水针疗法联合清热祛毒汤治疗寻常型银屑病(血热证)的疗效及其作用机制分析

目的观察分析水针疗法联合清热祛毒汤治疗寻常型银屑病(血热证)的疗效及其作用机制。方法选择2018年8月—2019年7月在我院接收治疗的112例寻常型银屑病患者作为分析对象,采取随机分组的办法将其分为对照组56例和研究组56例,对照组患者采取水针疗法治疗,研究组在对照组的基础上联合清热祛毒汤治疗。比较分析2组患者的疗效;治疗前后的中医证候评分、皮肤病生活质量指数(DLQI)评分;治疗前后皮损面积、浸润、鳞屑、红斑等评分;治疗前后肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、血管内皮生长因子(VEGF)水平变化情况。结果研究组患者治疗总有效率89.29%明显高于对照组73.21%(P<0.05);治疗前,2组患者的中医证候评分、DLQI评分、皮损面积、浸润、鳞屑、红斑等评分及TNF-α、IL-6、VEGF等水平比较(P>0.05);研究组患者治疗后的中医证候评分与DLQI评分明显低于治疗前(P<0.05);研究组患者治疗后的皮损面积、浸润、鳞屑、红斑等评分明显低于对照组(P<0.05);研究组患者治疗后的TNF-α、IL-6、VEGF等水平明显低于对照组(P<0.05)。结论对寻常型银屑病患者采取水针疗法联合清热祛毒汤治疗的疗效显著,能有效改善中医证候表现,提高生活质量,减轻皮损程度,降低炎症反应,其作用机制可能与炎症因子水平、皮损血管增生相关。     

余尚贞以六戊年麦门冬汤治疗高血压经验浅析

高血压病为临床最常见的慢性病,余尚贞根据多年临床经验辨证,结合开、阖、枢理论,以太阴阳明升降不和为病机,从太阴阳明入手论治高血压病,结合五运六气选方六戊年麦门冬汤,临床治疗多例,疗效甚佳。开、阖、枢理论源于内经,是对人体三阴三阳经生理功能、病理特点及其相互关系的概括,我们可从中窥得开、阖、枢理论之部分面貌,比如对太阴、阳明经的了解,并拓展中医在治疗高血压病方面的治疗思路。     

Rabs and axonal regeneration

Membrane trafficking processes are presumably vital for axonal regeneration after injury, but mechanistic understanding in this regard has been sparse. A recent loss-of-function screen had been carried out for factors important for axonal regeneration by cultured cortical neurons and the results suggested that the activity of a number of Rab GTPases might act to restrict axonal regeneration. A loss of Rab27b, in particular, is shown to enhance axonal regeneration in vitro, as well as in C. elegans and mouse central nervous system injury models in vivo. Possible mechanisms underlying this new finding, which has important academic and translational implication, are discussed.     

多原发结直肠癌的临床特征和预后

目的探讨多原发结直肠癌的临床特征和预后。方法回顾性分析南京医科大学第一附属医院2013年1月至2018年12月收治的42例多原发结直肠癌患者的临床资料,对其临床病理特征、诊治及预后进行总结。结果符合多原发结直肠癌诊断的患者42例,占同期收治的所有结直肠癌患者的1.20%(42/3499),病理类型以腺癌为主。其中,同时性多原发癌32例,年龄38~86岁,中位年龄66岁,共发现73处结直肠癌灶,多位于近端结肠、乙状结肠及直肠;共检出淋巴结527枚,阳性10枚(1.9%),淋巴结阳性患者占同时性多原发癌的37.5%(12/32);27例为双原发癌,3例为三原发癌,2例为五原发癌;1、3年总生存率分别为83.75%和74.38%。异时性多原发癌10例,年龄33~86岁,第一癌多位于直肠和乙状结肠区域,第二癌多位于升结肠区域;共检出淋巴结276枚,阳性率12.3%(34枚),1、3年总生存率分别为100.00%和66.67%。结论多原发结直肠癌在临床上不少见,其分布有一定规律。临床中应引起重视,提高早期诊断率。应早期手术治疗以提高患者的生存率。     

Protein kinase Cδ mediates trimethyltin-induced neurotoxicity in mice in vivo via inhibition of glutathione defense mechanism

