Tos改良联合进路钛听骨植入鼓室成形的疗效观察*

目的观察符合条件的慢性化脓性中耳炎患者行Tos改良联合入路清理病变并一期植入钛人工听骨行鼓室成形的效果。方法回顾性分析34例在该院施行Tos改良联合入路乳突开放并植入钛人工听骨行鼓室成形的慢性化脓性中耳炎病例,总结患者手术前后听力及影像学特点,观察手术前后言语频率气导听阈变化。结果以术中听骨破坏情况分组,镫骨板上结构缺失组植入全听骨赝复体(TORP)后听力改善(36.25±6.12)dB HL;砧蹬关节中段组植入部分听骨赝复体(PORP)后听力改善(13.18±3.37)dB HL。术后无钛听骨移位、感染,听力改善有效率97.06%(P0.05)。1~3个月全部干耳。结论 Tos改良联合入路鼓室成形并一期植入钛人工听骨能有效地清理中耳病变,尤其是清理后鼓室的隐匿病变,并有效提高听力,术前高分辨率CT(HRCT)发现乳突气化不良,尤其有乙状窦前移、脑板低位和面神经低位等不利于暴露的解剖变异时,可优先选择此术式。     

3D全胸腔镜不停跳房间隔缺损修补术CUSUM学习曲线分析*

目的探讨3D全胸腔镜不停跳房间隔缺损(ASD)修补术的学习曲线及安全性。方法 ASD患者206例,完成3D全胸腔镜ASD修补及三尖瓣成形术44例(腔镜组)。累积和(CUSUM)法确定3D胸腔镜ASD修补术的学习曲线。并与传统开胸手术(开胸组)行倾向性评分匹配(PSM),分析腔镜组学习期间手术的安全性。结果 CUSUM学习曲线显示手术失败率、手术时间、体外循环时间、术后并发症发生率分别在第34、21、29及39例患者后低于可接受水平。匹配后两组术前特征不存在系统差异。腔镜组体外循环时间长于开胸组(P=0.000);手术时间、呼吸机辅助时间、ICU住院时间、术后并发症及总住院费用两组比较差异无统计学意义(P0.05)。腔镜组术后引流量明显少于开胸组(P=0.000)。结论 3D胸腔镜不停跳ASD修补术使手术更简化,更安全,不增加术后并发症及住院费用,并能在39例后快速跨越学习曲线。     

不同调配方法对注射用奥美拉唑钠残留量的影响

目的选取注射用奥美拉唑钠较好的调配方法,探寻超药品说明书用药的合理性。方法采用高效液相色谱(HPLC)法测定不同调配方法调配后瓶内奥美拉唑钠残留量,比较调配方法的优劣。结果选用10mL溶剂所调配药物溶液的残留量较小。结论在调配注射用奥美拉唑钠时,溶剂的选择方面,超说明书用药具有合理性,而溶剂的用量还需遵照药品说明书的规定。     

高效液相色谱质谱联用法测定射干合剂中8种中药成分的含量

目的:建立一种高效液相色谱质谱联用法同时测定黄芩苷、野黄芩苷、汉黄芩素、咖啡酸、麻黄碱、射干苷、次野鸢尾黄素、黄芩素等8种中药成分的含量及其在我院自有制剂射干合剂中的应用。方法:色谱条件:色谱柱为ZORBAX SB-C18(2.1 mm×50 mm,1.8μm),流动相为0.1%甲酸水溶液-乙腈,梯度洗脱,流速为0.3 ml·min-1,柱温:35℃;质谱条件:采用电喷雾离子源(ESI),多反应离子监测(MRM),结合正负离子扫描切换,其中咖啡酸、野黄芩苷、射干苷采用负离子模式检测,黄芩苷、汉黄芩素、次野鸢尾黄素、黄芩素、麻黄碱采用正离子模式检测。结果:黄芩苷、野黄芩苷、汉黄芩素、咖啡酸、麻黄碱、射干苷、次野鸢尾黄素、黄芩素的定量限分别为1.44×10-4,4.20×10-3,2.95×10-4,7.80,4.90×10-3,4.6×10-2,3.18×10-4,4.85 ng·ml-1,检测限分别为4.32×10-5,1.3×10-3,8.84×10-5,0.77,2.90×10-4,3.33×10-4,9.5×10-5,1.46 ng·ml-1;在相应的线性范围内R2>0.992 3;日内和日间精密度(RSD)均小于5%,平均回收率均在80%~120%。结论:本方法在20 min内实现这8种化合物的分离和测定,简单、快速、灵敏、准确,可用于射干合剂多成分含量测定。     

山风化学成分研究

摘 要 目的： 研究中药材山风的化学成分。方法: 采用薄层色谱、硅胶及凝胶柱色谱法对山风进行分离纯化,通过理化方法和波谱数据进行结构鉴定。结果: 从山风中分离得到10个化合物,通过波谱数据及理化性质分别鉴定为油酸(1)、亚油酸(2)、槲皮素(3)、木犀草素(4)、柚皮素(5)、橙皮素(6)、没食子酸(7)、β 谷甾醇(8)、胡萝卜苷(9)和橙皮苷(10)。结论:化合物1、2、5、6、7、10为首次从山风中分离得到。     

用于抗肿瘤的ATP竞争性纺锤体驱动蛋白抑制药的研究进展

纺锤体驱动蛋白(kinesin spindle protein,KSP)抑制药是抗肿瘤药物研究的一个重要方向,已有数个KSP抑制药进入临床研究。ATP竞争性KSP抑制药的发现,为克服因为结合位点突变而引起的对ATP非竞争性KSP抑制药耐药提供了新的研究思路。本文综述了近年来报道的ATP竞争性KSP抑制药,为进一步的研究提供了参考。     

