Purpose: Chlamydia psittaci pneumonia is an uncommon type of pneumonia characterized by non-specific clinical manifestations. Current knowledge regarding its clinical features is insufficient. Therefore, we aimed to elucidate its epidemiological profile, clinical characteristics, and distinctions between severe and non-severe cases. Patients and Methods: Clinical data of 186 patients diagnosed with C. psittaci pneumonia using next-generation sequencing (NGS) were systematically collected from seven hospitals in Guangdong Province, China, between January 2019 and June 2025. Epidemiological characteristics, clinical presentations, laboratory results, chest computed tomography (CT) features, bronchoscopy findings, and treatment outcomes were analyzed, with comparisons by disease severity. Results: Of 186 patients (58.1% male, 50-74 years), 43.5% presented with severe disease, and 67.2% developed complications. Most cases occurred during autumn or winter (67.2%), and a history of bird or poultry exposure was reported in 68.3%. Prevalent clinical symptoms included fatigue (98.9%), high fever (90.3%), and headache (73.7%). Laboratory findings showed elevated serum levels of C-reactive protein, procalcitonin, fibrinogen, and D-dimer in most patients (over 90%). Additionally, over 70% had increased neutrophilia, alanine transaminase, aspartate transaminase, and lactate dehydrogenase levels, with reduced lymphocyte counts. Chest CT findings frequently revealed pulmonary consolidation (100%), ground-glass opacities (97.8%), and air bronchograms (81.2%). Severe cases showed extensive bilateral and multilobar consolidation, with increased prevalence of pleural and pericardial effusions. The median time from admission to diagnosis was 3 (2-4) days, with 96.2% of patients improving following targeted antimicrobial therapy and being discharged, while 3.2% died. Conclusion: C. psittaci pneumonia is characterized by a high incidence of severe cases and both intrapulmonary and extrapulmonary complications. Its clinical manifestations are diverse and multifaceted, with hallmark features including high fever, relative bradycardia, normal white blood cell counts, elevated transaminases, and pulmonary consolidation. Early diagnosis through NGS and targeted antimicrobial therapy are associated with positive patient outcomes.

Vasculogenic mimicry (VM), a process in which cancer cells form endothelial cell-independent vascular networks, is a hallmark of tumor aggressiveness in lung adenocarcinoma (LUAD) and supports tumor growth and metastasis. This study aims to identify and validate key genes associated with VM formation in LUAD, and to elucidate their functional roles and clinical significance. Transcriptomic data from LUAD samples were analyzed using differential expression analysis (DEA) and weighted gene co-expression network analysis (WGCNA) to identify VM-associated genes. Machine learning algorithms were applied to refine the selection and identify hub genes. Functional enrichment and immune infiltration analyses were performed. The role of SULF1 in VM was further validated through in vitro and in vivo experiments. We identified 10,810 differentially expressed genes. WGCNA revealed 101 VM-associated genes, predominantly within the “yellow” and “brown” modules. Machine learning pinpointed three key regulators: downregulated decorin (DCN) and upregulated nucleoplasmin 3 (NPM3) and sulfatase 1 (SULF1). Functional enrichment analysis highlighted their involvement in extracellular matrix (ECM) organization and ribosomal pathways. Immune infiltration analysis indicated a positive correlation between DCN and immune cell presence, whereas NPM3 and SULF1 showed negative correlations. Critically, SULF1 overexpression promoted VM formation in vitro by enhancing cell migration and invasion, mediated through the vascular endothelial growth factor (VEGF)/transforming growth factor beta (TGF-β)/Vimentin signaling axis, and accelerated tumor growth in vivo. We identified DCN, NPM3, and SULF1 as key biomarkers of VM in LUAD. SULF1, in particular, plays a central role in driving VM formation and tumor progression. These findings offer novel mechanistic insights and highlight potential therapeutic targets for LUAD treatment.

