The Sixth People's Hospital of Shenyang

ObjectiveThis study examined the correlation between changes in peripheral blood neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) before and after treatment, and Exacerbations of Chronic Pulmonary Disease Tool - Patient Reported Outcome (EXACT-PRO) scores in patients with acute exacerbations of COPD (AECOPD), to assess the clinical utility of EXACT-PRO in measuring disease severity.MethodsHospitalized patients diagnosed with AECOPD underwent pulmonary function testing, and peripheral blood NLR and PLR levels were recorded before and after treatment. Participants completed the EXACT-PRO, COPD Assessment Test (CAT), and modified Medical Research Council (mMRC) Dyspnea Scale questionnaires. Patients with AECOPD were classified into mild, moderate, and severe groups according to the 2026 GOLD classification criteria. Baseline characteristics were compared across the three groups. Pearson’s correlation analysis was performed to evaluate the relationship between changes in NLR, PLR, and EXACT-PRO scores. ROC curves of post-treatment NLR and EXACT-PRO scores were further constructed to evaluate the discriminative performance of NLR, and a scatter plot was used to visually illustrate the correlation between the two variables.ResultsAfter applying the exclusion criteria to the initial cohort of 112 patients, a total of 60 patients with AECOPD were ultimately included in the analysis. According to the 2026 GOLD classification criteria, 13 patients were classified as mild, 29 as moderate, and 18 as severe. Blood samples were collected within 24 hours of hospital admission before treatment and on the day of discharge after treatment. Post-treatment NLR levels showed a statistically significant reduction compared to pre-treatment levels (p < 0.05, 95% CI: 1.12–5.60). A positive correlation was observed between post-treatment NLR levels and EXACT-PRO scores.ConclusionPeripheral blood NLR levels demonstrated potential clinical relevance in patients with AECOPD and may support the development of a simple and effective quantitative tool for assessing disease severity.

The circadian rhythm syndrome (CircS) is closely linked to metabolism; however, its association with nonalcoholic fatty liver disease (NAFLD) and liver fibrosis remains inadequately explored. This study aims to explore the association of CircS with NAFLD and liver fibrosis. A cross-sectional analysis was performed using data from the National Health and Nutrition Examination Survey, and 3 multivariable logistic regression models were constructed to examine the association of CircS with NAFLD and liver fibrosis. Additionally, subgroup and interaction analyses were conducted to identify potential influencing factors. The study enrolled a total of 2597 participants. In models adjusted for all covariates, the odds ratios (OR) of CircS for NAFLD and liver fibrosis were (OR = 4.85, 95% CI: 3.99–5.89) and (OR = 1.73, 95% CI: 1.29–2.34), respectively. Subgroup and interaction analyses revealed a stronger positive association of CircS with NAFLD and liver fibrosis in younger age groups (<60 years) (P = .049, P = .004). Furthermore, CircS participants with diabetes showed a stronger positive correlation with NAFLD (P = .002). This indicates that in U.S. adults, CircS is significantly associated with the prevalence of both NAFLD and liver fibrosis. The association between CircS and NAFLD is stronger in individuals under 60 years of age and those with diabetes, while the association of CircS with liver fibrosis is more pronounced in individuals under 60 years of age.

