Association between triglyceride-glucose index and hypertension: a cohort study based on the China Health and Nutrition Survey (2009-2015).

AIM: Insulin resistance (IR) may participate in the pathogenesis of hypertension by mediating low-grade systemic inflammation. The triglycerides-glucose (TyG) index has recently been suggested as a reliable alternative biochemical marker of IR compared with traditional methods. Herein, we speculated TyG index may also be associated with hypertension. METHODS: Data of adults were extracted from the China Health and Nutrition Survey (CHNS) in 2009-2015 in this retrospective cohort study. The TyG index was calculated using the formula: TyG = Ln [fasting triglycerides (mg/dL) ×fasting glucose (mg/dL)/2]. Associations between TyG index and hypertension were evaluated by univariate and multivariate logistic regression analyses with odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup analyses of age and gender were also performed. In addition, we assessed the interaction effect between TyG index and body mass index (BMI) on hypertension in participants with different age and gender. RESULTS: Among 3,413 eligible participants, 1,627 (47.67%) developed hypertension. The average TyG index in hypertension group and non-hypertension group was 8.58 and 8.39 respectively. After adjusting for covariates, we found that compared with participants with TyG index ≤ 8.41 (median value), those who had higher TyG index seemed to have higher odds of hypertension [OR = 1.17, 95%CI: (1.01-1.37)]. Similarly, this association was also discovered in participants who aged ≤ 65 years old [OR = 1.19, 95%CI: (1.01-1.39)] or were female [OR = 1.35, 95%CI: (1.10-1.65)]. Additionally, there was a potential additive interaction effect between obesity and TyG index on hypertension. CONCLUSION: High TyG index was associated with high odds of hypertension in general population in China, but the causal relationship between them needed further exploration.

Effect of preoperative intensive statin on the efficacy and inflammatory response of acute ST-segment elevation myocardial infarction after emergency percutaneous coronary intervention.

It was to explore the application value of individualized nursing oriented by solution-focused nursing mode in postoperative nursing of patients with pelvic fractures. 90 patients with ST-segment elevation myocardial infarction (STEMI) undergoing emergency percutaneous coronary intervention (PCI) were enrolled. They were randomly grouped into a control group and an experimental group, with 45 cases in each group. Patients in the general group were treated with conventional treatment, and patients in the enhancement group were treated with high-dose rosuvastatin based on conventional treatment. The experimental group was compared for indicators such as serum inflammatory factors, cardiac function, overall efficacy, and follow-up prognosis before and after the operation. After treatment, the total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in the enhancement group were better as against the control group (P<0.05). Through treatment, the concentration of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in the enhancement group was lower compared to the general group. The total effective rate of the enhancement group (95.56%) was higher relative to the general group (86.67%) (P<0.05). In patients with STEMI, preoperative intensive statin therapy can improve the efficacy of PCI, and reduce the inflammatory response and the incidence of cardiovascular events.

The Association between Standardized Serum 25-Hydroxyvitamin D Concentration and Risk of Anemia: A Population-Based Cross-Sectional Study.

The relationship between standardized serum 25-hydroxyvitamin D (25(OH)D) concentration and incident anemia in the United States (U.S.) is unclear. The purpose of our study was to examine the association between serum 25(OH)D and anemia risk. We performed a cross-sectional analysis of the U.S. population participating in the National Health and Nutrition Examination Survey (NHANES) between 2001 and 2018. A generalized linear model and restricted cubic spline (RCS) plot curve were constructed to assess the relationship between serum 25(OH)D concentration and anemia incidence. Additionally, the association between serum 25(OH)D concentration and red blood cell (RBC) count and hemoglobin (HB) levels was investigated using generalized additive models with smooth functions. Subgroup analysis also was performed. A total of 29933 individuals were included in our research. After adjusting for known confounding variables, compared with the lowest quartile, the odds ratios (ORs) with 95% confidence intervals (CIs) for association of serum 25(OH)D with anemia across the second, third, and fourth quartiles were 0.735 (0.651, 0.829), 0.527 (0.461, 0.602), and 0.696 (0.611, 0.792), respectively. Serum 25(OH)D concentration was associated with anemia risk in a U-shaped pattern, as shown by an RCS plot (P for nonlinearity <0.001). In addition, RBC count and Hb levels initially increased and then decreased as serum 25(OH)D levels increased. Serum 25(OH)D concentration and risk of anemia are associated with a U-shaped curve in the U.S. general population. Serum 25(OH)D concentration in the range 59.7-70.3 nmol/l was associated with anemia incidence <1. Therefore, the risk of anemia can be reduced by close monitoring and appropriate vitamin D supplementation.