BackgroundPleural effusion (PE), frequently encountered in clinical practice, can arise from a variety of underlying conditions. Accurate differential diagnosis of PE is crucial, as treatment and prognosis are heavily dependent on the underlying etiology. However, diagnosing the cause of PE remains challenging, relying on mycobacteriological methods that lack sensitivity and are time-consuming, or on histological examinations that require invasive biopsies. The recent advancements in metagenomic next-generation sequencing (mNGS) have shown promising applications in the diagnosis of infectious diseases. Despite this, there is limited research on the utility of mNGS as a comprehensive diagnostic tool for simultaneously identifying the causes of PE, particularly in cases of tuberculosis or malignancy.MethodsThis study aimed to assess the efficacy of mNGS in detecting tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE). A total of 35 patients with PE were included, and their PE samples were analyzed using mNGS.ResultsAmong the participants, 8 were ultimately diagnosed with TPE, and 10 were diagnosed with MPE, with lung adenocarcinoma being the most prevalent pathological type (50%, 5/10), according to established diagnostic criteria. Additionally, 7 patients were diagnosed with non-infectious PE. However, mNGS identified only 2 cases of TPE and 8 cases of MPE. The sensitivity of mNGS for detecting Mycobacterium tuberculosis was 25% (2/8), while the specificity was 100%. For tumor detection, mNGS demonstrated a sensitivity of 80%, a specificity of 92.6%, and an AUC of 0.882.ConclusionmNGS is effective in distinguishing MPE from non-MPE, but is not suitable for diagnosing TPE.

Background:Some patients with Chlamydia psittaci pneumonia exhibit liver function abnormalities. In this study, we aimed to elucidate the characteristics of liver function changes and the factors influencing liver injury in patients with Chlamydia psittaci pneumonia, providing a reference for clinical treatment. Methods:The clinical data of patients with Chlamydia psittaci pneumonia admitted to three tertiary Grade A hospitals in Guangdong Province, China, from January 2020 to February 2025 were retrospectively collected. Changes in liver parameters and related influencing factors upon admission were analyzed. Results:Overall, 120 cases were included: 100 (83.3%) exhibited liver function abnormalities and 55 (45.8%) had liver injury. The incidence of liver function abnormalities and liver injury was significantly higher in the severe group than that in the mild group. Liver function abnormalities and injury associated with Chlamydia psittaci pneumonia were characterized by elevations in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (GGT) levels. AST and ALT levels exceeded three times the upper limit of normal (ULN) in 43 (35.8%) and 20 (16.7%) cases, respectively, while GGT exceeded twice the ULN in 25 (20.8%) cases. ALT (70 [47-115] vs 51 [26-73] U/L, p = 0.002) and AST (122 [72-252] vs 52 [30-76] U/L, p = 0.000) were significantly different between the severe and mild groups. Hepatocellular injury was the most common type of liver injury upon admission, followed by mixed and cholestatic types. Compared to patients without liver injury, those with liver injury had a higher prevalence of alcohol consumption history, dyspnea, higher pneumonia severity index scores, and longer hospital stays. Conclusion:Patients with Chlamydia psittaci pneumonia, particularly severe cases, are prone to concurrent liver function abnormalities and liver injury. Liver injury, predominantly hepatocellular injury, was associated with factors such as alcohol consumption history, pneumonia severity, and elevated inflammatory responses, leading to prolonged hospital stays. Monitoring liver function may aid in early identification of severe cases.

BackgroundAcute respiratory distress syndrome (ARDS) is a life-threatening condition frequently encountered in critically ill patients, including those with advanced non-small cell lung cancer (NSCLC). Almonertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), has shown promise as a first-line treatment for NSCLC with classical EGFR mutations. However, its efficacy in NSCLC patients suffering from ARDS has not been well-documented.Case PresentationWe report the case of a 63-year-old Chinese Han female with severe NSCLC complicated by ARDS. Upon hospital admission, the patient exhibited progressive dyspnea and required intubation to maintain oxygenation. Pathological analysis of bronchoalveolar lavage fluid sediment confirmed lung adenocarcinoma, and genetic testing of blood identified an EGFR E19 mutation. The patient was treated with almonertinib, resulting in significant clinical improvement and successful extubation after nine days. Radiographic imaging showed substantial reduction in pulmonary lesions, highlighting the efficacy of almonertinib.ConclusionThis case represents the first documented successful treatment of ARDS induced by EGFR E19 mutated NSCLC using almonertinib. The favorable clinical response observed in this critically ill patient suggests that almonertinib may be a viable therapeutic option for managing severe complications in NSCLC. Further research is necessary to corroborate these findings and optimize dosage and toxicity management strategies for broader clinical application.

