Wuhan Hankou Hospital

BackgroundInhaled corticosteroids (ICS) combined with long-acting β2-agonists (LABAs) remain the cornerstone of maintenance therapy in persistent asthma. Although multiple trials have demonstrated short-term efficacy, there is a lack of comprehensive, long-term data on the impact of ICS/LABA therapy on asthma control, exacerbation frequency, and pulmonary function in real-world clinical settings. This study aims to fill this gap by evaluating the effects of ICS/LABA therapy over a 24-month period in a real-world cohort.MethodsWe conducted a retrospective cohort study involving 237 adult patients with moderate-to-severe persistent asthma treated at Wuhan Hankou Hospital between January 2021 and December 2023. Eligible participants had ≥12 months of documented ICS/LABA use. Patients were evaluated for asthma control using the Asthma Control Test (ACT), frequency of acute exacerbations requiring systemic corticosteroids, pulmonary function (FEV1 % predicted), and adverse drug reactions. Data were collected at baseline, 12 months, and 24 months.ResultsAfter 24 months, the proportion of patients achieving well-controlled asthma (ACT ≥20) increased significantly from 42.6% at baseline to 73.0% (P < 0.001). Mean FEV1 improved from 72.1 ± 10.4% to 79.8 ± 11.2% predicted (P = 0.002). The annualized exacerbation rate declined from 2.1 ± 1.0 to 0.8 ± 0.6 episodes per patient (P < 0.001). Medication adherence, defined as ≥80% refill rate, was significantly associated with greater improvements in ACT and FEV1. Reported side effects included oropharyngeal candidiasis (8.0%), dysphonia (5.1%), and tremors (3.8%), but no serious adverse events were documented.ConclusionContinuous use of inhaled corticosteroids in combination with long-acting β-agonists was associated with sustained improvements in asthma control, enhanced lung function, and a reduction in the frequency of exacerbations. These findings support the continued use of ICS/LABA therapy as an effective and safe strategy for long-term asthma management in clinical practice.

Abstract Study design: Cross-sectional study. Objectives This study aimed to investigate the mechanism by which miR-99b-5p regulates microglial polarization via targeting AKT1, and to evaluate its potential as a prognostic biomarker and therapeutic target for spinal cord injury (SCI). Setting: The study was conducted at Wuhan Hankou Hospital and Nedong District People's Hospital, China. Methods A total of 90 individuals with SCI and 70 healthy controls were enrolled. Serum levels of miR-99b-5p, inflammatory cytokines, and microglial polarization markers were quantified. Functional outcomes were assessed using the AIS, FIM, SCIM-III, and WISCI-II scales. In vitro investigations included cell transfection, LPS-induced polarization, co-culture, and dual-luciferase reporter assays. Results Serum miR-99b-5p was significantly elevated in SCI individuals (AUC = 0.872) and positively correlated with AIS grade and functional outcomes (FIM, SCIM-III, WISCI-II). The miR-99b-5p mimic selectively inhibited M1 polarization in microglia, downregulating markers such as iNOS and TNF-α, while exhibiting no significant effect on macrophages. AKT1 was identified as a direct target of miR-99b-5p, and its overexpression reversed the inhibitory effect of miR-99b-5p on microglial polarization. Furthermore, miR-99b-5p alleviated neuronal inflammation and apoptosis, as evidenced by decreased Bax and increased Bcl-2 expression, through its regulatory action on microglia. Conclusion miR-99b-5p targets AKT1 to suppress microglial M1 polarization, thereby alleviating neuroinflammation and neuronal damage in SCI. Its serum level serves as a promising prognostic biomarker and potential therapeutic target.

Acute kidney injury (AKI) involves a sudden loss of renal function and is associated with high mortality. MicroRNA (miR)-489-3p may serve as a critical molecule in AKI according to previous studies. The study aimed to explore the functional roles of miR-489-3p in AKI and underlying mechanisms. An in vitro model of sepsis-induced cell injury was established by treating human proximal tubular epithelial cells (HK-2) with lipopolysaccharide (LPS). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed to examine expression levels of kidney injury molecule-1 (KIM-1), miR-489-3p, and downstream mRNAs. After silencing miR-489-3p, receptor-interacting protein kinase 4 (RIPK4), or β-catenin signaling, HK-2 cell viability was measured using cell counting kit-8 assays. Apoptosis was assessed by TdT-mediated dUTP nick-end labeling (TUNEL) assay and flow cytometry analysis. Western blot analysis was performed to examine protein levels of apoptotic markers, RIPK4, and β-catenin. Luciferase reporter assays were conducted to explore the interaction between miR-489-3p and RIPK4. Immunofluorescence staining was performed to evaluate the distribution of β-catenin in LPS-stimulated HK-2 cells. MiR-489-3p was significantly upregulated in LPS-treated HK-2 cells. Its inhibition attenuated the pro-apoptotic effects induced by LPS, increased cell viability, and reduced KIM-1 level. MiR-489-3p directly targeted 3′ untranslated region of RIPK4 and suppressed its expression. Knockdown of RIPK4 rescued the suppressive effect of miR-489-3p inhibition on cell apoptosis. Moreover, miR-489-3p was found to inactivate the β-catenin signaling by reducing RIPK4 expression. IWR-1 treatment similarly rescued the suppressive effect of miR-489-3p inhibition on cell apoptosis. In conclusion, miR-489-3p promotes LPS-induced HK-2 cell damage by targeting RIPK4 and inactivating β-catenin signaling.

