社区获得性肺炎证候及其特征的专家咨询问卷分析

目的:探讨社区获得性肺炎常见证候及变证的特征.方法:采用德尔菲(Delphi)法,编制肺炎中医证候特征专家咨询问卷,向全国30位专家发送.回收的资料使用Epidata3.0版软件建立数据库,运用SAS 6.12统计软件进行均数和变异系数的统计描述和X2检验.结果:回收有效问卷27份.专家积极系数为90%,权威系数为0.7758,协调系数为0.356(X2=455.65,P=0.001).肺炎常见证候有外寒内热证、风热袭肺证、痰热壅肺证、痰湿壅肺证、肺脾气虚证和气阴两虚证,变证有热入心包证和邪陷正脱证,并对其主次症特征作了分析.结论:肺炎常见证候有6种,变证有2种.肺炎证候及其特征可作为制定肺炎诊疗标准的参考.     

自拟化痰降浊汤治疗糖调节受损期的临床研究

目的:探讨化痰降浊法对糖调节受损(IGR)发病机制的治疗作用.方法:治疗40例运用自拟化痰降浊汤治疗60 d,比较治疗前后胰岛素(INS)的变化,并与单纯控制血糖的对照组比较.结果:治疗组空腹血糖(FBG),糖化血红蛋白(HBAIC)均有下降(P＞0.05),胰岛素敏感指数(IAI)较治疗前改善(P＜0.01),明显优于对照组.结论:痰浊内阻是IGR的重要发病机制,是IGR、糖尿病(DM)多种变证的核心所在,化痰降浊法是治疗IGR的有效方法,应贯彻始终.     

加味苓桂术甘汤合抗痨药治疗结核性胸腔积液

应用苓桂术甘汤加味联合抗痨药治疗结核性胸腔积液３９例,与单纯抗痨药治疗３７例作疗效对照观察。结果表明：治疗组在促进胸腔积液吸收、改善胸膜肥厚粘连方面疗匀明显优于对照组（Ｐ〈０．０５￣０．０１）,且具有缩短疗程,防止肝脏损害和降低复发率的作用。     

CDK4/6 and autophagy inhibitors synergize to suppress the growth of human head and neck squamous cell carcinomas

Head and neck squamous cell carcinoma (HNSCC) accounts for over 10,000 deaths in the United States annually. Approximately 80% of HNSCC are human papillomavirus (HPV)-negative which have an overall poorer prognosis compared to the HPV-positive disease. Treatment options are mainly nontargeted chemotherapy, radiation, and surgery. The cyclin-d -CDK4/6-RB pathway, which regulates cell cycle progression, is often deregulated in HNSCC, making it an attractive therapeutic target. In the current study, we investigated the therapeutic effects of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors in preclinical models of HNSCCs. Our results show that the specific CDK4/6 inhibitor, abemaciclib, inhibited cell growth, and induced apoptosis in HNSCC cell lines. We also demonstrated that both the pro-survival autophagy pathway and the ERK pathway in HNSCC cells were activated with abemaciclib treatment through the generation of reactive oxygen species (ROS). Coinhibition of CDK4/6 and autophagy synergistically decreased cell viability, induced apoptosis, and inhibited tumor growth in both in vitro and in vivo preclinical HNSCC models. These results reveal a potential therapeutic strategy that supports the rationale for further clinical development of a combination of CDK4/6 and autophagy inhibitors in HNSCC.