Atherosclerosis is a chronic inflammatory disease, and vascular smooth muscle cells(VSMC) play a central role in its pathological process. Single-cell RNA sequencing reveals the central role of VSMC in the atherosclerotic microenvironment. Inflammatory factors and oxidized lipids in the atherosclerotic plaque microenvironment affect VSMC phenotype switching and function in various ways, thereby affecting plaque stability. This article summarizes the phenotypic transformation rules, biological behaviors, and interaction mechanisms of VSMC with immune cells in the inflammatory microenvironment of atherosclerosis, and reviews the progress of new anti-inflammatory strategies and models targeting the VSMC-inflammatory axis, in order to provide a theoretical basis and translational direction for the precise treatment of atherosclerosis.

AIM:To investigate the role of serum high-sensitivity C-reactive protein(hsCRP)in the pathogenesis and progression of diabetic retinopathy(DR)in patients with type 2 diabetes mellitus(T2DM).METHODS:A nested case-control study was conducted involving 187 T2DM patients(187 eyes)who attended at Eye Center, Beijing Tongren Hospital, Capital Medical University from June 2017 to October 2024. Patients were categorized into three groups: the diabetes mellitus(DM)group, non-proliferative DR(NPDR)group, and proliferative DR(PDR)group. Baseline information was collected, including age, sex, duration of DM, and duration of hypertension. All patients underwent fasting biochemical tests and comprehensive ophthalmic examinations.RESULTS: A positive correlation was observed between hsCRP and fasting blood glucose(FBG; P=0.004)and glycated hemoglobin A1c(HbA1c; P=0.048)by Spearman's rank correlation coefficient analysis. After adjusting for confounding factors, multivariable Logistic regression identified hsCRP as a significant risk factor for DR(OR=2.67, 95% CI: 1.19-5.96, P=0.017). CONCLUSION:Serum hsCRP is positively correlated with FBG and HbA1c and can serve as an important predictor of the severity of DR.

Rice (Oryza sativa L.) is an important food crop. The appearance of lesion mimics in rice leads to phytohormone disorders, which affects rice adaptation to environmental stresses and ultimately reduces the yield and quality. To explore whether the changes in the adaptability of rice lesion-mimic mutants to stressful environments are caused by the disorder of phytohormone metabolism in plants. In this study, we screened an ethyl methane sulfonate-treated population of the japonica cultivar 'Taipei 309' for a mutant with rust-like spots on leaves at the early tillering stage and brown-red spots at maturity and named it rsl1 (rust spotted leaf 1). Compared with the wild type, rsl1 showed decreases in plant height, panicle length, primary branch number, secondary branch number, filled grains per panicle, seed-setting rate, and 1 000-grain weight, and an increase in number of effective panicles. Genetic analysis indicated that rsl1 was controlled by a single recessive nuclear gene. RSL1 was localized between two molecular markers, B7-7 and B7-9, on rice chromosome 7 by map-based cloning. PCR sequencing of the annotated genes in this interval revealed a mutation of C1683A on the eighth exon of SPL5 (LOC_Os07g10390) in rsl1, which resulted in premature termination of protein translation. Exogenous phytohormone treatments showed that rsl1 was less sensitive to salicylic acid (SA), abscisic acid (ABA), and indo-3-acetic acid (IAA) and more sensitive to methyl jasmonate (MeJA) and gibberellin acid (GA) than the wild type. In addition, the survival rate of rsl1 was lower than that of the wild type under salt, alkali, drought, and high temperature stresses, and it was higher than that of the wild type under cold stress. Quantitative real-time polymerase chain reaction (qRT-PCR) results showed that RSL1 was involved in the regulation of ABA, SA, MeJA, IAA, and GA-related genes under abiotic stresses. The present study showed that the RSL1 mutation led to the appearance of lesion mimics and affected the growth, development, and stress resistance of rsl1 under abiotic stresses. The study of the functional mechanism of this gene can provide theoretical guidance for the research on rice stress resistance.
Oryza/microbiology* ; Stress, Physiological/genetics* ; Plant Diseases/genetics* ; Cloning, Molecular ; Chromosome Mapping ; Plant Growth Regulators/metabolism* ; Plant Proteins/genetics* ; Mutation ; Cyclopentanes ; Genes, Plant ; Plant Leaves/genetics* ; Oxylipins

Military training represents one of the most essential activities for troops during peacetime,of which the prevention and treatment of training-induced injuries are a very important part.Recent findings of research suggest that cold atmospheric plasma(CAP)exhibits a distinctive and multifaceted superiority in terms of broad-spectrum sterilization,rapid blood coagulation and healing promotion for wounds.Consequently,CAP has good prospects of applications in diverse fields such as clinical medicine,emergency rescue and military medicine.Based on a review of the research progress in plasma medicine,the applicability of CAP in the prevention and treatment of military training injuries was discussed in this paper by focusing on the urgent issues related to military training injury,including the typical application scenarios and methods for CAP,the safety and effectiveness of plasma trauma prevention and treatment,and the key issues facing the prevention and treatment of military training injuries.

