腰椎间盘突出症的非手术治疗

目前国内学者认为腰椎间盘突出症患者80%以上可通过非手术治疗获得治愈和缓解,非手术疗法已成治疗该病的首选方法。进一步探讨非手术疗法治疗腰椎间盘突出症的临床疗效及进展,以指导临床实践。通过对各种非手术治疗方法资料的分析、评价,得出结论:非手术疗法是治疗腰椎间盘突出症的发展方向。综合治疗可取长补短,安全简便,疗效确切,易于患者接受。     

腰椎间盘突出症的非手术治疗

目的观察非手术治疗腰椎间盘突出症的效果。方法回顾性分析30例典型腰椎间盘突出症采用为期2周的非手术综合治疗情况。结果 30例患者中痊愈22例,显效4例,有效2例,无效2例,总有效率为93.3%。结论非手术治疗是大部分患者希望采用的治疗方式,且疗效肯定,不良反应少,应在临床上广泛推广。     

七叶皂甙钠治疗急性期腰椎间盘突出症

目的探讨急性期腰椎间盘突出症安全可靠规范的非手术疗法。方法作者采用七叶皂甙钠静滴治疗急性期腰椎间盘突出症420例，观察其疗效。结果治愈307例，好转103例，未愈10例，总有效率97．6％。结论七叶皂甙钠治疗急性期腰椎间盘突出症较为可靠，规范，安全，疗效满意的非手术疗法。     

非手术治疗54例腰椎间盘突出症临床分析

目的:探讨非手术疗法治疗腰椎间盘突出症的疗效.方法:对54例腰锥间盘突出症采用牵引、静脉输液,结合手法复位、推拿按摩、针灸等综合性治疗.结果:临床治愈18例,好转13例,显效21例,无效2例,总有效率96.29%。结论:非手术治疗对腰椎间盘突出症(除椎间盘钙化型和髓核破裂游离型外)有满意的疗效.     

中西医结合治疗腰椎间盘突出症212例临床分析

目的 探讨治疗腰椎间盘突出症有效的中西医结合非手术治疗方法。方法 本组198例腰椎间盘突出症患者采用手法、练功、中药脱水及针灸的方法治疗。结果 198例获得随访，其中175例治疗后无自觉症状，体检阴性，恢复工作，随访1年以上无复发。结论 手术治疗腰椎间盘突出症前可通过非手术的中西医结合方法能得到有效的治疗。     

非手术治疗腰椎间盘突出症44例临床疗效分析

目的分析和评价非手术治疗腰椎间盘突出症的临床疗效。方法回顾性总结分析3年来成都市新都区中医医院44例腰椎间盘突出症患者经针灸理疗、药物、局部封闭非手术综合治疗的疗效,按照其优良可差属性进行评价。结果治疗后评分为优、良、可、差分别为14例(31.8%)、20例(45.5%)、7例(15.9%)、2例(4.5%)与治疗前相比均有非常显著的差异(P<0.001)。治疗后优良率达到77.3%,与治疗前31.8%相比,有非常显著差异(P<0.001)。结论非手术治疗能缓解椎间盘突出症的症状,有很好的治疗作用,目前基层医院仍将是作为临床上的常规和首选方案。     

非手术综合疗法治疗腰椎间盘突出症60例

目的观察针灸治疗腰椎间盘突出症的临床效果。方法运用针刺、艾灸、推拿疗法治疗腰椎间盘突出症。结果治愈31例,显著进步16例,好转8例,无效5例,总有效率92%。结论非手术综合疗法治疗腰椎间盘突出症有显著疗效,是一种理想的治疗方法。     

非手术治疗腰椎间盘突出症临床分析

目的:探讨非手术疗法治疗腰椎间盘突出症的疗效。方法:对54例腰椎问盘突出症采用牵引、静脉输液,结合手法复位、推拿按摩、针灸等综合性治疗。结果:临床治愈18例,显效21例,好转13例,无效2例,总有效率96.29%.结论:非手术治疗对腰椎问盘突出症(除椎间盘钙化型和髓核破裂游离型外)有满意的疗效。     

脊柱非手术减压系统治疗腰椎间盘突出症疗效观察

目的探讨DRX9000脊柱非手术减压系统治疗腰椎间盘突出症的疗效。方法DRX9000脊柱非手术减压系统治疗腰椎间盘突出症前评分，治疗1、2、4、6周后同样方法评分，比较治疗前后评分，观察治疗效果。结果88例患者治疗前综合评分10分，其中85例患者随着治疗时间的延长，综合评分逐渐增高，治疗结束时综合评分20分，较治疗前明显增高，有效率96．7％，观察6周内无复发病例，3例患者因不属于适应证治疗4次后无效而放弃继续本方法治疗。结论DRX9000脊柱非手术减压系统治疗腰椎间盘突出症是一种全新、安全、有效、舒适的治疗方法。     