Predictive Value of Arterial Blood Lactic Acid Concentration on the Risk of in-Hospital All-Cause Death in Patients with Acute Heart Failure.

The study aims to examine the predictive value of arterial blood lactic acid concentration for in-hospital all-cause mortality in the intensive care unit (ICU) for patients with acute heart failure (AHF). We retrospectively analyzed the clinical data of 7558 AHF patients in the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. The exposure variable of the present study was arterial blood lactic acid concentration and the outcome variable was in-hospital all-cause death. The patients were divided into those who survived (n = 6792) and those who died (n = 766). The multivariate logistic regression model, restricted cubic spline (RCS) plot, and subgroup analysis were used to evaluate the association between lactic acid and in-hospital all-cause mortality. In addition, receiver operating curve (ROC) analysis also was performed. Finally, we further explore the association between NT-proBNP and lactic acid and in-hospital all-cause mortality. Compared with the lowest quartiles, the odds ratios with 95% confidence intervals for in-hospital all-cause mortality across the quartiles were 1.46 (1.07-2.00), 1.48 (1.09-2.00), and 2.36 (1.73-3.22) for lactic acid, and in-hospital all-cause mortality was gradually increased with lactic acid levels increasing (P for trend <0.05). The RCS plot revealed a positive and linear connection between lactic acid and in-hospital all-cause mortality. A combination of lactic acid concentration and the Simplified Acute Physiology Score (SAPS) II may improve the predictive value of in-hospital all-cause mortality in patients with AHF (AUC = 0.696). Among subgroups, respiratory failure interacted with an association between lactic acid and in-hospital all-cause mortality (P for interaction <0.05). The correlation heatmap revealed that NT-proBNP was positively correlated with lactic acid (r = 0.07) and positively correlated with in-hospital all-cause mortality (r = 0.18). There was an inverse L-shaped curve relationship between NT-proBNP and in-hospital all-cause mortality, respectively. Mediation analysis suggested that a positive relationship between lactic acid and in-hospital all-cause death was mediated by NT-proBNP. For AHF patients in the ICU, the arterial blood lactic acid concentration during hospitalization was a significant independent predictor of in-hospital all-cause mortality. The combination of lactic acid and SAPS II can improve the predictive value of the risk of in-hospital all-cause mortality in patients with AHF.

Effect of S-Nitrosylation of RIP3 Induced by Cerebral Ischemia on its Downstream Signaling Pathway.

OBJECTIVES: Our preliminary experiments indicate that receptor-interacting protein 3 (RIP3) is S-nitrosylated and contributes to its autophosphorylation (activation) after 3 h of rat brain ischemia/reperfusion mediated by activation of the N-methyl-D-aspartate receptor (NMDAR)-dependent neuronal NO synthase (nNOS) and is involved in the process of neuronal injury. Here, we will to demonstrate whether S-nitrosylation of RIP3 facilitates the activation of the downstream signaling pathway and finally exacerbates ischemic neuron death. MATERIALS AND METHODS: Adult male Sprague-Dawley rat transient brain ischemia/reperfusion and cortical neurons oxygen and glucose deprivation (OGD)/reoxygenation models were performed. The hippocampal CA1 regions or cultured cells were homogenized and the cytosolic fraction were collected as tissue samples. Coimmunoprecipitation and western blot analysis were carried out for detecting phosphorylation of RIP1 and mixed lineage kinase-like domains (MLKL) and the Cleaved-Caspase8 (Cl-Caspase8). The activities of Glycogen phosphorylase (PYGL), Glutamate-ammonia ligase (GLUL) and Glutamate dehydrogenase (GLUD1) were detected with ultraviolet absorption method. RESULTS: This study showed that active RIP3 could phosphorylate RIP1 and MLKL through its kinase activity, promote the conversion of Caspase8 to active Cl-Caspase8, enhance the activities of PYGL, GLUL and GLUD1, and finally aggravate neuronal injury in cerebral ischemia/reperfusion. The inhibition of RIP3 S-nitrosylation inhibited the phosphorylation of RIP1 and MLKL, inhibited the activities of Caspase8, PYGL, GLUL, and GLUD1, and alleviated neuronal damage in cerebral ischemia/reperfusion. CONCLUSIONS: S-nitrosylation of RIP3 increased RIP1 and MLKL phosphorylation levels, Cl-Caspase8 content and PYGL, GLUL and GLUD1 activities and aggravated neuronal damage during cerebral ischemia/reperfusion and regulating the S-nitrosylation of RIP3 and its downstream signaling pathway might be a therapeutic target for stroke.

