This study was to evaluate the prognostic value of the Naples prognostic score (NPS) in adult patients with asthma. Data on 44 601 participants from the 1999–2018 National Health and Nutrition Examination Survey (NHANES) were analyzed. The NPS was calculated based on serum albumin, total cholesterol, neutrophil-to-lymphocyte ratio (NLR), and lymphocyte-to-monocyte ratio (LMR), and participants were divided into 3 groups. Self-administered questionnaires were used to collect information on asthma, and mortality was identified using the National Death Index through December 31, 2019. Multiple logistic regressions were used to analyze the relationship between NPS and its components and the prevalence of asthma. Kaplan-Meier survival analysis, Cox proportional regressions, and the random survival forest (RSF) were used to assess the significance of NPS and its components in predicting all-cause and cause-specific (cardiovascular, cancer, and respiratory diseases) mortality in asthma patients. The mean age of the participants was 47.59 ± 0.18 years, and 48.47% were male. The prevalence of asthma was 13.11%. The participants were categorized into 3 groups: 8306 (18.6%) participants were in group 0 (NPS 0), 30 842 (69.2%) were in group 1 (NPS 1 or 2), and 5453 (11.2%) were in group 2 (NPS 3 or 4). Compared to the reference group, participants in group 2 had a higher prevalence of asthma (odds ratio [OR] = 1.40 [1.24–1.56]). Participants with asthma in group 2 had a significantly increased risk of all-cause mortality (hazard ratio [HR] = 2.42 [1.67–3.50]), cardiovascular mortality (HR = 2.68 [1.50–4.79]), cancer mortality (HR = 2.10 [1.00–4.45]), and respiratory disease mortality (HR = 3.00 [1.18–7.65]) compared to those with asthma in group 0. The RSF showed that NPS had the highest value in predicting all-cause mortality in adults with asthma, compared to its components. The results of this study indicate that the NPS is a powerful prognostic indicator for outcomes in asthma patients.

Janus kinase (JAK) 2 plays a pivotal role in the tumorigenesis of signal transducers and activators of transcription (STAT) 3 constitutively activated solid tumors. JAK2 mutations are involved in the pathogenesis of various types of hematopoietic disorders, such as myeloproliferative disorders, polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Thus, small-molecular inhibitors targeting JAK2 are potent for therapy of these diseases. In this study, we screened 1,062,608 drug-like molecules from the ZINC database and 2080 natural product chemicals. We identified a novel JAK family kinase inhibitor, dehydrocrenatidine, that inhibits JAK-STAT3–dependent DU145 and MDA-MB-468 cell survival and induces cell apoptosis. Dehydrocrenatidine represses constitutively activated JAK2 and STAT3, as well as interleukin-6–, interferon-α−, and interferon-γ–stimulated JAK activity, and STAT phosphorylation, and suppresses STAT3 and STAT1 downstream gene expression. Dehydrocrenatidine inhibits JAKs-JH1 domain overexpression–induced STAT3 and STAT1 phosphorylation. In addition, dehydrocrenatidine inhibits JAK2-JH1 kinase activity in vitro. Importantly, dehydrocrenatidine does not show significant effect on Src overexpression and epidermal growth factor–induced STAT3 activation. Our results indicate that dehydrocrenatidine is a JAK-specific inhibitor.

Objective: To investigate the risk factors of pulmonary embolism in patients with lung cancer and develop and validate a novel nomogram scoring system-based prediction model. Method: We retrospectively analyzed the clinical data and laboratory characteristics of 900 patients with lung cancer who were treated, including patients with lung cancer without pulmonary embolism (LC) and patients with lung cancer with pulmonary embolism (LC + PE). The patients were randomly divided into derivation and internal validation groups in a 7:3 ratio. Using logistic regression analysis, a diagnostic model of the nomogram scoring system was developed by incorporating selected variables in the derivation group and validated in the internal and external validation groups (n = 108). Result: Seven variables (adenocarcinoma, stage III-IV LC, indwelling central venous catheter, chemotherapy, and the levels of serum albumin, hemoglobin, and D-dimer) were identified as valuable parameters for developing the novel nomogram diagnostic model for differentiating patients with LC and LC + PE. The scoring system demonstrated good diagnostic performance in the derivation (area under the curve [AUC]; 95% confidence interval [CI], 0.918; 0.893, 0.943; sensitivity, 88.5%; specificity, 80.5%), internal validation (AUC; 95% CI, 0.921; 0.884, 0.958; sensitivity, 90.5%; specificity, 80.4%), and external validation (AUC; 95% CI, 0.929; 0.875, 0.983; sensitivity; 85.0%; specificity; 87.5%) groups. Conclusion: In this study, we constructed and validated a nomogram scoring system based on 7 clinical parameters. The scoring system exhibits good accuracy and discrimination between patients with LC and LC + PE and can effectively predict the risk of PE in patients with LC.