非手术治疗腰椎间盘突出症216例分析

目的探讨非手术治疗腰椎间盘突出症临床疗效,降低患者的痛苦及减少治疗费用,方法回顾性总结216例腰椎间盘突出症患者,经过中西药等非手术治疗临床疗效满意,治疗费用减少。结果临床症状消失或减轻,随访两年无复发及加重,结论非手术治疗腰椎间盘突出症,近期临床疗效满意,可在基层医院推广。     

川芎嗪抗大鼠心肌缺血及抗心肌细胞凋亡作用

目的研究川芎嗪对心肌缺血大鼠模型及心肌细胞凋亡的影响。方法建立大鼠心肌缺血模型,将24只大鼠按随机化原则分为对照组、高剂量组、低剂量组、假手术组。各组均测定心肌缺血和梗死范围以及CPK、LDH指标,并应用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法（TUNEL法）测定各组心肌细胞凋亡及凋亡指数,比较各组间差异。结果高剂量组较对照组和低剂量组能明显降低心肌缺血大鼠模型的危险指数,降低心肌中CPK、LDH的升高。高剂量组能明显降低心肌细胞的凋亡指数,对心肌细胞凋亡的保护作用均明显高于生理盐水和低剂量组,与假手术组无统计学差异。结论川芎嗪对心肌缺血大鼠模型心肌梗死有明显保护作用,其作用机制可能与抗心肌细胞凋亡作用有关。     

3′-大豆苷元磺酸钠对心肌缺血/再灌注损伤及抗氧化作用的影响

目的利用离体心脏灌流模型,研究3′-大豆苷元磺酸钠对离体心脏缺血/再灌注损伤的保护作用,并探讨其抗氧化作用的机制。方法应用Langendorff离体心肌缺血/再灌注损伤模型,在灌流液中加入高、中、低剂量的3′-大豆苷元磺酸钠,测定再灌注过程中冠脉流量、左心室收缩压的变化;比色法测定心肌组织中LDH、SOD、GSH-Px的活性。结果3′-大豆苷元磺酸钠可使缺血/再灌注后心脏灌流量及左心室收缩压增大,使心肌组织中LDH、SOD、GSH-Px的活性升高。结论3′-大豆苷元磺酸钠对离体心脏缺血/再灌注损伤具有保护作用,其保护机制与其增强抗氧化作用有关。     

青少年腰椎间盘突出症的诊断与治疗

目的分析研究青少年腰椎间盘突出症的病因及治疗。方法对9例青少年腰椎间盘突出症患者行小切口单侧/双侧开窗减压、髓核摘除术。结果9例均获得随访,随访时间12～72个月,平均38个月,7例腰痛及下肢放射痛完全消失;2例劳累后有轻微症状,休息后可缓解。结论外伤所致骺离骨折为青少年腰椎间盘突出重要病因,直腿抬高试验阳性为重要体征,腰椎CT可确诊。对于保守治疗无效或症状明显、CT证实硬膜囊及神经根明显受压者,应积极手术治疗。     

姜黄素通过抑制程序性坏死改善丙烯晴的神经毒性

目的 研究姜黄素抑制丙烯晴神经细胞毒性的具体机制.方法 CCK-8、乳酸脱氢酶(LDH)检测试剂盒、ELISA试剂盒检测HMGB1释放评价丙烯晴对大脑皮层星形胶质细胞(AST)的毒性;谷胱甘肽检测试剂盒检测细胞谷胱甘肽水平、DCF-DA检测细胞活性氧水平;Western blot 法检测细胞坏死信号通路蛋白水平.结果 1,2,4 mmol/L丙烯晴处理大鼠神经AST 24 h,细胞活力显著降低、LDH和高迁移率族蛋白(HMGB1)释放显著增加,程序性坏死抑制剂necrostatin-1抑制丙烯晴诱导的细胞活力降低.姜黄素可增加丙烯晴降低的谷胱甘肽水平,抑制丙烯晴诱导的氧自由基增加及RIP-1激活,抑制丙烯晴诱导的AST活力下降.结论 姜黄素可通过上调谷胱甘肽水平抑制程序性坏死改善丙烯晴的神经毒性.     