Cost-Effectiveness of Evolocumab Therapy for Myocardial Infarction: The Chinese Healthcare Perspective.

PURPOSE: Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are an indispensable lipid-lowering treatment option, but their cost-effectiveness has been questioned. This study aimed to perform a health economic evaluation of evolocumab versus placebo in patients with myocardial infarction (MI) in China. METHODS: A Markov cohort state-transition model was developed in decision analysis software to estimate the incremental cost-effectiveness ratio (ICER), defined as cost per quality-adjusted life-year (QALY) saved. The simulation subjects could undergo non-fatal MI and/or stroke, or vascular or non-vascular death event. We integrated the Chinese population-specific demographics and event rates with the risk reduction of evolocumab based on the FOURIER trial and/or lowering of low-density lipoprotein cholesterol (LDL-C). Age-related change, event costs and utilities were included from published sources. RESULTS: At its current list price [33,748 Chinese yuan (CNY) annually per person], the ICER for evolocumab therapy was 927,713 CNY per QALY gained when integrating the FOURIER trial with absolute reduction of LDL-C. The probability of cost-effectiveness of evolocumab versus placebo was 1.96%, with a generally accepted threshold of 212,676 CNY per QALY gained. A reduction in acquisition price by approximately 70% (to less than 10,255 CNY annually) was needed to be cost-effective. Alternative scenario analyses of therapeutic benefit showed that the ICER for evolocumab in MI patients with uncontrolled familial hypercholesterolemia (FH) was 187,736 CNY per QALY gained. CONCLUSION: Evolocumab in patients with MI was not cost-effective based on the price in 2019 in China; however, treatment with evolocumab was more favorable in MI patients with FH.

gB co-immunization with GP96 enhances pulmonary-resident CD8 T cells and exerts a long-term defence against MCMV pneumonitis.

Human cytomegalovirus (HCMV) infection in the respiratory tract leads to pneumonitis in immunocompromised hosts without available vaccine. Considering cytomegalovirus (CMV) mainly invades through the respiratory tract, CMV-specific pulmonary mucosal vaccine development that provides a long-lasting protection against CMV challenge gains our attention. In this study, N-terminal domain of GP96 (GP96-NT) was used as a mucosal adjuvant to enhance the induction of pulmonary-resident CD8 T cells elicited by MCMV glycoprotein B (gB) vaccine. Mice were intranasally co-immunized with 50 µg pgB and equal amount of pGP96-NT vaccine 4 times at 2-week intervals, and then i.n. challenged with MCMV at 16 weeks after the last immunization. Compared with pgB immunization alone, co-immunization with pgB/pGP96-NT enhanced a long-lasting protection against MCMV pneumonitis by significantly improved pneumonitis pathology, enhanced bodyweight, reduced viral burdens and increased survival rate. Moreover, the increased CD8 T cells were observed in lung but not spleen from pgB/pGP96-NT co-immunized mice. The increments of pulmonary CD8 T cells might be mainly due to non-circulating pulmonary-resident CD8 T-cell subset expansion but not circulating CD8 T-cell populations that home to inflammation site upon MCMV challenge. Finally, the deterioration of MCMV pneumonitis by depletion of pulmonary site-specific CD8 T cells in mice that were pgB/pGP96-NT co-immunization might be a clue to interpret the non-circulating pulmonary-resident CD8 T subset expansion. These data might uncover a promising long-lasting prophylactic vaccine strategy against MCMV-induced pneumonitis.