BACKGROUND:Benralizumab is indicated as add-on therapy in patients with uncontrolled, severe eosinophilic asthma; it has not yet been evaluated in a large Asian population with asthma in a clinical trial. OBJECTIVE:To evaluate the efficacy and safety of benralizumab in patients with severe asthma in Asia. METHODS:MIRACLE (NCT03186209) was a randomized, Phase 3 study in China, South Korea, and the Philippines. Patients aged 12-75 years with severe asthma receiving medium-to-high-dose inhaled corticosteroid/long-acting β2-agonists, stratified (2:1) by baseline blood eosinophil count (bEOS) (≥300/μL; <300/μL), were randomized (1:1) to benralizumab 30 mg or placebo. Endpoints included annual asthma exacerbation rate (AAER; primary endpoint), change from baseline at Week 48 in pre-bronchodilator (BD) forced expiratory volume in 1 second (pre-BD FEV1) and total asthma symptom score (TASS). Safety was evaluated ≤ Week 56. RESULTS:Of 695 patients randomized, 473 had baseline bEOS ≥300/μL (benralizumab n = 236; placebo n = 237). In this population, benralizumab significantly reduced AAER by 74% (rate ratio 0.26 [95% CI 0.19, 0.36], p < 0.0001) and significantly improved pre-BD FEV1 (least squares difference [LSD] 0.25 L [95% CI 0.17, 0.34], p < 0.0001) and TASS (LSD -0.25 [-0.45, -0.05], p = 0.0126) versus placebo. In patients with baseline bEOS <300/μL, there were numerical improvements in AAER, pre-BD FEV1, and TASS with benralizumab versus placebo. The frequency of adverse events was similar for benralizumab (76%) and placebo (80%) in the overall population. CONCLUSIONS:MIRACLE data reinforces the efficacy and safety of benralizumab for severe eosinophilic asthma in an Asian population, consistent with the global Phase 3 results.

Background This study examined the association between chest muscles and chronic obstructive pulmonary disease (COPD) and the relationship between chest muscle areas and acute exacerbations of COPD (AECOPD). Methods There were 168 subjects in the non-COPD group and 101 patients in the COPD group. The respiratory and accessory respiratory muscle areas were obtained using 3D Slicer software to analysis the imaging of computed tomography (CT). Univariate and multivariate Poisson regressions were used to analyze the number of AECOPD cases during the preceding year. The cutoff value was obtained using a receiver operating characteristic (ROC) curve. Results We scanned 6342 subjects records, 269 of which were included in this study. We then measured the following muscle areas (non-COPD group vs. COPD group): pectoralis major (19.06 ± 5.36 cm 2 vs. 13.25 ± 3.71 cm 2 , P < 0.001), pectoralis minor (6.81 ± 2.03 cm 2 vs. 5.95 ± 1.81 cm 2 , P = 0.001), diaphragmatic dome (1.39 ± 0.97 cm 2 vs. 0.85 ± 0.72 cm 2 , P = 0.011), musculus serratus anterior (28.03 ± 14.95 cm 2 vs.16.76 ± 12.69 cm 2 , P < 0.001), intercostal muscle (12.36 ± 6.64 cm 2 vs. 7.15 ± 5.6 cm 2 , P < 0.001), pectoralis subcutaneous fat (25.91 ± 13.23 cm 2 vs. 18.79 ± 10.81 cm 2 , P < 0.001), paravertebral muscle (14.8 ± 4.35 cm 2 vs. 13.33 ± 4.27 cm 2 , P = 0.007), and paravertebral subcutaneous fat (12.57 ± 5.09 cm 2 vs. 10.14 ± 6.94 cm 2 , P = 0.001). The areas under the ROC curve for the pectoralis major, intercostal, and the musculus serratus anterior muscle areas were 81.56%, 73.28%, and 71.56%, respectively. Pectoralis major area was negatively associated with the number of AECOPD during the preceding year after adjustment (relative risk, 0.936; 95% confidence interval, 0.879–0.996; P = 0.037). Conclusion The pectoralis major muscle area was negative associated with COPD. Moreover, there was a negative correlation between the number of AECOPD during the preceding year and the pectoralis major area.

