Because cigarette smoke can induce COPD/emphysema through accelerating senescence with or without an incomplete repair system. However, the pathogenesis of COPD following lung senescence induced by CS is not fully understood. Airspace enlargement and airway epithelial cell senescence are common finding during the COPD development. We investigated the lung tress response to CS and demonstrated that a stress-responsive transcription factor, FOXO3, was regulated by deacetylase. SIRT1 inhibited FOXO3 acetylation and FOXO3 degradation, leading to FOXO3 accumulation and activation in airway epithelial cells. CS exposure activated SIRT1 contributed to FOXO3 activation and functioned to protect lungs, as deletion of SIRT1 decreased CS-induced FOXO3 activation and resulted in more severe airway epithelial cells senescence airspace enlargement. Strikingly, deletion of FOXO3 during the development of COPD aggravated lung structural and functional damage, leading to a much more profound COPD phenotype. We show that deletion of FOXO3 resulted in decreased autophagic response and increased senescence, which may explain lung protection by FOXO3. Our study indicates that in the COPD, stress-responsive transcription factors can be activated for adaptions to counteract senescence insults, thus attenuating COPD development.

Abstract Background LncRNAs pays an important roles in the regulation of alveolar cells in cigarette smoke (CS) induced chronic obstructive pulmonary disease (COPD). However, the role of lncRNA SAL-RNA1 in promoting mitophagy and reduces senescence of alveolar cells in COPD is unknow. Methods This study is aims to elucidate the underlying mechanism of LncRNA SAL-RNA1 and phosphatase and tensin homolog (PTEN)-induced putative protein kinase 1 (PINK1) expression were upregulated in alveolar of emphysema mice and CS treated alveolar epithelial cells. LncRNA SAL-RNA1 knockdown suppressed mitophagy and induced senescence of alveolar cells while overexpressing lncRNA SAL-RNA1 promoted mitophagy and reduced the senescence of alveolar cells. In addition, lncRNA SAL-RNA1 interacted with Sirt1 and regulated the upgradation of Sirt1. Results We further found lncRNA SAL-RNA1 regulated Pink1 expression through Sirt1. Mechanistically, lncRNA SAL-RNA1 regulated PinK1-mediated mitophagy and senescence of alveolar cells through regulation Sirt1. Conclusion Finally, overexpression lncRNA SAL-RNA1 promote mitophagy and relieved emphysema.

BACKGROUND:Lung cancer with pulmonary tuberculosis (TB) refers to the occurrence of lesions simultaneously or sequentially in the lung(s) of the same patient, and the pathological examination and sputum TB examination diagnose them as lung cancer and TB, respectively. The occurrence of endobronchial TB (EBTB) with endobronchial tumor sequentially in the same bronchus lesion of the same patient is relatively rare.CASE SUMMARY:A 62-year-old female patient was admitted to a local hospital on June 18, 2019 after a 3-mo history of dyspnea. She was a farmer and had no history of smoking and alcohol misuse. The patient had neither family nor work contact indicating exposure to TB. Emergency chest computed tomography (CT) examination showed that the right main bronchus was occupied and malignant tumor was possible. Histopathologic examination of a bronchial biopsy showed granulomatous inflammation with caseification and the presence of acid fast bacilli (AFB). However, after 6 mo of antitubercular treatment, repeat bronchoscopy and biopsy histological examination showed squamous cell carcinoma. The patient has started on systemic chemotherapy with carboplatin. After another two cycles of therapy, chest CT showed complete resolution of the lesions. Bronchoalveolar lavage and bronchial aspirate were negative for AFB and cancer cells.CONCLUSION:It is not only more likely that a patient presenting with what appears to be TB will concurrently have a pulmonary malignancy than someone who does not have a TB infection, but also that it is of greater urgency to make an expedited diagnosis of the malignancy.

目的 通过测定慢性阻塞性肺疾病(COPD)患者血浆生长分化因子(GDF-15)的水平,探讨GDF-15在COPD严重程度分级和判断预后中的作用.方法 纳入2014年4月～2019年2月我院收治的99例COPD住院患者作为COPD组,按严重程度分为中度组(n=35)、重度组(n=33)、极重度组(n=31),记录各组的基线资料,并对相关指标进行比较.对COPD患者进行14个月随访,记录COPD不良事件.采用Spearman相关分析研究COPD中度、重度、极重度的GDF-15和CRP之间的相关性.并比较GDF-15和CRP区分对照组和COPD组的诊断效能,预测COPD组不良事件.结果 与对照组相比,COPD组患者CRP、GDF-15水平明显升高,CRP、GDF-15随COPD严重程度增加而明显升高(均P<0.05),在中度组COPD患者中,血浆中GDF-15与CRP浓度呈正相关(r=0.952,P<0.001),在重度组COPD患者中,血浆中GDF-15与CRP浓度呈正相关(r=0.951,P<0.001),在极重度组COPD患者中,血浆中GDF-15与CRP浓度呈正相关(r=0.973,P<0.001).ROC曲线表明,血浆CRP、GDF-15对COPD诊断的AUC分别为0.764、0.900,最佳诊断临界值分别为10.45 mg/L、485.50 ng/mL.CRP、GDF-15二者联合诊断的AUC为0.091,血浆CRP、GDF-15对COPD不良事件预测的AUC分别为0.855、0.859,最佳诊断临界值分别为18.45 mg/L、720.95 ng/mL.CRP、GDF-15二者联合诊断的AUC为0.864.结论 GDF-15和CRP均有助于判断COPD的严重程度,对预测患者病情的严重程度和预后有着积极的临床意义.

