目的 了解青海省北京/W系结核分枝杆菌分布特征。方法 收集青海地区结核分支杆菌临床分离株,采用RD105缺失基因检测鉴定北京/W系结核分枝杆菌。结果 共收集237株结核分枝杆菌临床分离株,采用RD105缺失基因检测鉴定北京/W系结核分枝杆菌220株,占92.8%,非北京/W结核分枝杆菌,共17株,占7.2%。北京/W系结核分枝杆菌在青海地区性别与民族分布差异没有统计学意义(P＞0.05)。结论 北京/W结核分枝杆菌为青海地区流行菌株,在人群易于发生感染和传播。

Objective To ascertain the epidemiological characteristics of Beijing/W lineage Mycobacterium tuberculosis in Qinghai Province. Methods M. tuberculosis clinical isolates were collected and identified with an RD105 deletion test.Statistical analysis was performed by using the test. Results Totally, 237 clinical isolates of M. tuberculosis were collected in which 220 strains (92.8%) belonged to the Beijing/W lineage of M. tuberculosis while 17strains (7.2%) belonged to the non-Beijing/W lineage of M. tuberculosis according to the RD105 deletion test. There were no significant differences in the distribution of Beijing/W lineage of M. tuberculosis in the gender and nationality (P＞0.05). Conclusion Beijing/W lineage of M. tuberculosis were prevalent in Qinghai province and prone to having infection and transmission in the crowd.

       目的   研究SOCS6/STAT6通路在前列腺细胞炎性增殖作用中的调控作用。方法  使用人前列腺细胞株RWPE-1建立炎症模型，将细胞分为对照（CON）组和炎症刺激（INF）组，后者通过添加脂多糖（LPS）模拟炎症环境。采用ELISA检测白细胞介素-1β（IL-1β）-1β、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）表达水平，蛋白免疫印迹法检测细胞因子信号抑制物-6（SOCS6）、信号转导和转录激活因子-6（STAT6）及磷酸化STAT6蛋白的表达水平。结果  经过LPS处理后，RWPE-1细胞中的SOCS6蛋白表达水平显著下降（P＜0.01），而磷酸化STAT6表达水平上升（P＜0.01）。结论  SOCS6/STAT6通路可能通过调节炎症环境下STAT6的磷酸化水平，参与调节前列腺细胞的炎性增殖作用。

       Objective   To explore the  regulatory  role of  SOCS6/STAT6  pathway in the inflammatory  proliferation of 

prostate cells．Methods  The human prostate cell line RWPE-1 was used to establish an inflammation model．Cells were divided into a control（CON）group and an inflammation-stimulated（INF）group，with the latter subjected to lipopolysaccharide（LPS）treatment to simulate an inflammatory environment．The expression levels of interleukin（IL）-1β、IL-6 and  IL-8 were detected by ELISA，and the expression levels of suppressor of cytokine signaling 6（SOCS6），signal transducer and activator oftranscription-6，（STAT6），and phosphorylated STAT6 proteins were detected by Western blot．Results  The  results showed that after LPS treatment，the expression of SOCS6 protein in RWPE-1 cells significantly decreased，while the expression of phosphorylated STAT6 increased．Conclusions  The SOCS6/STAT6 pathway may be involved in  regulating the inflammatory proliferation of prostate cells by modulating the phosphorylation level of STAT6 under inflammatory conditions．

        目的   分析达格列净联合沙库巴曲缬沙坦治疗射血分数降低的心力衰竭（HFrEF）效果。方法  连续抽取2021年1月—2023年6月在广州市第一人民医院心内科住院的射血分数降低的心力衰竭（HFrEF）患者203例，随访至少6个月，按照接受的治疗进行分组。对照组予常规治疗和沙库巴曲缬沙坦治疗；观察组予常规治疗、沙库巴曲缬沙坦和达格列净治疗；对比两组疗效，观察指标包括住院时间，入院及出院后6个月的心功能状态（NYHA纽约心脏病协会心功能分级）、心脏超声指标左室射血分数（LVEF）、左室舒张末内径（LVEDD）、左室收缩末内径（LVSDD）、血液指标-端脑钠肽前体（NT-proBNP N）、糖化血红蛋白（HBA1c）、血肌酐（Cr）、6个月时的再住院率及全因死亡率。结果   观察组心脏监护病房（CCU）停留时间（2.54±1.26）d，短于对照组的（3.73±1.21）d；观察组6个月时观察组心功能NYHA改善≥2级比例为95.05%高于对照组的86.27%，差异有统计学意义（P＜0.05）；观察组6个月时的LVEDD、LVESD水平分别为（48.22±7.35）（34.61±4.32）mm，低于对照组的（51.47±8.02）（43.07±5.33）mm，LVEF为（51.49±5.40）%，高于对照组的（46.18±4.21）%，差异有统计学意义（P＜0.05）；6个月时观察组的NT-proBNP为（415.58±31.57）pg/mL，低于对照组的（520.23±385.56）pg/mL，差异有统计学意义（P＜0.05）；两组的住院时间、血清肌酐（Cr）、HBA1c、6个月时的再住院率、全因病死率对比，差异不显著（P＞0.05）。观察组HBA1c值为（6.04±0.66）mmol/L，高于对照组的（5.20±0.56）mmol/L（P＜0.05）。结论  HFrEF患者采取达格列净+沙库巴曲缬沙坦治疗，可通过协同作用，缩短CCU停留时间，改善患者6个月时的心功能状态，降低NT-proBNP值，减少心脏扩大趋势，提高LVEF水平。

