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关键词： Ancianos   Benign prostatic hyperplasia   Diagnosis   Diagnóstico   Elderly   Hiperplasia prostática benigna   Homocysteine   Homteína   IL-6  

摘要： OBJECTIVE:To investigate the diagnostic value of serum metabolic markers such as HCY, sdLDL-C, Crea, inflammatory factor IL-6 and prostate-specific antigen in elderly patients with prostatic hyperplasia (BPH). METHODS:150 senile patients with hyperplasia of prostate were selected as observation group and 169 healthy senile patients were selected as control group. The tPSA, fPSA, fPSA/t PSA and prostate size data of the two groups were collected, and serum samples of the subjects were collected for the detection of HCY, sdLDL, Crea, IL-6 and other indicators. Univariate analysis, correlation analysis and Logistic regression analysis were conducted to analyze the relationship between each index and senility prostatic hyperplasia. The diagnostic efficiency of each serum metabolite was analyzed by receiver operating characteristic curve (ROC). RESULTS:Serum levels of tPSA, fPSA, Crea, HCY, sdLDL-C and IL-6 were significantly increased, fPSA/tPSA ratio and HDL were significantly decreased, and TCHO, TG and LDL had no statistical significance. Serum tPSA and fPSA levels were positively correlated with prostate size, serum IL-6, Crea and HCY levels were positively correlated with tPSA and fPSA levels, and serum sdLDL-C levels were negatively correlated with fPSA levels. Logistic regression analysis showed that tPSA, fPSA, prostate size, HCY, Crea and IL-6 were risk factors for prostate hyperplasia. HDL and fPSA/tPSA are protective factors for benign prostatic hyperplasia. ROC curve analysis showed that the sensitivity and specificity of fPSA/tPSA and IL-6 were 82.7% and 72%, 83.4% and 80.5%, and the area under ROC curve were 0.840 and 0.825, respectively. tPSA and fPSA combined with HCY, IL-6 and Crea had the best diagnostic efficiency, with the area under ROC curve reaching 0.881, specificity and sensitivity reaching 84% and 77.3%, respectively. CONCLUSION:The combined detection of prostate-specific antigen, HCY, Crea and IL-6 can significantly improve the diagnostic effi

关键词： Hepatitis B virus   Peg-IFN-alpha   LY6E   TRIM6  

摘要： BackgroundPegylated interferon alpha (Peg-IFN-alpha) has the potential to eradicate hepatitis B surface antigen (HBsAg). This study aimed to investigate whether the expression levels of lymphocyte antigen 6 family member E (LY6E) and tripartite motif-containing protein 6 (TRIM6) mRNAs in peripheral blood mononuclear cells (PBMCs) of hepatitis B e antigen (HBeAg)-negative chronic hepatitis B virus (HBV) patients is associated with the response to Peg-IFN-alpha treatment and HBsAg *** this prospective study, HBeAg-negative chronic HBV patients treated with Peg-IFN-alpha were followed for 48 weeks. The participants were classified into two groups, the virological response (VR) group and nonvirological response (NVR) group, according to the changes in HBV DNA and HBsAg levels observed at week 48 of treatment. Furthermore, these patients were divided into a serological response (SR) group and a nonserological response (NSR) group, depending on whether they exhibited a loss of serum HBsAg or evidence of seroconversion. The expression levels of LY6E and TRIM6 mRNAs in PBMCs were evaluated using real-time quantitative PCR with fluorescence detection. The diagnostic performance of LY6E and TRIM6 was assessed by analyzing the receiver operating characteristic (ROC) curve and calculating the area under the ROC curve (AUC).ResultsAfter the treatment period, the observed VR and SR rates were 44.64% and 28.57%, respectively. Dynamic changes in LY6E and TRIM6 mRNA levels were significantly different between the VR and NVR groups and between the SR and NSR groups. Multivariate analysis revealed that TRIM6 was independently associated with VR at weeks 12 and 24 of Peg-IFN-alpha therapy and with SR at week 12;in addition, LY6E was independently associated with VR at week 12 and SR at week 24. At week 24, the area under the curve (AUC) for LY6E in the prediction of VR was 0.6942, and the AUC for the prediction of SR was 0.7766;at week 12, TRIM6 had AUCs of 0.7600 for t

关键词： Chlamydia trachomatis   Helicobacter pylori   Varicella zoster virus   Alzheimer   Cytokines   Real-time RT-PCR  

