Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

BACKGROUND: Targeted therapy for patients with driver genes positive and immunotherapy for patients with driver gene-negative but high programmed death ligand 1 (PD-L1) expression are the standards of first-line treatment for patients with advanced non-small cell lung cancer (NSCLC). The treatment options for patients with driver gene positive and high PD-L1 expression are still worth exploring. METHODS: The characteristics of 315 patients with NSCLC were identified to analyze the clinicopathological characteristics of patients with driver gene positive and high PD-L1 expression, and the efficacy of targeted therapy. RESULTS: Among the 315 patients, the total positive rate of driver genes was 62.2%, and the high PD-L1 expression rate (≥50.0%) was 11.2%. The proportion of patients with driver gene positive and high PD-L1 expression was 10.7%. PD-L1 was highly expressed in patients with epidermal growth factor receptor (EGFR) mutation, KRAS mutation, ALK fusion, BRAF mutation, and MET 14 exon skip mutation, the proportions were 7.8% (11/141), 18.2% (4/22), and 23.1%, (3/13), 50.0% (2/4) and 100.0% (1/1) respectively. EGFR mutation positive with PD-L1 high expression was mainly in patients with stage IV lung adenocarcinoma. KRAS mutation positive with PD-L1 high expression was mainly in patients with a history of smoking. Among them, two patients were followed in detail for targeted therapy, who with ALK fusion-positive and PD-L1 high expression (90.0%), EGFR L858R mutation and PD-L1 high expression (70.0%) respectively. The total OS of the patients was 5 months, 2 months. CONCLUSIONS The high PD-L1 expression rate in NSCLC patients with different driver gene mutations was variable, which maybe correlated with distinct clinicopathological characteristics. Patients with sensitive mutations and high PD-L1 expression may be less benefit from targeted therapy and have poor prognosis.

Background and objective Non-small cell lung cancer (NSCLC) has been transformed from the treatment according to histological type to genotype treatment model. The epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) genes are the most important drivers in lung cancer. The aim of this study is to explore the clinical characteristics and prognostic factors of patients with advanced NSCLC with different genotypes. Methods We retrospectively reviewed the clinical data of 553 advanced NSCLC patients with EGFR mutations and ALK positive who were hospitalized in the Beijing Chest Hospital from July 2004 to December 2015, and the independent prognostic factors of pa-tients were analyzed by Cox proportional hazards regression model. Results The clinical data of 553 patients (227 with EGFR mutations, 58 with ALK positive, 2 with EGFR and ALK co-mutation and 266 with wild-type) with advanced NSCLC were enrolled in this study. The median survival time of 227 patients with EGFR mutations was 28.7 mo (95%CI: 22.160-35.240), and the performance status (PS) score (0-1) (HR=4.451; 95%CI: 2.112-9.382; P<0.001) and EGFR-tyrosine kinase inhibitors(TKIs) targeted therapy (HR=2.785; 95%CI: 1.871-4.145; P<0.001) were the independent prognostic factors for the survival of patients harboring EGFR mutations. The median survival time of 58 patients with ALK positive was 15.5 mo (95%CI:10.991-20.009), and treatment with crizotinib (P=0.022) was the independent influence factor for the survival of ALK positive patients. The median survival time of 266 patients with wild-type was 12.1 mo (95%CI: 10.660-13.540), and the PS score (0-1) (HR=2.313; 95%CI: 1.380-3.877; P=0.001) and treatment with chemotherapy (HR=1.911; 95%CI: 1.396-2.616; P<0.001) were the independent prognostic factors for the survival of wild-type patients. Conclusion The prognosis of patients with advanced NSCLC is associated with genetic mutation, and targeted therapy has a improvement on survival for patients with EGFR mutations or ALK rearrangement.