Incompatibility of silver nanoparticles with lactate dehydrogenase leakage assay for cellular viability test is attributed to protein binding and reactive oxygen species generation

A growing number of studies report that conventional cytotoxicity assays are incompatible with certain nanoparticles (NPs) due to artifacts caused by the distinctive characteristics of NPs. Lactate dehydrogenase (LDH) leakage assays have inadequately detected cytotoxicity of silver nanoparticles (AgNPs), leading to research into the underlying mechanism. When ECV304 endothelial-like umbilical cells were treated with citrate-capped AgNPs (cAgNPs) or bare AgNPs (bAgNPs), the plasma membrane was disrupted, but the LDH leakage assay failed to detect cytotoxicity, indicating interference with the assay by AgNPs. Both cAgNPs and bAgNPs inactivated LDH directly when treated to cell lysate as expected. AgNPs adsorbed LDH and thus LDH, together with AgNPs, was removed from assay reactants during sample preparation, with a resultant underestimation of LDH leakage from cells. cAgNPs, but not bAgNPs, generated reactive oxygen species (ROS), which were successfully scavenged by N-acetylcysteine or ascorbic acid. LDH inhibition by cAgNPs could be restored partially by simultaneous treatment with those antioxidants, suggesting the contribution of ROS to LDH inactivation. Additionally, the composition of the protein corona surrounding AgNPs was identified employing liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. In sum, the LDH leakage assay, a conventional cell viability test method, should be employed with caution when assessing cytotoxicity of AgNPs.     

非小细胞肺癌恶性胸腔积液的临床特征及预后影响因素

目的 研究非小细胞肺癌（NSCLC）恶性胸腔积液患者的临床特征及影响疗效、预后的因素。方法 选择安徽省胸科医院2013年1月至2014年12月收治的91例伴恶性胸腔积液NSCLC患者,回顾分析患者临床资料、胸腔积液情况、胸腔积液治疗情况等,分析各因素对疗效及生存期的影响。结果 血性胸水患者RR为48.7%,显著低于非血性胸水患者（P<0.05）;胸腔局部应用IL-2生物治疗RR为70.3%,显著高于不用IL-2进行局部治疗者（P<0.05）。非血性胸水中位生存期位13个月,较血性胸水生存有优势,胸腔局部应用含IL-2生物治疗中位生存期为12个月,较不用IL-2治疗生存有优势,在腺癌患者中EGFR-TKI联合化疗生存优于单纯化疗,而后者生存优于单纯EGFR-TKI治疗（P<0.05）。结论 血性胸水疗效及预后差,胸腔局部应用IL-2生物治疗疗效较好、生存有优势。     

Protection of renal tubular cells against the cytotoxicity of cadmium by glycine

Glycine treatment is reported to protect against the nephrotoxicity of cadmium (Cd) in rats. The purpose of the present study was to explore the mechanism of this protection using a renal epithelial cell line, LLC-PK(1). The cells were incubated with 10-30 microM Cd in serum-free DMEM and cytotoxicity was evaluated by LDH leakage into the incubation medium. Under these conditions, 20 and 30 microM Cd concentrations were cytotoxic. As compared to the non-Cd-exposed cells, the LDH release was elevated more than six-fold in cells exposed to 30 microM Cd for 24h. Co-treatment with 5-50mM glycine was cytoprotective in a concentration-dependent manner. Prior treatment with 50 mM glycine for 16 h, or co-treatment for 24h, reduced LDH leakage due to 30 microM Cd exposure by 60 and 66%, respectively. Co-incubation with 50 mM alanine was also protective but only about half as effective as with glycine. During the first 4h, prior to the onset of any significant cell membrane damage, the Cd-exposed cells accumulated 0.55 microg Cd/mg protein. Glycine pre-treatment or co-treatment reduced Cd accumulation by about one-quarter or one-half, respectively. To delineate the mechanism of glycine's effect on Cd accumulation, the efflux of Cd was studied after a 30 min pulse exposure. The results suggested that pre-treatment reduced Cd accumulation by increasing its efflux from the cells. In contrast, co-treatment reduced Cd efflux, suggesting that the co-treatment lowered Cd accumulation by suppressing its uptake. When co-incubated, Cd and glycine formed a complex that was apparently responsible for the marked reduction in Cd uptake. It is concluded that, regardless of the mode of treatment, glycine is cytoprotective against Cd and that it may do so by lowering the intracellular Cd burden.     

