Aviation General Hospital

ABSTRACTDepression is a common comorbidity in CKD patients. The purpose of this study was to define the age‐specific association between the dietary inflammatory index (DII) and depression among patients with chronic kidney disease (CKD). Data in this cross‐sectional study were collected from the 2005–2018 National Health and Nutritional Examination Survey (NHANES). Weighted multivariable logistic regression models were conducted to assess the relationship between DII and depression in CKD patients across different age groups. A mediation analysis was constructed to clarify the mediating role of inflammation and renal function. A total of 5501 CKD patients were enrolled in this study. A significant association between DII and depression was demonstrated in patients with CKD aged ≤ 70 years, and a linear correlation was uncovered (p for nonlinear > 0.05). However, no significant effect was present in patients aged > 70 years. Additionally, residual renal function slightly mediated the role of DII on depression in CKD patients. DII was associated with depressive disorder in CKD patients partially through renal function. Younger CKD patients were more affected, and targeting age‐specific anti‐inflammatory diets could be an intervention strategy to prevent depression in patients with CKD.

Uromodulin, also called Tamm-Horsfall protein, is a kidney-specific glycoprotein primarily synthesized in the thick ascending limb of Henle’s loop. This review summarizes recent advances in its multifaceted physiological roles across urinary, interstitial, and circulatory compartments. In urine, It inhibits urinary tract infections and prevents renal stones by modulating calcium/magnesium reabsorption via ion channels. In the interstitium, preclinically and observationally, uromodulin regulates water-salt balance via the sodium-potassium-2-chloride cotransporter 2/sodium-chloride cotransporter (NKCC2/NCC) phosphorylation, influences blood pressure, and exerts dual immunomodulatory effects. Serum uromodulin (sUMOD) exhibits systemic antioxidant activity (preclinical models) and mitigates vascular calcification (in vitro/animal studies), with associations to multiple disease outcomes—suggesting biomarker potential. Despite progress, unresolved questions remain regarding uromodulin’s secretory regulation, post-translational modifications, and therapeutic potential. Key future research priorities are standardizing its detection methods (addressing assay heterogeneity) and clarifying its role in chronic kidney disease (CKD), acute kidney injury (AKI), and cardiovascular diseases. This review comprehensively synthesizes literature to clarify these aspects, emphasizing its physiological roles and observational clinical associations to guide potential clinical translation. Clinical trial number Not applicable.

Endometrial cancer (EC) is a common gynecologic malignancy with high morbidity and mortality. Kinesin Family member 22 (KIF22) is regarded as a critical oncogene, but its functions in EC progression remained elusive. Hence, this research elucidated the role of KIF22 in EC development and studied the possible mechanism. KIF22 expression in EC and the relationship with the overall survival of EC cases were determined by GEPIA and online K-M plotter. After transfection with sh-KIF22, cell viability and invasion were evaluated utilizing CCK-8 and Transwell assays. The content of IFN-γ, IL-2, and TNF-α was assessed utilizing an ELISA assay. The protein levels of p-STAT3, STAT3, and PD-L1 were examined using western blot. A xenograft tumor was constructed to assess tumor growth. KIF22 was elevated in EC, with high KIF22 levels presenting poor overall survival. Additionally, silenced KIF22 restrained EC cell viability, invasion ability, and STAT3/PD-L1 pathway, enhanced the viability of CD8+ T cells, and elevated the levels of IFN-γ, IL-2, and TNF-α. Moreover, the rescue assay revealed that STAT3 overexpression counteracted the inhibitory effect of silenced KIF22 on EC cell proliferation, invasion and immune escape. Furthermore, silenced KIF22 repressed EC tumor growth and p-STAT3 and PD-L1 levels, and elevated the IFN-γ level in vivo. The findings demonstrated that KIF22 was elevated in EC and correlated with a poor prognosis. Silenced KIF22 repressed cell proliferation, invasion, and immune escape via suppressing the STAT3/PD-L1 pathway in EC.

ObjectiveHealthcare workers (HCWs) are at potential risk of Helicobacter pylori (H. pylori) infection due to occupational exposure, yet epidemiological data in this population remain scarce. This study aimed to investigate the prevalence, risk factors, eradication efficacy and antibiotic resistance patterns of H. pylori infection among HCWs.DesignRetrospective cohort study.SettingA tertiary hospital in Beijing, China.Participants725 HCWs who underwent H. pylori testing via urea breath test between January 2020 and December 2023.Primary and secondary outcome measuresDemographic characteristics, lifestyle factors, symptomatic presentations, treatment regimens and antibiotic resistance profiles were extracted from electronic medical records. Univariate analyses using χ² tests identified associations between variables, followed by multivariate logistic regression to adjust for confounders and determine independent predictors of H. pylori eradication failure.ResultsThe overall H. pylori positivity rate was 22.9% (166/725). Male gender (OR=1.76, 95% CI 1.20 to 2.59) and alcohol consumption (OR=2.40, 95% CI 1.26 to 4.58) were identified as independent risk factors. Notably, H. pylori-positive individuals had a lower incidence of acid reflux symptoms (9.1% vs 17.3%, p=0.011). The eradication rate was 92.0% (95% CI 84.3% to 96.7%), but clarithromycin resistance reached 47.1% (95% CI 36.4% to 58.0%), with 12.8% (95% CI 6.6% to 21.5%) showing dual resistance to clarithromycin and quinolones.ConclusionsTargeted screening for male HCWs and alcohol users, along with bismuth-containing quadruple therapy, is recommended. High clarithromycin resistance underscores the need for local antibiotic stewardship.

