Objective To explore the predictive value of serum inducible nitric oxide synthase(iNOS), Kruppel-like factor 5(KLF5), and peroxiredoxin 6(Prdx6) for the failure of mechanical ventilation weaning in patients with acute respiratory failure(ARF). Methods A total of 95 ARF patients admitted to the Department of Emergency Medicine at the Second Affiliated Hospital of Bengbu Medical College from January 2023 to October 2025 were selected and divided into a weaning failure group(n=31) and a weaning success group(n=64) based on whether weaning from mechanical ventilation failed. Serum levels of iNOS, KLF5, and Prdx6 were measured by ELISA. Logistic regression analysis was used to identify factors influencing weaning failure in ARF patients, and forest plots were generated using Empower Stats and the R statistical software package. Relative risk analysis was used to evaluate the risk of weaning failure at different levels of iNOS, KLF5, and Prdx6. ROC curves were used to assess the predictive value of these markers for weaning failure in ARF patients. Results Serum levels of iNOS and KLF5 in the weaning failure group were significantly higher than those in the weaning success group, while serum Prdx6 levels were significantly lower(t/P=7.319/<0.001, 7.149/<0.001, 7.180/<0.001). iNOS, KLF5, and Prdx6 were independent predictors of weaning failure from mechanical ventilation in ARF patients [OR(95%CI)=3.089(1.405-6.792), 2.571(1.362-4.852), 0.382(0.186-0.784)]. Relative risk analysis showed that patients with high expression of iNOS and KLF5 had 1.985-fold(95%CI:1.409-2.797) and 1.982-fold(95%CI:1.382-2.841) higher risks of weaning failure, respectively, while patients with high Prdx6 expression had a 0.380-fold(95%CI:0.192-0.753) risk compared with those with low expression. The AUCs of serum iNOS, KLF5, Prdx6 alone, and their combination for predicting weaning failure were 0.798, 0.827, 0.775, and 0.935, respectively. The combined prediction was significantly superior to individual markers(Z/P= 2.517/0.008, 2.503/0.009, 2.532/0.005). Conclusion Serum iNOS, KLF5, and Prdx6 demonstrate high predictive efficiency for weaning failure from mechanical ventilation in ARF patients. Furthermore, the combination of these three markers provides superior predictive value for weaning failure in ARF patients undergoing mechanical ventilation.

This study reports the clinical data of two patients with ruptured juvenile cystic adenomyoma and conducts a literature review and analysis.

This paper traces the origin of the collateral disease theory, elucidates the ideological connotation of the qi collaterals theory, and discusses the correlation between qi collaterals and peripheral nerves. Based on the theory of qi collaterals, the pathogenesis of diabetic peripheral neuropathy(DPN) is proposed as "collateral deficiency with malnutrition" and "phlegm-dampness, stasis, and heat obstructing the collaterals." In view of the above pathogenesis, the treatment principles for DPN are proposed as "tonifying the collaterals, promoting blood circulation, and unblocking the collaterals, " "removing dampness and phlegm, tonifying qi, and unblocking the collaterals, " and "tonifying qi and unblocking the collaterals, clearing heat and removing toxins." This paper aims to provide readers with new ideas for the treatment of DPN.

Bruton's tyrosine kinase inhibitors(BTKis) have become core targeted agents for B-cell malignancies and have markedly improved patient prognosis. However, acquired resistance remains a formidable clinical challenge. The first-generation irreversible BTKi ibrutinib has demonstrated proven efficacy, but its off-target toxicities and resistance conferred by the C481S mutation limit its clinical application. As second-generation highly selective BTKis, zanubrutinib, orelabrutinib, and acalabrutinib exhibit superior efficacy and safety, and have replaced first-generation agents as the first-line standard of care for various B-cell malignancies; nevertheless, drug resistance remains unresolved. The third-generation non-covalent BTKi pirtobrutinib can overcome C481S-mediated resistance, and BTK protein degraders provide a novel strategy for managing multiple resistance mechanisms. This article reviews the classification, clinical treatment advances, and resistance mechanisms of BTKis, aiming to provide a reference for clinical practice.

In recent years, the continuous advancement of surgery, perioperative chemotherapy, targeted therapy, and immunotherapy has improved the survival outcomes of patients with advanced gastric cancer. However, treatment-related toxicity, acquired drug resistance, an immunosuppressive tumor microenvironment, malnutrition, and decreased quality of life remain major clinical challenges. Traditional Chinese medicine(TCM) posits that the core pathogenesis of gastric cancer can be summarized as spleen-stomach deficiency and qi-blood deficiency as the root causes, with phlegm-dampness, blood stasis, heat-toxin, and cancer-toxin interaction as the manifest symptoms. This condition is characterized by a deficiency of healthy qi and an excess of pathogenic factors, with a dynamic interplay between deficiency and excess. The Fuzheng Quxie Method is based on strengthening healthy qi through approaches such as invigorating the spleen and replenishing qi, nourishing blood and harmonizing the stomach, and nourishing yin and warming yang, while simultaneously eliminating pathogenic factors via heat-clearing and detoxification, phlegm-resolving and mass-eliminating, blood-activating and stasis-removing, and softening and dissipating mass therapies. This method has shown research value in perioperative rehabilitation, reducing radiotherapy and chemotherapy toxicity while enhancing efficacy, maintenance therapy for advanced disease, intervention in precancerous lesions, and prevention of recurrence and metastasis. Modern research suggests that the Fuzheng Quxie Method exerts its effects through multiple mechanisms, including regulation of the tumor immune microenvironment, inhibition of inflammation-cancer transformation, induction of apoptosis/autophagy/ferroptosis, interference with metabolic reprogramming, suppression of epithelial-mesenchymal transition and angiogenesis, regulation of exosome communication, improvement of the gastrointestinal mucosal barrier, and reversal of drug resistance. This review summarizes the theoretical basis, modern mechanistic insights, clinical research progress, and future research directions of the Fuzheng Quxie Method in gastric cancer treatment, with the aim of providing a reference for integrated traditional Chinese and Western medicine approaches to gastric cancer management.