保健品,不要被礼品边缘化

现在的消费者已经不再像从前一样无知而冲动了.消费者被各式各样的理论灌输多了,自己俨然成为一个保健专家,谈起保健也头头是道.更糟糕的是消费者都被骗怕了,不会轻易把钱扔出去.     

白藜芦醇在骨关节炎中的作用及机制研究进展

骨关节炎（osteoarthritis, OA）是由衰老、肥胖、创伤、遗传等多因素引起的慢性退行性疾病,是临床上骨科医生面临的棘手疾病,该病给患者及其家庭带来了沉重的负担。白藜芦醇是一种具有抗炎、抗氧化等作用的天然化合物,可通过影响软骨衰老、软骨基质代谢、软骨损伤等作用参与OA的发生发展进程,这一过程可能与核因子-κB（NF-κB）、Toll样受体4（TLR4）、细胞外信号调节激酶（ERK）等信号通路的调控有关。本文拟就白藜芦醇在OA进程中的作用及其可能机制的研究进展作一综述,以期为相关研究提供参考。     

低成本营销成功法则:如何让产品决胜市场?

低成本营销,在我看来,就是在充分考虑和规避市场风险的前提下,以最经济最合理的投入、实现市场最大化的利益回报,这就需要企业能集中自身现有的资源,洞悉市场发展规律,针对消费文化的多元格局,审时度势走出一条细分化、差异化道路。同时通过多种宣传手段的组合运用,准确细分,以     

京万红治疗褥疮的疗效观察

京万红是一种治疗大面积烧伤的药物,其主要成份为地榆、桅子、大黄、冰片等中药。该药有促进局部血液循环、抗菌消炎,去腐生肌,加速伤口愈合之功效。根据京万红的药理作用,我们将此药用于治疗褥疮,取得了良好的效果。现报告如下。1 临床资料1.1 一般资料 我们使用京万红治疗褥疮患者12例,年龄58～85岁,其褥疮均为院外带入,其中Ⅱ期(炎性浸润期)5例,Ⅲ期(浅度溃烂期)6例,Ⅳ期(坏死溃疡期)1例,Ⅲ Ⅳ期褥疮创面均有感染。创面分泌物经细菌培养显示有大肠杆菌生长,药物敏感试验对菌必治、复达欣敏感。     

HPLC测定冬凌草药材及片剂中的冬凌草甲素

目的 采用HPLC法测定冬凌草药材及片剂中的冬凌草甲素.方法 用Hypersil C_(18)(250 mm×4.6 mm,5μm)色谱柱,甲醇-水(50:50)为流动相,流速0.8 mL·min~(-1);检测波长238 nm;柱温25 ℃;进样量20μL.结果 冬凌草甲素20～200 mg·mL~(-1)与峰面积有良好的线性关系(r=0.9999),最低检出限50 ng.按<中国药典>方法对样品预处理后进样测量,在药材中可检出冬凌草甲素,但片剂中无法检出.对供试品脱脂后,片剂中仍未检出冬凌草甲素.结论 所建方法简便、重复性好、准确度高,可用于冬凌草片剂的质量控制.文中所选的冬凌草片剂中未检测出冬凌草甲素,说明其质量有待提高.     

增强化学发光法测定盐酸恩诺沙星的含量

目的 采用增强化学发光法快速测定痕量盐酸恩诺沙星.方法 利用加入Tb3+和盐酸恩诺沙星后可以使Ce4+-Na2SO3体系的化学发光显著增强的原理,测定盐酸恩诺沙星的含量.结果 增强的化学发光强度与盐酸恩诺沙星0.1～10μg·mL-1和10～100μg·mL-1呈良好的线性关系(r分别为0.9984、0.9980),检测限为0.033 μg·mL-1,RSD=1.29%(n=11).结论 所建方法快捷、简便、灵敏度高,测定了自制牛奶样品中盐酸恩诺沙星的含量,结果满意.     

孕产妇及新生儿梅毒血清学检测常用方法的评价

目的评价酶联免疫吸附试验（ELISA）、梅毒螺旋体抗体明胶颗粒凝集试验（TPPA）和胶体金免疫层析试验（GICA）对孕产妇及新生儿梅毒患者的诊断价值。方法随机抽取经TPPA试验确诊的阳性血清标本65例和阴性血清标本70例,同时用上述3种方法检测,以TPPA试验作为确认试验,比较其它两种方法的灵敏度和特异度。结果ELISA法的灵敏度及特异度分别为98．46％、95．71％;GICA法的灵敏度及特异度分剐为95．38％、94．29％;ELISA及GICA的试验结果与TPPA试验结果无统计学意义（Y。一0．25,0;P〉0．05）,具有一致性。随着S／C．O．值的增高,GICA法与ELISA法的阳性符合率也增高。结论GICA的灵敏度及特异度较ELISA、TPPA方法偏低,可作为一种辅助试验。ELISA方法和TPPA方法一致性较好,可作为梅毒螺旋体抗体血清学检测的确证试验。     

Effects of SIRT1 gene knock-out via activation of SREBP2 protein-mediated PI3K/AKT signaling on osteoarthritis in mice

This study investigated the effects of SIRT1 gene knock-out on osteoarthritis in mice, and the possible roles of SREBP2 protein and the PI3K/AKT signaling pathway in the effects. Mice were randomly divided into a normal group and a SIRT1 gene knock-out group (6 mice in each group). In these groups, one side of the knee anterior cruciate ligament was traversed, and the ipsilateral medial meniscus was cut to establish an osteoarthritis model of knee joint. The countralateral synovial bursa was cut out, serving as controls. The knee joint specimens were then divided into four groups: SIRT1^+/+ control group (group A, n=6); SIRT1^+/+ osteoarthritis group (group B, n=6); SIRT1^–/– control group (group C, n=6); SIRT1^–/– osteoarthritis group (group D, n=6). HE staining, Masson staining, Safranin O-Fast Green staining and Van Gieson staining were used to observe the morphological changes in the articular cartilage of the knee. Immunohistochemical staining was employed to detect the expression of SIRT1, SREBP2, VEGF, AKT, HMGCR and type II collagen proteins. SA-β-gal staining was utilized to evaluate chondrocyte aging. The results showed clear knee joint cartilage destruction and degeneration in the SIRT1^–/– osteoarthritis group. The tidal line was twisted and displaced anteriorly. Type II collagen was destroyed and distributed unevenly. Compared with the SIRT1^+/+ osteoarthritis group and SIRT1^–/– control group, SIRT1 protein expression was not obviously changed in the SIRT1^–/– osteoarthritis group (P>0.05), while the expression levels of the SREBP2, VEGF and HMGCR proteins were significantly increased (P<0.05) and the levels of AKT and type II collagen proteins were significantly decreased (P<0.05). SIRT1 gene knock-out may aggravate cartilage degeneration in osteoarthritis by activating the SREBP2 protein-mediated PI3K/AKT signalling pathway, suggesting that SIRT1 gene may play a protective role against osteoarthritis.