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Glomerular hypertension is an important factor exacerbating glomerular diseases to end-stage renal diseases because, ultimately, it results in glomerular sclerosis (especially in hypertensive and diabetic nephropathy). The precise mechanism of glomerular sclerosis caused by glomerular hypertension is unclear, due partly to the absence of suitable in vitro or in vivo models capable of mimicking and regulating the complex mechanical forces and/or organ-level disease processes. We developed a “glomerulus-on-a-chip” (GC) microfluidic device. This device reconstitutes the glomerulus with organ-level glomerular functions to create a disease model-on-a chip that mimics hypertensive nephropathy in humans. It comprises two channels lined by closely opposed layers of glomerular endothelial cells and podocytes that experience fluid flow of physiological conditions to mimic the glomerular microenvironment in vivo . Our results revealed that glomerular mechanical forces have a crucial role in cellular cytoskeletal rearrangement as well as the damage to cells and their junctions that leads to increased glomerular leakage observed in hypertensive nephropathy. Results also showed that the GC could readily and flexibly meet the demands of a renal-disease model. The GC could provide drug screening and toxicology testing and create potential new personalized and accurate therapeutic platforms for glomerular disease.

To investigate the relationships between LncRNA NNT-AS1, CRP, PCT and their interactions and the refractory mycoplasma pneumoniae pneumonia (RMPP) in children. Serum levels of LncRNA NNT-AS1 of RMPP and non-RMPP (NRMPP) patients were detected by real-time PCR, and were analyzed together with serum c-reactive protein (CRP) and procalcitonin (PCT). Correlations between LncRNA NNT-AS1 and CRP and PCT were analyzed by Pearson correlation test. The ROC curve was used to analyze the potential of LncRNA NNT-AS1, CRP and PCT as biomarkers for predicting RMPP. Logistic regression crossover model and the Excel compiled by Andersson et al. were used to analyze the interactions among the biomarkers. We found that LncRNA NNT-AS1, CRP and PCT were all highly expressed in patients with RMPP. LncRNA NNT-AS1 could positively correlate with the expressions of CRP and PCT, and jointly promote the occurrence of RMPP. The combined diagnosis of LncRNA NNT-AS1, CRP and PCT could predict the occurrence of RMPP.

This study included patients with thyroid eye disease (n = 81) and Graves’ disease (n = 165) for a cross-sectional study. Then, peripheral blood mononuclear cells (PBMCs) were collected from patients with thyroid eye disease (n = 5), Graves’ disease (n = 15), and normal individuals (n = 5) for RNA-seq. WGCNA analysis was conducted on the RNA-seq results to identify genes related to thyroid eye disease, and these genes were verified by RT-qPCR. The results suggest that: (1) Neutrophil counts were elevated in the TED group compared to the GD group. (2) Ten hub genes, MMP9, BPI, CD177, MPO, CEACAM8, CEACAM1, SLPI, AZU1, KCNJ15 and TNFRSF10C, were identified. The above hub genes were positively correlated with neutrophils.

Background Activation of pericytes leads to renal interstitial fibrosis, but the regulatory mechanism of pericytes in the progression from AKI to CKD remains poorly understood. CD36 activation plays a role in the progression of CKD. However, the significance of CD36 during AKI-CKD, especially in pericyte, remains to be fully defined. Methods GEO and DISCO database were used to analyze the expression of CD36 in pericyte during AKI-CKD; IRI to conduct AKI-CKD mouse model; Hypoxia/Reoxygenation (H/R) to induce the cell model; RT-qPCR and Western blotting to detect gene expression; IP and confocal-IF to determine the core fucosylation (CF) level of CD36. Flow cytometry (AV/PI staining) to detect the cell apoptosis and JC-1 staining to react to the change of mitochondrial membrane potential. Results During AKI to CKD progression, CD36 expression in pericytes is higher and may be influenced by CF. Moreover, we confirmed the positive association of CD36 expression with pericyte-myofibroblast transition and the progression of AKI-CKD in an IRI mouse model and hypoxia/reoxygenation (H/R) pericytes. Notably, we discovered that FUT8 upregulates both CD36 expression and its CF level, contributing to the activation of the mitochondrial-dependent apoptosis signaling pathway in pericytes, ultimately leading to the progression of AKI-CKD. Conclusion These results further identify FUT8 and CD36 as potential targets for the treatment in the progression of AKI-CKD.

