推拿和电脑中频联合治疗肩周炎疗效观察

[目的]探讨推拿结合电脑中频治疗肩周炎疗效。[方法]对166例肩周炎患者随机分为推拿组、电脑中频组和两者联合治疗之综合组分别进行治疗。[结果]综合治疗组治愈率为62·5%;对照组治愈率分别为23·68%和31·58%。[结论]推拿结合电脑中频治疗肩周炎疗效明显高于单纯推拿或电脑中频治疗肩周炎疗效。     

双极等离子体电切镜治疗膀胱肿瘤76例报告

目的探讨利用双极等离子体电切镜治疗膀胱肿瘤的优点。方法本组均采用双极等离子体电切镜进行电切，以生理盐水作为介质。结果本组病人手术时间为20～40min（25．3＋6．2min），术中出血约为2—20ml（12＋6．2m1）。术后给予抗炎治疗3天，4—7天拔除尿管，术后病人均未出现膀胱痉挛，无出血。平均住院日数9天。结论双极等离子体电切刀为双极，有自体回流，不导电，可以使用生理盐水作为介质，不易出现闭孔反射。术后病人恢复快，不产生膀胱痉挛，出血少，病人痛苦小，住院时间短。对于早期膀胱肿瘤，采用双极等离子体电切治疗不失为最好的方法。     

超声引导经皮微波消融治疗早期原发性肝癌的远期疗效

目的评价经皮微波消融治疗早期肝细胞肝癌患者的远期疗效。方法自1994年5月至2004年6月,216例直径≤5.0 cm的原发肝细胞肝癌患者共275个结节进行了经皮微波消融治疗(男性193例,女性23例;平均年龄54.68岁),所有病例均在我院诊治并签署知情同意书同意接受微波治疗。分析了肿瘤完全坏死率、远期生存率、复发率及并发症。结果本组平均随访期为40个月±24个月(6~127个月)。随访中159例(73.61%)存活,57例(26.39%)死亡。微波消融后95.64%(263/275)的肿瘤呈完全灭活,患者1、2、3、4和5年的累计生存率分别为94.87%、88.81%、80.44%、74.97%和68.63%。微波消融后1、2、3、4和5年的累计复发率分别为20.01%、32.04%、39.57%、44.97%和52.90%,3例发生较严重的并发症,包括针道种植1例,胆瘘2例,1例于治疗后一周死于肺部感染。结论超声引导经皮微波消融早期肝细胞肝癌在大部分病例可达到肿瘤完全坏死且并发症发生率较低,具有满意的远期临床疗效。     

富锗金针菇多糖对小鼠肝脏的保护作用

目的：研究富锗金针菇多糖（cFVP）对急性肝损伤小鼠转氨酶活性的影响及对肝脏的保护作用，在此基础上研究其精制品FVP1对cCl4损伤的小鼠原代肝细胞的保护作用。方法：采用0．2％CCl4灌胃造成小鼠急性肝损伤模型，以CFVP和阳性对照联苯双酯灌胃给药，测定血清中谷丙转氨酶（ALT）的活性，并对小鼠肝脏进行切片观察；采用二步分离法制备小鼠原代肝细胞，检测FVP1对CCl4损伤的原代肝细胞ALT活力的影响。结果：CFVP高、中剂量组对CCl4致急性肝损伤小鼠ALT活性的升高具有显著的降低作用，与造模组相比有极显著性差异（P〈0．01）；低剂量组与造模组相比有显著性差异（P〈0．05），CFVP对CCl4致小鼠急性肝损伤有明显的保护作用；FVP1中剂量组、低剂量组可使培养液中的ALT活性明显低于模型组，具有极显著性差异（P〈0．01），即ALT明显减少，说明FVP1对CCl4损伤的原代小鼠肝细胞具有保护作用，结论：富锗金针菇多糖具有保护肝脏细胞，防止肝细胞坏死的作用。     

中药三棱的化学成分及药理研究进展

近年来国内外中药三棱化学成分与药理作用研究进展的概述。三棱化学成分主要为黄酮类、皂苷类、苯丙素类、挥发油等;主要有抗血小板聚集、抗肿瘤、心血管系统活性、镇痛等药理作用。     

HPLC法测定新肤螨灵软膏中甲硝唑的含量

目的采用高效液相色谱法测定新肤螨灵软膏甲硝唑含量。方法色谱柱为Diamonsil-C18柱(250mm×4.6mm,5μm),甲醇-水(20∶80)为流动相,流速为1.0ml.min-1,检测波长为315nm。结果线性范围为7.614~38.07μg.ml-1(r=0.9996),甲硝唑的平均回收率为100.3%,RSD为0.66%。结论该法简便、灵敏、准确。     

薢瓜方治疗痛风性关节炎的临床疗效研究

目的:观察薢瓜方治疗痛风的临床疗效.方法:将180例急性痛风性关节炎患者按2:1比例随机分为两组,治疗组(120例)采用薢瓜方治疗,对照组(60例)单纯使用西药治疗,观察治疗前后血尿酸的变化及临床疗效.结果:血尿酸变化治疗组与对照组相比,具有统计学差异(P＜0.05);总有效率治疗组为95.8%,对照组为93.3%,两组间疗效无统计学差异(P＞0.05);治疗组患者用药期间未见明显不良反应.结论:薢瓜方治疗痛风性关节炎疗效确切,且无明显不良反应.     

