ObjectiveTo analyze the epidemiological characteristics of latent tuberculosis infection (LTBI) among newly detained populations in eastern China, to identify high-risk groups, and to provide a scientific basis for formulating tuberculosis prevention and control strategies in the prison system. MethodsA cross-sectional study was conducted among the newly admitted detainees in two prisons in eastern China in 2022. Data on demographic characteristics, behavioral risk factors and previous disease history of the research subjects were collected through a structured questionnaire survey. The LTBI status of the detainees was determined using the QuantiFERON-TB Gold In-Tube (QFT-GIT) method. Lasso regression was used to screen variables, followed by multivariate logistic regression analysis to investigate the influencing factors of LTBI. ResultsA total of 305 detainees were included in the study. The median age of detainees was 35 (31, 43) years. The study population was predominantly male (67.21%), of Han ethnicity (95.41%), had a junior or senior high school education (59.34%), and was unemployed (31.80%). A history of smoking was reported by 52.79% of participants, while 57.70% reported no alcohol consumption. The majority had no history of hypertension (85.90%), diabetes mellitus (93.77%), human immunodeficiency virus (HIV) infection (97.38%), familial genetic diseases (95.08%), surgery or trauma (73.77%), drug use (92.79%), or hepatitis (93.77%). The LTBI rate was 14.75%. After comparing the demographic characteristics of LTBI and non-infected groups, it was found that smoking history (χ²=7.40, P=0.025), drug use history (χ²=5.49, P=0.019), and HIV infection (χ²=8.12, P=0.004) were statistically correlated with LTBI infection. The results of multivariate logistic regression analyses showed that smoking [adjusted odds ratio (aOR)=4.08, 95%CI: 1.60‒10.42, P=0.003], HIV infection (aOR=11.57, 95%CI: 2.50‒53.51, P=0.002) and drug use (aOR=3.04, 95%CI: 1.02‒9.09, P=0.046) were risk factors for LTBI. ConclusionThe LTBI rate among newly detainees in two prisons in eastern China is slightly lower than that among long-term detainees. Early screening and intervention should be implemented for newly detainees, with particular attention focused on high-risk groups such as those with a history of smoking, HIV infection, or drug use.

Tumor drug resistance is an important problem in the failure of chemotherapy and targeted drug therapy, which is a complex process involving chromatin remodeling. SWI/SNF is one of the most studied ATP-dependent chromatin remodeling complexes in tumorigenesis, which plays an important role in the coordination of chromatin structural stability, gene expression, and post-translation modification. However, its mechanism in tumor drug resistance has not been systematically combed. SWI/SNF can be divided into 3 types according to its subunit composition: BAF, PBAF, and ncBAF. These 3 subtypes all contain two mutually exclusive ATPase catalytic subunits (SMARCA2 or SMARCA4), core subunits (SMARCC1 and SMARCD1), and regulatory subunits (ARID1A, PBRM1, and ACTB, etc.), which can control gene expression by regulating chromatin structure. The change of SWI/SNF complex subunits is one of the important factors of tumor drug resistance and progress. SMARCA4 and ARID1A are the most widely studied subunits in tumor drug resistance. Low expression of SMARCA4 can lead to the deletion of the transcription inhibitor of the BCL2L1 gene in mantle cell lymphoma, which will result in transcription up-regulation and significant resistance to the combination therapy of ibrutinib and venetoclax. Low expression of SMARCA4 and high expression of SMARCA2 can activate the FGFR1-pERK1/2 signaling pathway in ovarian high-grade serous carcinoma cells, which induces the overexpression of anti-apoptosis gene BCL2 and results in carboplatin resistance. SMARCA4 deletion can up-regulate epithelial-mesenchymal transition (EMT) by activating YAP1 gene expression in triple-negative breast cancer. It can also reduce the expression of Ca²⁺ channel IP3R3 in ovarian and lung cancer, resulting in the transfer of Ca²⁺ needed to induce apoptosis from endoplasmic reticulum to mitochondria damage. Thus, these two tumors are resistant to cisplatin. It has been found that verteporfin can overcome the drug resistance induced by SMARCA4 deletion. However, this inhibitor has not been applied in clinical practice. Therefore, it is a promising research direction to develop SWI/SNF ATPase targeted drugs with high oral bioavailability to treat patients with tumor resistance induced by low expression or deletion of SMARCA4. ARID1A deletion can activate the expression of ANXA1 protein in HER2+ breast cancer cells or down-regulate the expression of progesterone receptor B protein in endometrial cancer cells. The drug resistance of these two tumor cells to trastuzumab or progesterone is induced by activating AKT pathway. ARID1A deletion in ovarian cancer can increase the expression of MRP2 protein and make it resistant to carboplatin and paclitaxel. ARID1A deletion also can up-regulate the phosphorylation levels of EGFR, ErbB2, and RAF1 oncogene proteins.The ErbB and VEGF pathway are activated and EMT is increased. As a result, lung adenocarcinoma is resistant to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). Although great progress has been made in the research on the mechanism of SWI/SNF complex inducing tumor drug resistance, most of the research is still at the protein level. It is necessary to comprehensively and deeply explore the detailed mechanism of drug resistance from gene, transcription, protein, and metabolite levels by using multi-omics techniques, which can provide sufficient theoretical basis for the diagnosis and treatment of poor tumor prognosis caused by mutation or abnormal expression of SWI/SNF subunits in clinical practice.