We investigated whether protein kinase C (PKC) is involved in trimethyltin (TMT)-induced neurotoxicity. TMT treatment (2.8 mg/kg, i.p.) significantly increased PKCδ expression out of PKC isozymes (i.e., α, βI, βII, δ, and ?) in the hippocampus of wild-type (WT) mice. Consistently, treatment with TMT resulted in significant increases in cleaved PKCδ expression. Genetic or pharmacological inhibition (PKCδ knockout or rottlerin) was less susceptible to TMT-induced seizures than WT mice. TMT treatment increased glutathione oxidation, lipid peroxidation, protein oxidation, and levels of reactive oxygen species. These effects were more pronounced in the WT mice than in PKCδ knockout mice. In addition, the ability of TMT to induce nuclear translocation of Nrf2, Nrf2 DNA-binding activity, and upregulation of γ-glutamylcysteine ligase was significantly increased in the PKCδ knockout mice and rottlerin (10 or 20 mg/kg, p.o. × 6)-treated WT mice. Furthermore, neuronal degeneration (as shown by nuclear chromatin clumping and TUNEL staining) in WT mice was most pronounced 2 days after TMT. At the same time, TMT-induced inhibition of phosphoinositol 3-kinase (PI3K)/Akt signaling was evident, thereby decreasing phospho-Bad, expression of Bcl-xL and Bcl-2, and the interaction between phospho-Bad and 14-3-3 protein, and increasing Bax expression and caspase-3 cleavage were observed. Rottlerin or PKCδ knockout significantly protected these changes in anti- and pro-apoptotic factors. Importantly, treatment of the PI3K inhibitor LY294002 (0.8 or 1.6 µg, i.c.v.) 4 h before TMT counteracted protective effects (i.e., Nrf-2-dependent glutathione induction and pro-survival phenomenon) of rottlerin. Therefore, our results suggest that down-regulation of PKCδ and up-regulations of Nrf2-dependent glutathione defense mechanism and PI3K/Akt signaling are critical for attenuating TMT neurotoxicity.     

大病保险对我国中老年人家庭灾难性卫生支出影响实证分析

目的:考察大病保险对我国中老年人家庭灾难性卫生支出的影响,为完善我国大病保险制度提供建议。方法:以中国健康与养老追踪调查数据库(2011年与2015年)中45岁及以上的城乡中老年人家庭作为研究对象,利用描述性统计法和两部模型法分析大病保险对我国中老年人家庭灾难性卫生支出的影响。结果:目前的大病保险政策从总体上降低了中老年人家庭灾难性卫生支出的发生率,但没有显著降低其发生强度。结论:目前的大病保险并未达到其预期的效果,只是解决了"面"的问题,从总体上降低了灾难性卫生支出发生的可能性,但并没有解决"点"的问题,没有有效降低其大额的医疗卫生支出进而减少其医疗经济负担。建议各地各级政府相关部门应进一步完善大病保险制度,从而真正有效减轻居民重大疾病医疗经济负担。     

黄蜀葵花治疗2型糖尿病肾病早期蛋白尿40例临床观察

目的:探讨黄蜀葵花干预2型糖尿病肾病(T2DKD)早期蛋白尿的临床疗效.方法:将80例T2DKD早期患者随机分为治疗组和对照组,每组各40例.对照组给予西医常规治疗,治疗组在对照组的基础上加用黄蜀葵花片治疗.2组疗程均为6个月.观察2组治疗前后血糖、血脂、肝肾功能、肾小球滤过率(eGFR)、尿白蛋白与尿肌酐比值(UACR)的变化.结果:治疗组脱落2例,对照组脱落1例.2组血压、血糖、血脂、肝肾功能、eGFR、合并用药情况治疗后组间比较,差异均无统计学意义(P＞0.05),而UACR及UACR下降程度治疗后组间比较,差异均有统计学意义(P＜0.05).结论:黄蜀葵花可明显减轻T2DKD早期患者尿蛋白水平,该疗效不依赖于血压和糖脂代谢的变化.     

益气化瘀解毒方对MRP、GST-π和Topo Ⅱ基因在Sorafenib获得性耐药人肝癌QGY7702细胞表达的干预研究

目的探讨益气化瘀解毒方干预后对Sorafenib获得性耐药人肝癌QGY7702细胞(QGY7702/Sora)增殖及MRP、GST-π和Topo Ⅱ基因表达的影响。方法培养QGY7702/Sora细胞和QGY7702细胞,利用Cell Counting Kit-8(CCK-8)法检测Sorafenib对细胞的半数抑制率浓度(IC50值),计算耐药指数RI;观察益气化瘀解毒方对耐药细胞的增殖影响;采用荧光定量PCR检测药物干预前后2种细胞中MRP、GST-π和Topo Ⅱ基因表达水平。结果亲本细胞和耐药细胞Sorafenib的IC50值分别为(7.993±0.522)μmol/L和(19.651±1.216)μmol/L,RI约为2.5。益气化瘀解毒方可抑制耐药细胞的增殖活性。2种细胞的MRP、GST-π、Topo Ⅱ表达量无明显差异(P>0.05)。Sorafenib组可促进耐药细胞MRP 、GST-π基因的过表达(P<0.05),益气化瘀解毒方组可抑制GST-π基因的过表达(P<0.01),且联合Sorafenib可显著提高Topo Ⅱ基因的表达量(P<0.01)。结论 QGY7702/Sora细胞MRP、GST-π和Topo Ⅱ的表达水平与亲本细胞无显著差异。耐药细胞对Sorafenib敏感性降低与MRP、GST-π过表达相关,而益气化瘀解毒方拮抗Sorafenib耐药与抑制GST-π过表达相关。