TDZD-8 alleviates delayed neurological sequelae following acute carbon monoxide poisoning involving tau protein phosphorylation.

Objective: Acute carbon monoxide （CO）poisoning can cause delayed neurological sequelae (DNS). Glycogen synthase kinase 3ß (GSK-3ß) /Tau protein pathway is reported to play a key role in neurological abnormalities. In the present study, we aimed to determine the role of GSK-3ß/Tau in DNS following acute CO poisoning.Methods: 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), a specific non-competitive inhibitor of GSK-3ß, was used to inhibit GSK-3ß. Twenty-four male Sprague-Dawley rats were randomly assigned to the three groups: Control group, CO group and CO-TDZD-8 group. Rats breathed 1000 ppm CO for 40 minutes and then 3000 ppm for up to 20 minutes until they lost consciousness. TDZD-8 (1 mg/kg) was administered intravenously three times after the end of CO exposure at 0, 24, 48 hours late. Learning and memory abilities were observed using the Morris Water Maze (MWM). Brain histological changes were evaluated by hematoxylin-eosin staining. Moreover, the expression levels of Tau and GSK-3ß were detected after acute carbon monoxide poisoning.Results: TDZD-8 significantly attenuated the learning and memory dysfunction induced by acute CO poisoning, ameliorated the histology structure of damaged neural cells in cortex and hippocampus CA1 area. TDZD-8 clearly decreased p-Tau expression, reversed the reduction of p-GSK-3ß induced by acute CO poisoning.Conclusions: The therapeutic effect of TDZD-8 in alleviating DNS caused by acute CO poisoning is related to the inactivation of Tau by intensifying the level of GSK-3ß phosphorylation.

[Impact of left atrium size on left atrial thrombus in patients with non-valvular persistent atrial fibrillation].

OBJECTIVE: This study sought to investigate the impact of left atrium size on left atrial (LA) thrombus in patients with non-valvular persistent atrial fibrillation (AF). METHODS: In a prospectively established database, patients with AF underwent transesophageal echocardiography prior to AF ablation were screened from January 2007 to June 2010. Exclusive criteria included paroxysmal AF, vavular AF, deep vein thrombus, pulmonary embolism, on warfarin, redo procedure. Of 1 524 patients, 367 patients (male 267, female 100) with age 26-89 (mean 56±11) were enrolled. The patients were divided into LA thrombus group and non-thrombus group. Receptor-operating curves were used to test the value of CHA2DS2Vasc score and LA diameter predicting LA thrombus. Logistic analysis were used to find the independent predictor of LA thrombus. RESULTS: Thirty-two (8.7%) patients had LA thrombus. The LA diameter, left ventricular end diastolic diameter, left ventricular end systolic diameter were significantly larger in thrombus group than non-thrombus group. Left ventricular ejection fraction was significantly lower in thrombus group than non-thrombus group. CHA2DS2Vasc score did not differ between the two groups. The area under the receptor-operating curve for LA diameter predicting LA thrombus was 0.656 (0.563-0.750), the best cut-off point was 42.5 mm. The incidence of LA thrombus was significantly higher in patients with LA diameter≥42.5 mm than those with LA<42.5 mm (14.0% vs. 5.1%, χ2=8.888, P=0.003). In univariate analysis, LA diameter≥42.5 mm increased the risk of LA thrombus with odds ratio 3.05 (95% confidence interval 1.42-6.53, P=0.004. The sensitivity and specificity of LA diameter≥42.5 mm in predicting LA thrombus were 67.7% and 61.5%, respectively. In multivariate analysis, after adjustment of CHA2DS2Vasc score, left ventricular end diastolic diameter, left ventricular end systolic diameter, left ventricular ejection fraction, LA diameter≥42.5 mm was an independent risk factor of LA thrombus (odds ratio 2.77, 95% confidence interval 1.17-6.57, P=0.021). CONCLUSION: LA enlargement is an independent risk factor of LA thrombus in patients with non-vavular persistent AF.

Predictors of recurrence after a repeat ablation procedure for paroxysmal atrial fibrillation: role of left atrial enlargement.