CONTEXT.—:Covert severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections could be seeding new outbreaks. How to identify asymptomatic SARS-CoV-2 infections early has become a global focus.OBJECTIVE.—:To explore the roles of immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies detection, nucleic acid tests, and computed tomography (CT) scanning to identify asymptomatic SARS-CoV-2 infection.DESIGN.—:The clinical data of 389 individuals with close contacts, including in general characteristics, SARS-CoV-2 etiology, serum-specific IgM and IgG antibody detection and CT imaging results, were systematically analyzed.RESULTS.—:The present study showed that only 89 of 389 individuals with close contacts were positive after the first nucleic acid test, while 300 individuals were still negative after 2 nucleic acid tests. Among the 300 individuals, 75 did not have pneumonia, and the other 225 individuals had pulmonary imaging changes. A total of 143 individuals were eventually diagnosed as having asymptomatic infection through IgM antibody and IgG antibody detection. The sensitivity, specificity, and false-negative rate of IgM and IgG antibody detection were approximately 97.1% (347 of 357), 95.3% (204 of 214), and 4.67% (10 of 214), respectively. It also indicated that during approximately 2 weeks, most individuals were both IgM positive and IgG positive, accounting for 68.57% (72 of 105). During approximately 3 weeks, the proportion of IgM-positive and IgG-positive individuals decreased to 8.57% (9 of 105), and the proportion of IgM-negative and IgG-positive individuals increased to 76.19% (80 of 105).CONCLUSIONS.—:There are highlighted prospects of IgM/IgG antibody detection as a preferred method in identifying the individuals with asymptomatic SARS-CoV-2 infection, especially combined with nucleic acid tests and pulmonary CT scanning.

卒中后抑郁(PSD)是卒中后最常见的神经精神并发症之一.其诊断比较困难,目前仅基于临床量表评估.近年来,国内外学者发现了与PSD相关的血液生物标志物,如血浆5-羟色胺、多种细胞因子、瘦素、神经营养因子及其相关分子、总胆红素、丙氨酸、碱性磷酸酶、血尿酸、丙二醛、超氧化物歧化酶、谷胱甘肽过氧化物酶、血清8-羟基-2-脱氧鸟苷等.但截至目前,没有发现任何高度特异性的血液生物标志物可以应用于临床进行PSD诊断.

目的 探讨非间断性口服艾司唑仑联合唑吡坦对高龄失眠患者认知功能的影响.方法 根据镇静催眠药种类将61例高龄失眠患者分为艾司唑仑组29例、唑吡坦联合艾司唑仑组32例,比较两组平均睡眠时间评估和简易智力状态检查量表(MMSE)评分.结果 治疗4周后,两组日间功能障碍评定量表中困倦、精神差、反应迟钝、共济失调、判断力下降五个项目差异均有统计学意义(均P＜0.05);两组注意力和计算力、回忆能力、语言能力差异均有统计学意义(均P＜ 0.05).结论 非间断性应用艾司唑仑联合唑吡坦对高龄失眠患者认知功能的影响低于单用艾司唑仑片.

目的 观察痒觉刺激对卒中后抑郁的临床干预效果.方法 将2015年10月~2017年4月新发脑梗死经评估确诊为卒中后抑郁的患者随机分为试验组和对照组,各30例,两组均采用内科基础治疗,试验组在康复训练的基础上进行痒觉刺激治疗,对照组进行单纯的康复训练.两组在入院24 h内、住院7 d、发病14 d、发病1个月和3个月时分别进行汉密尔顿抑郁量表(HAMD)及入院24 h内、住院7 d、发病14 d NIHSS测评.结果 试验组治疗14 d和1个月、3个月时HAMD评分分别为(12.93±3.63)分、(9.70±3.50)分、(5.93±4.88)分与对照组分别为(16.90±3.35)分、(11.67±3.47)分、(9.30±3.57)分进行比较,差异具有统计学意义(P<0.01、P<0.05、P<0.01),而两组间住院7 d、发病14 d NIHSS测评对比差异无统计学意义(P>0.05).结论 痒觉刺激早期实施可有效干预卒中后抑郁,降低抑郁程度.