BackgroundThe world has witnessed a steady rise in neurological diseases, which represent a heterogeneous group of disorders characterized by complex pathogenesis involving disruptions at multiple molecular levels, including genomic, transcriptomic, proteomic, and metabolomic levels. These disorders, often caused by genetic mutations, metabolic imbalances, immune dysregulation, and environmental factors, pose significant challenges to global public health due to their high prevalence, mortality, and disability burden.ResultsThe advent of high-throughput technologies, such as next-generation sequencing and mass spectrometry, has provided valuable insights into the underlying mechanisms of disease, especially the development of multi- and high-spatial-resolution omics technologies, enabling the interaction of multiple levels of biology and analysis of the complex molecular networks and pathophysiological processes.ConclusionsThis review provides a comprehensive analysis of the latest advancements in multi- and high-spatial-resolution omics, with a focus on their applications in precision diagnostics, biomarker discovery, and therapeutic target identification in brain diseases. The study also highlights the current challenges in the clinical implementation and discusses the future directions, with artificial intelligence being anticipated to enhance clinical translation and diagnostic accuracy significantly.

The treatment methods for patients with localized low-risk prostate cancer whose life expectancy is > 10 years mainly include radical prostatectomy, radiotherapy, active surveillance (AS), and focal therapy of low-risk prostate cancer. Research shows that only 3% of patients with low-risk prostate cancer experience disease progression or death, which indicates that there is overtreatment. The number of patients who choose active monitoring is increasing, but in the process of treatment, they often suffer great psychological pressure. Therefore, we are trying to adopt a more active treatment mode than active surveillance-Super Active Surveillance (Super-AS). Super-AS involves the application of 18F-PSMA PET/MR multimodal medical imaging, combined with real-time fusion of intraoperative transrectal ultrasound images, thereby enabling precise navigation for targeted argon-helium cryoablation therapy. The significance of Super-AS lies in its ability to effectively manage tumors in oncology while exerting minimal impact on functionality. Even if the focal therapy fails, the subsequent radical prostatectomy makes no significant difference in the overall oncological control, functional (urinary orifice and sexual function), and postoperative complications. Therefore, precise focal therapy can be an alternative transitional treatment for patients, from active monitoring to radical treatment, and it can also be seen as a "future bridge" for the treatment of localized prostate cancer. Consequently, Super-AS is a potentially promising therapeutic option for patients who meet the indications.

ABSTRACTBackgroundMicroglia polarization and inflammatory response are closely related to cerebral ischemia–reperfusion injury (CIRI). The diterpenoid compound Jolkinolide B (JB) possesses anti‐inflammatory properties, but the effects of JB and the mechanism on CIRI remain unclear.MethodsAn middle cerebral artery occlusion/reperfusion (MCAO/R) rat model and an oxygen–glucose deprivation/reoxygenation (OGD/R)‐induced HAPI cell model were used to evaluate the neuroprotective effects and mechanisms of JB. Neurological deficits and histopathological changes were assessed using Longa scoring, corner turn tests, TTC, HE, Nissl, and TUNEL staining. ELISA, flow cytometry, Western blot, and immunofluorescence were employed to analyze pro‐inflammatory cytokines, JAK2/STAT3 pathway proteins, and microglial polarization. In vitro, JB's effects on cell viability and apoptosis were evaluated using CCK‐8 and LDH release assays. Validation experiments were conducted using the JAK2‐specific inhibitor WP1066 and activator Broussonin E.ResultsJB exhibited dose‐dependent neuroprotective effects in MCAO/R rats, improving neurological function, reducing infarction area, neuronal apoptosis, cerebral edema, and neuroinflammation. JB suppressed JAK2/STAT3 signaling by downregulating p‐JAK2, p‐STAT3, and M1 markers (iNOS, CD16) while upregulating M2 markers (Arg‐1, CD206) and reducing pro‐inflammatory cytokines (IL‐1β, TNF‐α, IFN‐γ). Both in vivo and in vitro, JB inhibited the JAK2/STAT3 signaling pathway and promoted microglial polarization from M1 to M2, alleviating CIRI. In vitro, JB enhanced HAPI cell viability, decreased apoptosis, and reduced LDH leakage.ConclusionThe ability of JB to modulate microglial polarization through JAK2/STAT3 inhibition presents a promising pharmacological approach for cerebral ischemia–reperfusion injury management in stroke therapy.

Functional tendon regeneration faces dual challenges: limited self-healing capacity and the complexity of three hierarchical interfaces-the myotendinous junction (MTJ), tendon proper, and bone-tendon junction (BTJ). Conventional repair strategies often fail to address these critical barriers, resulting in a higher probability of re-tear after the surgery. 3D bioprinting emerges as a transformative approach, enabling recapitulation of these multiscale interfaces through precise structural design, functional material gradients, and bioactive integration. This review comprehensively analyzes recent advances in bioprinted tendon scaffolds, focusing on tripartite structural-biological requirements across MTJ, tendon proper, and BTJ microenvironments. Critical examination is given to the synergistic regulation of bioprinting technologies and material diversity for replicating native mechanobiological cues. Furthermore, innovative scaffold design strategies target each interface's unique regeneration challenges: anisotropic muscle-tendon integration, load-bearing tendon remodeling, and mineralized osteotendinous regeneration. Finally, translational roadblocks and future directions are assessed, emphasizing in vivo functional reintegration of the muscle-to-bone continuum and scalable manufacturing for clinical adoption.