Evidence for the treatment of patients with mild-to-moderate chronic obstructive pulmonary disease (COPD) is limited. The efficacy of N-acetylcysteine (an antioxidant and mucolytic agent) for patients with mild-to-moderate COPD is uncertain. In this multicentre, randomised, double-blind, placebo-controlled trial, we randomly assigned 968 patients with mild-to-moderate COPD to treatment with N-acetylcysteine (600mg, twice daily) or matched placebo for two years. Eligible participants were 40–80 years of age and had mild-to-moderate COPD (forced expiratory volume in 1 second [FEV 1 ] to forced vital capacity ratio < 0.70 and an FEV 1 ≥ 50% predicted value after bronchodilator use). The coprimary outcomes were the annual rate of total exacerbations and the between-group difference in the change from baseline to 24 months in FEV 1 before bronchodilator use. COPD exacerbation was defined as the appearance or worsening of at least two major symptoms (cough, expectoration, purulent sputum, wheezing, or dyspnoea) persisting for at least 48 hours. Assessment of exacerbations was conducted every three months, and lung function was performed annually after enrolment. The differences between the N-acetylcysteine group and the placebo group in the annual rate of total exacerbations were not significant (0.65 vs. 0.72 per patient-year; relative risk [RR], 0.90; 95% confidence interval [CI], 0.80–1.02; P = 0.10). There was no significant difference in FEV 1 before bronchodilator use at 24 months. Long-term treatment with high-dose N-acetylcysteine did not significantly reduce the annual rate of total exacerbations and did not improve lung function in patients with mild-to-moderate COPD. Chinese Clinical Trial Registration: ChiCTR-IIR-17012604.

AbstractEvidence for the treatment of patients with mild-to-moderate chronic obstructive pulmonary disease (COPD) is limited. The efficacy of N-acetylcysteine (an antioxidant and mucolytic agent) for patients with mild-to-moderate COPD is uncertain. In this multicentre, randomised, double-blind, placebo-controlled trial, we randomly assigned 968 patients with mild-to-moderate COPD to treatment with N-acetylcysteine (600 mg, twice daily) or matched placebo for two years. Eligible participants were 40-80 years of age and had mild-to-moderate COPD (forced expiratory volume in 1 second [FEV1] to forced vital capacity ratio <0.70 and an FEV1 ≥ 50% predicted value after bronchodilator use). The coprimary outcomes were the annual rate of total exacerbations and the between-group difference in the change from baseline to 24 months in FEV1 before bronchodilator use. COPD exacerbation was defined as the appearance or worsening of at least two major symptoms (cough, expectoration, purulent sputum, wheezing, or dyspnoea) persisting for at least 48 hours. Assessment of exacerbations was conducted every three months, and lung function was performed annually after enrolment. The difference between the N-acetylcysteine group and the placebo group in the annual rate of total exacerbation were not significant (0.65 vs. 0.72 per patient-year; relative risk [RR], 0.90; 95% confidence interval [CI], 0.80–1.02; P = 0.10). There was no significant difference in FEV1 before bronchodilator use at 24 months. Long-term treatment with high-dose N-acetylcysteine neither significantly reduced the annual rate of total exacerbations nor improved lung function in patients with mild-to-moderate COPD. Chinese Clinical Trial Registration: ChiCTR-IIR-17012604.

目的:建立小鼠慢性阻塞性肺疾病(COPD)模型,探讨噻托溴铵(TIO)是否能够通过调控核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体活性发挥肺保护作用.方法:全身暴露香烟烟雾法构建COPD小鼠模型,部分采用TIO进行干预,分析小鼠的一般情况、肺功能指标、病理改变和肺部炎症细胞数量的变化.ELISA法检测小鼠支气管肺泡灌洗液(BALF)上清中白细胞介素1β(IL-1β)和IL-18的水平;Western blot法检测小鼠肺组织NLRP3及caspase-1蛋白的表达.结果:与对照组比较,COPD组小鼠体重、第100毫秒用力呼气容积(FEV100)、FEV100/用力肺活量(FVC)和动态肺顺应性(Cdyn)均明显下降(P＜0.05),气道阻力(RI)明显升高(P＜0.05),FVC水平无显著差异,肺组织平均肺泡间隔、BALF中炎症细胞、IL-1β和IL-18水平和肺组织中NLRP3及caspase-1蛋白表达均显著升高(P＜0.05).与COPD组比较,COPD+TIO组小鼠体重、FVC和Cdyn水平无显著差异,FEV100和FEV100/FVC明显升高(P＜0.05),RI明显下降(P＜0.05),肺组织平均肺泡间隔,BALF中炎症细胞、IL-1β和IL-18水平,以及肺组织中NLRP3和caspase-1蛋白表达均显著降低(P＜0.05).结论:TIO可以减轻COPD模型小鼠肺部炎症损伤,其机制可能与抑制NLRP3炎症小体的活化有关.

