全膝关节置换应用股神经阻滞镇痛与自控静脉镇痛的系统评价

背景：目前对全膝关节置换围手术期采用何种镇痛方法的效果差异存在争议. 目的：系统评价全膝关节置换术中应用股神经阻滞镇痛与患者自控静脉镇痛的疗效和安全性. 方法：全面搜索国内外关于全膝关节置换中应用股神经阻滞镇痛和患者自控静脉镇痛的随机对照研究资料,按照既定的纳入、排除标准,核定检出符合评价标准的文献,提取所需研究数据,采用RevMan 5.0.18软件进行Meta分析.评价指标包括术后24,48 h静息和活动时的目测类比评分、恶心呕吐胃肠道症状发生率、嗜睡等镇静过度发生率以及患者满意率. 结果与结论：纳入随机对照研究19篇,样本共计952膝,股神经阻滞组和患者自控静脉镇痛组分别为481膝和471膝.荟萃分析加权后,股神经阻滞与患者自控静脉镇痛相比,术后24,48 h静息和活动目测类比评分均较低（P 〈0.05）,无论是单次股神经阻滞还是连续股神经阻滞,差异均有显著性意义.在并发症发生率方面,股神经阻滞术后恶心呕吐及嗜睡发生率低于患者自控静脉镇痛（P 〈0.05）.结果提示,全膝关节置换术中采用股神经阻滞镇痛,无论是镇痛效果还是并发症发生率都优于患者自控静脉镇痛,且股神经阻滞镇痛患者满意度较高.但二者间的比较仍需大规模多中心的随机对照试验来进一步研究.     

健脾补肾法对核苷类似物治疗慢性乙型肝炎的增效作用及对CD4、CD8的影响

目的:观察健脾补肾法对核苷类似物治疗慢性乙型肝炎(CHB)的增效作用及其对CD4、CD8的影响。方法:将120例患者随机分为对照组和观察组,每组60例,对照组予核苷类似物治疗,观察组予核苷类似物加健脾补肾方药治疗,疗程均为52周。结果:观察组患者肝功能、HBV DNA复常率明显高于对照组;e抗原血清转换率、完全应答率明显高于对照组(P<0.05);CD4、CD4/CD8比值明显高于对照组(P<0.05)。结论:健脾补肾法可明显提高核苷类似物治疗CHB的疗效,减少拉米夫定致乙型肝炎病毒(HBV)YMDD变异,其增效的机理可能与提高CD4及CD4/CD8比值有关。     

大鼠鞘内腺苷同类物CHA抗神经病理性疼痛作用

目的 探讨大鼠鞘内注射腺苷同类物CHA(Cyclohexyladenosine)抗神经病理性疼痛作用.方法 雄性SD大鼠,鞘内留置PE-10导管,一周后制作大鼠脊神经结扎神经病理性疼痛模型(SNL).将30只SNL大鼠随机分成5组(n=6):对照组(生理盐水)、CHA组(CHA 0.1,0.5,1.0 nmol)、拮抗组(CHA 1.0 nmol 格列本脲2.0 μg).测定各组鞘内给药前、给药后10,20,30,40,50,60 min各时点的大鼠机械撤足阈值,计算对应时点的最大效应百分比(%MPE),评价抗神经病理性疼痛效果.结果 CHA 0.5及1.0 nmol组抗神经病理性疼痛最大效应百分比均明显高于生理盐水组(P＜0.05).CHA 1.0 nmol 格列本脲2.0 μg组抗神经病理性疼痛最大效应百分比明显低于CHA 1.0 nmol组(P＜0.05).结论 鞘内注射CHA具有明显的抗神经病理性疼痛作用,鞘内预注格列本脲(三磷酸腺苷敏感型K 通道阻滞剂)能拮抗CHA抗神经病理性疼痛作用.     