Objective To investigate the prevalence rate of healthcare-associated infection(HAI)in Xiangya Hospital,and provide reference for preventing and controlling HAI.Methods The cross sectional surveys on preva-lence rates of HAI,cross-sectional antimicrobial use,and bacterial detection among all hospitalized patients on the given days in 2000-2014 (except 2006)were carried out by combination of bedside investigation and medical record reviewing.Results The prevalence rates of HAI in 2000-2014 decreased from 6.30% to 3.91%,difference was statistically significant (χ2 = 35.14,P < 0.001 );prevalence rates of community-associated infection(CAI)were 15.61%-15.76%,there was no significant difference among each year.General intensive care unit (ICU)had the highest prevalence rate;respiratory tract was the most common site of both HAI and CAI;urinary catheterization rate showed a decreased tendency,arteriovenous catheterization rate showed a increased tendency,difference were both significant(χ2 = 5.21,96.24,respectively,both P <0.001).In 2008 - 2014,pathogenic detection rates for specimens from patients receiving therapeutic antimicrobial agents were 36.37%-44.51%,from patients with HAI were 34.00%-44.99%,detection rate of pathogens causing HAI were 41.57%-68.48%,all showed a increased tendency,difference was significant (χ2 = 22.78,10.03,26.49,respectively,all P < 0.001 ).Gram-negative bacteria were the main pathogens causing infection;both cross sectional and combination antimicrobial usage rates declined (P < 0.05 ).Conclusion Prevention and control of HAI,and antimicrobial management has achieved preliminary success,prevalence rate of HAI and cross sectional antimicrobial usage rate declined obviously,the main pathogen is gram-negative bacteria,and the major infection site is lower respiratory tract.

Background and objective Kirsten rat sarcoma viral oncogene (KARS) mutation is one of the major driver genes of non-small cell lung cancer (NSCLC). KARS is a resistant predictor of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which raises controversy because of its role in chemotherapy sensitivity and prognosis. hTe aim of this study is to accumulate clinical experience in treating NSCLC patients harboringKARSmutation.MethodsA total of 107 NSCLC patients harboringKARSmutation were analyzed retrospectively. hTe effcacy was analyzed in terms of ifrst-line chemotherapy or EGFR-TKIs therapy.Results hTe objective response rate (ORR) to ifrst-line chemotherapy of 52 pa-tients with advanced disease harboringKARS mutation was 9.6%. hTe disease control rate (DCR) was 53.8%, and the median progression-free survival (PFS) was 3 months. hTe ORR to EGFR-TKIs therapy in 21 patients harboringKARS mutation and EGFR/KARS co-mutation was 9.5%; the DCR was 23.8%, and the median PFS was 1 month. hTe ORR and DCR to EGFR-TKIs therapy of patients withEGFR/KARS co-mutation were signiifcantly higher than those of patients withKARS mutation (50%vs 0,P=0.029; 75%vs 11.8%,P=0.043); the median PFS was also signiifcantly longer (3 monthsvs 1 month,P=0.004). Conclusion hTe effcacy to ifrst-line chemotherapy and EGFR-TKIs therapy in NSCLC patients harboringKARS mutation was poor; thus, new drugs should be developed. Furthermore, the existence ofEGFR/KARS co-mutation was conifrmed. Hence, EGFR-TKIs therapy should be administered to patients withEGFR/KARS co-mutation.

Background and objectiveAnaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC) is an important subtype of lung cancer. hTe standard modality of ALK-positive NSCLC with brain metastases re-mains uncertain.MethodsWe collected data on clinical characteristics and treatment of patients with ALK-positive NSCLC and brain metastases between March 2013 and March 2016 and retrospectively analyzed patient outcomes.Results In 84 ALK-positive patients with advanced NSCLC, 22 (26.2%) had brain metastases during the initial diagnosis of lung cancer, among which 3 patients with EGFR mutation were excluded, and 19 patients were analyzed. Median intracranial progression-free survival (PFS) was 12.0 months. PFS for patients who received first-line local brain therapy (P=0.021) and crizotinib therapy (P=0.030) was superior to PFS for patients without such therapies. PFS for patients who received ifrst-line crizotinib combined with local brain therapy was 27.0 months and only 4.2 months for those who received crizotinib alone.Conclusion First-line crizotinib therapy combined with local brain treatment can improve intracranial PFS for ALK-positive NSCLC with brain metastases. hTis ifnding should be conifrmed further through multicenter, prospective clinical trials with large sample size.