摘要： Objectives: This study aimed to use the real-time RT-PCR method to detect the gene expression cytokines IL-10, TNF alpha, IFN-gamma, and TGF-(3 in the serum of Alzheimer's patients. Methods: This study was conducted on 100 serum samples of Alzheimer's patients. DNA extraction was performed on the samples with the Cinnaclone kit and PCR techniques were used to detect the presence of Helicobacter pylori, Chlamydia trachomatis, and Varicella zoster virus. Real-time RT-PCR was performed to measure the expression of TNF alpha, IFNT, TGF(3, and IL-10 genes with a Smobio kit. Results: The relative changes in the expression of TNF alpha, IFNT, TGF(3, and IL-10 genes were observed in Alzheimer's patients compared to the control samples without microorganisms, and a significant increase was observed (P < 0.05). Conclusion: This study showed that the cytokines TNF alpha, IFNT, TGF(3, and IL-10, have an increase in Alzheimer's patients(P < 0.05). Therefore, the presence of the microorganisms accompanied by the rise and inducing the expression of cytokines compared to the groups without the mentioned microorganisms causes a significant increase in the production of cytokines effective in the occurrence or exacerbation of Alzheimer's disease.

关键词： Ventriculomegaly   ASD   MIA   IFN-gamma   Choroid plexus   Ependyma  

摘要： Maternal immune activation (MIA) is a principal environmental risk factor contributing to autism spectrum disorder (ASD) and can be causally linked to ASD symptoms. In our study, we found that MIA triggered by poly (I: C) injection caused ventriculomegaly in offspring due to the dysfunction of the choroid plexus (Chp) and ependyma. We subsequently identified a sustained enhancement of interferon-gamma (IFN-gamma) signaling in the brain and serum of MIA offspring. Further study revealed that increased IFN-gamma signaling could disrupt the barrier function of Chp epithelial cells by activating macrophages, and suppress the differentiation of primary ependymal cells via the signal transducer and activator of transcription 1/3 signaling. The effects of MIA on the offspring were mitigated by administration of IFNGR-blocking antibody in pregnant dams, while systemic maternal administration of IFN-gamma was sufficient to mimic the effect of MIA. Overall, our findings revealed that ventriculomegaly caused by IFN-gamma signaling could be a critical factor in compromising fetal brain development in MIA-induced ASD and provide a mechanistic framework for the association between maternal inflammation and abnormal development of ventricles in the offspring.

关键词： Subacute sclerosing panencephalitis   Measles   IL-12   IFN-gamma   Gene expression   Cytokines  

摘要： Background: Subacute sclerosing panencephalitis (SSPE) is a rare but fatal neurological syndrome resulting from persistent measles virus infection in the central nervous system. Despite the availability of a measles vaccine, SSPE continues to pose a significant health burden, and immunogenetic risk factors remain unclear. We aimed to study the role of the interleukin 12 (IL-12)/interferon-gamma (IFN-gamma) axis, known for it's significance in antiviral defense, in the development of SSPE. Methods: This cross-sectional case-control study recruited consecutive age and sex-matched SSPE cases (n = 51) and controls (n = 51). Gene expressions were quantified for IL-12B, IFNG, IL-12RB1, STAT4, IFNGR1, IFNGR2, STAT1, IRF8, and ISG15 genes using quantitative realtime PCR. Additionally, plasma levels of IL-12p40, IL12p70, and IFN-gamma were measured using the multiplex suspension array platform. Furthermore, single nucleotide polymorphisms (SNPs) in IL-12B, IL-12RB1, IFNG, IFNGR1, IFNGR2, and ISG15 genes were examined using TaqMan SNP genotyping assays. Statistical analyses compared gene expressions, cytokine levels, and alleles and genotypes frequencies between SSPE patients and controls. Results: Significant alterations in the expression of key IL-12 pathway-related genes were observed in SSPE patients compared to controls, including lower STAT4 (p = 0.0445) and higher IFNGR1 (p = 0.0005) and IRF8 (p = 0.0229). Elevated plasma levels of IL-12p70 (p = 0.0015) and IFN-gamma (p = 0.0381) were also observed in SSPE patients. Additionally, associations with SSPE were found for the rs3212227 SNP in IL-12B (p = 0.048), the rs1059293 SNP in IFNGR2 (p = 0.052), and the rs1921 SNP in ISG15 (p = 0.054) genes. Notably, gene-gene interactions among these genes exhibited associations with SSPE. Conclusion: This study provides novel insights into the dysregulation of the IL-12/IFN-gamma immune axis in SSPE and underscores the complex interplay between host genetics and viral infection in

