针灸联合关节松动术治疗肩周炎的网状Meta分析＊

目的 运用网状Meta分析方法评价针灸联合关节松动术治疗肩周炎的疗效。方法 运用计算机检索Web of Science、PubMed、Cochrane Library、EMbase、维普（VIP）、中国知网（CNKI）、万方（Wanfang）、中国生物医学文献数据库（CBM），搜寻有关针灸联合关节松动术治疗肩周炎的随机对照试验。所有研究人员均独立纳排文献、提录资料、风险评估，对符合质量标准的RCT研究采用Stata16.0和Review Manager 5.4软件进行分析。结果 共检索出6561篇文献，最终纳入37项研究，涉及10种针灸联合关节松动术方法。总样本量2890例，其中试验组1432例，对照组1458例。网状Meta分析所得结果表明：①在总有效率方面，最好的3种治疗方法为内热针联合组、温针联合组、动筋针联合组；②在降低VAS评分方面，最好的3种治疗方法为内热针联合组、动筋针联合组、针刀联合组。结论 针灸联合关节松动术治疗肩周炎疗效总体优于单独使用，且内热针联合组具有最佳的疗效。     

不孕与情志关系初探

认为情志异常是影响女子不孕的重要因素。肝失疏泄可使气机失调,影响月经周期阴阳消长转化,导致排卵障碍,破坏肾气-天癸-冲任-胞宫生殖轴的协调与平衡,导致不孕。治疗当以疏肝解郁为主,辅以养血理脾,并应注重情志调节。     

经外踝入路关节内环锯法行踝关节融合术

[目的]介绍经外踝入路关节内环锯法行踝关节融合术的方法与临床效果。[方法]利用环锯(14mm、16 mm、18 mm)对20例踝关节严重病损病人行关节融合术,均采用踝关节外侧入路,腓骨下段截骨并下翻显露关节,利用环锯关节内融合即原锯心骨旋转90°原位回植,外踝骨块螺钉固定旁靠植骨。术后关节予以石膏固定。[结果]经随访6个月~4 a,平均26个月。术后2周刀口Ⅰ期愈合,4周可见骨痂形成,12周病人疼痛明显缓解或消失,足部外形改善。X线片示胫距关节牢固融合。[结论]采用经外踝入路关节内环锯法行踝关节融合术,方法简单,融合率高。其优点为:切口显露良好;对胫距关节干扰小,保证了关节的正常高度和下肢长度;锯心骨原位回植无需再次植骨,外踝旁靠植骨提高了植骨强度。     

《金匮要略》对耳鼻喉科临床的影响

从主张治未病、重视整体性、注重从脏腑经络辨治、强调辨病与辨证相结合以及灵活运用内治法和外治法五个方面,阐述了《金匮要略》辨证论治的思想对后世耳鼻喉科疾病治疗的影响。认为现代耳鼻喉疾病的发生虽然与古代有所不同,但是《金匮要略》的论治思想和治疗法则仍然对现代耳鼻喉科的临床发挥着重要的指导作用。     

活血熄风方对局灶性脑缺血大鼠内皮素1和一氧化氮含量的影响

目的观察活血熄风方对局灶性脑缺血模型大鼠血液和脑组织中内皮素1（ET-1）和一氧化氮（NO）含量的影响，探讨其脑保护的作用机制。方法雄性WiStar大鼠40只随机分为5组：假手术组、模型组及活血熄风方高、中、低剂量组，每组8只。采用光化学法建立局灶性脑缺血大鼠模型，造模前7d灌胃给药，活血熄风方高、中、低剂量组分别给予活血熄风方20、10、5g／（kg·d），假手术组和模型组给予等体积蒸馏水灌胃，造模后24h分别取血及脑组织，放射免疫法测定模型大鼠血浆及脑组织中ET-1含量，分光光度法测定血清及脑组织中N0的含量。结果活血熄风方能降低模型大鼠血浆及脑组织中ET-1含量，降低脑组织中NO含量，升高血清中N0含量，与模型组比较，差异有统计学意义（P〈0．05或P〈0．01）。结论活血熄风方对局灶性脑缺血模型大鼠的保护作用可能与其降低血浆及脑组织中ET-1含量，降低脑组织中N0含量，升高血清N0含量，从而调节ET-1／N0比值有关。     

基于复杂网络的《新针灸学》与《经络腧穴学》比较分析研究（英文）

提取《新针灸学》《经络腧穴学》中穴位名称、主治病症信息,基于复杂网络建立穴-症网络,分析两者穴位数量、相互关联程度及主治规律变化,借助拓扑学数据解释变化原因,为传统针灸知识体系的结构化、标准化研究提供具体思路和方法。共纳入《新针灸学》386穴、773种症状、形成152163个穴位配伍对,《经络腧穴学》403穴、253种症状、28755个穴位配伍对。两本教材的穴-症网络存在丰富的差异性,其所载的病症结构化程度随医学知识的更新而提升。《新针灸学》模型具有更加典型的小世界效应,或因其以病症为主要分类手段的优势体现。两本教材穴位定位与主治方面发生许多变化,学科发展、时代背景等方面是变化的主要原因。     

Ferulic acid enhances insulin secretion by potentiating L-type Ca2+ channel activation