Psittacosis and Guillain-Barré syndrome are both rare clinical diseases with low incidence, and their combination has rarely been reported. Here, we report a case of Chlamydia psittaci pneumonia combined with Guillain-Barré syndrome. The patient initially presented with high fever, difficulty breathing, and fatigue. Chest computerised tomography indicated large consolidation opacities in both lungs. Metagenomic next-generation sequencing clearly identified the pathogen as C. psittaci. The patient's fever subsided after targeted antibiotic treatment, but difficulty breathing and fatigue worsened, and the patient developed symmetric limb numbness and weakness. Lumbar puncture, electrophysiological examination, and clinical characteristics were suggestive of Guillain-Barré syndrome, and the symptoms improved after treatment with human immunoglobulin. The results of this study suggest that metagenomic next-generation sequencing is useful for the rapid diagnosis of pulmonary infectious agents. Psittacosis is closely associated with the development of Guillain-Barré syndrome; however, more cases are needed to support this conclusion, and early targeted antibiotic treatment, immunotherapy, and basic supportive treatment are essential for improving outcomes.

Background: Extensively drug-resistant Acinetobacter baumannii (XDRAB) can acquire drug resistance genes, which are rapidly cloned and transmitted, leading to worldwide spread and posing significant treatment challenges. This study aimed to clarify effective treatment methods during XDRAB infection and factors affecting patient prognosis. Methods: Clinical features, treatment, and prognosis of 65 patients with hospital-acquired XDRAB pneumonia clinically diagnosed at Guangzhou First People's Hospital between January 2019 and December 2020 were retrospectively analyzed. Results: Of 65 subjects, only 37 survived. There was no significant difference in anti-A. baumannii activity according to type or combination of antibiotics administered between patients that survived and those that died (p > 0.05). The use of antibacterial drugs during infection did not effectively improve clinical outcomes. Advanced age, multiple organ failure, and disease severity were significantly negatively correlated while effective airway management was positively associated with bacterial clearance (p < 0.05). In multivariate analysis, age and APACHE score were independent risk factors affecting prognosis. Tracheotomy during infection was a protective factor contributing to survival (p < 0.05). Advanced age and disease severity independently affected patient prognosis, while use and type of antibacterial treatment did not substantially affect the prognosis. Conclusions: Advanced age and severe disease are independent risk factors that affect patient prognosis. Timely and effective airway management is key to improving the prognosis of patients with hospital-acquired XDRAB infection.

Glutamate ionotropic receptor kainate type subunit 3 (GRIK3) is a predominant excitatory neurotransmitter receptor in the mammalian brain. While it is known that GRIK3 is involved in normal neurophysiologic processes, its biological functions in tumor progression are still poorly understood due to limited investigation. In this study, we reported for the first time that GRIK3 expression was downregulated in non-small cell lung cancer (NSCLC) tissues as compared to paracarcinoma tissues. Additionally, we observed that GRIK3 expression was strongly correlated with the prognosis of NSCLC patients. We also noted that GRIK3 suppressed the cell proliferation and migration capability of NSCLC cells, thereby inhibiting xenografts growth and metastasis. Mechanistically, GRIK3 deficiency increased the expression of ubiquitin-conjugating enzyme E2 C (UBE2C) and cyclin-dependent kinase 1 (CDK1), which resulted in the activation of the Wnt signaling pathway and enhanced NSCLC progression. Our findings suggest that GRIK3 plays a role in regulating NSCLC progression and that its expression may serve as an independent prognostic indicator for NSCLC patients.