关键词： genetic diversity   HLA   immunogenetics   Kazakhstan   linkage disequilibrium   polymorphisms  

摘要： Background: The human leukocyte antigen (HLA) system represents the most polymorphic segment within human DNA sequences and constitutes a core component of immune defense responses and in understanding population genetics. This research investigates the distribution of HLA class I and II polymorphisms across different ethnic groups in Kazakhstan, offering valuable insights into the genetic diversity and demographic evolution within this region. Methods: We performed an in-depth examination of HLA class I and II polymorphisms across diverse ethnic communities living in Kazakhstan, including Kazakhs, Russians, Uzbeks, Ukrainians, Germans, Tatars, and Koreans. Utilizing data from high-resolution HLA typing studies allowed us to assess allele frequencies alongside haplotype distributions while analyzing genetic interrelations between these populations. Additionally, we performed comparative assessments with global HLA databases to determine the genetic affiliations between these groups and their relationships with neighboring and more distant populations. Results: Our study revealed over 200 HLA alleles within the analyzed populations, and significant variations were observed in their allele and haplotype frequencies. Notably, the Kazakh group exhibited strong genetic ties to Asian and Siberian demographics;conversely, other ethnicities showed associations reflective of their historical roots. Notable alleles included HLA-A*02:01, B*07:02, C*07:02, DRB1*07:01, and DQB1*03:01, commonly observed across various groups. Linkage disequilibrium analysis revealed the presence of population-specific haplotypes, highlighting distinct genetic structures within these communities. Conclusions: The findings highlight the significant genetic diversity in Kazakhstan, influenced by its geographical location at the crossroads of Europe and Asia. These results are pertinent to immunogenetics, transplantation medicine, and personalized healthcare within Kazakhstan and adjacent regions. Fu

关键词： Idiopathic nephrotic syndrome   Steroid-sensitive nephrotic syndrome   Frequently relapsing   Steroid dependent   Human leukocyte antigen  

摘要： BackgroundManagement of patients with steroid-sensitive nephrotic syndrome (SSNS) is challenging because of frequent relapses. Causal variants in the human leukocyte antigen (HLA) class II region that are associated with relapse remain *** collected a cohort of East Asian individuals comprising 206 pediatric patients with SSNS and 435 healthy controls from Southwest China. Ninety children with steroid-sensitive nephrotic syndrome without relapse (SSNSWR) and 116 children with steroid-dependent and/or frequent relapse nephrotic syndrome (SDNS/FRNS) were genotyped using Sanger sequencing. We then measured the transcriptional level, allele expression imbalance (AEI) and functional proteins of HLA-DQA1 and HLA-DQB1 in different stages of SDNS/***1464545187 in ANKRD36 was associated with an approximately 1.69-fold greater risk for SSNSWR (P = 0.04;95% confidence interval [CI], 1.05-2.72). Clustered risk variants in HLA-DQA1 and HLA-DQB1 were significantly associated with SDNS/FRNS (rs1047989: P = 2.26E-07, odds ratio [OR] = 2.25, 1.65-3.05;rs9273471: P = 5.45E-05, OR = 1.84, 1.37-2.46;HLA-DQB1*06:02: P = 0.017, OR = 0.19, 0.04-0.77). The genotype distributions of rs1047989, 2:171713702, rs1049123, rs9273471, and HLA-DQB1*06:02 in patients with SSNS were significantly different from those in healthy controls. rs1047989 (HLA-DQA1) was significantly associated with a greater number of infections at relapse in SDNS/FRNS patients (P = 0.045, OR = 6.79, 95% CI: 1.29-168.52). Flow cytometry showed that the proportion of cells expressing HLA-DQA1+/DQB1+ (HLA-DQA1+, P = 0.0046;HLA-DQB1+, P = 0.0045) was lowest in the relapse stage. In addition, the mRNA levels of HLA-DQA1 and HLA-DQB1 were significantly greater in the relapse group than in the remission group (HLA-DQA1, P = 0.03;HLA-DQB1, P = 0.002). No significant AEIs were detected in the different stages of SDNS/FRNS. The rs1047989 variant is likely to affect the structure and stability of HLA-DQA