胡椒碱胶囊自乳化释药系统的处方筛选及体外质量评价

摘 要 目的： 研究胡椒碱自乳化释药系统的处方及其体外特性。方法: 通过溶解度、处方配伍试验以及伪三元相图的绘制来筛选处方,并考察空白处方、含药处方对自乳化效率的影响以及自乳化后乳滴的粒度分布,考察了胡椒碱自乳化胶囊的溶出速率和稳定性。结果: 胡椒碱自乳化胶囊的最终处方为油酸乙酯、Tween 80、Transcutol P,三者之比为30∶55∶15（w∶w∶w）,药物为辅料总量的2.5%,粒径约为90 nm,胡椒碱自乳化胶囊60 min溶出度是自制的胶囊剂6倍;低温和常温稳定性考察药物含量无明显变化。结论:所制备的胡椒碱自乳化胶囊自乳化效率高、能力强、性质稳定,体外溶出率高。     

卡介菌多糖核酸干预豚鼠急性过敏反应的研究

目的:研究卡介菌多糖核酸对豚鼠急性过敏反应的作用及可能的机制,探讨卡介菌多糖核酸的质量控制效力模型的提高方法。方法:建立牛血清白蛋白诱导豚鼠产生急性过敏反应模型。激发后30 min内观察豚鼠全身反应,并根据致敏性症状评分标准分级。取血用ELISA法测致敏前、攻击前及攻击后豚鼠血清总Ig E和组胺水平。结果:攻击后,模型组和卡介菌多糖核酸低剂量组豚鼠出现不同程度的急性过敏反应症状,而卡介菌中、高剂量组豚鼠急性过敏反应症状明显缓解。模型组在攻击前、后采集的血清总Ig E水平分别为1.637 0±0.158 6,1.683 1±0.228 1μg·ml-1,较正常对照组显著升高(P<0.01),而同时给予卡介菌多糖核酸后,卡介菌高剂量和中剂量处理组在攻击前、后采集的血清总Ig E水平与模型组比较均显著降低(P<0.01)。经牛血清蛋白致敏后,在攻击前后,模型组血清中组胺水平分别为1.499 7±0.133 1,1.512 1±0.050 6μg·ml-1,与阴性对照组相比均显著升高(P<0.01),而同时给予卡介菌多糖核酸后,卡介菌高、中、低各剂量处理组在攻击前、后采集的血清中组胺水平与模型组比较有明显降低(P<0.01)。结论:卡介菌多糖核酸可剂量依赖性抑制牛血清蛋白引起的急性过敏反应。其抗急性过敏反应的可能机制与降低血清总Ig E和组胺水平有关。     

Mushroom Consumption and Cardiovascular Health: A Systematic Review

IntroductionEdible mushrooms have a great nutritional value including high protein, essential amino acids, fiber, vitamins (B₁, B₂, B₁₂, C, and D), minerals (calcium [Ca], potassium [K], magnesium [Mg], sodium [Na], phosphorus [P], copper [Cu], iron [Fe], manganese [Mn], and selenium [Se]), low fatty foods, and sodium. The objective of this systematic review was to determine the relationship between edible mushroom consumption and overall cardiovascular risk.MethodsWe systematically searched Ovid MEDLINE, Embase, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science from database inception from 1966 through August 2020 for observational studies that reported the association between edible mushroom consumption and cardiovascular risk. Two investigators independently reviewed data. Conflicts were resolved through consensus discussion.ResultsOf 1479 studies, we identified 7 prospective studies. Edible mushroom consumption may have favorable effects on lipid profiles by changing some metabolic markers such as low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, total cholesterol, and triglycerides. Moreover, edible mushroom consumption is probably associated with reduced mean blood pressure. The beneficial overall cardiovascular risk, stroke risk, and coronary artery disease of edible mushroom consumption are not consistent.ConclusionsEdible mushroom consumption has not been shown to conclusively affect cardiovascular risk factors to date. However, potential health benefits may exist, including a favorable alteration of lipid profiles and blood pressure reduction.     

Hepatoprotective effects of kaempferol 3-O-rutinoside and kaempferol 3-O-glucoside from Carthamus tinctorius L. on CCl4-induced oxidative liver injury in mice

Safflower (Carthamus tinctorius L.) is a traditional medicinal and edible herb with a long history of use in China. In this study, a model of hepatotoxicity induced by carbon tetrachloride (CCl₄) in mice was used to investigate the hepatoprotective effects of kaempferol 3-O-rutinoside (K-3-R) and kaempferol 3-O-glucoside (K-3-G), two kaempferol glycosides isolated from C. tinctorius L. K-3-R and K-3-G, at doses of 200 mg/kg and 400 mg/kg, were given orally to male mice once/d for 7 days before they received CCl₄ intraperitoneally. Our results showed that K-3-R and K-3-G treatment increased the level of total protein (TP) and prevented the CCl₄-induced increases in serum aspartate aminotransferase (AST), serum alkaline phosphatase (ALP), and hepatic malondialdehyde (MDA) levels. Additionally, mice treated with K-3-R and K-3-G had significantly restored glutathione (GSH) levels and showed normal catalase (CAT) and superoxide dismutase (SOD) activities, compared to CCl₄-treated mice. K-3-R and K-3-G also mitigated the CCl₄-induced liver histological alteration, as indicated by histopathological evaluation. These findings demonstrate that K-3-R and K-3-G have protective effects against acute CCl₄-induced oxidative liver damage.