       Objective  To analyze the efficacy of  dapagliflozin combined with  sacubitril/valsartan in the treatment of heart failure with reduced ejection fraction（HFrEF）．Methods  A total of 203 patients with HFrEF who were hospitalized in the cardiology department of the hospital between January 2021 and June 2023 were enrolled and followed up for at least six months．Patients were divided into groups based on their treatment regimens：the control group received conventional treatment plus sacubitril/valsartan，while the observation group received conventional treatment plus sacubitril/valsartan and dapagliflozin．The two groups were compared for clinical outcomes，including length of hospital stay，cardiac function（NYHA classification）at admission and six months after discharge，echocardiographic indicators（LVEF，LVEDD，LVESD），blood indicators（NT-proBNP，HbA1c，creatinine），six-month rehospitalization rate，and all-cause mortality．Results  The observation group had a shorter CCU stay（2.54±1.26 days）compared to the control group（3.73±1.21 days）．At sixth month，the proportion of patients in the observation group with an NYHA improvement ≥2 grades（95.05%）was significantly higher than that in the control group（86.27%）（P＜0.05）．The observation group demonstrated lower LVEDD（48.22±7.35 mm）and LVESD（34.61±4.32 mm）levels and higher LVEF（51.49±5.40%）compared to the control group（LVEDD：［51.47±8.02］ mm，LVESD：［43.07±5.33］mm，LVEF：［46.18±4.21］%）（P＜0.05）．NT-proBNP levels in the observation group（［415.58±31.57］ pg/mL）were significantly lower than those in the control group（［520.23±385.56］ pg/ml）（P＜0.05）．There were no significant differences between the two groups in length of total hospital stay，serum creatinine，HbA1c，six-month rehospitalization rate，or all-cause mortality（P＞0.05）．However，HbA1c levels in the observation group（［6.04±0.66］ mmol/L）were higher than those in the control group（［5.20±0.56］ mmol/L）（P＜0.05）．Conclusions  The combination of dapagliflozin and sacubitril/valsartan in the treatment of HFrEF patients can exert a synergistic effect，shorten CCU stay，improve cardiac function at sixth month，reduce NT-proBNP levels，mitigate cardiac dilation，and increase LVEF．

       目的   探讨谷氨酸对HT22细胞线粒体自噬和细胞凋亡的影响，并评估虾青素预处理的保护作用及其分子机制。方法   用谷氨酸及虾青素处理HT22细胞，通过蛋白印迹及聚合酶联反应等评估其对线粒体自噬的影响。结果   谷氨酸处理显著抑制线粒体初级自噬（PINK1、Parkin、pULK1^ser555和LC3Ⅱ）和次级自噬（LAMP1和Rab7），上调cleaved Caspase-3的表达（P＜0.05）。虾青素预处理减少细胞凋亡，恢复了线粒体自噬，PINK1、Parkin、pULK1^ser555和LC3Ⅱ的表达水平上升（分别为2.3倍、2.6倍、83.3%及81.1%）（P＜0.05），该作用被自噬抑制剂BafA1阻断。此外，谷氨酸抑制Nrf2核内转移和NLRX1表达，而预处理显著促进Nrf2的核内转移并上调NLRX1，分别上调25.8%、33.2%。生物信息学分析显示NLRX1启动子区域含有3个Nrf2结合位点，提示Nrf2通过调控NLRX1转录活性发挥作用。结论   文章揭示虾青素通过Nrf2/NLRX1通路激活线粒体自噬，展现神经保护作用。

       Objective  To explore the effects of glutamate on mitophagy and apoptosis in HT22 cells and evaluate the protective effects and molecular mechanisms of astaxanthin pretreatment．Methods  HT22 cells were treated with glutamate and astaxanthin．The effects on mitophagy were assessed using Western Blot and PCR．Results  Glutamate treatment  significantly inhibited primary mitophagy（PINK1，Parkin，pULK1^ser555 and LC3II）and secondary mitophagy（LAMP1 and Rab7）while upregulating cleaved Caspase-3 expression．Astaxanthin pretreatment notably reduced apoptosis and restored mitophagy，the expression levels of PINK1，Parkin，pULK1^ser555 and LC3II were significantly upregulated（by 2.3-fold，2.6-fold，83.3% and 81.1% respectively，P＜0.05），but this effect was blocked by the autophagy inhibitor BafA1．Additionally，glutamate suppressed Nrf2 nuclear translocation and NLRX1 expression，whereas astaxanthin promoted Nrf2 nuclear translocation and increased NLRX1 expression by 25.8% and 33.2%，respectively．Bioinformatics analysis  revealed three Nrf2 binding sites in the NLRX1 promoter region，suggesting that Nrf2 may regulate NLRX1 transcriptional activity．Conclusions  The study demonstrates that astaxanthin exhibited potential neuroprotective effect by activating mitophagy through the Nrf2/NLRX1 pathway．