ABSTRACT Aims The tolerance of patients with compensated hepatitis B cirrhosis to interferon (IFN) therapy remains controversial. Therefore, this study aimed to evaluate the safety of pegylated interferon‐alpha in chronic hepatitis B (CHB) patients with compensatory cirrhosis. Methods Data from two prospective cohorts (the OASIS Project and CHESS 2306) from January 2018 to January 2024 were synthesized and analyzed. Patients with Child‐Pugh Class A hepatitis B cirrhosis who received IFN‐based therapy ( n = 920) were included. The control groups included patients with compensated hepatitis B receiving nucleos(t)ide analog (Nuc) monotherapy ( n = 714) and patients without cirrhosis receiving IFN‐based therapy ( n = 4111), respectively. Propensity score matching was used to control for confounding factors; 566 versus 566 cases were analyzed among patients with cirrhosis treated with IFN‐based therapy or Nuc monotherapy, and 785 versus 785 cases were analyzed among patients with and without cirrhosis treated with IFN‐based therapy. Primary outcomes included decompensation events, and secondary outcomes included severe adverse events, overall adverse events, and treatment‐related hospitalizations or deaths. Results In patients with hepatitis B virus‐related cirrhosis, the incidence of decompensation events was similar between IFN‐based therapy and Nuc monotherapy (6/566 [1.1%] vs. 3/566 [0.5%], p = 0.506). No hospitalizations or deaths were associated with adverse events during the observation period (48 weeks). The incidences of severe adverse events were similar in patients with cirrhosis under IFN‐based therapy or Nuc monotherapy (severe neutropenia: 1/450 [0.2%] vs. 0/378 [0], p = 0.999; severe thrombocytopenia: 4/435 [0.9%] vs. 0/296 [0], p = 0.153; severe alanine aminotransferase level elevation: 1/523 [0.2%] vs. 1/458 [0.2%], p = 0.999; and severe total bilirubin [TBIL] level elevation: 5/419 [1.2%] vs. 3/385 [0.8%], p = 0.727). The incidences of severe adverse events were similar between patients with and without cirrhosis receiving IFN‐based therapy, except that severe TBIL level elevation was more frequent in patients with cirrhosis who already had mildly to moderately elevated TBIL levels at baseline than in those without (6/153 [3.9%] vs. 0/118 [0], p = 0.040). Conclusion IFN‐based therapy demonstrates favorable safety in Child‐Pugh A compensated cirrhosis. It did not increase decompensation events or severe adverse events compared to Nuc monotherapy, and adverse event profiles were largely similar between cirrhotic and non‐cirrhotic patients, except for a higher risk of severe hyperbilirubinemia in those with pre‐existing TBIL elevation. ClinicalTrials.gov identifier: NCT04896255. Chinese Clinical Trial Registry number: ChiCTR2500107592.

Metabolic dysfunction-associated steatotic liver disease (MASLD) with clinically significant fibrosis substantially elevates the risk of liver-related complications and mortality. The American Diabetes Association consensus report specifically recommends systematic risk stratification for MASLD and hepatic fibrosis in patients with type 2 diabetes mellitus (T2DM), with particular emphasis on those presenting with obesity. This multicenter study demonstrates that obese patients with T2DM exhibit a substantially elevated prevalence of MASLD with clinically significant fibrosis compared to their non-obese counterparts (26.7% vs. 8.4%). Furthermore, the prevalence escalates progressively with the accumulation of cardiometabolic risk factors, highlighting the synergistic impact of multiple metabolic abnormalities on hepatic fibrosis development. Our findings underscore the critical need for routine screening and integrated management of MASLD with clinically significant fibrosis in patients with T2DM, particularly those presenting with obesity and multiple cardiometabolic risk factors.

ObjectiveTo investigate the dynamic relationship and interaction between symptom burden and exercise adherence in olderly patients with Chronic obstructive pulmonary disease (COPD) undergoing remote pulmonary rehabilitation, and to establish a foundation for enhancing remote rehabilitation interventions.MethodsA total of 340 olderly patients with COPD, admitted to the Respiratory Center of Nantong Sixth People’s Hospital between May 2023 and February 2025, were selected using a convenience sampling method. The Symptom Burden Scale (SSS-8) and Exercise Adherence Scale were employed to assess symptom burden and exercise adherence levels at baseline (T1), 5 weeks (T2), 9 weeks (T3), and 12 weeks (T4). A cross-lag model was constructed to analyze the causal relationship between these variables.ResultsSymptom burden exhibited a decreasing trend at each stage (F = 36.74, p < 0.001). Exercise compliance demonstrated a gradual increase (F = 38.92, p < 0.001). The cross-lag model indicated that symptom burden and exercise compliance in the early stage (T1-T2) were mutually causal (β = −0.32, p = 0.002; β = −0.24, p = 0.011). Symptom burden in the middle stage (T2-T3) significantly negatively predicted exercise compliance (β = −0.39, p < 0.001). No significant predictive relationship was found between them in the late stage (T3-T4; p > 0.05).ConclusionThe symptom burden of olderly patients with COPD during remote pulmonary rehabilitation is moderate to severe, while exercise compliance is at a moderate level. The dynamic relationship between symptoms and behavior shifts from a bidirectional effect in the early stage to symptom dominance in the middle stage, with no influence in the later stage. It is essential to implement precise interventions tailored to the characteristics of the three-stage trajectory, addressing both symptoms and behavioral obstacles in the early stage, focusing on symptom management in the middle stage, and reinforcing behavioral habits in the later stage.