眼镜蛇毒活性组分抑制内皮细胞生长及其生化机制初探

目的探讨中华眼镜蛇毒活性组分(CCVAF)抑制新生牛肺主动脉血管内皮细胞(BAVEC)生长的作用及其生化机制。方法用MTT法测定CCVAF抑制BAVEC的增殖活性,用伊红-考马斯亮蓝法观察细胞骨架,罗丹明-鬼笔环肽荧光探针F-actin骨架蛋白定位,荧光标记流式细胞法测荧光强度表胞内钙离子浓度[Ca2+]i及分光光度法测细胞上清液中乳酸脱氢酶(LDH)及一氧化氮(NO)的含量。结果CCVAF(0.625~20μg/mL)剂量依赖性地抑制内皮细胞的生长,IC50=2.45μg/mL。CCVAF与BAVEC共同孵育后,引起细胞间连接减少,细胞F-actin分布混乱;细胞上清液中LDH活力及NO的含量及胞内[Ca2+]i分别增加。结论CCVAF抑制BAVEC增殖,可能与CCVAF导致细胞骨架改变,LDH及NO分泌量及胞内Ca2+浓度增加等生化机制有关。     

Depletion in vitro of mitochondrial glutathione in rat hepatocytes and enhancement of lipid peroxidation by adriamycin and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)

Treatment of isolated rat hepatocytes with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and adriamycin (ADR) produced a complete depletion of cellular glutathione accompanied by a significant increase in lactate dehydrogenase (LDH) leakage. Separation of the mitochondrial and cytoplasmic pools of glutathione by digitonin disruption showed that, although BCNU, a specific inhibitor of glutathione, completely depleted the cytoplasmic pool of glutathione, the mitochondrial supply was not entirely expended and LDH leakage was only moderately stimulated. Only after depletion of the mitochondrial supply of glutathione by ADR and BCNU did LDH leakage increase markedly. Measurement of lipid peroxidation, by monitoring malondialdehyde through the thiobarbituric acid procedure, showed that malondialdehyde accumulated more extensively and at a rate mirroring release of LDH from ADR/BCNU treated cells. The time of increase in LDH leakage and malondialdehyde production corresponded to the time of depletion of mitochondrial glutathione to less than 10% of the initial pool size. No such increase in LDH leakage was observed with BCNU or ADU treatment alone or when aminopyrine, an inhibitor of lipid peroxidation, was included. Aminopyrine was found to prevent, in a dose-dependent manner, both LDH leakage and malondialdehyde production stimulated by ADR/BCNU treatment. The protective effect peaked at 5 mM aminopyrine, and higher concentrations produced significant LDH leakage exhibiting LDH release kinetics different than those observed with ADR/BCNU. Although aminopyrine had no effect on the rate or extent of cytoplasmic glutathione depletion by ADR/BCNU treatment, the mitochondrial pool was conserved significantly in those cells protected by aminopyrine. These data suggest that enhanced hepatocyte damage observed after treatment with a combination of ADR and BCNU versus BCNU or ADR alone is due to the extensive depletion of mitochondrial glutathione supported by ADR after glutathione reductase inhibition. Further, enhancement of lipid peroxidation is strongly implicated in the mechanism of adriamycin toxicity.     

槐果碱对感染CVB3搏动心肌细胞的保护作用

目的：应用柯萨奇病毒B3(CVB3)感染SD大鼠乳鼠心肌细胞造成病毒性心肌炎模型,观察槐果碱对该模型的作用。方法：(1)将乳鼠心肌细胞分成4组：感染组,感染CVB3；治疗组,感染病毒后加入100mg·L~(-1)的槐果碱；同时设立药物对照组和细胞对照组。在处理的d 2,3,5观察各组细胞病变效应(CPE)、细胞搏动频率并测定细胞上清液中乳酸脱氢酶浓度。(2)将心肌细胞感染CVB3后加入不同浓度的槐果碱(12．5～400mg·L~(-1)),设立病毒、细胞及药物对照。在处理后d 2,3,5观察CPE并测定细胞上清中的乳酸脱氢酶(LDH)浓度。结果：(1)100mg·L~(-1)的槐果碱对感染CVB3的乳鼠心肌细胞有保护作用,治疗组的CPE较感染组减轻,上清液中的LDH浓度降低。(2)槐果碱在12．5～300mg·L~(-1)之间均对感染CVB3的乳鼠心肌细胞有保护作用,它可以减轻病毒导致的CPE,并减少LDH释放。在400mg·L~(-1)反而会加重CPE,增加LDH释放。结论：一定浓度的槐果碱在体外对感染CVB3的心肌细胞有保护作用。