Fucoidan(FUC)is a natural seaweed-derived drug.Previously,our experiments have shown that FUC can significantly inhibit the cell viability of human osteosarcoma 143B cells and induce cell death,but the mechanism remains unclear.Ferroptosis,a novel form of cell death,has emerged as an important target for tumor therapy.This study aims to investigate whether FUC induces ferroptosis of 143B cells and elucidate its underlying molecular mechanisms.CCK-8 and LDH assays result showed that FUC(10,100,400 μg/mL)significantly reduced cell viability of 143B cells and induced cell death.Calce-in-AM staining,FeRhoNox-1 staining,and C11 BODIPY 581/591 staining indicated that FUC obviously increased the levels of labile iron pool(LIP),Fe2+,and lipid reactive oxygen species(Lip ROS)in 143B cells.Chemical colorimetric analysis revealed that FUC markedly decreased intracellular Glutathi-one(GSH)contents.Real-time quantitative PCR showed that FUC dramatically reduced the mRNA lev-els of ferroptosis-related factors solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4),while increasing the mRNA levels of prostaglandin endoperoxide synthase 2(PTGS2)and acyl-CoA synthetase long-chain family member 4(ACSL4).Western blotting analysis demonstrated that FUC significantly reduced the protein levels of SLC7A11 and GPX4,and the ratios of p-PI3K/PI3K,p-AktSer473/Akt,and p-AktThr308/Akt,but increased the protein level of ACSL4.Immunofluorescence staining showed that FUC obviously inhibited the nuclear translocation of p-AktSer473.The ferroptosis in-hibitor ferrostatin-1(Fer-1)and iron chelator deferoxamine(DFO)remarkably suppressed cell death in-duced by FUC in 143B cells.Additionally,the PI3K/Akt pathway activator 740Y-P significantly inhibi-ted FUC-induced iron overload and lipid peroxidation in 143B cells,and restored the protein levels of SLC7A11 and GPX4.In conclusion,FUC can induce ferroptosis of 143B cells by inhibiting the PI3K/Akt signaling pathway,which may be a potential target for the prevention and treatment of osteosarcoma.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