Background The benchmark dose (BMD) method calculates the dose associated with a specific change in response based on a specific dose-response relationship. Compared with the traditional no observed adverse effect level (NOAEL) method, the BMD method has many advantages, and the 95% lower confidence limit of benchmark dose lower limit (BMDL) is recommended to replace NOAEL in deriving biological exposure limits. No authority has yet published any health-based guideline for rare earth elements. Objective To evaluate genotoxicity threshold induced by acute exposure to neodymium nitrate in mice using BMD modeling through micronucleus test and comet assay. Methods SPF grade mice (n=90) were randomly divided into nine groups, including seven neodymium nitrate exposure groups, one control group (distilled water), and one positive control group (200 mg·kg⁻¹ ethyl methanesulfonate), 10 mice in each group, half male and half female. The seven dose groups were fed by gavage with different concentrations of neodymium nitrate solution (male: 14, 27, 39, 55, 77, 109, and 219 mg·kg⁻¹; female: 24, 49, 69, 97, 138, 195, and 389 mg·kg⁻¹) twice at an interval of 21 h. Three hours after the last exposure, the animals were neutralized by cervical dislocation. The bone marrow of mice femur was taken to calculate the micronucleus rate of bone marrow cells, and the liver and stomach were taken for comet test. Results The best fitting models for the increase of polychromatophil micronucleus rate in bone marrow of female and male mice induced by neodymium nitrate were the exponential 4 model and the hill model, respectively. The BMD and the BMDL of female mice were calculated to be 31.37 mg·kg⁻¹ and 21.90 mg·kg⁻¹, and those of male mice were calculated to be 58.62 mg·kg⁻¹ and 54.31 mg·kg⁻¹, respectively. The best fitting models for DNA damage induced by neodymium nitrate in female and male mouse hepatocytes were the exponential 5 model and the exponential 4 model, respectively, and the calculated BMD and BMDL were 27.15 mg·kg⁻¹ and 11.99 mg·kg⁻¹ for female mice, and 16.28 mg·kg⁻¹ and 10.47 mg·kg⁻¹ for male mice, respectively. The hill model was the best fitting model for DNA damage of gastric adenocytes in both female and male mice, and the calculated BMD and BMDL were 36.73 mg·kg⁻¹ and 19.92 mg·kg⁻¹ for female mice, and 24.74 mg·kg⁻¹ and 14.08 mg·kg⁻¹ for male mice, respectively. Conclusion Taken the micronucleus rate of bone marrow cells, DNA damage of liver cells and gastric gland cells as the end points of genotoxicity, the BMDL of neodymium nitrate is 10.47 mg·kg⁻¹, which can be used as the threshold of genotoxic effects induced by acute exposure to neodymium nitrate in mice.

Healthy lifestyles and good living habits are effective strategies and important approaches to prevent chronic non-communicable diseases. With the development of evidence-based medicine, the evidence translation system has made some achievements in clinical practice. There is, however, no comprehensive, professional and efficient system for translating lifestyle evidence globally. Therefore, the Health Lifestyle Evidence (HLSE) Group of Lanzhou University constructed the HLSE Evidence Translation System (https://hlse.cn/), with the aim of synthesizing, evaluating, translating, and applying lifestyle-related evidence resources. This paper aims to introduce the functional module design of the evidence translation system, the system development process and testing, introduce the interface design and function demonstration, and explain the significance of constructing the HLSE.

Healthy lifestyles and good living habits are effective strategies and important approaches to prevent chronic non-communicable diseases. With the development of evidence-based medicine, the evidence translation system has made some achievements in clinical practice. There is, however, no comprehensive, professional and efficient system for translating lifestyle evidence globally. Therefore, the Health Lifestyle Evidence (HLSE) Group of Lanzhou University constructed the HLSE Evidence Translation System (https://hlse.cn/), with the aim of synthesizing, evaluating, translating, and applying lifestyle-related evidence resources. This paper aims to introduce the functional module design of the evidence translation system, the system development process and testing, introduce the interface design and function demonstration, and explain the significance of constructing the HLSE.

