Background:Although tobacco smoking is one of the established risk factors for liver cancer, results from epidemiological studies remain inconclusive on the relationship between second-hand smoke (SHS) and liver cancer, particularly among nonsmokers.Objectives:This study aimed to examine the association between SHS and liver cancer, and to assess its potential interaction with major risk factors such as hepatitis B virus (HBV) infection.Methods:A population-based case-control study was conducted in Jiangsu, China, from 2003 to 2010, including 2011 newly diagnosed primary liver cancer cases and 7933 population-based controls. Data on SHS exposure at home and in the workplace, along with other major liver cancer risk factors such as alcohol consumption, were collected through self-reported questionnaires. SHS exposure was assessed as a dichotomous variable, categorizing participants as either exposed or unexposed to SHS. HBV infection status was determined by testing serum samples for serum hepatitis B virus surface antigen. Multivariable unconditional logistic regression models were used to examine the association between SHS and risk of liver cancer. Besides stratified analyses, interactions on additive and multiplicative scales were further evaluated between SHS and other risk factors for liver cancer.Results:Exposure to SHS was associated with liver cancer, shown as adjusted odds ratios (ORs) of 1.84 (95% confidence interval [CI]: 1.56, 2.18) in the overall population and 2.11 (95% CI: 1.67, 2.65) among never smokers. Stratified analyses showed that the association between SHS and liver cancer was stronger among HBV-positive participants (OR: 2.09, 95% CI: 1.48, 2.93) compared with HBV-negative participants (OR: 1.87, 95% CI: 1.54, 2.27) (P = 0.02). Both super-additive and super-multiplicative interactions were observed between SHS and HBV infection, with relative excess risk due to interaction (RERI) of 12.56 (95% CI: 6.60, 18.53) and ratio of ORs of 1.55 (95% CI: 1.07, 2.23) in the total population, and RERI of 12.87 (95% CI: 4.93, 20.81) and ratio of ORs of 1.78 (95% CI: 1.06, 2.99) among never smokers.Conclusion:SHS is independently associated with liver cancer, and this association is further modified by HBV infection, leading to a substantially elevated risk, particularly among nonsmokers.

Chronic inflammation drives vascular aging and stroke risk, yet circulating proteins linking immune activation to cerebrovascular events remain elusive. People with HIV (PWH) face elevated stroke risk beyond traditional vascular risk factors, even under antiretroviral therapy. We aimed to identify circulating proteomic signatures of HIV-associated stroke, characterize underlying biological pathways, and assess their longitudinal stability. We conducted a nested case-control study of 135 PWH with stroke (HIV + /Stroke + , mean age 64.2 years, 85.9% ischemic) and two matched control groups (HIV + /Stroke- and HIV - /Stroke - , n = 135 each), with longitudinal validation in 37 PWH who subsequently developed stroke (78.4% ischemic). Among 184 plasma proteins measured using Olink Cardiovascular panels, 16 were associated with stroke in PWH, centrally involving the tumor necrosis factor receptor superfamily (TNFRSF). TNFRSF proteins (TNFRSF10A, TRAIL-R2, TNFRSF14, and TNF-R1) were strongly inter-correlated (ρ > 0.77), with their co-expression module associated with stroke (adjusted OR = 1.75, P = 0.018). TNFRSF expression increased monotonically across HIV - /Stroke - , HIV + /Stroke - , and HIV + /Stroke+ groups. Longitudinal analysis confirmed post-stroke upregulation of these TNFRSF members, alongside MMP12 and TFF3, particularly in ischemic subtypes. These findings suggest coordinated TNFRSF upregulation as a potential signature associated with both HIV-related inflammation and cerebrovascular events, providing candidate biomarkers for future investigation.

