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Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease that reduces lung and respiratory function, with a high mortality rate. Severe and acute deterioration of COPD can easily lead to respiratory failure, resulting in personal, social, and medical burden. Recent studies have shown a high correlation between the gut microbiota and lung inflammation. In this study, we investigated the relationship between gut microbiota and COPD severity. A total of 60 COPD patients with varying severity according to GOLD guidelines were enrolled in this study. DNA was extracted from patients’ stool and 16S rRNA data analysis conducted using high-throughput sequencing followed by bioinformatics analysis. The richness of the gut microbiota was not associated with COPD severity. The gut microbiome is more similar in stage 1 and 2 COPD than stage 3+4 COPD. Fusobacterium and Aerococcus were more abundant in stage 3+4 COPD. Ruminococcaceae NK4A214 group and Lachnoclostridium were less abundant in stage 2–4, and Tyzzerella 4 and Dialister were less abundant in stage 1. However, the abundance of a Bacteroides was associated with blood eosinophils and lung function. This study suggests that no distinctive gut microbiota pattern is associated with the severity of COPD. The gut microbiome could affect COPD by gut inflammation shaping the host immune system.

Background Whether the long-term survival of patients with idiopathic pulmonary fibrosis (IPF) is worse than that of patients with IPF combined with emphysema after anti-fibrotic therapy is unclear. This study aimed to compare treatment outcomes between the two groups and identify potential predictors of mortality. Methods This retrospective cohort study was conducted in seven hospitals across Taiwan between August 2015 and August 2022 and included patients with IPF who received anti-fibrotic agents covered by national insurance. Based on the extent of emphysema observed on high-resolution chest tomography, patients with IPF were categorized into two groups: IPF only; and IPF with emphysema. Baseline characteristics and survival outcomes were compared between the groups. Cox proportional hazards models were used for multivariable analysis to identify factors associated with overall mortality during the follow-up period. Results Of the 275 patients included, 126 (45.8%) had IPF with emphysema and 149 (54.2%) had IPF only. The emphysema group had a higher proportion of males and patients with a smoking history, finger clubbing, comorbidities, or a definite usual interstitial pneumonia (UIP) pattern compared to the IPF-only group. Additionally, this group had a higher forced vital capacity (FVC, %) and forced expiratory volume in 1 s (FEV₁, L), while FEV₁ (%) was similar and FEV₁/FVC (%) was lower. During a median follow-up of 3.7 years, the overall survival rates were comparable (IPF only: 45.6%; IPF with emphysema: 48.4%). The overall survival of patients with probable UIP was significantly better than that of patients with definite UIP (53.5% vs. 34.6%). Likewise, the survival rate of the group with a diffusing capacity of the lung for carbon monoxide (DLCO) > 49% was higher than that of the group with DLCO ≤ 49% (53.9% vs. 31.4%). After adjusting for confounders, lower body mass index (BMI) (adjusted hazard ratio [aHR] = 0.95) and comorbid pulmonary hypertension (aHR = 2.27) were independently associated with increased overall mortality. Neither the presence of emphysema nor the type of anti-fibrotic agent was associated with mortality. Conclusions The survival outcomes of patients with IPF and emphysema and those of patients with IPF only are comparable after treatment with anti-fibrotic agents. Lower BMI and comorbid pulmonary hypertension are significant predictors of increased mortality.

Tracheal tumours can develop as primary neoplasms or as extensions from adjacent organs such as the lungs or larynx. We present a case of a man diagnosed with adenoid cystic carcinoma of the trachea. Tracheal tumours can develop as primary neoplasms or as extensions from adjacent organs such as the lungs or larynx. We present a case of a man with chronic and severe cough, diagnosed with adenoid cystic carcinoma of the trachea.

Key message Despite embolization being now considered the preferred treatment for PAVM, surgical intervention may be considered if the malformation involves large vessels. We present a case where surgical intervention was successful for the treatment of pulmonary arteriovenous malformation.

Key message Situs ambiguus is a rare congenital abnormality with outcomes ranging from asymptomatic to fatal. Here we present a woman with an incidental finding of situs ambiguus hinted by her chest radiograph. This case highlights the importance of actively seeking diagnosis when right sub‐diaphragmic air is noted when viewing a chest radiograph. We present a case of incidental finding of situs ambiguus hinted by chest radiograph. This case highlights the importance of actively seeking diagnosis when right sub‐diaphragmic air is noted when viewing a chest radiograph.

