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Background: Iron deficiency is prevalent in patients with chronic kidney disease (CKD), even in those without anemia. However, the effects of iron deficiency on CKD progression and all-cause mortality in non-dialysis-dependent CKD (NDD-CKD) patients without anemia remain incompletely understood. Methods: This multicenter retrospective nationwide cohort study included adult patients with non-anemia NDD-CKD from 24 hospitals across China. The study investigated the associations between serum ferritin or transferrin saturation (TSAT) levels and the risks of CKD progression and all-cause mortality. Results: Among 18,878 patients with NDD-CKD, 9,989 patients were included in the kidney outcome analysis, and 18,481 patients in the all-cause mortality analysis. Of the patients with the measurement, 2,450 (27.2%) had ferritin levels ≤ 100ng/mL and 2,440 (13.1%) had a TSAT level ≤ 20%. Compared with patients with TSAT level of > 20%, those with TSAT level of ≤ 20% had significantly higher risks of CKD progression (adjusted hazard ratio [aHR]: 1.66, 95% confidence intervals [CI]: 1.16–2.37; P = 0.005) and all-cause mortality (aHR: 2.21, 95% CI: 1.36–3.57; P = 0.001). The robustness of results was supported by subgroup analyses. However, there was no significant association found between ferritin levels and the risk of CKD progression or all-cause mortality (P > 0.05). Conclusion: Iron deficiency was prevalent in NDD-CKD patients without anemia, and TSAT could be a modifiable risk factor of CKD progression and all-cause mortality. The screening of iron biomarkers, especially TSAT, in the early stage of NDD-CKD is important to assess and improve prognosis. [ABSTRACT FROM AUTHOR]

Background: The effects of acute kidney injury (AKI) on liver-related outcomes in patients with hepatitis B virus (HBV) infection remain unclear. The study aimed to evaluate the association between AKI with liver-related mortality and complications in patients with HBV infection. Methods: The multicenter, retrospective cohort study included Chinese adults with HBV infection from 24 regional central hospitals between January 2000 and December 2022. AKI was defined as a ≥ 26.5 μmol/l increase in serum creatinine concentration within 48 h, or a ≥ 50% increase over the baseline within 7 days. The primary outcome was post-discharge liver-related mortality, while the secondary outcome was a composite of new-onset liver cirrhosis and hepatocellular carcinoma. Cox proportional hazard model was employed for analyses. Results: Of the 86,204 inpatients with HBV infection and without liver cancer or cirrhosis at baseline, 4407(5.1%) patients experienced AKI. During a mean follow-up of 4.6 ± 2.4 years, 334 (0.4%) patients died of liver-related events. After adjustment, AKI during hospitalization was significantly associated with a higher risk of liver-related mortality after discharge (adjusted hazard ratio (HR), 1.78; 95% confidence intervals (CI), 1.26–2.51, P = 0.001), especially in those with severe AKI. Similarly, AKI was associated with a higher risk of cirrhosis or new-onset hepatocellular carcinoma (adjusted HR, 1.33; 95%CI, 1.10–1.60, P = 0.004). The association between AKI and liver-related outcomes remained consistent across different subgroups. Conclusions: AKI during hospitalization was associated with substantial increased risk of liver-related mortality and incident liver-related complication. Our findings highlight the importance of monitoring AKI in patients with HBV infection for tailoring personalized treatments. [ABSTRACT FROM AUTHOR]

Inflammation is a complex factor in the pathogenesis of intracranial aneurysms (IA), but its specific cellular inflammatory factors remain uncertain. We collected two cohorts and measured the representation of vascular inflammation-related proteins using the Olink CVD II Vascular Inflammation Panel. We subsequently validated our findings using ELISA and RT-qPCR. Our proteomic analysis identified 11 vascular inflammation-related markers that were significantly differentially represented between the IA and control groups. These markers were implicated in leukocyte migration, immune response, triglyceride and lipoprotein metabolism, acute phase response, T cell regulation, and several key biological pathways, including PPAR, HIF-1, cytokine-cytokine interactions, and PI3K-AKT signaling. Further validation with ELISA and RT-qPCR confirmed the differential representation of IL6, PTX3, LPL, and OLR1 between the two groups. Notably, a combination marker incorporating these four factors demonstrated high diagnostic potential for the early detection of IA. Our study has identified a set of informative biomarkers (IL6, PTX3, LPL, and OLR1) that could be valuable for the early diagnosis of IA. Importantly, this is the first report of significantly elevated OLR1 representation in the plasma of IA patients. Further investigation into the role of OLR1 in the pathogenesis of IA is warranted. SIGNIFICANCE: This study significantly advances our understanding of the molecular mechanisms underlying intracranial aneurysm (IA) pathogenesis. By identifying a panel of novel biomarkers, including the previously unreported elevated expression of OLR1 in IA patients, we provide crucial insights into the inflammatory processes involved in aneurysm formation and development. These findings have important clinical implications, as the identified biomarkers could serve as valuable tools for early diagnosis and potentially targeted therapeutic interventions. Furthermore, the study highlights the complex interplay of inflammatory pathways in IA, suggesting that a multi-faceted approach may be necessary for effective management., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2025 Elsevier B.V. All rights reserved.)

Despite the worldwide prevalence of Parkinson's disease (PD), there are currently no effective methods for treating or preventing α-synucleinopathy. Research has demonstrated that small molecules are capable of preventing α-synuclein aggregation and the associated neurotoxicity. Nonetheless, the specific anti-amyloid mechanism of these compounds is not thoroughly comprehended in detail. In this study, the interaction between glycitein and α-synuclein was evaluated. Furthermore, the aggregation of α-synuclein in the presence of glycitein was examined utilizing several arrays. Thermodynamic results indicated that glycitein, an O-methylated isoflavone, binds to α-synuclein by creating a static complex, wherein non-covalent interactions, especially hydrophobic forces, served as the primary intermolecular forces stabilizing the complex. We further found that glycitein serves as a promising bioactive agent against α-synuclein amyloid fibrillation in a concentration-dependent fashion, modulating the formation of hydrophobic regions, the solution's surface tension, and the shift from natural random coil to β-sheet configurations, in addition to potential interactions with α-synuclein monomers and amyloid fibril formations. Moreover, we noted that glycitein prevents the neurotoxicity caused by α-synuclein aggregates by shielding PC12 cells from ROS production and caspase-3 activation. These results emphasize the significance of using bioactive small compounds for the prevention and treatment of PD., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)