关键词： 慢性骨髓增殖性肿瘤   调节性T细胞   细胞因子   免疫治疗  

摘要： 慢性骨髓增殖性肿瘤（myeloproliferative neoplasm，MPN）是肿瘤克隆和炎症相互作用的典型疾病模型，免疫微环境在其发生发展中发挥重要的调控作用。调节性T细胞（Regulatory T cells，Tregs）是免疫微环境中的重要组成部分，可受到IL-4、IL-10、IL-13和TGF-β等抗炎细胞因子以及肿瘤坏死因子-α、IL-2、IL-17、IFN-γ等促炎细胞因子的调控，同时也可分泌TGF-β、IL-10等多种细胞因子。目前Tregs在MPN中的具体作用机制尚不明确，本文综述了Tregs相关细胞因子在MPN中的表达及作用，并总结了目前MPN中靶向Tregs相关细胞因子的治疗方式，以期为Tregs及其相关细胞因子在MPN发病机制、临床应用等领域的研究提供思路。

关键词： glutamate   mGluR5   Crassostrea gigas   hemocyte   IL-17 expression  

摘要： Metabotropic glutamate receptor 5 (mGluR5) is a critical regulator of immune responses within the neuroimmune system, influencing cytokine secretion and immune cell function. Although extensively studied in mammals, its role in regulating IL-17 in invertebrate immunity is poorly understood. This study examines CgmGluR5 expression and downstream signaling activation in Pacific oyster (Crassostrea gigas) hemocytes following glutamate (Glu) and Vibrio splendidus treatment. Glu treatment significantly induced the expression of CgmGluR5 and key signaling molecules, including PLC, DAG, IP3, Ca-2(+), and PKC, while enhancing mRNA levels of CgIL17-1, CgIL17-5, and CgCaspase3. Elevated Ca-2(+) content and CgIL17 expression in hemocytes were observed at 12 h post-Glu exposure, indicating CgmGluR5-mediated immune regulation through the phosphoinositide pathway. A 1.14-fold increase in the apoptosis rate was found in the Glu treatment group compared to the control group. Knockdown of CgmGluR5 suppressed CgIL17-1 and CgIL17-5 expression and reduced granulocyte proportions, reflecting its role in immune regulation. This study shows that CgmGluR5 mediates long-term immune regulation in oysters through the phosphoinositide pathway, providing new theoretical insights for aquaculture immune management.

关键词： evolutionary divergence   HBV   HCC   human leukocyte antigen   zygosity  

摘要： Background and Aims:The human leukocyte antigen (HLA) locus is implicated in HCC among chronic HBV carriers. We investigated associations of HLA variants, amino acid polymorphisms, zygosity, and evolutionary divergence with HBV-related HCC in Han Chinese and explored biological mechanisms. Approach and Results:We examined the associations of HLA variants (imputed 4-digit classical alleles and amino acid polymorphisms), zygosity, and evolutionary divergence with HBV-related HCC in a discovery set (706 HBV-related HCC cases, 6197 chronic HBV carriers in Taiwan). Significant signals were validated in an independent set (636 cases, 560 controls in Qidong, Mainland China). We used logistic regression adjusted for sex, age, and top 10 genetic principal components, with a Bonferroni correction for multiple testing (p<1.6x10(-4)). We evaluated predicted peptide-binding affinities and control of viral load, viral population diversity, and inflammatory markers for significant signals. HLA-DQB1*03:01 was most significantly associated with HBV-related HCC in discovery and validation sets (ORmeta-analysis=1.33, p(meta-analysis)=2.6x10(-8)). Three amino acids within the DQ beta 1 peptide-binding region, HLA-DQ beta 1Ala13, HLA-DQ beta 1Tyr26, and HLA-DQ beta 1Glu45, were positively associated with HCC. HLA-DQB1*03:01 was associated with lower binding affinity of HBV nucleocapsid antigen and higher HBV DNA load and serum soluble programmed cell death 1 (sPD-1) (p<0.05). HLA-DQB1 heterozygosity was inversely associated with HCC independent of HLA-DQB1*03:01 (p(meta-analysis)=3.3x10(-3)). Conclusions: HLA-DQB1*03:01 and its 3 key amino acids are associated with an increased HBV-related HCC risk. This association may be explained by the low binding affinity to HBV antigen, resulting in poor control of viral load and increased inflammation, as evidenced by sPD-1 levels.