Diagnosing tuberculous pleural effusion (TPE) is challenging. There is a lack of cross-sectional lateral comparisons among TPE prediction models. We aimed to develop and validate a novel TPE prediction model and compare its diagnostic performance with that of existing models. Patients with pleural effusion were included in the training, testing, and external validation sets. Variable selection strategies included LASSO and logistic regression. The discriminability, calibration, and clinical efficacy of the prediction model were estimated in the three sets. The performance of the model was compared with that of two existing prediction models. Fever, tuberculosis interferon-gamma release assays, pleural adenosine deaminase, the pleural mononuclear cell ratio, the ratio of pleural lactate dehydrogenase to pleural adenosine deaminase, pleural carcinoembryonic antigen, and pleural cytokeratin 19 fragment were selected to establish the prediction model. The AUCs were 0.931 (0.903-0.958), 0.856 (0.753-0.959), and 0.925 (0.867-0.984) in the training, testing, and external validation sets, respectively. The AUCs of the two existing prediction models were 0.793 (0.737-0.850) and 0.854 (0.816-0.892). The calibration curves revealed that this model had good consistency. Decision curve analysis revealed the acceptable clinical benefit of this model. Compared with the existing models, the TPE prediction model developed in this study demonstrated good diagnostic performance.

ABSTRACT Objective Previous studies show DEX protects against focal cerebral ischemia by hindering autophagy. However, the exact mechanisms are unclear. This study hypothesizes DEX may protect neurons by regulating the crosstalk between autophagy and ferroptosis. Methods In this study, male C57/BL6 mice were used in an MCAO model divided into five groups. After MCAO and reperfusion, treatments with DEX, DEX+Erastin, or DEX+rapamycin were administered. Neurological deficits and cerebral infarction volumes were measured 24 hours later. Electron microscopy and molecular techniques were used to analyze autophagy and ferroptosis markers to explore DEX’s neuroprotective mechanism. Results Compared to sham controls, the model group showed significantly increased cerebral infarction volume and neurobehavioral scores (p < 0.05). DEX treatment reversed these effects, demonstrating neuroprotection against ischemic injury. Simultaneously, DEX treatment safeguards mitochondrial integrity by suppressing autophagy lysosomes. It also upregulates the expression of glutathione (GSH) protein, solute carrier family 7 member 11 (SLC7A11) protein, and glutathione peroxidase 4 (GPX4). Moreover, DEX inhibits the levels of malondialdehyde (MDA), ferrous ion (Fe2+), microtubule-associated protein 1A/1B-light chain 3 (LC3), and Beclin1 proteins (all p values < 0.05), thereby intervening in the crosstalk between the autophagy and ferroptosis pathways and ultimately exerting its neuroprotective function. Notably, DEX’s effects were negated by ferroptosis inducer Erastin or autophagy inducer RAPA. Conclusion Dexmedetomidine modulates the crosstalk between autophagy and ferroptosis pathways, thereby protecting the mouse brain against ischemia-reperfusion injury and providing novel insights for the future treatment of ischemic stroke.