HPLC测定龙血竭中龙血素A和龙血素B的含量

目的建立龙血竭中龙血素A和龙血素B的含量测定方法。方法采用HPLC法,用C18柱,乙腈-1%冰醋酸溶液(37∶63)为流动相,检测波长275nm,柱温30℃。结果方法线性关系良好,平均加样回收率龙血素A为100.25%,RSD=1.2%(n=6);龙血素B为101.32%,RSD=1.7%(n=6)。结论所用方法简便易行,结果准确,可用于龙血竭药材的质量控制。     

Sustained effect of inhaled diesel exhaust particles on T-lymphocyte-mediated immune responses against Listeria monocytogenes.

Studies have shown that exposure to diesel exhaust particles (DEP) suppresses pulmonary host defense against bacterial infection. The present study was carried out to characterize whether DEP exposure exerts a sustained effect in which inhaled DEP increase the susceptibility of the lung to bacterial infection occurring at a later time. Brown Norway rats were exposed to filtered air or DEP by inhalation at a dose of 21.2 +/- 2.3 mg/m3, 4 h/day for 5 days, and intratracheally instilled with saline or 100,000 Listeria monocytogenes (Listeria) 7 days after the final DEP exposure. Bacterial growth and cellular responses to DEP and Listeria exposures were examined at 3 and 7 days post-infection. The results showed that inhaled DEP prolonged the growth of bacteria, administered 7 days post DEP exposure, in the lung as compared to the air-exposed controls. Pulmonary responses to Listeria infection were characterized by increased production of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-12, and IL-10 by alveolar macrophages (AM) and increased presence of T lymphocytes and their CD4+ and CD8+ subsets in lung draining lymph nodes that secreted elevated levels of IL-2, IL-6, IL-10, and interferon (IFN)-gamma. Diesel exhaust particles were found to inhibit Listeria-induced production of IL-1beta and TNF-alpha, which are responsible for the innate immunity, and IL-12, which initiates the development of T helper (Th)1 responses, but enhance Listeria-induced AM production of IL-10, which prolongs Listeria survival in these phagocytes. The dual action of DEP on AM production of IL-12 and IL-10 correlated with an inhibition of the development of bacteria-specific T lymphocytes by DEP. Cytokine production by lymphocytes from DEP- and Listeria-exposed rats showed a marked decrease in the production of IL-2, IL-10, and IFN-gamma compared to Listeria infection alone, suggesting either that DEP inhibit the production of cytokines by lymphocytes or that these lymphocytes contained T-cell subsets that are different from those of Listeria infection alone and less effective in mediating Th1 immune responses. This study demonstrates that inhaled DEP, after a 7-day resting period, increase the susceptibility of the lung to bacterial infection occurring at a later time by inhibiting macrophage immune function and suppressing the development of T-cell-mediated immune responses. The results support the epidemiological observations that exposure to DEP may be responsible for the pulmonary health effects on humans.     

Exposure of brown Norway rats to diesel exhaust particles prior to ovalbumin (OVA) sensitization elicits IgE adjuvant activity but attenuates OVA-induced airway inflammation.

Exposure to diesel exhaust particles (DEP) during the sensitization process has been shown to increase antigen-specific IgE production and aggravate allergic airway inflammation in human and animal models. In this study, we evaluated the effect of short-term DEP exposure on ovalbumin (OVA)-mediated responses using a post-sensitization model. Brown Norway rats were first exposed to filtered air or DEP (20.6 +/- 2.7 mg/m3) for 4 h/day for five consecutive days. One day after the final air or DEP exposure (day 1), rats were sensitized with aerosolized OVA (40.5 +/- 6.3 mg/m3), and then again on days 8 and 15, challenged with OVA on day 29, and sacrificed on days 9 or 30, 24 h after the second OVA exposure or the final OVA challenge, respectively. Control animals received aerosolized saline instead of OVA. DEP were shown to elicit an adjuvant effect on the production of antigen-specific IgE and IgG on day 30. At both time points, no significant airway inflammatory responses and lung injury were found for DEP exposure alone. However, the OVA-induced inflammatory cell infiltration, acellular lactate dehydrogenase activity and albumin content in bronchoalveolar lavage (BAL) fluid, and numbers of T cells and their CD4+ and CD8+ subsets in lung-draining lymph nodes were markedly reduced by DEP on day 30 compared with the air-plus-OVA exposure group. The OVA-induced nitric oxide (NO) in the BAL fluid and production of NO, interleukin (IL)-10, and IL-12 by alveolar macrophages (AM) were also significantly lowered by DEP on day 30 as well as day 9. DEP or OVA alone decreased intracellular glutathione (GSH) in AM and lymphocytes on days 9 and 30. The combined DEP and OVA exposure resulted in further depletion of GSH in both cell types. These results show that short-term DEP exposure prior to sensitization had a delayed effect on enhancement of the sensitization in terms of allergen-specific IgE and IgG production, but caused an attenuation of the allergen-induced airway inflammatory responses.