AIMS: This study sought to explore the predictors of recurrence in patients with paroxysmal atrial fibrillation (AF) undergoing repeat catheter ablation, especially the impact of left atrial (LA) remodelling after the original procedure on the outcome of repeat procedure. METHODS AND RESULTS: Ninety-five patients undergoing repeat ablation were enrolled in this study. Repeat procedure endpoints were pulmonary vein isolation, linear block when linear ablation is performed, and non-inducibility of atrial tachyarrhythmia by burst pacing. Patients with LA enlargement between the pre-original procedure and pre-repeat procedure were categorized as Group 1 (35 patients), while individuals with no change or decrease of LA diameter were categorized as Group 2 (60 patients). The mean duration from the original procedure to the repeat procedure was 12 months (1-40 months). After 29.6 ± 20.5 (3-73) months follow-up from the repeat procedure, 33 patients experienced recurrence (34.7%). The recurrence rate was significantly higher in Group 1 than in Group 2 (51.4 VS. 25.0%, P = 0.017). In univariate analysis, LA remodelling was the only predictor of recurrence. In multivariate analysis, after adjustment for age and LA diameter, Group 1 had a greater risk of recurrence after the repeat procedure (hazard ratio = 2.22, 95% confidence interval: 1.02-4.81, P = 0.043). CONCLUSIONS: Left atrial enlargement after undergoing the original catheter ablation of paroxysmal AF was an independent risk factor of recurrence after repeat ablation.

Pacing or ablation: which is better for paroxysmal atrial fibrillation-related tachycardia-bradycardia syndrome?

BACKGROUND: Symptomatic prolonged sinus pauses on termination of atrial fibrillation (AF) are an accepted indication for pacemaker implantation. We evaluated the outcome of AF ablation in patients with paroxysmal AF-related tachycardia-bradycardia syndrome and compared the efficacy of catheter ablation with permanent pacing plus antiarrhythmic drugs (AADs). METHODS AND RESULTS: Patients with prolonged symptomatic sinus pauses on termination of AF were retrospectively analyzed. Forty-three consecutive patients who underwent catheter ablation (ABL group) were compared to 57 patients who underwent permanent pacing plus AADs (PM group). All 43 patients in the ABL group fulfilled Class I indication for pacemaker implantation at baseline but they actually underwent AF ablation. Reevaluation after 20.1 ± 9.6 months of follow-up showed that 41 patients (95.3%) did no longer need a pacemaker (Class III indication). Total cardiac-related rehospitalization was not significantly different between the two groups (P = 0.921). Tachycardia-related hospitalization was significantly higher in the PM group than the ABL group (14.0% and 0%, P = 0.029). More patients in the PM group were on AADs (PM 40.4%, ABL 4.7%, P < 0.001) while sinus rhythm maintenance was remarkably higher in the ABL group at the end of follow-up (83.7% vs 21.1% in PM group, P < 0.001). CONCLUSIONS: In patients with paroxysmal AF-related tachycardia-bradycardia syndrome, AF ablation seems to be superior to a strategy of pacing plus AAD. Pacemaker implantation can be waived in the majority of patients after a successful ablation.

Congenital anomalous coronary sinus ostium.

Congenital anomalous coronary sinus ostium is extremely rare. We describe a case of congenital left atrial coronary sinus ostium in a patient scheduled for ablation for atrial fibrillation. The anomalous coronary sinus ostium was found when contrast was injected during the ablation procedure and was confirmed by cardiac computed tomography.

Omega-3 fatty acids for postoperative atrial fibrillation: alone or in combination with antioxidant vitamins?

