小脑幕脑膜瘤显微手术治疗及手术入路选择

目的 探讨小脑幕脑膜瘤的手术治疗和手术入路选择。方法 回顾性分析2008年6月至2017年3月手术治疗的92例小脑幕脑膜瘤的临床资料。内侧型和外侧型向幕上发展者,采用扩大翼点入路10例,颞下入路23例,颞枕部入路18例;肿瘤全部或主体在颅后窝21例,采用枕下或枕部幕上下联合入路;20例镰幕型采用枕部经小脑幕入路。结果 肿瘤全切除86例,部分切除6例。无手术死亡病例。83例术后随访1~8年,正常工作、生活71例,生活自理8例,生活需要照顾4例;肿瘤复发再次手术7例（次全切除5例,全切除2例）。结论 手术全切除小脑膜脑膜瘤可获得满意效果及良好预后;根据肿瘤特点设计合适的手术入路以及熟练掌握局部神经解剖和显微神经外科技术是手术成功的关键;术中深静脉系统及大静脉窦的保护具有重要意义。     

川芎嗪通过减少肺癌A549细胞内活性氧的生成抑制细胞增殖及侵袭

目的:探讨川芎嗪(tetramethylpyrazine,TMP)对人肺癌A549细胞生长侵袭的干预作用与活性氧（reactive oxygen species,ROS）及其调控蛋白表达水平的相关性。方法:采用CCK-8法检测川芎嗪对A549细胞生长的影响,采用Transwell小室实验检测川芎嗪对A549细胞侵袭能力的影响,采用DCFH-DA荧光探针检测川芎嗪对A549细胞内ROS水平的影响,Western-blot法检测川芎嗪对HIF-1α、VEGF-C、MMP-9蛋白表达水平的影响。结果:川芎嗪呈浓度依赖性抑制肺癌A549细胞增殖和侵袭能力（P＜0.05）,同时减少细胞内ROS生成（P＜0.05）,抑制HIF-1α、VEGF-C、MMP-9蛋白表达（P＜0.05）。结论:川芎嗪可降低人肺癌A549细胞ROS水平,减轻氧化应激损伤,从而抑制肿瘤细胞的增殖及侵袭。     

第八届国际红斑狼疮学术会议会讯

由中华医学会放射肿瘤学分会和中国医科院肿瘤医院放疗科主办的“全国肿瘤放化疗综合治疗进展研讨会暨已故吴桓兴教授归国从医六十周年纪念会”于2006年6月22～23日在北京天坛饭店召开，来自国内近200位专家学者参加了会议。6月22日全天至23日上午为大会发言，23日下午在北京陕西大厦秦乐宫为西门子公司卫星会议和吴桓兴教授归国从医60周年纪念会。大会开幕式由中华医学会放射肿瘤学分会前任主任委员殷蔚伯教授和现任主任委员余子豪教授主持。首先由中国工程院院士、中国医科院肿瘤医院内科孙燕教授主讲了肿瘤内科治疗的现状和展望，他总结了40余年来国际国内肿瘤内科领域内的发展历程和现状，特别指出我国肿瘤内科治疗是在50年代末期由吴桓兴、金显宅等老前辈的支持和指导下开始的；     

抗乙酰肝素酶单抗联合紫杉醇对肺癌A549增殖及侵袭的影响

目的探讨抗乙酰肝素酶（heparanase,HPA）单抗联合紫杉醇对肺癌A549细胞的增殖及侵袭抑制作用。方法选用浓度梯度递增的抗HPA单抗和紫杉醇,单独或联合作用于A549细胞48 h后,采用MTT法检测细胞增殖,流式细胞仪检测细胞周期,细胞划痕试验、Transwell试验检测细胞侵袭,观察抗HPA单抗与紫杉醇对细胞增殖及转移的抑制作用。结果抗HPA单抗与紫杉醇联用后将抑制率从20%、31%、37%、45%、51%增大至52%、56%、60%、67%、77%。两药分别干预后细胞S期分别降低至4.7%、6.8%,联用后出现了36.5%的细胞凋亡期。在体外侵袭实验中抗HPA单抗、紫杉醇、紫杉醇联用抗HPA单抗使肺癌A549细胞侵袭能力分别下降（23.3±5.3）%、（63.3±3.9）%、（85.0±3.2）%。结论抗HPA单抗联合紫杉醇对肺癌A549细胞的增殖及侵袭能力的抑制作用比两药单用时更为显著。     