Under long-standing threat of seasonal influenza outbreaks, it remains imperative to understand the drivers of influenza dynamics which can guide mitigation measures. While the role of absolute humidity and temperature is extensively studied, the possibility of ambient ozone (O 3 ) as an environmental driver of influenza has received scant attention. Here, using state-level data in the USA during 2010–2015, we examined such research hypothesis. For rigorous causal inference by evidence triangulation, we applied 3 distinct methods for data analysis: Convergent Cross Mapping from state-space reconstruction theory, Peter-Clark-momentary-conditional-independence plus as graphical modeling algorithms, and regression-based Generalised Linear Model. The negative impact of ambient O 3 on influenza activity at 1-week lag is consistently demonstrated by those 3 methods. With O 3 commonly known as air pollutant, the novel findings here on the inhibition effect of O 3 on influenza activity warrant further investigations to inform environmental management and public health protection. Temperature and absolute humidity are associated with influenza activity, and recent data from Hong Kong have suggested ozone as an additional environmental driver. Here, the authors investigate the relationship between ozone and influenza transmission using surveillance data from the USA and find evidence for an inhibitory effect.

Background Inherited genomic susceptibility and associated transcriptomic patterns are crucial players in lung cancer etiology. Lung cancer susceptibility is getting rising attention in carcinogenesis. The present study aimed to investigate unique clinical features and transcriptomic profile in patients with familial lung cancer (FLC) in Yunnan-Guizhou Plateau, Wumeng-Mountain area of China. Methods 1,823 local lung cancer patients were enrolled (762 FLC, 1061 Sporadic). Clinicopathologic parameters were analyzed and summarized. 43 lung tissue samples (the adjacent nonmalignant tissue) were selected for Transcriptome/RNA-seq, the differential gene expression patterns were analyzed, significant functions and pathways were enriched and studied. Results Our FLC cohort showed unique characters: younger age; increased rate of adenocarcinoma, and early-stage cases; unbalance in blood types, anatomic sites and co-existing diseases; highlighted with significantly elevated comorbidity and early-onset of hypertension in FLC + population. Notably, our FLC + group exhibited a higher rate of bilateral lung cancers and multiple pulmonary nodules; beside, were more likely to develop different cysts, polyps, hyperplasia at a younger age. The transcriptome found that immune-related functions & pathways were significantly enriched in the familial cohort. E.g. “immune cells recruitment” with higher Neutrophils/ lower CD4 memory T cells. Collectively, these transcriptomic differences suggested: individuals with FLC may have baseline alterations in immune regulation, which could reflect a compromised immune surveillance or dysregulated inflammatory tone in their normal lung tissue. For the key gene, MUC16 may contribute to this process by influencing the assembly, structure & dynamical functions of pulmonary epithelial cilium; which could potentially impair mucociliary clearance, leading to prolonged retention of pollutants and carcinogens in the lung microenvironment. Conclusions Hereditary factors likely contribute to the susceptibility to both lung cancer and hypertension in this population, while chronic exposure to local air pollution may further promote their early-onset and comorbidity. Our findings highlighted the potential significance of MUC16 in familial lung cancer or even early-onset lung cancer; and provided useful data for early screening and personalized treatment strategies for lung cancer.

Chronic kidney disease (CKD) and renal fibrosis remain major global health burdens, with limited options for early diagnosis and effective therapy. Conventional approaches, such as kidney biopsy and imaging, are invasive or insensitive to early-stage changes. Microfluidic technology has emerged as a transformative platform that enables precise modeling of renal microenvironments, sensitive biomarker detection, and physiologically relevant drug testing. This review evaluates recent advances in microfluidics for CKD and fibrosis, with emphasis on mechanistic insights, diagnostic innovations, and therapeutic strategies. Mechanistic studies using organ-on-a-chip systems, including glomerulus- and tubule-on-a-chip, have replicated critical pathophysiological processes such as proteinuria-induced podocyte injury, epithelial-mesenchymal transition, FAO dysregulation in tubular cells, and immune cell-mediated inflammation. These models provide superior resolution compared with 2D culture or animal models and have identified novel fibrotic pathways-how they work: by perfusing media through microchannels to simulate shear stress; advantages: dynamic real-time monitoring; disadvantages: high cost and limited throughput; limitations: often lack full multi-cellular integration; translational value: patient-specific modeling for precision nephrology. Diagnostic innovations include microfluidic biosensors for non-invasive, high-sensitivity detection of CKD biomarkers such as albumin and neutrophil gelatinase-associated lipocalin (NGAL), as well as multiplex platforms that analyze multiple analytes in urine or blood simultaneously. Wearable epidermal patches have further extended applications to continuous monitoring of electrolytes and metabolites, enhancing patient-centered management. Therapeutically, microfluidic systems support high-throughput drug screening under physiologically relevant perfusion, enabling more predictive antifibrotic testing. Microfluidic-assisted nanodelivery platforms improve drug targeting and bioavailability, while organoid-on-chip systems enhance stem cell differentiation and regenerative potential. Integration with artificial intelligence and multi-omics further refines data interpretation, biomarker discovery, and personalized therapy design. Microfluidic technologies bridge the gap between bench and bedside by enabling mechanistic discovery, sensitive biomarker detection, and translational therapeutic testing in CKD and fibrosis. Despite significant advances, challenges remain in scalability, reproducibility, and regulatory approval. Addressing these hurdles through interdisciplinary collaboration will be essential. With continued innovation, microfluidic systems hold strong promise for advancing precision nephrology and improving patient outcomes.

