≤60 years (OR 1.33, 95% CI 1.15-1.53; p<0.001) than in patients aged >60 years (OR 1.11, 95% CI 1.01-1.23; p<0.05), and higher in males (OR 1.21, 95% CI 1.09-1.35; p<0.001) than in females (OR 1.16, 95% CI 1.03-1.31; p<0.05). Q4 (ALP >83.00 U/L) was significantly associated with increased risk of atherosclerosis in the inflammatory state (OR 1.48, 95% CI 1.18-1.86; p<0.001), and it remained after stratified analysis according to sex and age. CONCLUSIONS: The risk of atherosclerosis tended to increase with increasing ALP levels and the correlation between ALP and the degree of atherosclerosis was significantly stronger when ALP was >83.00 U/L. This relationship was more pronounced in inflammatory states, and there were sex and age differences. REGISTRATION: URL: https://www. CLINICALTRIALS: gov; Unique identifier: NCT04026724.

Identification of USP29 as a key regulator of nucleotide biosynthesis in neuroblastoma through integrative analysis of multi-omics data.

Cancer cells show enhanced nucleotide biosynthesis, which is essential for their unlimited proliferation, but the underlying mechanisms are not entirely clear. Ubiquitin specific peptidase 29 (USP29) was reported to sustain neuroblastoma progression by promoting glycolysis and glutamine catabolism; however, its potential role in regulating nucleotide biosynthesis in tumor cells remains unknown. In this study, we depleted endogenous USP29 in MYCN-amplified neuroblastoma SK-N-BE2 cells by sgRNAs and conducted metabolomic analysis in cells with or without USP29 depletion, we found that USP29 deficiency caused a disorder of intermediates involved in glycolysis and nucleotide biosynthesis. De novo nucleotide biosynthesis was analyzed using 13C6 glucose as a tracer under normoxia and hypoxia. The results indicated that USP29-depleted cells showed inhibition of nucleotide anabolic intermediates derived from glucose, and this inhibition was more significant under hypoxic conditions. Analysis of RNA sequencing data in SK-N-BE2 cells demonstrated that USP29 promoted the gene expression of metabolic enzymes involved in nucleotide anabolism, probably by regulating MYC and E2F downstream pathways. These findings indicated that USP29 is a key regulator of nucleotide biosynthesis in tumor cells.

Comparison of Analgesia Treatment Methods After Arthroscopic Rotator Cuff Repair: A Network Meta-analysis of 42 Randomized Controlled Trials.

Background: The optimal method for postoperative analgesia after arthroscopic rotator cuff repair (ARCR) is still unclear. Purpose: To compare the efficacy of postoperative analgesic methods after ARCR through network meta-analysis of randomized controlled trials and prospective controlled trials. Study Design: Systematic review; Level of evidence, 2. Methods: Following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we searched PubMed, Embase, and Web of Science from inception until April 12, 2022, for randomized controlled trials and prospective controlled trials evaluating neuraxial analgesia, peripheral nerve block, periarticular local anesthetic infiltration, intravenous patient-controlled analgesia, oral analgesia, or any combination of these methods for pain management after ARCR. Outcomes included pain scores at rest, morphine consumption, and complications (nausea and vomiting). Study quality was assessed using the Cochrane risk-of-bias tool. Network meta-analysis was used to assess the relative efficacy of the methods for postoperative analgesia. The best choice for postoperative analgesia was defined as the one with significant differences in pain scores and morphine consumption compared with placebo, with no significant difference in complications, during the initial 48 hours postoperatively. Results: Included were 42 studies with 3110 patients. Only suprascapular nerve block (SSNB) was significantly superior to placebo in pain scores (mean difference [MD], -0.93 [95% CI, -1.31 to -0.54] at 6 hours; MD, -2.34 [95% CI, -3.49 to -1.19] at 12 hours) and morphine consumption (MD, -17.70 [95% CI, -32.98 to -2.42] at 24 hours) (P < .05 for all), with no difference in complications (odds ratio, 0.96 [95% CI, 0.21 to 4.32]; P > .05). Pain scores were significantly lower with interscalene nerve block compared with SSNB (MD, -0.69 [95% CI, -1.17 to -0.20] at 6 hours; MD, -1.44 [95% CI, -2.21 to -0.67] at 12 hours) and with SSNB + axillary nerve block compared with SSNB (MD, -3.09 [95% CI, -4.18 to -1.99] at 6 hours; MD, -0.87 [95% CI, -1.71 to -0.03] at 12 hours) (P < .05 for all). Conclusion: Based on the current evidence, most analgesic methods lowered pain and morphine consumption compared with placebo. There were significant differences in pain scores between interscalene nerve block and SSNB during the first 12 hours postoperatively, and adding axillary nerve block to SSNB enhanced the analgesic effect.

Effect of Dan-Lou tablets on coronary heart disease revealed by microarray analysis integrated with molecular mechanism studies.

Dan-Lou tablets (DLT) effectively treat coronary heart disease (CHD). However, its pharmacological mechanism in CHD treatment requires further investigation. This study aimed to elucidate the underlying pharmacological mechanisms of DLT in the treatment of CHD through clinical trials, microarray research, bioinformatics analysis, and molecular mechanism research. In this study, DLT improved coagulation function, endothelial injury, and levels of lipids, metalloproteases, adhesion molecules, inflammatory mediators, and homocysteine. The results of molecular biology research demonstrated that DLT can increase the gene and protein expressions of meningioma expressed antigen 5 (MGEA5) and mouse doubleminute 2 (MDM2) and inhibited the gene and protein expressions of signal transcription and transcription activator 5 B (STAT5B), tropomyosin-1 (TPM1), and aromatic hydrocarbon receptor nuclear transpose (ARNT). The results indicate that DLT reduced the extent of vascular endothelial damage in CHD rats by reducing the expressions of STAT5B, TPM1, and MDM2; inhibiting the inflammatory reaction; and increasing the expressions of ARNT and MGEA5.