In June 2018,sows at a pig farm in Jiamusi,Heilongjiang Province,suffered a large num-ber of miscarriages,and subsequently weaned piglets at the farm began to show persistent high fe-ver symptoms at around 35 days of age,with some pigs having a fever of more than 41.5 ℃.In or-der to determine the cause of this outbreak,63 clinical samples from this farm were tested.The re-sults showed that 60 out of 63 samples were positive for the porcine reproductive and respiratory syndrome virus(PRRSV)antigen.Subsequently,PRRSV antigen-positive plasmid was transfected into African green monkey embryonic kidney cells(Marc-145),and after three generations of blind transmission,indirect immunofluorescence assay(IFA)was performed.The results showed that one PRRSV strain,named HLJ38,was successfully isolated.Then the whole genome of HLJ38 strain was sequenced and then analyzed in detail by bioinformatics software.Sequence analysis showed that there were three deletions of 131 amino acids(323-433 aa,483 aa and 504-522 aa)in the derived sequence of Nsp2 gene of HLJ38 strain,which was consistent with the molecular ge-netic marker of NADC30 PRRSV.The phylogenetic tree analysis showed that HLJ38 and NADC30 PRRSV in GenBank belong to lineage 1 subgroup,and the nucleotide homology of HLJ38 and NADC30 PRRSV in GenBank was only 85.2％and 84.6％.Recombinant analysis showed that HLJ38 was a recombinant NADC30-like PRRSV,and the recombinant gene fragments were de-rived from multiple strains,among which the fragment of 1-201 nt was provided by VR2332 strain and fragment of 6 641-8 061 nt derived from the HP-PRRSV strain.In summary,the re-sults showed that the outbreak in this pig farm may be caused by the recombination of PRRSV strains among different lineages,and the recombinant circulating strains not only have certain pathogenicity but also suggest that the existing commercial vaccines provide limited cross-protec-tion against them.Recombination between different lineages increases the genetic diversity of PRRSV and aggravates the difficulty of prevention and control of PRRS in pig farms.Therefore,it is necessary to continuously monitor the epidemic dynamics of PRRSV in pig farms and take effec-tive measures in time to curb the spread of PRRS.

Type 2 diabetes mellitus is a metabol-ic disease characterized by high blood sugar levels.Traditionally,amino acids are primarily viewed as the basic building blocks for proteins and peptide synthesis.However,in recent years,amino acids have gained increased attention as signaling mole-cules that play crucial roles in the maintenance and regulation of metabolic homeostasis.It has been found that there is a close correlation between the metabolism of branched-chain and/or aromatic amino acids and the occurrence or development of type 2 diabetes mellitus.Furthermore,there have been successive reports on the regulation mecha-nism involved.This article will focus on the meta-bolic processes,mechanisms and clinical value of branched-chain and aromatic amino acids in type 2 diabetes mellitus.It will also summarize and pro-vide an outlook on the current state of amino acid metabolism in the treatment of diabetes mellitus,with the aim of offering new ideas for the treat-ment of type 2 diabetes mellitus.

Objective To retrospectively analyze the association between metabolic factors and high-risk colorectal adenoma(CRA).Methods The medical records of patients aged 18-75 years who underwent their initial colonoscopy at Karamay Central Hospital of Xinjiang Uygur Autonomous Region from Jul 2000 to Mar 2017 were collected.The comparison between normal colonoscopy(NC)and high-risk CRA patients was conducted using an unpaired t-test,while chi-square test was used for categorical variables.Least absolute shrinkage and selection operator(LASSO)regression and Logistic regression were utilized to analyze the association between metabolic factors and high-risk CRA.Results A total of 1 798 patients meeting the inclusion and exclusion criteria were enrolled and divided into normal colonoscopy(NC)findings group(n=972)and high-risk CRA group(n=826).The high-risk CRA group exhibited significantly lower levels of high-density lipoprotein cholesterol(HDL-C)in comparison to the NC group,while uric acid and fibrosis 4(FIB-4)index levels were significantly higher than those observed in the NC group(all P<0.05).Based on LASSO regression analysis,we identified 12 variables that potentially influence the occurrence of high-risk CRA,including age,gender,smoking history,alcohol consumption history,non-alcoholic fatty liver disease(NAFLD),hypertension,coronary artery disease,hyperglycemia,hypercholesterolemia,low levels of HDL-C,elevated alanine aminotransferase,and elevated gamma-glutamyl transferase.Multivariate analysis revealed that individuals aged over 50 years,male gender,cigarette and alcohol consumption,low HDL-C levels,history of NAFLD and hypertension were identified as independent risk factors associated with high-risk CRA(P<0.05).In addition,without or with adjusting for age,sex,smoking,and drinking history,patients with a high TG/HDL-C ratio(the ratio≥2.68)had a significantly higher risk of high-risk CRA than those with a low TG/HDL-C ratio(the ratio<2.68)[odds ratios(ORs)were1.430 and 1.235 respectively,all P<0.05)].Without or with adjusting variables,the ORs for NAFLD patients with FIB-4 index>2.67 were 1.849(P=0.466)and 1.435(P=0.707),respectively.Conclusion A significant association exists between metabolic factors and high-risk CRA.Independent risk factors for high-risk CRA include older age(≥50 years),male,smoking history,alcohol consumption history,low levels of HDL-C,and a history of NAFLD and hypertension.Individuals exhibiting a TG/HDL-C ratio exceeding 2.68 manifest a significantly heightened susceptibility to the development of high-risk CRA.Therefore,elderly males with one or more aforementioned metabolic abnormalities should be considered a priority population for colorectal screening.

