Biomedical subjects

Dong-Yan Zhang

Publications and source records attributed to Dong-Yan Zhang.

4 recordsLinked to original sources

PubMed2026

Endothelial function in relation to low-level chronic residential air pollution in a general population: a cohort study.

BACKGROUND: Given the recently updated clean-air targets, this population study assessed endothelial function at low exposure to particulate matter with an aerodynamic diameter of ≤10 µm (PM10) and ≤2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC). METHODS: In 453 Flemish participants (47.7% women; mean age, 52.8 years), endothelial function was assessed by finger photoplethysmography after 5 min of ischaemia. The outcome measures were the maximal ischaemic-to-control ratio (Rmax) and the maximal difference (Dmax) in pulse amplitude between the test and control fingers. The air pollutants were related to Rmax and Dmax using mixed models accounting for coresidence, to cardiovascular endpoints by proportional hazards regression, and to residential address by high-resolution spatiotemporal interpolation. RESULTS: From 2010 to 2015, PM10, PM2.5, NO2 and BC decreased (p < 0.0001) with 6-year levels averaging 15.9, 12.8, 14.3 and 1.04 µg/m3. Irrespective of adjustment for risk factors, Dmax was inversely correlated with PM2.5, while associations of Rmax with PM2.5 and associations of both Dmax and Rmax with other pollutants were weaker (p values <0.10), but consistently inverse. Association sizes of Rmax and Dmax with PM10 and PM2.5 weakened over 6 years, paralleling the decreasing air pollutants (p ≤ 0.044). In adjusted analyses, the risk of a composite cardiovascular endpoint decreased (p ≤ 0.043) with higher Rmax and Dmax with hazard ratios ranging from 0.31 to 0.49. Finally, in the geographical analysis, endothelial dysfunction followed the spatial gradients in PM2.5. CONCLUSIONS: Long-term low-level air pollution is associated with subclinical endothelial dysfunction, the initial and critical step leading to adverse cardiovascular outcomes.

Humans↗

PubMed2026

Home blood pressure telemonitoring reveals race-specific patterns of target organ damage.

BACKGROUND: Racial differences in cardiac and renal target organ damage (TOD) may persist at comparable blood pressure levels. This study compared TOD in high-risk, non-African-American Black and White patients in relation to the home blood pressure (HBP). METHODS: UPRIGHT-HTM (NCT04299529) is an ongoing international trial comparing risk stratification strategies in asymptomatic patients, aged 55-75  years, with ≥5 risk factors. Patients engage in HBP telemonitoring (OMRON HEM 9210-T). After 34.7 months (median), 287 Black and 154 White patients underwent echocardiography. At baseline, their chronic kidney disease (CKD) grade was assessed by cross-classification of the race-free estimated glomerular filtration rate and albuminuria (2024 KDIGO guideline). HBP was stratified by the 2024 ESC thresholds. Linear and logistic regression models, including a race-by-HBP interaction term, were applied to assess associations with the home systolic HBP. RESULTS: The number of HBP readings was 252 215. Median systolic/diastolic HBP was 127/77 mmHg with 142 patients (32.2%) having home hypertension. Fewer Black patients received statins or combination therapy for hypertension or diabetes. Among nonhypertensive White compared to Black patients, left atrial dimensions, mitral annular s', and stroke volume had a steeper slope in relation to systolic HBP. All patients had concentric left ventricular remodeling, but only 4 Black and 13 White patients had an ejection fraction < 50%. CKD grade was worse in Black than White patients without association with HBP. CONCLUSIONS: TOD primarily affects the kidney in Black and the heart in White patients. Intensifying pharmacological treatment in sub-Saharan Africa, including antihypertensives, lipid-lowering agents, antidiabetic medications, and aspirin, should create an opportunity for improved overall cardiovascular and metabolic prevention.

Aged↗

PubMed2026

Integrative Pan-Cancer Characterization of lncRNA UPK1A-AS1 and Its Role in Hypoxia-Associated Sorafenib Resistance in Hepatocellular Carcinoma.

Long noncoding RNAs (lncRNAs) are emerging as critical regulators of tumor initiation and progression through transcriptional and posttranscriptional mechanisms. UPK1A antisense RNA 1 (UPK1A-AS1), a cancer-associated lncRNA, has been reported to participate in oncogenic processes; however, its overall landscape across human malignancies and its biological role in therapy resistance remain poorly understood. Given the increasing importance of identifying functional lncRNAs with prognostic and therapeutic potential, this study presents a comprehensive multiomics characterization of UPK1A-AS1 and its experimental validation in hepatocellular carcinoma (HCC). We integrated datasets from The Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression Project (GTEx), the cancer immunology data engine (CIDE), and the cBioPortal for cancer genomics (cBioPortal) to systematically assess its expression pattern, genomic alterations, clinical significance, and immunological associations. Our analyses revealed that UPK1A-AS1 is significantly upregulated in multiple tumor types, with copy-number amplification as the predominant genomic alteration driving its overexpression. Elevated UPK1A-AS1 expression was correlated with advanced disease stage, poor differentiation, immune exclusion, and unfavorable prognosis, supporting its potential as a cancer type-dependent biomarker. In parallel, functional studies demonstrated that hypoxia transcriptionally induces UPK1A-AS1 in HCC, where it promotes sorafenib resistance by suppressing apoptosis. Silencing UPK1A-AS1 restored apoptotic and enhanced sorafenib efficacy both in vitro and in vivo. Collectively, our findings suggest that UPK1A-AS1 is a hypoxia-inducible oncogenic lncRNA that plays dual roles in cancer, with cancer type-dependent associations with progression and immune modulation across malignancies and mechanistically mediating hypoxia-associated drug resistance in HCC.

Humans↗

PubMed2025

Ventricular-arterial coupling is preserved in prematurely born 11-year-old children but calls for life-long prevention of hemodynamic deterioration.

BACKGROUND: Premature birth disrupts the intra-uterine structural and functional maturation of the left ventricle (LV) and arteries. The study investigated the impact of premature birth on ventricular-arterial coupling (VAC), a potential precursor of cardiovascular disease in adulthood. METHODS: This case-control study in Northern Belgium (2011-2016) included 93 extremely-low-birth-weight (ELBW) cases and 87 sex and age-matched term-born controls. Main outcomes included SBP and DBP, central arterial properties, echocardiographic structure and function, and VAC. RESULTS: Compared with controls, cases were shorter by 4.1 cm [95% confidence interval (95% CI): 1.3-7.0] and lighter by 4.1 kg (95% CI: 1.3-6.9). Cases had higher central SBP/DBP (+7.3/3.0 mmHg; 95% CI: 4.7-9.9/1.1-4.8), lower left ventricular end-diastolic and end-systolic dimensions, and 9.2 g (95% CI: 3.7-14.6) lower left ventricular mass. Left ventricular volumes and mass correlated with body size without significant between-group differences ( P  ≥ 0.12). Cardiac output was 0.38 l/min lower in cases, who also had higher arterial resistance (29.5 vs. 24.4 mmHg × min/l) and augmentation ratio (1.10 vs. 1.05). The tension-time index was 231 mmHg × ms (95% CI: 128-335) higher in cases. Ea and Ees were higher in cases (0.40 and 0.65 mmHg/ml, respectively), but VAC did not differ between groups ( P  = 0.48). CONCLUSION: Compensatory mechanisms maintain the anatomical and functional integrity of the cardiovascular system in ELBW youth, but mask their vulnerability to cardiovascular disease in adulthood and necessitate careful follow-up during adolescence.

Humans↗