NMDA receptors (NMDARs) are widely distributed throughout the central nervous system (CNS) and play pivotal roles in normal physiological processes such as synaptic plasticity, learning, and memory. Substantial evidence indicates that NMDAR dysfunction, particularly excessive calcium influx, critically contributes to the pathogenesis of major neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS). Dysregulated glutamatergic signaling synergizes with pathological protein aggregation (e.g., Aβ, α-synuclein, mutant huntingtin) to drive neuronal loss. We systematically delineate NMDAR-related mechanisms underlying neurodegeneration, highlighting spatial-specific roles (e.g., synaptic NMDAR-mediated neuroprotection versus extrasynaptic NMDAR-mediated excitotoxicity) and crosstalk with mitochondrial dysfunction and oxidative stress. We critically evaluate current therapeutic strategies targeting NMDARs, including subunit-selective modulators, downstream effector modulation, and glutamate transporter modulation designed to restore NMDAR homeostasis. Consequently, NMDARs and their modulators represent promising therapeutic targets for these refractory conditions. This review comprehensively summarizes current research on the involvement of NMDARs and the glutamatergic system in neurodegenerative diseases. Furthermore, we discuss the clinical application of NMDAR-targeting agents and explore emerging therapeutic strategies focused on modulating NMDAR-related pathways. This article aims to provide a reference for elucidating the molecular mechanisms underlying these neurodegenerative disorders and to highlight potential avenues for future drug development.

ABSTRACTThe rising prevalence of metabolic dysfunction—associated steatotic liver disease (MASLD) demands a better understanding of its risk factors. This study aimed to explore the relationship between the hemoglobin to high density lipoprotein‐cholesterol ratio (HHR) and MASLD. Data from 3121 participants sourced from the National Health and Nutrition Examination Survey (NHANES) were analyzed. Weighted logistic regression models were constructed to evaluate the associations between HHR and MASLD. Subgroup analyses were conducted to probe potential heterogeneity, and sensitivity analyses, through redefining the CAP cut‐off for hepatic steatosis, were employed to affirm the robustness of the observed associations. Increased HHR was independently associated with a higher risk of MASLD. Notably, this association was pronounced among smokers. While a preliminary positive correlation between HHR and liver fibrosis in MASLD patients was noted, it dissipated upon full adjustment. Sensitivity analysis confirmed the stability of the association between HHR and MASLD. Our study reveals a significant positive correlation between HHR and MASLD, with smoking status emerging as a modulatory factor.

To investigate the levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) in patients with advanced lung cancer complicated by pulmonary infection during chemotherapy and their effects on the type of pathogenic bacteria. We retrospectively analyzed the clinical data of 196 patients from Wuhan Hankou Hospital (January 2021-June 2024). The incidence of pulmonary infection was assessed, and the levels of IL-6 and IL-8 were compared across different infection severities and pathogenic bacteria types. Spearman correlation analysis was used to determine associations, and logistic regression was performed to identify factors influencing different pathogenic bacteria infections. The lung infection rate was 24.49% (48/196). Pathogenic bacteria included 36 strains (64.29%) of Gram-negative bacteria (G-) and 20 strains (35.71%) of Gram-positive bacteria (G+). The levels of IL-6 and IL-8 were significantly higher in infected patients than in uninfected patients (P < 0.05). These levels increased with the severity of infection and were positively correlated with the degree of infection. Elevated IL-6 and IL-8 levels were identified as independent risk factors for Gram-negative bacterial (G-) infections in patients with pulmonary infection. The combined AUC, sensitivity, and specificity of IL-6 and IL-8 were 0.925, 81.80%, and 93.33%, respectively. In patients with advanced-stage lung cancer undergoing chemotherapy, elevated IL-6 and IL-8 levels were closely associated with pulmonary infection severity. Detection of these cytokines may help differentiate the types of pathogenic bacteria causing lung infections.

To identify the clinical and physiological factors associated with successful weaning from mechanical ventilation (MV) in patients with acute respiratory failure (ARF) treated in the Emergency department, and to evaluate their short-term prognosis. This retrospective study analyzed data from 248 ARF patients who underwent MV in the Emergency department from July 2021 to June 2024. Patients were categorized into weaning success and failure groups based on their ability to maintain spontaneous breathing for over 48 hours post-extubation. Collected variables included demographic characteristics, body mass index, MV duration, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, blood gas parameters, and diaphragm function metrics. Multivariate logistic regression was used to identify independent predictors of weaning success. Among the 248 patients, 165 (66.5%) were successfully weaned. Independent predictors of successful weaning included shorter MV duration, lower APACHE II scores, higher tidal volumes, and lower respiratory rates during spontaneous breathing trials. Diaphragmatic excursion was negatively associated with weaning failure, as was arterial oxygen partial pressure (PaO2). Patients in the failure group had longer hospital stays and higher rates of complications, invasive interventions, and readmissions (all P<0.05). Weaning success in ARF patients managed in the Emergency department is influenced by a combination of clinical severity, ventilatory parameters, and diaphragm function. Recognition of these factors may aid in optimizing weaning strategies and improving patient prognosis.