Both human immunodeficiency virus (HIV) infection and sexual behaviors, particularly among men who have sex with men (MSM), are known to influence gut microbial composition and immune regulation. However, their interacting effects on the gut microbiome and systemic immune-inflammatory responses remain unclear. This cross-sectional study included 378 adult men classified into 4 groups: HIV-positive MSM (PMSM), HIV-positive men who have sex with women (PMSW), HIV-negative MSM (NMSM), and HIV-negative MSW (NMSW). Fecal samples were analyzed via 16S rRNA (V3-V4) sequencing, and microbial diversity and composition were analyzed using QIIME2, LEfSe, and MaAsLin2. Immune and inflammatory markers (CD4 count, CD4/CD8 ratio, IL-1β, IL-10, hsCRP, D-lactate, and IP-10) were quantified and correlated with microbial features. HIV infection and sexual behavior each significantly shaped gut microbial diversity and composition, with observable interaction effects. Alpha diversity indices (Shannon and Simpson) were highest in the PMSM group (p < 0.001), and beta diversity differed significantly among all four groups (PERMANOVA, p = 0.001). Prevotella, Succinivibrio, and Alloprevotella were enriched in MSM compared with MSW, whereas Bacteroides and Ruminococcus gnavus group predominated in MSW. HIV infection was associated with enrichment of pro-inflammatory and opportunistic genera (Succinivibrio, Fusobacterium, Escherichia–Shigella) and depletion of short-chain fatty acid (SCFA)-producing genera (Faecalibacterium, Blautia, Lachnospira). Significant interaction effects were observed for Erysipelatoclostridium (positive) and Butyricicoccus (negative), indicating synergistic modulation of the microbiome by HIV and sexual behavior. Reduced SCFA producers correlated with lower CD4/CD8 ratios and elevated IL-1β, IP-10, and D-lactate levels, reflecting impaired mucosal barrier function and chronic immune activation. HIV infection and MSM sexual behavior exert independent and synergistic effects on the gut microbiome. Loss of SCFA-producing commensals and expansion of pro-inflammatory taxa may contribute to mucosal barrier disruption and systemic inflammation in HIV-positive men. These findings suggest the gut microbiome could be a potential therapeutic target to mitigate immune activation and enhance mucosal health in people living with HIV.

Abstract Urban subway systems represent important yet understudied environments for human exposure to airborne microorganisms. Therefore, we conducted an investigation of air microbiome across 43 underground stations spanning 13 lines of the Shanghai subway. Using stratified cluster sampling, we simultaneously collected total suspended particles (TSP, aerodynamic diameter ≤ 100 μm) and fine particulate matter (PM2.5, aerodynamic diameter ≤ 2.5 μm) at station entrances, halls, and platforms, integrating microbial taxonomy, transcriptional potential, PM2.5 chemical composition, microclimate, and network topology. We found bacteria dominated both particle-size fractions and accounted for the majority of transcriptional signals, whereas eukaryotic taxa were strongly enriched in TSP, reflecting pronounced particle-size filtering. Although transcriptional potential generally increased with abundance, dominant taxa such as Staphylococcus and Bacillus exhibited weak abundance–transcription coupling, indicating functional decoupling between numerical dominance and transcriptional contribution in subway air microbiomes. Microbial diversity and community composition remained broadly homogeneous across the subway network, consistent with extensive passenger mobility and high network connectivity. In contrast, finer-scale heterogeneity emerged within stations, particularly for eukaryotic communities, which declined from entrances to enclosed platform environments. Environmental associated factors exhibited kingdom-specific patterns: bacterial and viral diversity were primarily associated with local microclimatic conditions, especially temperature, whereas eukaryotic diversity was more strongly linked to urbanization and externally derived aerosol inputs. Overall, these findings demonstrate that subway airborne microbiomes are shaped by interacting effects of particle-size filtering, environmental selection, and network-driven microbial mixing.

