木耳菌丝体及其醇提物的药理作用

木耳菌丝体小鼠ip给药能明显提高外周血T淋巴细胞百分率,使环磷酰胺引起的半数溶血值HC₅₀减少恢复正常;其醇提物体内外均能明显抑制ADP诱导大鼠血小板聚集作用,缩短小鼠红细胞电泳时间。     

新的抗癌中药枫苓合剂的主要药效学

目的研究枫苓合剂体内抗癌作用及其他有关药理,为临床试验提供基础。方法采用对人体肿瘤移植的裸鼠体内人体胃癌MKN及人体肝癌QGY的抑制,对荷瘤和正常动物免疫功能的影响及与化学合成药合并用药等方面进行枫苓合剂的主要药效学研究。结果枫苓合剂对人体胃癌MKN 3个剂量组口服给药抑癌率分别为:74．68％-86．76％,49．86％- 59．31％及19．12％-21．68％;腹腔给药抑癌率分别为:78．72％-85．42％,55．32％-62．50％及26．69％-41．67％。对肝癌QGY口服给药抑癌率分别为:47．69％-49．33％,31．94％-33．63％及20．0％-26．0％。对荷Lewis肺癌小鼠显示提高机体NK细胞活力,有明显促进小鼠腹腔巨噬细胞的吞噬功能。对S180肉瘤的生长抑制,单独用环磷酰胺(CTX)15 mg·kg-1抑瘤率为45．16％,与枫苓合剂25 mL·kg-1合并用药抑瘤率为71．29％。结论高剂量枫苓合剂具有高的抗胃癌MKN的作用和中度的抗肝癌QGY的药效,且可提高免疫力,与CTX合用有增效作用。     

游戏教学法在学龄前儿童用力肺活量检查中的应用

目的 探讨游戏教学法在学龄前儿童用力肺活量检查中的应用效果.方法 选择2012年1月至2013年12月在我科肺功能室进行肺功能检查的学龄前儿童317例,随机分成两组,对照组118例,其中男82例,女36例;观察组199例,其中男133例,女66例.对照组儿童在做肺功能前由技术操作人员向患儿讲解操作规范、程序、如何用力、如何配合并演示,教导患儿用口深吸气一直到肺总量位置,然后以最快速度吹气,直到能够看见时间容积曲线显示呼气相平台之后,再用最快速度吸气至肺总量位置,然后用一张8cm×21 cm的小纸条让患儿练习直到把纸吹飞.观察组患儿采用游戏教学法,即让患儿先观看电脑画面,操作人员调出游戏软件中的蜡烛画面,一边让患儿看电脑里吹蜡烛的情景,一边做示范用力吹气,重点强调吹气时一定要用最大的力气尽量可能的长时间吹气,就像吹蜡烛一样,只有这样才能把蜡烛全部吹灭,吹灭的蜡烛越多获得的分数就越高,以奖励游戏的形式鼓励患儿进行检查.每一个患儿测定6次,每次间隔2分钟,不成功者休息20分钟再重新测试,2小时以内能完成并达到质控标准的视为成功,2小时内不能达到质控标准的视为不成功,记录患儿肺功能测定的成功率,比较两组患儿进行肺功能检查的成功率.结果 对照组118例中成功完成操作者78例,占66.1％,不成功者40例,占33.9％;观察组199例中成功者160例,占80.4％,不成功者39例,占19.6％.2组结果比较,x2值为8.096,P值为0.004,差异有显著性.结论 在学龄前儿童用力肺活量检查中,游戏教学法可以有效提高检查的成功率.     

占里侗族传统医药文化传承及保护浅析

占里侗族传统医药作为祖国宝贵的传统医药文化的重要组成部分,足占里侗族同胞智慧的结晶,长期以来在占里人民战胜疾病保障健康方面做出了卓越贡献,尤其在占里创造“中国计划生育第一村”的奇迹方面,占里医药作为控制计划生育的技术手段起了不可磨灭的贡献。但是研究表明,在占里医药自身的局限和现代经济、科技、生活方式等的综合影响下,占里统医药面临失传的危险。占里传统医药急需保护、研究和改进。为此提出了相关政策建议。     

Didymin attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress

Objective: This study was designed to investigate the protective effects of didymin (Did) on doxorubicin (DOX)-induced cardiotoxicity. Methods: After pretreatment with Did (2, 4, 8 mg/kg intraperitoneal i.p.) for 7 d, the male C57 mice were injected with single dose of DOX (20 mg/kg i.p.). The cardioprotective effect of Did was observed on the 7th day after DOX treatment. Results: DOX delayed body growth and caused cardiac tissue injury, oxidative stress, and mitochondrial dysfunction. Similar experiments in H9C2 cardiomyocytes showed that DOX reduced cell viability, increased generation of reactive oxygen species (ROS) and fragmentation of DNA, decreased mitochondrial membrane potential, and induced cardiomyocyte apoptosis. However, all of these adverse effects were suppressed by Did pretreatment. Did increased protein expression of glutamate-L-cysteine ligase catalytic subunit (GCL), heme oxygenase 1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2). Besides, Did also induced activation of PI3K/AKT. Conclusion: These findings indicated Did prevented DOX-induced cardiac injury and apoptosis via activating PI3K/AKT/Nrf2 signaling pathway.     