BACKGROUND: The effects of omega-3 polyunsaturated fatty acids (PUFA) on the prevention of postoperative atrial fibrillation (POAF) are inconclusive in current studies. Moreover, the most appropriate composition of PUFA to play the protective role is unclear. The aim of this meta-analysis was to ascertain the protective role of PUFA on POAF and the most appropriate composition. METHODS: Studies were identified through PubMed, CENTRAL, EMBASE, reviews and reference lists of relevant papers. The odds ratio (OR) was calculated for POAF. Statistical analyses were performed with Review Manager 5.0. RESULTS: Eleven randomised controlled trials with 3137 patients were included in the analysis. The use of PUFA alone did not reduce the incidence of POAF compared with the control (OR: 0.76; 95% confidence interval [CI]: 0.57-1.03; P=0.08; I(2)=52%). However, combination therapy with PUFA and vitamins C and E reduced the incidence of POAF by 68% (OR: 0.32; 95%CI: 0.17-0.60; P=0.0005; I(2)=38%). Subgroup analysis indicated that the ratio of EPA/DHA 1:2 was effective in preventing POAF (OR: 0.35; 95%CI: 0.24-0.50; P<0.00001; I(2)=0%), while the ratio not 1:2 failed. CONCLUSIONS: Combination therapy with PUFA and vitamins C and E is effective in the prevention of POAF while PUFA alone is not. The ratio of EPA/DHA may influence the incidence of POAF, and 1:2 may be most appropriate. Studies about PUFA on the prevention of POAF are still worthwhile to be conducted in the future.

The protective effect of karanjin against sepsis-induced acute lung injury in mice is involved in the suppression of the TLR4 pathway.

Sepsis-induced acute lung injury (ALI) is a severe complication of sepsis. Karanjin, a natural flavonoid compound, has been proved to have anti-inflammatory function, but its role in sepsis-stimulated ALI is uncertain. Herein, the effect of karanjin on sepsis-stimulated ALI was investigated. We built a mouse model of lipopolysaccharide (LPS)-stimulated ALI. The histopathological morphology of lung tissues was scrutinized by hematoxylin-eosin (H&E) staining. The lung injury score and lung wet/dry weight ratio were detected. The myeloperoxidase (MPO) activity and malondialdehyde (MDA) content were scrutinized by commercial kits. Murine alveolar lung epithelial (MLE-12) cells were treated with LPS to mimic a cellular model of ALI. The cell viability was scrutinized by the CCK-8 assay. The contents of proinflammatory cytokines were scrutinized by qRT-PCR and ELISA. The TLR4 and MyD88 contents were scrutinized by qRT-PCR and western blotting. Results showed that karanjin alleviated LPS-stimulated ALI in mice by inhibiting lung tissue lesions, edema, and oxidative stress. Moreover, karanjin inhibited LPS-stimulated inflammation and TLR4 pathway activation in mice. However, treatment with GSK1795091, an agonist of TLR4, attenuated the effects of karanjin on LPS-induced ALI. Furthermore, karanjin repressed LPS-stimulated inflammatory response and TLR4 pathway activation in MLE-12 cells. Overexpression of TLR4 attenuated karanjin effects on LPS-stimulated inflammatory responses in MLE-12 cells. In conclusion, karanjin repressed sepsis-stimulated ALI in mice by suppressing the TLR4 pathway.

Identification of key molecules in the formation of portal vein tumor thrombus in hepatocellular carcinoma based on single cell transcriptomics and in vitro experiments.

Background: The presence of portal vein tumor thrombus (PVTT) is a significant indicator of advanced-stage hepatocellular carcinoma (HCC). Unfortunately, the prediction of PVTT occurrence remains challenging, and there is a lack of comprehensive research exploring the underlying mechanisms of PVTT formation and its association with immune infiltration. Methods: Our approach involved analyzing single-cell sequencing data, applying high dimensional weighted gene co-expression network analysis (hdWGCNA), and identifying key genes associated with PVTT development. Furthermore, we constructed competing endogenous RNA (ceRNA) networks and employed weighted gene co-expression network analysis (WGCNA), as well as three machine-learning techniques, to identify the upstream regulatory microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) of the crucial mRNAs. We employed fuzzy clustering of time series gene expression data (Mfuzz), gene set variation analysis (GSVA), and cell communication analysis to uncover significant signaling pathways involved in the activation of these important mRNAs during PVTT development. In addition, we conducted immune infiltration analysis, survival typing, and drug sensitivity analysis using The Cancer Genome Atlas (TCGA) cohort to gain insights into the two patient groups under study. Results: Through the implementation of hdWGCNA, we identified 110 genes that was closely associated with PVTT. Among these genes, TMEM165 emerged as a crucial candidate, and we further investigated its significance using COX regression analysis. Furthermore, through machine learning techniques and survival analysis, we successfully identified the upstream regulatory miRNA (hsa-miR-148a) and lncRNA (LINC00909) that targeted TMEM165. These findings shed light on the complex regulatory network surrounding TMEM165 in the context of PVTT. Moreover, we conducted CIBERSORT analysis, which unveiled correlations between TMEM165 and immune infiltration in HCC patients. Specifically, TMEM165 exhibited associations with various immune cell populations, including memory B cells and CD8+ T cells. Additionally, we observed implications for immune function, particularly in relation to immune checkpoints, within the context of HCC. Conclusions: The regulatory axis involving TMEM165, hsa-miR-148a, and LINC00909 emerges as a crucial determinant in the development of PVTT in HCC patients, and it holds significant implications for prognosis. Furthermore, alterations in the TMEM165/hsa-miR-148a/LINC00909 regulatory axis exhibit a strong correlation with immune infiltration within the HCC tumor microenvironment, leading to immune dysfunction and potential failure of immunotherapy.