Complete blood count (CBC)-derived inflammatory markers are predictive biomarkers for the prognosis of many diseases. However, there was no study on patients with peritoneal dialysis-associated peritonitis (PDAP). We aimed to investigate the value of these markers in predicting treatment failure of acute peritonitis in chronic PD patients. The records of 138 peritonitis episodes were reviewed and divided into treatment success or failure groups in a single center for 10 years. CBC-derived markers and other routine data were recorded before peritonitis treatment was initiated. Univariate and multivariate regression analyses and the receiver operating characteristic (ROC) curve about the predictors of treatment outcomes were performed. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), systemic immune-inflammation index (SII), and derived NLR were significantly higher in the failure group. Univariate logistic regression results showed that NLR and PLR were risk factors of treatment outcomes. The backward stepwise multivariate logistic regression results demonstrated that NLR [adjusted odds ratio (aOR), 1.376; 95% confidence intervals (CI), 1.105-1.713; p = .004], PLR (aOR, 1.010; 95%CI, 1.004-1.017; p = .002) were risk factors, but hemoglobin-to-lymphocyte ratio (HLR) (aOR, 0.977; 95%CI, 0.963-0.991; p = .001), and SII (aOR, 0.999; 95%CI, 0.998-1.000; p = .040) were protective factors. A combination of age, PD vintage, Gram-positive peritonitis, staphylococcus aureus, culture-negative, NLR, PLR, HLR, and SII would improve prognostic performance. The area under this ROC curve was 0.85, higher than other factors. NLR, PLR, HLR, and SII were associated with PDAP outcomes. Age, PD vintage, NLR, and PLR were significant risk factors in PDAP patients.

Pericytes have been identified as a major source of myofibroblasts in renal interstitial fibrosis (RIF). The overactivation of several signaling pathways, mainly the TGF-β and PDGF pathways, initiates the pericyte-myofibroblast transition during RIF. Key receptors in these two pathways have been shown to be modified by fucosyltransferase 8 (FUT8), the enzyme that catalyzes core fucosylation. This study postulated that core fucosylation might play an important role in regulating the pericyte transition in RIF. The data showed that core fucosylation increased with the extent of RIF in patients with IgA nephropathy (IgAN). Similarly, core fucosylation of pericytes increased in both a unilateral ureteral occlusion (UUO) mouse model and an in vitro model of pericyte transition. Inhibition of core fucosylation by adenoviral-mediated FUT8 shRNA in vivo and FUT8 siRNA in vitro significantly reduced pericyte transition and RIF. In addition, the activation of both the TGF-β/Smad and PDGF/ERK pathways was blocked by core fucosylation inhibition. In conclusion, core fucosylation may regulate the pericyte transition in RIF by modifying both the TGF-β/Smad and PDGF/ERK pathways. Glycosylation might be a novel “hub” target to prevent RIF.

Background Epidemiological research on the association between heavy metals and congestive heart failure (CHF) in individuals with abnormal glucose metabolism is scarce. The study addresses this research gap by examining the link between exposure to heavy metals and the odds of CHF in a population with dysregulated glucose metabolism. Method This cross-sectional study includes 7326 patients with diabetes and prediabetes from the National Health and Nutrition Examination Survey from 2011 to 2018. The exposure variables are five environmental heavy metals—cadmium (Cd), lead (Pb), mercury (Hg), selenium (Se), and manganese (Mn)—and the endpoint is CHF, determined via face-to-face interviews. Logistic regression, weighted quantile sum (WQS), and Bayesian kernel machine learning (BKMR) models were employed to investigate the association between exposure to mixtures of five heavy metals and the odds of having CHF in individuals with diabetes and prediabetes. Result Multivariate logistic regression analysis Shows that only blood Cd exhibited a significant linear positive correlation with CHF odds (OR: 1.26, 95%CI 1.07–1.47, p = 0.005), there was a significant 14% decrease in the odds rate of CHF for each additional standard deviation of log10 Se (OR: 0.86,95%CI 0.76–0.96, P = 0.009). The WQS index for the metal mixture only marginally increased the odds of CHF by 1% (OR = 1.01, 95% CI 1.00–1.02, P = 0.032). BKMR analysis demonstrated a positive association between Cd levels and the odds of CHF, an inverse relationship with Se levels in patients with diabetes and prediabetes. However, no significant association was observed between the metal mixture and CHF. Conclusion This cross-sectional study demonstrates that increased Cd levels are associated with a higher odds of CHF in patients with diabetes and pre-diabetes, whereas elevated blood Se levels significantly mitigate this odds.