Background and objective Status of epidermal growth factor receptor (EGFR) gene is a predictor of response to EGFR tyrosine kinase inhibitor (TKI). However, lile is know about the relationship between EGFR status and response to chemotherapy. We evaluated the prediction value of EGFR mutation status on response to first-line chemotherapy in patients with advanced non-small-cell lung cancer (NSCLC). Methods e data of 181 patients with stage IIIb/IV NSCLC who diagnosed by histopathology from January 10, 2006 to December 20, 2013 in Beijing Chest Hospital, Capital Medical University were collected. e relationships between EGFR gene status, clinical characteristics and response and progression-free survival (PFS) were analyzed. Results All of the 181 patients’ EGFR statuses were determined. 75 (41.4%) patients har-bored EGFR-activating mutations and 106 (58.6%) patients were EGFR wild-type. All patients received first-line chemother-apy. e objective response rate (ORR) was 26.0% and disease control rate (DCR) was 70.2%. Patients with EGFR-activating mutations had a higher DCR than patients with EGFR wild-type (84.0% vs 60.4%, P=0.001) did. Subgroup analysis showed that the ORR and DCR in patients with EGFR exon 19 deletions were remarkably higher than those with EGFR wild-type (P= 0.049, 0.002, respectively). e DCR in patients with EGFR exon 21 L858R mutation was significantly higher than that in patients with EGFR wild-type (P=0.010). 168 patients were available for response evaluation in all of 181 patients and median PFS was 4.3 mo. e PFS of patients with adenocarcinoma was significantly higher than that patients with squamous cell carci-noma (4.7 mo vs 3.0 mo, P=0.036). e PFS in patients harbored EGFR-activating mutations was significantly higher than that in the patients with EGFR wild-type (6.3 mo vs 3.0 mo, P=0.002). e PFS of patients with a performance status (PS) of 0-1 was significantly higher than that in patients with a PS of 2 (4.4 months vs. 0.7 months, P= 0.016). Cox multivariate analysis indicates the EGFR-activating mutation is an independent factor aecting PFS (HR=0.654, 95%CI: 0.470-0.909, P=0.012). Conclusion EGFR-activating mutation is a predictor for PFS of first-line chemotherapy in advanced NSCLC patients.

Background and objective Activating mutations in epidermal growth factor receptor (EGFR) and KARS are important markers in non-small cell lung cancer. However, EGFR and KARS gene mutations in lung squamous cell carcinoma are rarely reported. hTe aim of this study was to analyze EGFR and KARS gene mutation rate and their relationship with clinical features in patients with lung squamous cell carcinomas. Methods A total of 139 patients undergoing treatment for na?ve lung squamous cell carcinomas with tumor tissue samples available for testing were recruited. EGFR and KARS mutation statuses of the tumor samples were detected using a mutant enriched liquid chip. Results Of the 139 cases of lung squamous cell carcinoma, EGFR mutations were detected in 25 cases (18%), KARS mutations were detected in 7 cases (5%), and the pres-ence of both EGFR and KARS mutations was detected in 1 case (0.7%). EGFR mutations occurred more otfen in females than in males (33.3%vs 16.5%) and in patients that never smoked than in those who smoke (29.6%vs 16.1%). However, the differ-ence did not reach statistical signiifcance (P>0.05). No signiifcant differences were observed in age, stage, and different biopsy type. KARS mutations occurred more otfen in males than in females (5.5%vs 0%), but the difference did not reach statistical signiifcance (P>0.05). No signiifcant differences were observed in age, stage, different biopsy type, and smoking status (P>0.05). Conclusion EGFR and KARS mutations were low in lung squamous cell carcinomas, and had no signiifcant correlation with clinical features. Before using tyrosine kinase inhibitor targeted therapy, EGFR and KARS mutations should be detected in pa-tients with lung squamous cell carcinomas.