Evaluation of prevention and treatment effects of fibroblast growth factor-21 in BLM-induced pulmonary fibrosis.

Pulmonary fibrosis is a progressive and fatal fibrotic lung disease and associated with a high mortality rate. In the study, the prevention and treatment effects of fibroblast growth factor-21 (FGF-21) in bleomycin (BLM)-induced pulmonary fibrosis were investigated in vivo and vitro. In the prevention of pulmonary fibrosis studies, the results showed that interdict of FGF-21 could reduce the related gene and protein expression levels of pulmonary fibrosis. In addition, FGF-21 significantly reduced both the aggregation of inflammatory cells and deposition of collagen in the lung by histopathology. In therapy of pulmonary fibrosis studies, the results indicated that treatment with FGF-21 resulted in an amelioration of the pulmonary fibrosis in mice with reductions of the pathological score, collagen deposition and transforming growth factor (TGF)-ß and α-smooth muscle actin (α-SMA) expressions in the lung tissues at fibrotic stage, and late administration was also able to reduce the degree of pulmonary fibrosis and even better than these in the prevention group. Furthermore, BLM-induced THP-1 macrophage model was verified using FGF-21; the result showed that FGF-21 decreased the related gene expression level of pulmonary fibrosis. FGF-21 may have preventive and therapeutic effects on BLM-induced pulmonary fibrosis via inhibiting myofibroblast differentiation and inflammatory. Thus, FGF-21 represents a potential drug for the prevention and treatment of pulmonary fibrosis.

Combined analyses of transcriptome and metabolome reveal the mechanism of exogenous strigolactone regulating the response of elephant grass to drought stress.

Elephant grass is widely used in feed production and ecological restoration because of its huge biomass and low occurrence of diseases and insect pets. However, drought seriously affects growth and development of this grass. Strigolactone (SL), a small molecular phytohormone, reportedly participates in improving resilience to cope with arid environment. But the mechanism of SL regulating elephant grass to response to drought stress remains unknown and needs further investigation. We conducted RNA-seq experiments and identified 84,296 genes including 765 and 2325 upregulated differential expression genes (DEGs) and 622 and 1826 downregulated DEGs, compared drought rehydration with spraying SL in roots and leaves, respectively. Combined with targeted phytohormones metabolite analysis, five hormones including 6-BA, ABA, MeSA, NAA, and JA had significant changes under re-watering and spraying SL stages. Moreover, a total of 17 co-expression modules were identified, of which eight modules had the most significant correlation with all physiological indicators with weighted gene co-expression network analysis. The venn analysis revealed the common genes between Kyoto Encyclopedia of Genes and Genomes enriched functional DEGs and the top 30 hub genes of higher weights in eight modules, respectively. Finally, 44 DEGs had been identified as key genes which played a major role in SL response to drought stress. After verification of its expression level by qPCR, six key genes in elephant grass including PpPEPCK, PpRuBPC, PpPGK, PpGAPDH, PpFBA, and PpSBPase genes regulated photosynthetic capacity under the SL treatment to respond to drought stress. Meanwhile, PpACAT, PpMFP2, PpAGT2, PpIVD, PpMCCA, and PpMCCB regulated root development and phytohormone crosstalk to respond to water deficit conditions. Our research led to a more comprehensive understanding about exogenous SL that plays a role in elephant grass response to drought stress and revealed insights into the SL regulating molecular mechanism in plants to adapt to the arid environment.

Association between the atherogenic index of plasma and carotid artery plaques in patients with coronary heart disease in different glucose metabolism states: an RCSCD-TCM study in Tianjin, China.

BACKGROUND: The atherogenic index of plasma (AIP) is considered a powerful biomarker of dyslipidemia and atherosclerosis (AS). However, limited evidence is available regarding the relationship between the AIP and carotid artery plaques (CAPs) in patients with coronary heart disease (CHD). METHODS: This retrospective study included 9281 patients with CHD who underwent carotid ultrasound. Participants were divided according to the AIP tertiles: T1, AIP < 1.02; T2, 1.02 ≤ AIP < 1.25; and T3, AIP ≥ 1.25. The presence or absence of CAPs was assessed using carotid ultrasound. Logistic regression was used to analyze the relationship between the AIP and CAPs in patients with CHD. The relationship between the AIP and CAPs was assessed according to sex, age, and glucose metabolic status. RESULTS: The baseline characteristics revealed significant differences in related parameters among patients with CHD after stratification into the three groups according to the AIP tertiles. Compared with T1, the odds ratio (OR) of T3 in patients with CHD was 1.53 (95% confidence interval [CI]:1.35-1.74). The association between AIP and CAPs was higher in females (OR: 1.63; 95% CI: 1.38-1.92) than in males (OR: 1.38; 95% CI: 1.12-1.70). The OR for patients aged ≤60 years (OR: 1.40; 95% CI: 1.14-1.71) was lower than that for patients aged >60 years (OR: 1.49; 95% CI: 1.26-1.76). AIP was significantly associated with the risk of CAPs formation in different glucose metabolic states, with diabetes having the highest OR value (OR: 1.31; 95% CI: 1.19-1.43). CONCLUSION: The AIP and CAPs were significantly associated in patients with CHD, and the association was higher in female than in male patients. The association was lower in patients aged ≤60 years than in patients aged >60 years. Under different glucose metabolism statuses, the association between the AIP and the CAPs among patients with CHD was highest in patients with diabetes.