OBJECTIVE:HIV infection may affect uric acid (UA) metabolism, but no large-scale population-based studies have investigated whether and how HIV infection affects incidence of hyperuricemia. DESIGN:Prospective, observational, noninterventional study. METHODS:We included 1836 people with HIV (PWH) who had normal UA level at baseline assessment and 1836 age-, sex-, and baseline UA level-matched people without HIV (PWoH) from the Comparative HIV and Aging Research in Taizhou (CHART) cohort. Hyperuricemia was defined as a serum UA level ≥7 mg/dl, following Chinese clinical guidelines. Logistic regression models were used to examine the association and potential effect modifiers. A generalized linear model (GLM) and bootstrap method were employed to assess the mediation effect. RESULTS:The three-year cumulative incidence of hyperuricemia was significantly lower in PWH than in PWoH overall [11.6% vs. 16.4%; adjusted odds ratio (aOR) = 0.67; 95% confidence interval (CI): 0.55, 0.82], and significantly lower in male PWH than in male PWoH (13.1% vs. 19.4%; aOR = 0.64, 95% CI: 0.52, 0.79) but comparable between female PWH and female PWoH (6.2% vs. 6.1%, aOR = 0.97, 95% CI: 0.55, 1.72). A significant additive interaction between sex and HIV infection was observed, with a relative excess risk due to interaction (RERI) of -1.18 (95% CI :  -2.87, -0.13). Among males, lower BMI and albumin to globulin ratio (AGR) mediated 36% and 12% of the association between HIV infection and lower risk of hyperuricemia, respectively. CONCLUSIONS:HIV infection was associated with a lower risk of hyperuricemia in men but not women, partially mediated by lower BMI and AGR, suggesting distinct metabolic and inflammatory profiles in male PWH.

Background: Despite antiretroviral therapy, neurocognitive impairment (NCI) remains common among people with HIV (PWH), but whether it is associated with a distinct metabolic phenotype remains unclear. We aimed to identify and externally validate plasma metabolic alterations associated with NCI in treated PWH and compare them with those in people without HIV (PWoH). Methods: In the discovery stage, targeted UPLC–MS/MS was used to quantify 540 small–molecule metabolites and 864 lipid species in 699 PWH and 699 age– and sex–matched PWoH from the CHART cohort. NCI was defined as an International HIV Dementia Scale score of 9 or lower. Metabolites associated with NCI were identified separately by HIV status at FDR < 0·1, followed by multivariable, HIV–metabolite interaction, pathway enrichment, and sensitivity analyses. Findings in PWH were tested in an independent cohort of 260 PWH, including 130 with NCI and 130 without NCI. Findings: This study identified a reproducible HIV–specific plasma metabolic signature of NCI in treated HIV infection. NCI was more prevalent in PWH than in PWoH (29·9% vs 21·9%; aOR 1·42, 95% CI 1·07–1·87). Among PWH, 23 metabolites were associated with NCI, including arachidonic acid (AA) and other long–chain polyunsaturated fatty acids (PUFAs), hydroxyeicosatetraenoic acids, ether–linked lysophosphatidylcholines, and glycerophospholipid intermediates. A total of 22 metabolites were lower in PWH with NCI, whereas oleamide was higher. All 23 metabolites remained associated with NCI after multivariable adjustment, 20 showed evidence of interaction with HIV status, and 18 remained significant after participants with major comorbidities were excluded. In the external cohort, 19 of the 23 metabolites were directionally concordant and significant at p < 0·05· Pathway analyses consistently identified arachidonic acid metabolism, biosynthesis of unsaturated fatty acids, and glycerophospholipid metabolism as significantly enriched pathways in PWH with NCI. Interpretation: IHDS–defined NCI in treated PWH was associated with a reproducible, HIV–specific pattern of relative depletion in AA–related lipids, PUFAs, and ether–linked lysophosphatidylcholines. These findings support altered membrane phospholipid remodeling and inflammatory lipid homeostasis in HIV–associated NCI and warrant further studies incorporating comprehensive neuropsychological assessments and broader metabolomic profiling to clarify the underlying metabolic mechanisms and intervenable targets.