Fisetin inhibits growth,induces G2/M arrest and apoptosis of human epidermoid carcinoma A431 cells: role of mitochondrial membrane potential disruption and consequent caspases activation

Non‐melanoma skin cancers (NMSCs), one of the most common neoplasms, cause serious morbidity and mortality. Therefore, identification of non‐toxic phytochemicals for prevention/treatment of NMSCs is highly desirable. Fisetin (3,3′,4′,7‐tetrahydroxyflavone), a dietary flavonoid, present in fruits and vegetables possesses anti‐oxidant and antiproliferative properties. The aim of this study was to investigate the chemotherapeutic potential of fisetin in cultured human epidermoid carcinoma A431 cells. Treatment of A431 cells with fisetin (5–80 μm ) resulted in a significant decrease in cell viability in a dose‐ and time‐dependent manner. Employing clonogenic assay, we found that fisetin treatment significantly reduced colony formation in A431 cells. Fisetin treatment of A431 cells resulted in G₂/M arrest and induction of apoptosis. Furthermore, treatment of A431 cells with fisetin resulted in (i) decreased expression of anti‐apoptotic proteins (Bcl2; Bcl‐xL and Mcl‐1); (ii) increased expression of pro‐apoptotic proteins (Bax, Bak and Bad); (iii) disruption of mitochondrial potential; (iv) release of cytochrome c and Smac/DIABLO from mitochondria; (v) activation of caspases; and (vi) cleavage of Poly(ADP‐ribose) polymerase (PARP) protein. Pretreatment of A431 cells with the pan‐caspase inhibitor (Z‐VAD‐FMK) blocked fisetin‐induced cleavage of caspases and PARP. Taken together, these data provide evidence that fisetin possesses chemotherapeutic potential against human epidermoid carcinoma A431 cells. Overall, these results suggest that fisetin could be developed as a novel therapeutic agent for the management of NMSCs.     

妈富隆治疗原发性痛经的初步研究

目的评价妈富隆治疗原发性痛经的有效性和安全性。方法采用随机,对照,双盲方法将原发性痛经患者分为对照组和实验组各30例。对照组服用安慰剂,实验组服用妈富隆各3个周期。采用总的痛经评分(Total Dysmenorrhea Score,TDS)和视觉模拟评分法(Visual Analog Scale,VAS)来评价药物的疗效,对比治疗前后痛经的改善情况和药物的副作用。结果治疗后实验组TDS和VAS较对照组明显降低(P<0.05)。实验组TDS和VAS在第2,3周期下降明显。实验组药物副作用发生率明显增高,但随时间的发展而下降,而在对照组无变化,无严重副作用发生。结论妈富隆治疗原发性痛经效果明显,比较安全,值得临床推广应用。     

线粒体促凋亡蛋白Smac/DIABLO及其与肿瘤的关系

Smac/DIABLO即第2个线粒体衍生的半胱天冬蛋白酶激活剂/低pI的IAP直接结合蛋白,是近年发现的一种线粒体促凋亡蛋白,存在于线粒体并通过拮抗凋亡抑制蛋白(IAPs)的作用激活caspase-9和caspase-3而诱导细胞凋亡,并可促进肿瘤坏死因子相关的凋亡促使配体(TRAIL)诱导的凋亡。Smac/DIABLO还可以通过其N-或C-末端促进肿瘤细胞凋亡、增强肿瘤免疫及影响肿瘤细胞周期等机制抗肿瘤,并且增加肿瘤对放化疗的敏感性。本文主要就Smac/DIABLO的结构功能、作用机制及与肿瘤发生和治疗的关系作一综述。     

Therapy of chronic wounds with water-filtered infrared-A (wIRA)