Objective To explore the protective effect of resveratrol on myocardial damage caused by sepsis in rats.Methods Forty SD rats were randomly divided into control group,model group,experimental group and combined group,with 10 rats in each group.Except the control group,the other rats were intraperitoneally injected with 20 mg·kg-1 lipopolysaccharide,while the control group was injected with the same amount of normal saline.Two hours before modeling,the experimental group and combinated group were given 50 mg·kg-1 resveratrol by gavage,and the control group and model group were given the same amount of normal saline by gavage.The combined group was injected with 10 nmol of micro RNA-155(miR-155)agomir through the tail vein,and the other group was injected with equal volume of normal saline through the tail vein.Left ventricular function parameters of rats were measured by echocardiography.The level of myocardial injury markers was detected by colorimetry.Quantitative reverse transcription polymerase chain reaction was used to detect the expression of miR-155.The expression of sirtuin 1(SIRT1)and related proteins of nuclear factor κB signaling pathway were detected by Western blot.Results The left ventricular ejection fraction of control group,model group and experimental group were(80.78±12.85)％,(55.92±7.86)％and(71.55±10.71)％,respectively;left ventricular fractional shortening were(34.08±5.75)％,(22.92±2.96)％,(28.72±4.25)％,respectively;left ventricular end disatolic diameter were(3.12±0.46),(6.34±0.69),(4.95±0.57)mm,respectively;the left ventricular end systolic diameter were(5.98±0.65),(7.24±0.80),(6.16±0.78)mm,respectively;the fractional shortening were(38.91±5.38)％,(22.67±3.53)％,(30.74±3.97)％,and the expression levels of creatine kinase-MB were(661.56±85.44),(1181.41±142.14),(915.02±105.19)U·L-1,respectively;the expressions levels of cardiac troponin Ⅰ were(148.17±28.48),(448.17±60.34)and(375.44±49.01)ng·mL-1,respectively.The expression of miR-155 in control group,model group,experimental group and combined group were 1.00±0.12,3.79±0.45,1.87±0.23 and 4.03±0.49,respectively;the protein relative expression levels of nuclear factor κB(NF-κB)were 1.00±0.08,5.04±0.59,2.73±0.35,5.58±0.63,respectively;the protein relative expression levels of inhibitor of NF-κB-β were 1.00±0.11,3.03±0.37,1.35±0.15 and 2.89±0.34,respectively;the protein relative expressions of inhibitor of NF-κB-α were 1.00±0.13,0.86±0.08,1.21±0.18,0.77±0.09,respectively;the protein relative expression levels of SIRT1 were 1.00±0.16,0.66±0.07,0.93±0.14,0.54±0.06,respectively.The above indicators of the model group were compared with the control group,the experimental group were compared with the model group,and the above indicators of the combined group were compared with the experimental group,and the differences were statistically significant(all P＜0.05).Conclusion Resveratrol can alleviate myocardial injury and improve cardiac function in sepsis rats,which may be achieved by down-regulating the expression of miR-155,up-regulating the level of SIRT1,and inhibiting the nuclear factor κB signaling pathway.

Metastatic Crohn's disease (MCD) represents one of the rare cutaneous extraintestinal manifestations in patients with Crohn's disease. The genital area, particularly the vulva in females, is the most commonly affected site in MCD. However, clinical cases of metastatic vulval Crohn's disease (MVCD) are relatively scarce, and the symptoms often lack specificity, making differential diagnosis challenging. This article aims to summarize the clinical characteristics, diagnostic approaches, and treatment modalities of MVCD, thereby providing a reference for the clinical management of this condition.