Merbecovirus is a subgenus of betacoronaviruses and exhibits high genetic diversity with a capacity for cross-species transmission. However, beyond Middle East respiratory syndrome coronavirus (MERS-CoV), our knowledge of the ecology and pathogenic potential of these viruses remains limited. Merbecoviruses were once thought to rely exclusively on dipeptidyl peptidase 4 for cell entry, but recent discoveries have revealed that several members can also engage with angiotensin-converting enzyme 2 or aminopeptidase N, expanding their receptor repertoire and potential host range. Here we summarize recent advances in understanding of the receptor usage of merbecoviruses and examine how these insights inform pandemic preparedness and risk assessment. We discuss the development of targeted diagnostics, broad-spectrum antivirals and vaccines, including pan-coronavirus strategies. Together, these advances provide a foundation for predictive surveillance and rational countermeasure design, enabling earlier detection and more effective containment of future merbecovirus spillover events before they escalate into epidemics.

Antiretroviral therapy (ART) is shifting the primary driver of mortality for people with HIV (PWH) from opportunistic infections to noncommunicable diseases (NCDs). Protein biomarkers differentiating both AIDS-related and NCDs-related deaths from PWH may help early and precise risk prediction and intervention. We conduct a nested case-control study where 126 HIV deaths, 162 age-sex-matched HIV survivors and 152 HIV-negative controls are analyzed with 92 protein biomarkers of the Olink Organ Damage panel by proximity extension assays (PEA). Using LASSO regression, logistic regression, and ROC analysis, twelve proteins are significantly associated with HIV death, of which six (SIRT5, PPM1B, PSMA1, GALNT10, VEGFC, PTN) are specifically associated with NCDs-related death, two (RCOR1, SERPINA9) are specifically associated with AIDS-related death, and four (CA12, CA14, RARRES1, EDIL3) are associated with both. Three of these proteins are replicable in the external validation sample. The adjusted protein panels consisting of significantly associated proteins selected through both LASSO and logistic regression model well predicted NCDs-related death (AUC = 0.970) and AIDS-related death (AUC = 0.960) in PWH. The selected proteins also displayed a significant correlation with traditional biomarkers of NCDs among PWH (P < 0.05). The potential clinical utility of these biomarkers could shed light on pathogenesis of end-stage organ dysfunction in PWH.

PURPOSE:To investigate longitudinal trends in clinical-epidemiological characteristics among surgically treated lung cancer patients and assess implications for prevention strategies. METHODS:A retrospective analysis was conducted on patients diagnosed with lung cancer and surgically treated at Fudan University Shanghai Cancer Center (2006-2021). Socio-demographics, clinical and pathological data were collected. Continuous and categorical data variables were analyzed using non-parametric tests and chi-square tests, respectively, with trend analysis conducted by linear regression. RESULTS:A total of 21,743 patients with a median age of 59 were included of whom 11,802 (54.3 %) were women. From 2006 to 2021, the female proportion surged from 29.9 % to 59.5 %, paralleled by an increase in patients aged < 45 years (6.2 % to 15.4 %), with young females rising from 3.4 % to 19.2 %. Non-smokers predominated (72.0 % in 2021 vs. 42.3 % in 2006), particularly among women (97.5 % non-smokers), and the overall proportion of female non-smokers increased from 26.8 % to 58.5 %. Adenocarcinoma prevalence increased from 51.7 % to 82.9 % in females, while squamous carcinoma declined from 31.0 % to 4.1 %. Early-stage diagnoses (Stage 0-I) increased from 37.1 % to 85.0 %, coinciding with health checkup-driven detection rising from 44.0 % to 70.5 %. The EGFR mutation rate in adenocarcinoma was notably high in females (69.4 %) and non-smokers (68.9 %). CONCLUSIONS:The rising percentage of non-smokers, growing incidence of lung cancer among young females, increase in early-stage lung cancer cases, and shift in major pathological subtypes present potential challenges and directions for lung cancer prevention and control in China. The emergence of lung cancer in young non-smoking females and its underlying factors warrant further research.