金黄色葡萄球菌类肠毒素W的超抗原活性位点预测与克隆表达

目的预测金黄色葡萄球菌类肠毒素W(SElW)与T细胞受体(TCR)的对接和超抗原活性位点, 并对SElW进行克隆表达和纯化。方法利用AlphaFold对SElW蛋白单体进行三维结构预测, 借助SAVES在线服务器使用ERRAT、拉氏图和Verify₃D等软件对蛋白模型进行评估。用ZDOCK服务器模拟SElW与TCR的对接构象, 并对SElW与其他肠毒素的氨基酸序列进行比对。设计引物扩增selw基因, 将该片段重组于pMD18-T载体中并进行测序;经限制性内切酶BamHⅠ和Hind Ⅲ双酶切后将目的片段重组于表达质粒pET-28a(+)中, 重组质粒鉴定后用IPTG诱导表达;用亲和层析法对表达于上清中的SElW蛋白进行纯化, 用BCA法对蛋白进行定量。结果三维结构预测结果显示, SElW蛋白由氨基末端和羧基末端两个结构域组成, 其中氨基末端结构域由3个α-螺旋和6个β-片层组成, 羧基末端结构域由2个α-螺旋和7个反向平行的β-片层组成。SElW蛋白模型的整体质量因素得分为98.08, 其中93.24%的氨基酸Verify₃D得分≥0.2, 且...     

HPLC法同时测定当归药材中6种成分的含量

目的:建立高效液相色谱法同时测定当归药材中阿魏酸、阿魏酸松柏酯、Z 型和 E 型藁本内酯及 Z 型和 E 型3-丁烯基苯酞的含量。方法:采用 Zorbax ODS C_(18)色谱柱(250 mm×4.6 mm,5 μm);流动相为1%醋酸(A)-乙腈(B),梯度洗脱(0min,10%B;7 min,33%B;55 min,33%B),流速1.0 mL·min~(-1);检测波长为324 nm(阿魏酸、阿魏酸松柏酯和 Z/E 型藁本内酯)和260 nm(Z 型和 E 型3-丁烯基苯酞)。结果:阿魏酸、阿魏酸松柏酯、Z-藁本内酯、Z 型和 E 型3-丁烯基苯酞的线性范围分别为3.31～139.50 μg·mL~(-1)(r=0.9999),38.00～380.00 μg·mL~(-1)(r=0.9995),2.11～445.00 μg·mL~(-1)(r=1.000),3.32～136.18 μg·mL~(-1)(r=0.9999),1.94～16.32 μg·mL~(-1)(r:0.9995);加样回收率分别为101.8%(RSD=2.5%),105.3%(RSD=3.2%),98.5%(RSD=1.6%),105.3%(RSD=2.4%),105.8%(RSD=1.9%)。结论:该方法准确、简便,具有良好的重复性和稳定性,有利于提高当归药材的质量控制。     

与细胞周期G_1→S调控点相关的几个重要元件及其与肿瘤的关系

在哺乳动物细胞周期调控中,G_1→S期之间的调控点(restriction point)是细胞内外信号经传递、整合汇集到细胞核,对细胞的增殖进行调控的关键点,该点调控的异常与肿瘤的发生、发展关系密切。在相关的因子中,Rb、cyclin D1、CDk4/6和p16组成的调控途径研究比较明确,目前被认为与G_1→S调控点关系最密切。本文综述了Rb、cyclinD1和p16的异常与某些肿瘤发生的关系;并初步探讨了这些成分的异常与肿瘤发展的特定阶段和特定组织来源的某些相关性,以及它们在基因表达水平可能存在的相互调控作用。     

交趾黄檀提取物对大鼠急性心肌缺血的保护作用及机制研究

目的 探讨交趾黄檀提取物对大鼠冠状动脉左前降支结扎所致急性心肌缺血的心脏保护作用及可能机制。方法 60只SD雄鼠随机分为假手术组、模型组、尼可地尔(3 mg·kg^-1)组、交趾黄檀提取物组(1.5、3和6 g·kg^-1),每组10只,通过结扎冠脉左前降支建立大鼠急性心肌缺血模型,造模24 h后给药,连续10 d每天给药1次,假手术组和模型组给予相应剂量的蒸馏水,末次给药1h后进行观察和取材。PowerLab电生理记录仪检测大鼠血流动力学指标动脉收缩压(systolic blood pressure, SBP)、动脉舒张压(diastolic blood pressure, DBP)、平均血压(mean blood pressure, MBP)、左室收缩压(left ventricular systolic pressure, LVSP)、等容收缩期左心室内压最大上升和下降速率(±maximal left ventricular pressure rising rate,±dp/dt_max);HE染色观察心肌病理变化;生化...     