Objective:To identify a novel reassortant H3N2 avian influenza virus using nanopore sequencing technology and analyze its genetic characteristics.Methods:The positive samples of the H3N2 avian influenza virus, collected from the external environment in the farmers' market of Guangzhou, were cultured in chicken embryos. The whole genome was sequenced by targeted amplification and nanopore sequencing technology. The genetic characteristics were analyzed using bioinformatics software.Results:The phylogenetic trees showed that each gene fragment of the strain belonged to the Eurasian evolutionary branch, and the host source was of avian origin. The HA gene was closely related to the origin of the H3N6 virus. The NA gene was closely related to the H3N2 avian influenza virus from 2017 to 2020. The PB1 gene was closely related to the H5N6 avian influenza virus in Guangxi Zhuang Autonomous Region and Fujian Province from 2016 to 2022 and was not related to the PB1 gene of the H5N6 avian influenza epidemic strain in Guangzhou. The other internal gene fragments had complex sources with significant genetic diversity. Molecular characteristics indicated that the strain exhibited the molecular characteristics of a typical low pathogenic avian influenza virus and tended to bind to the receptors of avian origin. On important protein sites related to biological characteristics, this strain had mutations of PB2-L89V, PB1-L473V, NP-A184K, M1-N30D/T215A, and NS1-P42S/N205S.Conclusions:This study identified a novel reassortant H3N2 avian influenza virus by nanopore sequencing, with the PB1 gene derived from the H5N6 avian influenza virus. The virus had a low ability to spread across species, but further exploration was needed to determine whether its pathogenicity to the host was affected.

To monitor and analyze the molecular variation of the H3N2 influenza virus in Guangzhou during the COVID-19 pandemic, respiratory samples of influenza-like cases from influenza monitoring sentinel hospitals were collected from influenza monitoring sentinel hospitals for virus isolation and whole genome sequencing. The results showed that during COVID-19, there was only one peak of H3N2 influenza in the second quarter of 2022 in Guangzhou (the positive rate was 52.23%), and the epidemic intensity and duration were both higher than those in 2019. The HA gene and NA gene of the epidemic strain in Guangzhou in 2022 belonged to the 3C.2a1b. 2a. 1a. 1 branch, which had a good antigenic site matching with the vaccine strain (A/Cambodia/e0826360/2020) from 2021 to 2022 and had no antigen drift. In 2022 strains, the variation of antigen determinant mainly occurred in the I48T of C region, while no variation occurred in the A, B, D, and E regions. The binding site of the HA protein receptor was consistent with the vaccine strain (A/Cambodia/e0826360/2020). Most of the strains in 2022 carried 13 glycosylation sites on the HA protein, but an outbreak of strains caused a loss of glycosylation sites at 24-NST. In conclusion, the strains that caused the epidemic of H3N2 influenza in Guangzhou in 2022 were not evolved or transmitted from the local strains in 2019 during the COVID-19 pandemic.

To monitor and analyze the molecular variation of the H3N2 influenza virus in Guangzhou during the COVID-19 pandemic, respiratory samples of influenza-like cases from influenza monitoring sentinel hospitals were collected from influenza monitoring sentinel hospitals for virus isolation and whole genome sequencing. The results showed that during COVID-19, there was only one peak of H3N2 influenza in the second quarter of 2022 in Guangzhou (the positive rate was 52.23%), and the epidemic intensity and duration were both higher than those in 2019. The HA gene and NA gene of the epidemic strain in Guangzhou in 2022 belonged to the 3C.2a1b. 2a. 1a. 1 branch, which had a good antigenic site matching with the vaccine strain (A/Cambodia/e0826360/2020) from 2021 to 2022 and had no antigen drift. In 2022 strains, the variation of antigen determinant mainly occurred in the I48T of C region, while no variation occurred in the A, B, D, and E regions. The binding site of the HA protein receptor was consistent with the vaccine strain (A/Cambodia/e0826360/2020). Most of the strains in 2022 carried 13 glycosylation sites on the HA protein, but an outbreak of strains caused a loss of glycosylation sites at 24-NST. In conclusion, the strains that caused the epidemic of H3N2 influenza in Guangzhou in 2022 were not evolved or transmitted from the local strains in 2019 during the COVID-19 pandemic.