三七开花习性观察

本文报道了在云南省文山州气候条件下三七的开花、散粉规律，可为三七的杂交育种工作提供依据。     

驳骨煎剂促进骨折愈合的实验研究

为探讨驳骨煎剂促进骨折愈合的作用机理。选用体重２０－３０ｇ的ＮＩＨ小白鼠１２０只,雌雄各半,随机分为正常组,给药组、对照组。除正常组外,其它各组均采用定点手法折骨术造成小鼠右下肢胫骨中段闭合性骨折,术后７、１４、２１、２８天分批处死小鼠,处死前４８小时,经腹腔注射同一批号０．２ｍｌ＾４５Ｃａ－ＣａＣｌ２溶液,４８小时后,断头取向,并解剖出左右胫骨,测定骨痂生长状况及钙沉 积量的变化。结果显示,给药     

Regulation of PPAR-γ activity in lipid-laden hepatocytes affects macrophage polarization and inflammation in nonalcoholic fatty liver disease

BACKGROUNDLipid metabolism disorder and inflammatory-immune activation are vital triggers in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Various studies have shown that PPAR-γ exerts potent anti-inflammatory and immunomodulatory properties. However, little is known about the regulation of PPAR-γ activity in modulating cell crosstalk in NAFLD.AIMTo investigate whether the regulation of PPAR-γ activity in lipid-laden hepatocytes affects macrophage polarization and inflammation.METHODSPrimary hepatocytes were isolated from wild-type C57BL6/J mice or hepatocyte-specific PPAR-γ knockout mice and incubated with free fatty acids (FFAs). Macrophages were incubated with conditioned medium (CM) from lipid-laden hepatocytes with or without a PPAR-γ agonist. Wild-type C57BL/6J mice were fed a high-fat (HF) diet and administered rosiglitazone.RESULTSPrimary hepatocytes exhibited significant lipid deposition and increased ROS production after incubation with FFAs. CM from lipid-laden hepatocytes promoted macrophage polarization to the M1 type and activation of the TLR4/NF-κB pathway. A PPAR-γ agonist ameliorated oxidative stress and NLRP3 inflammasome activation in lipid-laden hepatocytes and subsequently prevented M1 macrophage polarization. Hepatocyte-specific PPAR-γ deficiency aggravated oxidative stress and NLRP3 inflammasome activation in lipid-laden hepatocytes, which further promoted M1 macrophage polarization. Rosiglitazone administration improved oxidative stress and NLRP3 inflammasome activation in HF diet-induced NAFLD mice in vivo.CONCLUSIONUpregulation of PPAR-γ activity in hepatocytes alleviated NAFLD by modulating the crosstalk between hepatocytes and macrophages via the reactive oxygen species-NLRP3-IL-1β pathway.     

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.     

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.