藿香正气散正气思想探微

藿香正气散之精要在于正气二字,一扶正气,其外证之生在于中气不足,脾胃虚弱,故治疗时,不仅仅祛湿寒之邪,更重视恢复人体的正常生理活动,以白术、茯苓、甘草扶中气、健脾运;二正气机,其内证乃三焦津凝气滞而生,尤以中焦气机升降出入失常为主,故调畅中焦气机,使脾气得升,胃气得降,气津得散,局部正气得复,后邪自祛,病自安。三祛邪气,已生之寒湿当化之,寒湿不去,津气难散,甚者湿郁成痰,或从热化,或湿盛而阳微,或变生他病,当使邪有出路,邪祛而正自安。藿香正气散为治湿之方,却没有单纯运用治湿的药物,而是从补益、疏通、祛邪三个方面帮助人体恢复肺、脾功能,使湿得治。     

Protective effect of breviscapine against brain injury induced by intrauterine inflammation in preterm rats and its mechanism北大核心CSCD

Objective To study the protective effect of breviscapine against brain injury induced by intrauterine inflammation in preterm rats and its mechanism. Methods A preterm rat model of brain injury caused by intrauterine inflammation was prepared by intraperitoneal injections of lipopolysaccharide in pregnant rats. The pregnant rats and preterm rats were respectively randomly divided into 5 groups: control, model, low-dose breviscapine (45 mg/kg), high-dose breviscapine (90 mg/kg), and high-dose breviscapine (90 mg/kg) +ML385 [a nuclear factor erythroid 2-related factor 2 (Nrf2) inhibitor, 30 mg/kg] (n=10 each). The number and body weight of the live offspring rats were measured for each group. Hematoxylin-eosin staining was used to observe the pathological morphology of the uterus and placenta of pregnant rats and the pathological morphology of the brain tissue of offspring rats. Immunofluorescent staining was used to measure the co-expression of ionized calcium binding adaptor molecule-1 (IBA-1) and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) in the cerebral cortex of offspring rats. ELISA was used to measure the levels of interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-1β (IL-1β) in the brain tissue of offspring rats. Western blotting was used to measure the expression of Nrf2 pathway-related proteins in the brain tissue of offspring rats. Results Pathological injury was found in the uterus, and placenta tissue of the pregnant rats and the brain tissue of the offspring rats, and severe microglia pyroptosis occurred in the cerebral cortex of the offspring rats in the model group. Compared with the control group, the model group had significant reductions in the number and body weight of the live offspring rats and the protein expression levels of Nrf2 and heme oxygenase-1 (HO-1) in the brain tissue of the offspring rats (P<0.05), but significant increases in the relative fluorescence intensity of the co-expression of IBA-1 and NLRP3, the levels of the inflammatory factors IL-6, IL-8, and IL-1β, and the protein expression levels of NLRP3 and caspase-1 in the brain tissue of the offspring rats (P<0.05). Compared with the model group, the breviscapine administration groups showed alleviated pathological injury of the uterus and placenta tissue of the pregnant rats and the brain tissue of the offspring rats, significant increases in the number and body weight of the live offspring rats and the protein expression levels of Nrf2 and HO-1 in the brain tissue of the offspring rats (P<0.05), and significant reductions in the relative fluorescence intensity of the co-expression of IBA-1 and NLRP3, the levels of the inflammatory factors IL-6, IL-8, and IL-1β, and the protein expression levels of NLRP3 and caspase-1 in the brain tissue of the offspring rats (P<0.05). The high-dose breviscapine group had a significantly better effect than the low-dose breviscapine (P<0.05). ML385 significantly inhibited the intervention effect of high-dose breviscapine (P<0.05). Conclusions Breviscapine can inhibit inflammatory response in brain tissue of preterm rats caused by intrauterine inflammation by activating the Nrf2 pathway, and it can also inhibit microglial pyroptosis and alleviate brain injury. © 2023 Xiangya Hospital of CSU. All rights reserved.