Background: Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are considered as the first-line treatment for advanced EGFR mutation-positive non-small cell lung cancer (NSCLC). We aimed to analyze the efficacy of EGFR-TKIs treatment in patients with advanced NSCLC of different smoking habits. Methods: We conducted a search for meta-analyses and systematic reviews on the PubMed, MEDLINE, Embase, and the Cochrane Library to address this knowledge gap. Patients were divided into 2 groups: (1) experimental group: treated with EGFR-TKIs or EGFR-TKIs combined with chemotherapy, immunotherapy, antiangiogenesis, radiotherapy and (2) control group: treated with chemotherapy. Progressive-free survival (PFS) and total survival (OS) were adopted for evaluating the efficacy of EGFR-TKIs between experimental group and control group. Results: Eleven studies including 6760 patients were included in the meta-analysis. The results showed that smoking (including previous and current smoking) significantly reduces the PFS and OS in comparison to non-smoking group in the treatment of NSCLC with EGFR-TKIs. In addition, EGFR-TKIs combined with anti-vascular endothelial growth factor therapy can reduce the risk of disease progression in smokers. Conclusions: Our study indicated that smoking significantly reduced the PFS and OS in comparison to non-smoking group in the treatment of NSCLC with EGFR-TKIs.

Since COVID-19 might have a lasting impact on global public health, it is crucial to analyze its effect on drug-resistant bacterial infections in the respiratory system for the prevention and control of hospital infections. This work aimed to investigate the impact of the COVID-19 outbreak on the clinical distribution and antibiotic resistance of bacterial infection among hospitalized patients in the respiratory unit in order to establish strategies to control antibiotic-resistant infections. Electronic clinical data registry records from 2018 to 2022 were retrospectively analyzed. A total of 36,829 clinical specimens, including sputum, bronchoalveolar lavage fluid, blood, and urine, were collected from 16,073 patients admitted to the Guangzhou First People’s Hospital from January 2018 to December 2022. Among them, 2209 samples were culture-positive. The bacterial isolation rates of different types of samples showed a similar trend from 2019 to 2022, with an increase in 2020 and 2022 and a decrease in 2021. Different bacterial species were separated from different types of samples. The most reported pathogens were identified in sputum samples. Gram-positive isolates were prevalent in urine samples, while Gram-negative bacilli were the predominant pathogenic bacteria isolated from respiratory tract and blood samples. Pseudomonas aeruginosa (P. aeruginosa), Acinetobacter baumannii (A. baumannii) complex, and Klebsiella pneumoniae (K. pneumoniae) were the most abundant Gram-negative bacteria in sputum samples, of which A. baumannii complex had the highest resistance to all tested antibiotics except colistin. Notably, there has been a substantial prevalence of carbapenem-resistant P. aeruginosa, A. baumannii, and K. pneumoniae in the past five years. This alarming situation calls for greater attention and precaution with prescribed antibiotics to limit the generation and spread of new multidrug-resistant bacteria and improve therapeutic management.

Sex-related differences in cancer epidemiology, tumor biology, immune system activity, and pharmacogenomics have been suggested to be important considerations for precision cancer control. Here we elucidated systematically sex biases in genetic variants, gene expression profiles, and immunological landscapes of lung adenocarcinoma patients (LUADs) with different ancestry and smoking status. Somatic mutation and mRNA expression data of Asian and Non-Asian LUADs were obtained from public databases. Sex-biased genetic mutations, gene expression, biological pathways, and immune infiltration were identified in the context of smoking status and race. Among nonsmokers, male-biased mutations were prevalent in Asian LUADs, while few sex-biased mutations were detected in Non-Asian LUADs. EGFR was the only mutation whose frequency was significantly higher in females than males in both Asian and Non-Asian nonsmokers. More genes exhibited sex-biased expression in Non-Asian LUADs compared to Asian LUADs. Moreover, genes distinctly expressed in females were mainly related to immune-related pathways, whereas those in males were more involved in activation of DNA repair, E2F_targets, and MYC_targets pathways. We also detected sex-specific immune infiltration in the context of genetic variation. In EGFR-mutant LUADs, males had a significantly increased infiltration of CD8 + T cells, whereas resting CD4 + memory T cells were more abundant in females. Additionally, in KRAS-mutant LUADs, CD8 + and CD4 + T cells were more abundant in females than males. In addition, we detected all female patients with high SCGB3A2 expression were exclusively sensitive to immunotherapy, while this phenomenon was not observed in male patients. Our findings provided evidence that sex-related molecular and cellular components are involved in shaping tumor distinct genetic and immune features, which might have important impact on personalized targeted and immune therapy.