[Objectives]To investigate the molecular epidemiological characteristics of HIV-1 infection among men who had sex with men(MSM)in Taizhou City,Zhejiang Province,and to provide a scientific reference for acquired immune deficiency syndrome prevention and control efforts.[Methods]The research subjects were all newly reported MSM population in Taizhou City from 2020 to 2023.Blood samples without antiviral therapy were collected.The HIV-1 pol gene was amplified and sequenced,and the sequences were submitted to the Stanford University drug resistance database to identify the mutation sites and drug resistance.MEGA 11.0 software was used to analyze the nucleic acid sequences,construct phylogenetic tree,and calculate genetic distance of gene sequences.The molecular transmission network diagram of HIV-1 was constructed using Cytoscape_v3.10.1,and the influencing factors of network entry were analyzed by logistic regression.[Results]A total of 363 newly reported HIV-infected MSM patients were included,with a median age[M(P25,P75)]of 34(26,47)years old.The majority had an educational level of junior high school or below(55.65%).A total of eight subtypes were found,mainly CRF07_BC and CRF01_AE.The primary drug resistance rate was 10.47%(38/363).The optimal molecular network gene distance was 0.019,with a network access rate of 42.70%(155/363),and a total of 47 molecular clusters were formed.Multivariate logistic analyses showed that compared with the CRF01_AE subtype,the clustering risk of CRF07_BC subtype was higher(OR=1.916,95%CI:1.191-3.109),cases with drug resistance had a higher risk of cluster formation than those without drug resistance(OR=2.011,95%CI:1.006-4.080),and recent infected patients had a lower risk of entering the largest molecular cluster than long-term infected patients(OR=0.376,95%CI:0.137-0.928).[Conclusion]The newly diagnosed infections among the MSM population are active in Taizhou City,Zhejiang Province,with a high level of primary drug resistance.Individuals carrying drug-resistant strains are more likely to cluster.Drug resistance monitoring should be strengthened to prevent further spread of drug-resistant strains in the network.

ObjectiveTo investigate the therapeutic effects of direct-acting antiviral agents (DAAs) combined regimens for hepatitis C virus (HCV) patients in Dehong Prefecture, Yunnan Province from 2022 to 2024, to analyze the characteristics of treatment failure patients, so as to provide a basis for discovering more effective treatment regimens in the future.MethodsData on HCV prevention and treatment in Dehong Prefecture was extracted from the China Disease Control and Prevention Information System. A total of 617 patients with HCV antiviral therapy were included, and the differences in variable characteristics among patients with different genotypes were analyzed using comparative statistical tests, including basic socio-demographic characteristics, biochemical testing indicators, and information on previous treatment and current treatment. In addition, the cure rate of HCV patients with diverse characteristics was compared, and the potential causes of treatment failure were explored simultaneously.ResultsThe cure rate of HCV was 96.8%, and statistically significant differences were observed in aspartate transaminase (AST) and alanine transaminase (ALT) levels, previous antiviral therapy history and initial treatment regimens among patients with different HCV genotypes (all P<0.05). Among the multi-type combination regimens, the cure rate of sofosbuvir (SOF)-containing regimens was 97.00%, that of velpatasvir (VEL)-containing regimens was 95.45%, and the cure rate of other treatment regimens, including the regimens with ribavirin (RIB) intervention, was 93.10%. Among the patients with treatment failure, 45.00% had genotype 3, 40.00% had abnormal abdominal ultrasound results, and all presented with elevated baseline AST test levels.ConclusionThe clinical treatment of HCV patients should consider the differences in genotype and biochemical test results. DAAs combined regimens for HCV have achieved a high cure rate in Dehong Prefecture and are applicable to HCV patients with diverse clinical characteristics, providing research evidence for wider application.