Objective. This study aimed to investigate the efficacy of the colloidal gold immunochromatography method in the detection of Cryptococcus antigen in bronchoalveolar lavage fluid (BALF) for pulmonary cryptococcosis (PC) diagnosis. Methods. A total of 111 patients with clinically suspected PC who were finally diagnosed with nonhuman immunodeficiency virus infection and hospitalized in the Ningbo First Hospital from March 2017 to December 2021 were retrospectively analyzed. All the confirmed cases were divided into two groups as follows: the PC group (33 cases) and the non-PC group (78 cases). All the patients were subjected to serum and BALF cryptococcal capsular polysaccharide antigen-lateral flow immunochromatographic assay (CrAg-LFA) and etiological culturing. Results. In the PC group, serum CrAg-LFA was positive for 24 and negative for 9 cases, serum Cryptococcus culture was positive for 1 and negative for 32 cases, BALF CrAg-LFA was positive for 31 and negative for 2 cases, and BALF Cryptococcus culture was positive for 9 and negative for 24 cases. In the non-PC group, serum CrAg-LFA was positive for 1 and negative for 77 cases, serum culture was negative in all the cases, and both BALF CrAg-LFA and culture were negative in all the cases. The sensitivity, specificity, and accuracy of BALF CrAg-LFA for PC diagnosis were 93.9%, 100%, and 98.2%, respectively, whereas those of BALF culture were 27.3%, 100%, and 78.4%, respectively. The sensitivity and accuracy of BALF CrAg-LFA were higher than that of serum CrAg-LFA and BALF etiological culture with statistically significant differences ( ). Conclusion. The diagnostic value of BALF CrAg-LFA for PC is superior to that of serum CrAg-LFA and BALF etiological culture.

Although alectinib is a well-tolerated and highly effective inhibitor of a second-generation anaplastic lymphoma kinase, special attention should be paid to the possibility of potentially severe and fatal adverse events such as interstitial pneumonia. We report a case of a patient with advanced non-small cell lung cancer treated with alectinib who developed immunohistochemically positive anaplastic lymphoma kinase (ALK(IHC +)) . However, due to the rapid emergence of drug-induced interstitial lung disease, alectinib treatment was halted. Once the interstitial lung disease had been successfully treated, we reluctantly chose crizotinib as a second-line treatment for ALK + NSCLC in this patient as he refused all other available treatments. Contrary to expectation, crizotinib performed well both in terms of its safety and efficacy. Our results suggest that crizotinib may provide a promising therapy option for patients with ALK + NSCLC accompanied by alectinib-induced interstitial lung disease. To our knowledge, this is a rare report of successful treatment of ALK + NSCLC with crizotinib after alectinib-induced interstitial lung disease.

Background: Systemic inflammation is closely associated with adverse outcomes in pulmonary embolism (PE). This study aimed to develop and evaluate a novel inflammatory prognostic score (IPS) derived from multiple inflammation‐related biomarkers to predict long‐term all‐cause mortality in patients with acute PE. Methods: This retrospective cohort study included 1642 patients with confirmed acute PE admitted between January 2016 and January 2024 at the First Affiliated Hospital of Ningbo University and the Affiliated People Hospital of Ningbo University. The primary outcome was all‐cause mortality. Follow‐up was conducted in January 2025. Fifteen inflammatory biomarkers were analyzed, including C‐reactive protein (CRP), white blood cell count (WBC), neutrophil count (NEU), lymphocyte count (LYM), monocyte count (MON), red cell distribution width (RDW), platelet count (PLT), and eight derived indices: neutrophil‐to‐lymphocyte ratio (NLR), derived NLR (dNLR), monocyte‐to‐lymphocyte ratio (MLR), neutrophil–MLR (NMLR), platelet‐to‐lymphocyte ratio (PLR), systemic immune‐inflammation index (SII), systemic inflammation response index (SIRI), and inflammatory burden index (IBI). IPS was constructed using least absolute shrinkage and selection operator (LASSO) Cox regression. Prognostic performance was assessed using Kaplan–Meier survival analysis, multivariable Cox regression, time‐dependent receiver operating characteristic (ROC) analysis, and random survival forest (RSF). Results: During a median follow‐up of 43.87 months, 262 patients (16.0%) died. The IPS was calculated as: IPS = 0.395 × IBI + 0.236 × RDW + 0.208 × SIRI + 0.115 × MLR + 0.040 × CRP. Patients with high IPS (≥0.55) had a significantly higher risk of all‐cause mortality compared to those with low IPS (adjusted hazard ratio [HR] = 2.55, 95% confidence intervals [CI]: 1.92–3.38; p < 0.001). Time‐dependent area under the curve (AUC) for IPS were 0.756, 0.768, and 0.773 at 1, 3, and 5 years, respectively. When added to the baseline clinical model—including age, length of hospital stay, deep vein thrombosis, diastolic blood pressure, body mass index (BMI), lactate, log‐transformed serum creatinine, blood urea nitrogen (BUN), log‐transformed D‐dimer, left ventricular ejection fraction (LVEF), pulmonary artery systolic pressure (PASP), and computed tomography pulmonary angiography (CTPA)‐based embolism location (main pulmonary artery)—IPS improved the AUC from 0.820 to 0.886 at 3 years ( p < 0.001, DeLong test). RSF analysis further identified IPS as the most informative inflammatory predictor of mortality. Conclusions: The IPS, derived from five routinely available inflammatory biomarkers, was independently associated with long‐term mortality and significantly enhanced risk stratification beyond traditional clinical predictors in patients with acute PE. This score may support early prognostic assessment and individualized management.