Additional file 7: Table S18. The DEGs identified from the comparison between female and male smokers with LUAD in the TCGA cohort (Non-Asian).

BACKGROUND:Small cell lung cancer (SCLC) is an aggressive disease with poor survival. Although molecular and clinical characteristics have been established for SCLC in western patients, limited investigation has been performed for Chinese SCLC patients.OBJECTIVE:In this study, we investigated the genomic features of Chinese SCLC patients.METHODS:A total of 75 SCLC patients were enrolled. Genomic alterations in 618 selected genes were analyzed by targeted next-generation sequencing.RESULTS:Here, we showed that TP53 (77.30%) and RB1 (30.70%) were the most prevalent genes alterations, followed by KMT2D, ALK, LRP1B, EGFR, NOTCH3, AR, CREBBP, ROS1, and BRCA2. And the most common genetic alterations were enriched in the cell cycle signaling pathway (84.00%) of Chinese SCLC patients. DNA damage repair (DDR) pathway analysis showed that the most frequently enriched DDR pathways were fanconi anaemia (FA, 29.41%) and homology recombination (HR, 21.57%). Notably, 9.33% SCLC patients in our cohort had pathogenic or likely pathogenic germline gene variants. Compared with the U Cologne cohort, a higher prevalence in EGFR, AR, BRCA2, TSC1, ATXN3, MET, MSH2, ERBB3 and FOXA1 were found in our cohort; while compared to the data from the Johns Hopkins cohort, a higher mutated frequency in TP53, KMT2D, ALK, and EGFR were found in our cohort. Moreover, a significant association was found between high tumor mutation burden (TMB) and mutations involved in TP53, CREBBP, EPHA3, KMT2D, ALK and RB1. Approximately 33.33% of patients with SCLC harbored at least one actionable alteration annotated by OncoKB, of which one patient had alterations of level 1; seventeen patients had level 3; fifteen patients possessed level 4.CONCLUSION:Our data might provide an insightful meaning in targeted therapy for Chinese SCLC patients.

目的 本研究对广州地区5家教学医院的鲍曼不动杆菌进行分子流行病学分析.方法 5家教学医院共采集138株鲍曼不动杆菌,利用多位点序列分型(multilocus sequence typing,MLST)及eBURST算法评价菌株之间的遗传关系.结果 MLST将138株鲍曼不动杆菌分为8个已有序列类型(STs),分别为ST195、ST208、ST457、ST136、ST254、ST548、ST445和ST53,还发现17个新STs.其中ST195的数量最多,占所有分离株的35.5％(49/138),其次为ST208,占所有分离株的21.0％(29/138).eBURST算法分析显示以ST195为预测祖先型的克隆复合体(clonal complex,CC)195在医院环境中广泛传播.结论 鲍曼不动杆菌CC195是广州地区的流行克隆,各家医疗机构应根据其自身实际制定感染防控策略.

Lung adenocarcinoma (LUAD) accounts for almost 40% of lung cancers, leading to significant associated morbidity and mortality rates. However, the mechanism of LUAD tumorigenesis remains far from clear. Here, we scanned down‐regulated genes involved in LUAD sourced from The Cancer Genome Atlas and Gene Expression Omnibus data and focused on G protein‐coupled receptor 133 ( GPR133 ). We offer compelling evidence that GPR133 was expressed at low levels in the setting of LUAD, and higher expression was positively related to a better prognosis among patients with LUAD. Functionally, GPR133 inhibited cell proliferation and tumor growth in vitro and in vivo . Regarding the mechanism, flow cytometry assays and western blot assays showed that GPR133 enhanced p21 and decreased cyclin B1 expression, thus triggering LUAD cells at G2/M‐phase arrest. Consistent with this, we evaluated the expression levels of cell‐cycle biomarkers and found that bioinformatics analysis combined with N 6 ‐methyladenosine (methylation at the N6 position in adenosine) RNA immunoprecipitation‐qPCR assay indicated that GPR133 expression was down‐regulated by this modification. Moreover, we observed that methyltransferase‐like 3 was impaired in LUAD, and that it is able to significantly increase levels of GPR133 by enhancing its RNA stability. In conclusion, we found that GPR133 expression was down‐regulated in LUAD via N 6 ‐methyladenosine modification. Increasing GPR133 levels could suppress LUAD cell proliferation and tumor growth.