Polyalthia belong to the Annonaceae family and are a type of evergreen tree distributed across many tropical and subtropical regions. Polyalthia species have been used long term as indigenous medicine to treat certain diseases, including fever, diabetes, infection, digestive disease, etc. Recent studies have demonstrated that not only crude extracts but also the isolated pure compounds exhibit various pharmacological activities, such as anti-oxidant, anti-microbial, anti-tumor, anti-cancer, etc. It is known that the initiation of cancer usually takes several years and is related to unhealthy lifestyle, as well as dietary and environmental factors, such as stress, toxins and smoking. In fact, natural or synthetic substances have been used as cancer chemoprevention to delay, impede, or even stop cancer growing. This review is an attempt to collect current available phytochemicals from Polyalthia species, which exhibit anti-cancer potentials for chemoprevention purposes, providing directions for further research on the interesting agents and possible clinical applications.

Cordycepin is an adenosine derivative isolated from Cordyceps sinensis, which has been used as an herbal complementary and alternative medicine with various biological activities. The general anti-cancer mechanisms of cordycepin are regulated by the adenosine A3 receptor, epidermal growth factor receptor (EGFR), mitogen-activated protein kinases (MAPKs), and glycogen synthase kinase (GSK)-3β, leading to cell cycle arrest or apoptosis. Notably, cordycepin also induces autophagy to trigger cell death, inhibits tumor metastasis, and modulates the immune system. Since the dysregulation of autophagy is associated with cancers and neuron, immune, and kidney diseases, cordycepin is considered an alternative treatment because of the involvement of cordycepin in autophagic signaling. However, the profound mechanism of autophagy induction by cordycepin has never been reviewed in detail. Therefore, in this article, we reviewed the anti-cancer and health-promoting effects of cordycepin in the neurons, kidneys, and the immune system through diverse mechanisms, including autophagy induction. We also suggest that formulation changes for cordycepin could enhance its bioactivity and bioavailability and lower its toxicity for future applications. A comprehensive understanding of the autophagy mechanism would provide novel mechanistic insight into the anti-cancer and health-promoting effects of cordycepin.

The introduction of anti-PD-1/PD-L1 therapies revolutionized treatment for advanced non-small cell lung cancer (NSCLC), yet response rates remain modest, underscoring the need for predictive biomarkers. While a T cell inflamed gene expression profile (GEP) has predicted anti-PD-1 response in various cancers, it failed in a large NSCLC cohort from the Stand Up To Cancer-Mark (SU2C-MARK) Foundation. Re-analysis revealed that while the T cell inflamed GEP alone was not predictive, its performance improved significantly when combined with gene signatures of myeloid cell markers. These additional signatures, however, showed negative contributions to prediction, hinting at immune alterations affecting therapy. Based on this, we proposed a combination biomarker approach that integrates the T cell inflamed GEP with immune-altered signatures, derived from the SU2C-MARK cohort using a machine-learning approach, as novel biomarkers. These signatures consisted of genes highly expressed in myeloid and stromal cells. We then assessed the predictive ability of these combined biomarkers in six independent cancer cohorts treated with anti-PD-1. The combined biomarkers demonstrated enhanced performance in NSCLC and gastric cancer cohorts, but not in melanoma cohorts. Our study introduces new biomarkers for predicting anti-PD-(L)1 response in NSCLC and offers mechanistic insights into treatment efficacy.

A clerodane diterpene compound 16-hydroxycleroda-3,13-dien-15,16-olide (CD) is considered a therapeutic agent with pharmacological activities. The present study investigated the mechanisms of CD-induced apoptosis in T24 human bladder cancer cells. CD inhibited cell proliferation in a concentration and time-dependent manner. CD-induced overproduction of reactive oxygen species and reduced mitochondrial membrane potential, associated with reduced expression of Bcl-2 and increased levels of cytosolic cytochrome c, cleaved PARP-1 and caspase-3. In addition, CD treatment led to cell cycle arrest at the G0/G1 phase and inhibited expression of cyclin D1 and cyclin-dependent kinases 2 and 4 and led to increased levels of p21, p27Kip1 and p53. All of these events were accompanied with a reduction of pEGFR, pMEK1/2, pERK1/2, pAkt, pmTOR, pP70S6K1, HIF-1α, c-Myc and VEGF. RNAseq-based analysis revealed that CD-induced cell death was characterised by an increased expression of stress and apoptotic-related genes as well as inhibition of the cell cycle-related genes. In summary, CD induces apoptosis in T24 bladder cancer cells through targeting multiple intracellular signaling pathways as a result of oxidative stress and cell cycle arrest.