ObjectiveTo investigate the effect of ferulic acid, a natural compound, on pancreatic beta cell viability, Ca²⁺ channels, and insulin secretion.MethodsWe studied the effects of ferulic acid on rat insulinoma cell line viability using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide viability assay. The whole-cell patch-clamp technique and enzyme-linked immunosorbent assay were also used to examine the action of ferulic acid on Ca²⁺ channels and insulin secretion, respectively.ResultsFerulic acid did not affect cell viability during exposures up to 72 h. The electrophysiological study demonstrated that ferulic acid rapidly and concentration-dependently increased L-type Ca²⁺ channel current, shifting its activation curve in the hyperpolarizing direction with a decreased slope factor, while the voltage dependence of inactivation was not affected. On the other hand, ferulic acid have no effect on T-type Ca²⁺ channels. Furthermore, ferulic acid significantly increased insulin secretion, an effect inhibited by nifedipine and Ca²⁺-free extracellular fluid, confirming that ferulic acid-induced insulin secretion in these cells was mediated by augmenting Ca²⁺ influx through L-type Ca²⁺ channel. Our data also suggest that this may be a direct, nongenomic action.ConclusionThis is the first electrophysiological demonstration that acute ferulic acid treatment could increase L-type Ca²⁺ channel current in pancreatic β cells by enhancing its voltage dependence of activation, leading to insulin secretion.     

关联分析和互信息熵联合探究《中国药典》胃病相关中药成方制剂用药规律

目的 基于关联分析和互信息熵对《中国药典》2020年版一部与胃病相关的中药成方制剂进行药物配伍应用规律研究。方法 锁定“胃”“脘”“宽中”“纳呆”“呕恶”“食积”等为检索词,收集《中国药典》中胃病相关成方制剂,结合药智数据网、蒲标网及中国知网（CNKI）辅助检索其药材相关信息,使用Microsoft Excel 2019软件建立数据库。运用SPSS Modeler 18.0的Apriori算法对高频中药进行关联规则分析,并使用Cytoscape 3.9.1完成网络可视化。用互信息熵（mutual information entropy,MIE）量化药对关联程度,选择高MIE药对在Cytoscape 3.9.1中构建药材配伍网络,并采用Glay算法对网络节点进行聚类分析。并将以上2种方法进行组合分析,先用Apriori算法收集所有核心中药组合,再计算并筛选出高MIE值药对。结果 《中国药典》2020年版一部共收录263个胃病相关成方制剂,剂型以丸剂、胶囊剂、片剂为主;涉及352味药材,主要包括清热药、补虚药、祛风湿药等,药味以苦、辛、甘为主,药性以温、寒居多。其中有13味名贵中药,34味...     

Clinical observation on treatment of tubal pregnancy by chinese herbal medicine combined with tubal intubation administration of methotrexate under uteroscope

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miR-146a-5p regulates autophagy and NLRP3 inflammasome activation in epithelial barrier damage in the in vitro cell model of ulcerative colitis through the RNF8/Notch1/mTORC1 pathway

Ulcerative colitis (UC) is a chronic inflammatory disease affecting the colon that can be influenced by microRNAs (miRNAs). This study aims to investigate the impact of miR-146a-5p on lipopolysaccharide (LPS)-induced Caco-2/HT-29 cell autophagy and NLRP3 inflammasome activation and the underlying mechanism, with the aim of identifying potential therapeutic targets. We used LPS to establish Caco-2/HT-29 cell models and measured cell viability by CCK-8. The levels of miR-146a-5p, RNF8, markers of NLRP3 inflammasome activation and autophagy, proteins involved in the Notch1/mTORC1 pathway, and inflammatory factors were assessed by RT-qPCR, Western blot, and ELISA. Intestinal epithelial barrier function was evaluated by measuring transepithelial electrical resistance. Autophagic flux was measured using tandem fluorescent-labeled LC3. miR-146a-5p was highly-expressed in LPS-induced Caco-2/HT-29 cells, and autophagy flux was blocked at the autolysosomal stage after LPS induction. Inhibition of miR-146a-5p suppressed NLRP3 inflammasome activation, reduced intestinal epithelial barrier damage, and facilitated autophagy inhibition in LPS-induced Caco-2/HT-29 cells. The autophagy inhibitor NH4Cl partially nullified the inhibitory effects of miR-146a-5p inhibition on NLRP3 inflammation activation. miR-146a-5p targeted RNF8, and silencing RNF8 partly abrogated the action of miR-146a-5p inhibition on promoting autophagy and inhibiting NLRP3 inflammasome activation. miR-146a-5p inhibition suppressed the Notch1/mTORC1 pathway activation by upregulating RNF8. Inhibition of the Notch1/mTORC1 pathway partially nullified the function of silencing RNF8 on inhibiting autophagy and bolstering NLRP3 inflammasome activation. In conclusion, miR-146a-5p inhibition may be a potential therapeutic approach for UC, as it facilitates autophagy of LPS-stimulated Caco-2/HT-29 cells, inhibits NLRP3 inflammasome activation, and reduces intestinal epithelial barrier damage by upregulating RNF8 and suppressing the Notch1/mTORC1 pathway.