中医诊断技能实训教学方法文献计量学研究

目的 分析目前中医诊断技能实训教学方法的研究现状,为今后中诊技能实践教学提供参考和借鉴,为更好地提高学生"四诊"技能水平提供思路.方法 利用中国知网、万方数据库和维普数据库,检索2016-2020年国内公开正式发表的有关中医诊断技能实训相关的文献,选取符合纳入标准的文章,采集提取发表年度、发表期刊、基金支持类别、教学方...     

Louki Zupa decoction attenuates the airway inflammation in acute asthma mice induced by ovalbumin through IL-33/ST2-NF-κB/GSK3β/mTOR signalling pathway

ContextAsthma is a common respiratory system disease. Louki Zupa decoction (LKZP), a traditional Chinese medicine, presents a promising efficacy against lung diseases.ObjectiveTo investigate the pathogenic mechanism of asthma and reveal the intervention mechanism of LKZP.Materials and methodsForty-eight female Balb/c mice were randomly divided into 6 groups: normal control group (NC), ovalbumin (OVA)/saline asthma model group, OVA/LL group, OVA/LM group, OVA/LH group and OVA/DEX group (n = 8 per group). The asthmatic mice were modelled through intraperitoneal injecting and neutralizing OVA. LKZP decoction was administrated by gavage at the challenge stage for seven consecutive days (2.1, 4.2 and 8.4 g/kg/day). We investigated the change in lung function, airway inflammation, mucus secretion and TH-1/TH-2-related cytokines. We further verify the activated status of the IL-33/ST2/NF-κB/GSK3β/mTOR signalling pathway.ResultsLKZP was proved to improve asthmatic symptoms, as evidenced by the down-regulated airway resistance by 36%, 58% and 53% (p < 0.01, p < 0.001 vs. OVA/saline group), up-regulated lung compliance by 102%, 114% and 111%, decreased airway inflammation and mucus secretion by 33%, 40% and 33% (p < 0.001 vs. OVA/saline group). Moreover, the content of cytokines in BALF related to airway allergy (such as IgE) and T helper 1/T helper 2 cells (like IL-2, IL-4, IL-5, IL-13, TNF-α and IFN-γ), were also markedly reduced by 13–65% on LKZP intervention groups compared with model group. Mechanistic research revealed that the IL-33/ST2-NF-κB/GSK3β/mTOR signalling pathway was activated in the OVA/saline group and LKZP significantly down-regulated this pathway.Discussion and conclusionLKZP improves lung function, airway inflammation, mucus secretion and correct immune imbalance by intervening with the IL-33/ST2-NF-κB/GSK3β/mTOR signalling pathway, presenting a promising therapeutic choice for asthma.     

7,7'-Dimethoxyagastisflavone-induced apoptotic or autophagic cell death in different cancer cells

7,7'-Dimethoxyagastisflavone (DMGF), a biflavonoid isolated from the needles of Taxus × media cv. Hicksii, was evaluated for its antiproliferative and antineoplastic effects in three human cancer cell lines. Interestingly, DMGF caused cell death via different pathways in different cancer cells. DMGF induced apoptosis, activated caspase-3 activity and changed the mitochondrial membrane potential in HT-29 human colon cancer cells. However, the apoptotic pathway is not the major pathway involved in DMGF-induced cell death in A549 human lung cancer cells and HepG2 human hepatoma cells. Treatment with 3-MA, an inhibitor of autophagy, significantly decreased DMGF-induced cell death in HepG2 and A549 cells, but did not affect DMGF-induced cell death in HT-29 cells. Following DMGF treatment, the HepG2 cells increased expression of LC3B-II, a marker used to monitor autophagy in cells. Thus, DMGF induced apoptotic cell death in HT-29 cells, triggered both apoptotic and autophagic death in A549 cells and induced autophagic cell death in HepG2 cells.     

大鼠长期脾虚和热证造模的胃黏膜主细胞超微结构观察

目的模拟慢性病证是动物实验的主要难点。本实验观察比较大鼠长期(26周)脾虚和热证造模动物胃黏膜主细胞的超微结构。方法将Wistar大鼠随机分为对照组、脾虚组、热证组。对照组正常饲养26周;脾虚组用耗气破气加饥饱失常法造模26周;热证组灌喂熟附子、肉桂、干姜、女贞子煎剂26周。另取幼年大鼠为幼年组作为对照。实验结束后取胃体后壁组织,透射电镜观察胃黏膜主细胞超微结构。结果对照组主细胞粗面内质网排列基本整齐,部分内质网池略呈小泡状扩张。脾虚组主细胞粗面内质网池扩张,从小泡状至池状之间,甚至呈湖状。胞质内出现髓鞘样小体或髓鞘样结构。热证组主细胞粗面内质网池扩张,呈小泡状,失去正常的同心性层状结构。幼年组主细胞粗面内质网排列比较整齐。结论热证组和脾虚组动物胃黏膜主细胞超微结构均有变化,以脾虚组更为严重。由于实验时间较长,实验结束时大鼠已近1岁龄,所以对照组动物胃黏膜主细胞超微结构也略有衰老改变。