CSF3 aggravates acute exacerbation of pulmonary fibrosis by disrupting alveolar epithelial barrier integrity.

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive respiratory disorder characterized by poor prognosis, often presenting with acute exacerbation. The primary cause of death associated with IPF is acute exacerbation of IPF (AE-IPF). However, the pathophysiology of acute exacerbation has not been clearly elucidated yet. This study aims to investigate the underlying pathophysiological molecular mechanism in a mouse AE-PF model. C57BL/6J mice were intratracheally administered bleomycin (BLM, 5 mg/kg) to induce pulmonary fibrosis. After 14 days, lipopolysaccharide (LPS, 2 mg/kg) was injected via the trachea route. Histological assessments, including H&E and Masson staining, as well as inflammatory indicators, were included to evaluate the induction of AE-PF by BLM and LPS in mice. Transcriptomic profiling of pulmonary tissues identified CSF3 as one of the top 10 upregulated DEGs in AE-PF mice. Indeed, administration of exogenous CSF3 protein exacerbated AE-PF in mice. Mechanistically, CSF3 disrupted alveolar epithelial barrier integrity and permeability by regulating specialized cell adhesion complexes such as tight junctions (TJs) and adherens junctions (AJs) via PI3K/p-Akt/Snail pathway, contributing to the aggravation of AE-PF in mice. Moreover, the discovery of elevated sera CSF3 indicated a notable increase in IPF patients during the exacerbation of the disease. Pearson correlation analysis in IPF patients revealed significant positive associations between CSF3 levels and KL-6 levels, LDH levels, CRP levels, respectively. These results provide mechanistic insights into the role of CSF3 in exacerbating of lung fibrotic disease and indicate monitoring CSF3 levels may aid in early clinical decisions for alternative therapy in the management of rapidly progressing IPF.

A rapid expansion of hospitals: the adaptation of multi-campus hospitals under the Chinese healthcare system.

In recent years, China's healthcare system has undergone significant changes to meet the increasing demands of its growing population. One notable development is the rapid expansion of hospitals, particularly the adaptation of multi-campus hospitals. These multi-campus hospitals have become increasingly popular due to the many advantages that single-campus hospitals lack, including the ability to; improve medical service quality, reduce operating costs, and facilitate the development of healthcare services in rural areas. In this study, we discuss the advantages that this type of medical facility offers and identify existing and potential problems that could hinder the development of multi-campus hospitals. Additionally, we propose appropriate solutions to mitigate these problems. Overall, we propose that there should be more communication between multi-campus hospitals and other healthcare providers.

Efficacy of two hemodialyses in patients with chronic renal failure complicated by massive intracerebral hemorrhage.