OBJECTIVE:This study aimed to identify risk factors for physical frailty incidence among people with HIV (PWH) and HIV-negative individuals and further explore the dynamic relationship between major chronic diseases and frailty. METHODS:PWH and HIV-negative individuals aged at least 40 years from the Comparative HIV and Aging Research in Taizhou (CHART) cohort were included. Univariate and multivariate Cox regression models were used to estimate the hazard ratio and 95% confidence interval (95% CI) of the association between risk factors and physical frailty. RESULTS:A total of 3968 participants (1279 cases and 2689 controls) were included. Regardless of HIV status, the overall trend of physical frailty incidence density increased with age, and aging significantly elevated the risk of frailty. Central obesity [adjusted hazard ratio (aHR) = 2.15, 95% CI: 1.09-4.23], hypertension (aHR = 2.06, 95% CI: 1.03-4.11), and current unsuppressed HIV viral load (aHR = 2.20, 95% CI: 1.01-4.80) increased the risk of frailty incident among PWH, while depression (aHR = 1.93, 95% CI: 1.06-3.50) and diabetes (aHR = 1.85, 95% CI: 1.18-2.90) increased the risk of frailty among HIV-negative controls. Dynamic Change analyses showed that incident depression, incident neurocognitive impairment, and persistent hypertension during a 3.18-year follow-up were associated with a higher risk of frailty among PWH. In contrast, incident depression, persistent depression, and persistent diabetes were significantly associated with frailty incidence among HIV-negative controls. CONCLUSION:Aging was significantly associated with a higher risk of physical frailty regardless of HIV status. Risk factors and the association between dynamic changes in major chronic diseases and frailty were different between HIV-positive and HIV-negative individuals.

BACKGROUND:We aimed to examine the associations of handgrip strength and walking pace with the risk of incident diabetes mellitus (DM) among people with HIV (PWH). DESIGN:A cohort study. SETTING:This study was conducted in Taizhou City Center for Disease Control and Prevention in Zhejiang Province, mainland China. PARTICIPANTS:A total of 1916 participants (mean age 43.3±14.2 years, 77.7% male) without diagnosed or unknown DM at baseline from the Comparative HIV and Aging Research in Taizhou cohort were included. OUTCOME MEASURES:The primary outcome was incident DM, defined by fasting glucose >7.0 mmol/L, HbA1c concentration >6.5% or diagnosed with DM by a doctor during the period of follow-up. RESULTS:During a mean follow-up of 3.2 years, 184 incident DM cases were identified. Overall, there was a significant inverse association between both handgrip strength and walking pace with the risk of incident DM in PWH. Compared with participants with lower handgrip strength (<32.1 and <20.3 kg for males and females) or slower walking pace (<2.1 miles/hour), those with higher handgrip strength (≥32.1 and ≥20.3 kg for males and females) or faster walking pace (≥2.1 miles/hour) had a lower risk of incident DM, the adjusted HR (aHRs) (95% CI were 0.60 (0.42 to 0.85) and 0.59 (0.42 to 0.83), respectively. A higher handgrip strength and a faster walking pace were responsible for 38.0% and 39.7% of DM cases, respectively. Moreover, the lowest risk of incident DM was observed in participants with both higher handgrip strength and faster walking pace (aHR, 0.44; 95% CI 0.25 to 0.76). CONCLUSION:Higher handgrip strength or faster walking pace was significantly associated with a reduced risk of incident DM among PWH.

Despite its rapid economic rise over the past four decades, China now grapples with the challenge of accommodating and supporting its expanding aging population. In 2020, 18