The central portion of chronic wounds is often hypoxic and relatively hypothermic, representing a deficient energy supply of the tissue, which impedes wound healing or even makes it impossible. Water-filtered infrared-A (wIRA) is a special form of heat radiation with a high tissue penetration and a low thermal load to the skin surface. wIRA produces a therapeutically usable field of heat and increases temperature, oxygen partial pressure and perfusion of the tissue. These three factors are decisive for a sufficient tissue supply with energy and oxygen and consequently as well for wound healing, especially in chronic wounds, and infection defense. wIRA acts both by thermal and thermic as well as by non-thermal and non-thermic effects. wIRA can advance wound healing or improve an impaired wound healing process and can especially enable wound healing in non-healing chronic wounds. wIRA can considerably alleviate the pain and diminish wound exudation and inflammation and can show positive immunomodulatory effects.In a prospective, randomized, controlled study of 40 patients with chronic venous stasis ulcers of the lower legs irradiation with wIRA and visible light (VIS) accelerated the wound healing process (on average 18 vs. 42 days until complete wound closure, residual ulcer area after 42 days 0.4 cm² vs. 2.8 cm²) and led to a reduction of the required dose of pain medication in comparison to the control group of patients treated with the same standard care (wound cleansing, wound dressing with antibacterial gauze, and compression garment therapy) without the concomitant irradiation. Another prospective study of 10 patients with non-healing chronic venous stasis ulcers of the lower legs included extensive thermographic investigation. Therapy with wIRA(+VIS) resulted in a complete or almost complete wound healing in 7 patients and a marked reduction of the ulcer size in another 2 of the 10 patients, a clear reduction of pain and required dose of pain medication, and a normalization of the thermographic image. In a current prospective, randomized, controlled, blinded study patients with non-healing chronic venous stasis ulcers of the lower legs are treated with compression garment therapy, wound cleansing, wound dressings and 30 minutes irradiation five times per week over 9 weeks. A preliminary analysis of the first 23 patients of this study has shown in the group with wIRA(+VIS) compared to a control group with VIS an advanced wound healing, an improved granulation and in the later phase of treatment a decrease of the bacterial burden. Some case reports have demonstrated that wIRA can also be used for mixed arterial-venous ulcers or arterial ulcers, if irradiation intensity is chosen appropriately low and if irradiation is monitored carefully. wIRA can be used concerning decubital ulcers both in a preventive and in a therapeutic indication. wIRA can improve the resorption of topically applied substances also on wounds. An irradiation with VIS and wIRA presumably acts with endogenous protoporphyrin IX (or protoporphyrin IX of bacteria) virtually similar as a mild photodynamic therapy (endogenous PDT-like effect). This could lead to improved cell regeneration and wound healing and to antibacterial effects. In conclusion, these results indicate that wIRA generally should be considered for the treatment of chronic wounds.     

Inhibition of proliferation of PC-3 human prostate cancer by antagonists of growth hormone-releasing hormone: lack of correlation with the levels of serum IGF-I and expression of tumoral IGF-II and vascular endothelial growth factor

BACKGROUND: Antagonists of growth hormone-releasing hormone (GHRH) such as JV-1-38 can inhibit androgen-independent prostate cancer directly by several mechanisms and/or indirectly by suppressing growth hormone/insulin-like growth factor-I (GH/IGF-I) axis. To shed more light on the mechanisms involved, the effects of JV-1-38 on PC-3 human prostate cancer were compared with those of somatostatin analog RC-160 in vivo and in vitro. METHODS: Nude mice bearing PC-3 tumors received JV-1-38 (20 microg), RC-160 (50 microg) or a combination of JV-1-38 and RC-160. The concentration of IGF-I in serum and the expression of mRNA for IGF-II and vascular endothelial growth factor (VEGF) in tumor tissue were investigated. RESULTS: In vivo, the final volume of PC-3 tumors treated with JV-1-38 was significantly lowered by 49% (P < 0.01), whereas RC-160 exerted only 30% inhibition (NS), compared with controls. Combined use of both compounds augmented tumor inhibition to 63% (P < 0.001). Serum IGF-I levels were decreased only in mice treated with RC-160. JV-1-38 suppressed mRNA for IGF-II in PC-3 tumors by 42%, whereas RC-160 alone or in combination with JV-1-38 caused a 65% reduction. JV-1-38 and RC-160 used as single drugs decreased the expression of VEGF by 50%, and their combination caused a 63% reduction. In vitro, JV-1-38 inhibited the proliferation of PC-3 cells by 39%. This effect could be partially reversed by addition of IGF-I to the serum-free medium. RC-160 alone did not affect the PC-3 cell growth in vitro, but in combination with JV-1-38 it augmented the antiproliferative effect of the GH-RH antagonist to 72%. Exposure to JV-1-38 in vitro reduced the expression of mRNA for IGF-II in PC-3 cells by 55% but did not change VEGF mRNA levels, whereas RC-160 had no effect. CONCLUSIONS: The antiproliferative effect of JV-1-38 was not associated with the suppression of serum IGF-I and was only partially correlated with the expression of IGF-II and VEGF in PC-3 tumors, suggesting that other mechanisms play a role in the antitumor action of GHRH antagonists. Nevertheless, the stronger inhibition of tumor growth after combined treatment with JV-1-38 and RC-160 indicates that the interference with multiple local stimulatory factors leads to an enhanced inhibition of prostate cancer.