OBJECTIVE: To compare the efficacy of intermittent hemodialysis (IHD) and continuous veno-venous hemofiltration (CVVH) in patients with chronic renal failure complicated by massive intracerebral hemorrhage. METHODS: Sixty-two patients were randomly and equally divided into IHD and CVVH groups. The clinical variables were compared, including National Institutes of Health Stroke Scale (NIHSS) score as the primary indicator, cerebral edema volume, hospital-acquired pneumonia (HAP) incidence, acute heart failure (AHF) incidence, rehemorrhage incidence, hospital stay length, and modified Rankin Scale (mRS) score. RESULTS: The CVVH group had lower NIHSS scores and edema volumes than the IHD group on postoperative days 7 and 14. Moreover, in the CVVH group, (i) the NIHSS scores on postoperative days 3 and 7 were higher than those on postoperative day 1; (ii) there was no significant difference in NIHSS scores between days 14 and 1; and (iii) no significant difference in cerebral edema volume was found between postoperative days 1 and 3, 7, and 14. In the IHD group, the NIHSS scores and cerebral edema volume on postoperative days 7 and 14 were significantly higher than those on postoperative day 1. The CVVH group had a lower incidence of HAP, AHF, and adverse events and shorter hospital stay length than the IHD group. The proportions of patients with mRS scores of 1 and 2 in the CVVH group were higher than those in the IHD group on day 30 after discharge. INTERPRETATION: CVVH is more effective than IHD in the treatment of patients with chronic renal failure complicated by massive intracerebral hemorrhage.

Trend analysis of mortality rates and causes of death in children under 5 years of age in Xuzhou, China from 2016 to 2020.

Objectives: To analyze the trends in mortality and causes of death among children under 5 years of age in Xuzhou, China between 2016 and 2020, in order to protect children's health and provide a basis for formulating child survival, development, and protection strategies. Methods: A population-based epidemiological study was conducted. Data were obtained from the Xuzhou Center for Disease Control Prevention. We input the data into the excel database and analyzed with SPSS20.0. Results: There were 1,949 children under 5 years of age died in Xuzhou, The number of deaths from 2016 to 2020 were 573 (29.40%), 577 (29.60%), 371 (19.04%), 334 (17.14%), and 94 (4.82%) respectively, mortality in children showed a downward trend. The number of deaths was relatively high in January (195 cases, 10.01%), February (190 cases, 9.75%), and May (180 cases, 9.24%), while was relatively small in July (147 cases, 7.54%), August (139 cases, 7.13%), and September (118 cases, 6.05%). The leading causes of death (COD) in children under 5 years of age were neonatal suffocation and hypoxia (323 cases, 16.57%). Pizhou (528 cases, 27.09%) showed the highest number of deaths in children under 5 years of age in China, and the Kaifa (25 cases, 1.28%) zone showed the lowest death toll. Conclusions: Our research suggested that the current strategies for reducing child mortality should prioritize the actions on neonatal deaths and conduct targeted interventions for the main cause.

An interpretable machine learning approach for predicting 30-day readmission after stroke.

BACKGROUND: Stroke is the second leading cause of death worldwide and has a significantly high recurrence rate. We aimed to identify risk factors for stroke recurrence and develop an interpretable machine learning model to predict 30-day readmissions after stroke. METHODS: Stroke patients deposited in electronic health records (EHRs) in Xuzhou Medical University Hospital between February 1, 2021, and November 30, 2021, were included in the study, and deceased patients were excluded. We extracted 74 features from EHRs, and the top 20 features (chi-2 value) were used to build machine learning models. 80% of the patients were used for pre-training. Subsequently, a 20% holdout dataset was used for verification. The Shapley Additive exPlanations (SHAP) method was used to explore the interpretability of the model. RESULTS: The cohort included 6,558 patients, of whom the mean (SD) age was 65 (11) years, 3,926 were males (59.86 %), and 132 (2.01 %) were readmitted within 30 days. The area under the receiver operating characteristic curve (AUROC) for the optimized model was 0.80 (95 % CI 0.68-0.80). We used the SHAP method to identify the top 10 risk factors (i.e., severe carotid artery stenosis, weak, homocysteine, glycosylated hemoglobin, sex, lymphocyte percentage, neutrophilic granulocyte percentage, urine glucose, fresh cerebral infarction, and red blood cell count). The AUROC of a model with the 10 features was 0.80 (95 % CI 0.69-0.80) and was not significantly different from that of the model with 20 risk factors. CONCLUSIONS: Our methods not only showed good performance in predicting 30-day readmissions after stroke but also revealed risk factors that provided valuable insights for treatments.