Background: The incidence and prevalence of chronic liver diseases (CLD) and liver cancer are increasing worldwide. Objectives: This study aimed to evaluate the associations between the intake levels of high-fat and low-fat dairy products and CLD mortality and liver cancer incidence. Methods: This study included eligible participants from the NIH-American Association of Retired Persons Diet and Health Study cohort established between 1995 and 1996. Epidemiological data, including dietary factors, were collected using a self-administered validated questionnaire. Portion size and frequency of intake of dairy products were recorded. Cox proportional hazard models were used to examine the associations. Results: A total of 485,931 eligible participants, 59.8% male, with an average age of 61.5 y (SD = 5.4 y) at baseline were included in this analysis after excluding those with pre-existing cancer diagnoses or extreme caloric intakes. During a median follow-up of 15.5 y, 993 deaths from CLD and 940 incident liver cancer cases occurred. CLD mortality was positively associated with intake of high-fat dairy [hazard ratio (HR)(21+ compared with 0-<3.5 serv/wk) = 1.51, 95% confidence interval (CI): 1.24, 1.84, P-trend = 0.009] and high-fat milk (HR14+ compared with 0 serv/wk = 2.03, 95% CI: 1.31, 3.14, P-trend <0.001), and was inversely associated with low-fat dairy (HR21+ compared with 0-<3.5 serv/wk =0.62, 95% CI: 0.46, 0.84, P-trend = 0.002), low-fat milk (HR14+ compared with 0 serv/wk =0.54, 95% CI: 0.41, 0.70, P-trend = 0.028) and yogurt (HR4+ compared with 0 serv/wk = 0.60, 95% CI: 0.37, 0.97, P-trend = 0.057). Total dairy intake (HR21-<28 compared with 0-<7 serv/wk = 1.26, 95% CI: 0.99, 1.59, P-trend = 0.040) and high-fat dairy (HR14-<21 compared with 0-<3.5 serv/wk = 1.35, 95% CI: 1.07, 1.70, P-trend = 0.14) showed marginally positive association with liver cancer risk. Milk intake was positively associated with risk of hepatocellular carcinoma (HCC). Conclusions: High-fat dairy intake is positively associated with CLD mortality, and low-fat dairy shows an inverse association. Total dairy intake is marginally positively associated with liver cancer, and milk intake is positively associated with HCC.

Objective: To determine the prevalence and associates of hyperuricemia (HUA) among the middle- and older-aged population of the island and mountainous areas in Taizhou City of Zhejiang Province. Methods: A cross-sectional study was conducted on individuals aged 45 and above in the island and mountainous area of Taizhou City. The study included questionnaires, physical examinations, and laboratory tests. Data were primarily collected on sociodemographic characteristics, chronic disease history, lifestyle factors, waist circumference, blood pressure, and serum uric acid levels. The association between hyperuricemia and these factors was analyzed by logistic regression. Results: A total of 971 individuals were included in the study, comprising 468 from island and 503 from mountainous area. The prevalence of hyperuricemia was 17.9%, with a significantly higher prevalence in the island area (25.6%) compared to the mountainous area (10.7%). Stratified by gender and age, differences in the prevalence of hyperuricemia between island and mountainous areas were observed in males aged 55 to 64, females aged 45 to 54, 55 to 64, 75 and above (all P<0.05). Multiple logistic regression analysis showed that high intake of sea food (>3 times/week) was positively associated with hyperuricemia (OR=2.10, 95%CI:1.33-3.34). Furthermore, separate regionally stratified logistic regression analyses showed that in the island area, male gender (OR=3.15, 95%CI:1.78-5.66), central obesity (OR=2.38, 95%CI:1.46-3.93), and hypertriglyceridemia (OR=2.00, 95%CI:1.22-3.30) were positively correlated with hyperuricemia (all P<0.05). In the mountainous area, the age group of 65 and above (OR=3.50, 95%CI:1.09-12.50), male (OR=6.79, 95%CI:2.87-17.81), those employed in enterprises and institutions (OR=6.57, 95%CI:1.92-23.73) and hypertension (OR=3.68, 95%CI:1.66-8.87) were positively correlated with hyperuricemia (all P<0.05). Conclusions: The prevalence of hyperuricemia among the middle- and older-aged population in the island of Taizhou City is significantly higher than that in the mountainous areas. Targeted comprehensive behavioral interventions such as routine screening of chronic diseases, low-fat diet, alcohol control, reduced seafood intake, enhanced exercise, weight management, and blood pressure control are warranted.

Background Whether and how sex plays differential roles in aging-related multimorbidity among people with HIV (PWH) is poorly characterized. Methods We included 2479 PWH and 5376 people without HIV from the baseline assessment of the CHART cohort (Comparative HIV and Aging Research in Taizhou). Ten non-AIDS comorbidities were investigated. Multiple logistic regression was used to assess the correlates of multimorbidity, defined as the coexistence of >= 2 non-AIDS comorbidities. Multimorbidity patterns were identified through hierarchical cluster analysis. Results The prevalence of multimorbidity was higher in PWH than in people without HIV (74.6% vs 66.9%, P < .001). This difference was particularly pronounced in women in each age group from 18 through 59 years and among men in each age group from 18 through 49 years. A significant interaction between sex and HIV on multimorbidity was identified (P < .001), with the strength of the association between HIV infection and multimorbidity being stronger in women than in men. Women with HIV presented a unique aggregation pattern of multimorbidity, where neuropsychiatric disorders (depression, neurocognitive impairment) clustered with cardiometabolic diseases. In contrast, all men and women without HIV manifested a similar multimorbidity pattern, where depression and neurocognitive impairment were clustered with hematologic abnormalities but not with cardiometabolic diseases. Conclusions Earlier onset and higher burden of multimorbidity in PWH, as well as disproportionate vulnerability to and a unique multimorbidity pattern among women with HIV, underscore the urgent need for early and sexually oriented integrative interventions and health services targeting multimorbidity in PWH.

The aim of this study is to identify the distribution of HPV31 and HPV33 lineages and sublineages, characterize their genetic variability, explore associations between cervical lesions, persistent/multiple infections, and HPV31/33 genetic variations, and estimate selective pressures and divergence times for both genotypes. In this study, a total of 94 samples were collected, with 276 full-length gene sequences obtained for analysis. Phylogenetic analysis evaluating genetic variant diversity was performed using MEGA software. Correlation analyses were conducted using SPSS 20.0. Selective pressure and divergence time estimations were performed using the Datamonkey web server and BEAST v1.8.3, respectively. Lineage A, B, and C variants were identified in 26.1

OBJECTIVES:Lipid metabolism plays an important role in HIV-associated atherosclerosis. However, the interplay between lipid metabolism, uncontrolled inflammation, and subclinical carotid atherosclerosis (SCA) in HIV infection remains poorly understood. This study aimed to characterize lipidome signatures that, together with inflammatory patterns, may predispose HIV-positive individuals to incident SCA. METHODS:A nested case-control study was conducted within the Comparative HIV and Aging Research Cohort in Taizhou, China, including 115 HIV-positive individuals with incident SCA, 112 age- and sex-comparable HIV-positive normal controls, and 117 HIV-negative normal controls. Untargeted lipidomic profiling and inflammatory marker assessments were performed at baseline and follow-up. A total of 649 plasma lipid species were annotated, and 20 plasma inflammatory markers were quantified. RESULTS:Three distinct baseline lipidomic signatures were identified: 1 upregulated in HIV infection, 1 downregulated, and 1 upregulated in HIV-associated SCA (showing a decreasing or increasing trend from HIV-negative normal controls to HIV-positive normal controls to SCA cases). The latter 2 signatures were enriched in glycerophospholipid metabolism, particularly involving lysophospholipids and short-chain fatty acyls. Lipid species within each signature exhibited distinct correlation patterns with subsets of inflammatory proteins, a pattern that persisted after the onset of SCA. Network analysis revealed that IL-18 was the only inflammatory protein showing divergent associations across lipidomic signatures, displaying positive correlations in the HIV-associated SCA-upregulated lipidomic signature and negative correlations in the other 2. DISCUSSION:Our findings underscore specific lipidomic-inflammatory networks that may underlie the heightened risk of atherosclerosis in HIV infection. The differential involvement of IL-18 suggests a central role of NLRP3 inflammasome activation in HIV-associated vascular inflammation. The observed alterations in lysophospholipid and short-chain fatty acyl metabolism warrant further mechanistic investigation as potential mediators of HIV-related atherogenesis.