敌草快是全球第三大灭生性除草剂,其与百草枯均为联吡啶类除草剂,被世界卫生组织归为中等毒性农药类管理[1].近年来,随着百草枯的禁用,敌草快在农业生产中应用越来越多,其中毒患者也逐年增加,但由于敌草快中毒病死率高,且无特效解毒剂,已成为现代中毒治疗学的研究热点之一[2].近期某医院成功收治了1例敌草快中毒患者,患者治愈出院.现报告如下,以期为此类患者的救治提供参考.

目的:探讨药物光毒性反应患者的药学监护要点.方法:临床药师通过参与1例药物光毒性不良反应患者的治疗,协助医生及时确定患者的光毒性反应,可能由左氧氟沙星氯化钠注射液引起,并参与治疗方案的调整,期间对患者进行了全程的药学监护.结果:患者药物光毒性反应得到了及时的识别与治疗,患者病情好转后出院.结论:临床药师参与临床药物治疗,能帮助患者及时识别药品不良反应,保障患者用药安全有效.

1例肝癌患者在使用信迪利单抗治疗过程中,出现胸痛、胸闷、阵发性呼吸困难等症状,结合患者既往病史、实验室检查结果等,考虑为免疫相关性心肌炎.临床药师参与了该患者的治疗过程,并结合相关文献分析不良反应发生的机制、梳理治疗过程,对治疗方案提出药学建议.经过临床药师与医师的密切合作,患者心功能逐渐恢复,病情好转出院.临床药师应参与到抗肿瘤药物的监测与管理中,为提升抗肿瘤药物治疗的安全性和有效性发挥作用.

目的:分析本院2020年第二类精神药品的使用情况和用药合理性,为临床合理用药提供参考依据.方法:通过医院信息系统(HIS)调取本院2020年1～12月第二类精神药品的门诊处方、住院医嘱,查看该类药品的使用情况,统计分析限定日剂量(DDD)、用药频度(DDDs)、日均费用(DDDc)和排序比(B/A)等指标.结果:本院2020年第二类精神药品消耗数量排名前3位的是艾司唑仑片、劳拉西泮片(规格1mg)和右佐匹克隆片;销售金额排序前3位的是地佐辛注射液、艾司唑仑片、右佐匹克隆;DDDs排序前3位的是艾司唑仑片、劳拉西泮片(规格1mg)和右佐匹克隆片;DDDc排序前3位的是艾司唑仑注射液、酒石酸布托啡诺注射液、地佐辛注射液.地佐辛注射液、盐酸曲马多注射液、咪达唑仑注射液、氨酚羟考酮片、酒石酸布托啡诺注射液、艾司唑仑注射液的B/A<1.结论:本院2020年第二类精神药品消耗数量较大,使用基本合理,但个别药品销售金额较大、价格较高,需加强监管.

目的 探讨玉屏风颗粒对正常BALB/c小鼠免疫系统的影响及机制.方法 将100只BALB/c小鼠随机分为空白组(Control)和玉屏风颗粒组(YPF),每组50只,YPF组按临床剂量换算为小鼠用剂量2.5 g·kg-1,以0.1 mL/10 g进行灌胃给药28 d;分离提取腹腔巨噬细胞和脾淋巴细胞、以ConA与LPS诱导脾淋巴细胞增殖、NK细胞毒力测定等实验.结果 玉屏风颗粒对正常小鼠体重、免疫器官指数、血常规、CD4+/CD8+T细胞比值和脾淋巴细胞的凋亡没有显著性的影响,而对脾淋巴细胞增殖、NK细胞活性、巨噬细胞吞噬活性、吞噬指数和抗体生成能力具有显著性的影响.结论 玉屏风颗粒对正常小鼠具有免疫增强作用.

目的 统计我院脑苷肌肽注射液的使用情况,对临床用药的合理性进行分析与评价,为临床合理用药提供参考.方法 采取回顾性研究方法,利用PASS系统,抽取我院2018年1～6月295例使用脑苷肌肽注射液的住院病例,从患者的性别、年龄、住院科室,药品适应证、用法用量、给药疗程、溶媒及溶媒量、联合或交替用药等方面进行统计分析.结果 我院295例使用脑苷肌肽注射液的患者中,临床不合理用药类型主要有:适应证不适宜17例次(5.76％)、用法用量不适宜8例次(2.71％)、给药疗程不适宜233例次(78.98％)、溶媒选择不适宜13例次(4.41％)、溶媒量不适宜138例次(46.78％)、联合或交替用药不适宜65例次(22.03％).结论 我院脑苷肌肽注射液临床使用存在一定不合理情况,建议临床医生应严格按照药品说明书内容及结合相关指南合理使用;另外,临床药师亦须加强监管,规范临床使用,以确保患者用药安全、有效、合理、经济.

目的:探讨在临床药师培养过程中应用品管圈活动的效果.方法:在临床药师培养过程中引入品管圈活动,以临床实际问题和需求为牵引,每期选定一个活动主题,按品管圈活动的各步骤实施各项活动,评价有形成果和无形成果,全活动循环进行.结果:临床药师的临床医学理论知识、药学理论知识、临床实践能力、解决问题能力、自信心、责任心等多项能力得到了提高,活动前后培训效果具有统计学差异.结论:品管圈活动应用于临床药师培养过程中是可行的,可作为临床药师在职培养的一种模式.

1例长期卧床的87岁男性偏瘫患者,入院时诊断为吸入性肺炎、营养不良(重度)、脑出血后遗症.住院期间患者感染疥疮,给予硫软膏、林旦乳膏、甲硝唑片等抗疥疮药物治疗.治疗2周后明显好转,治疗3周后基本痊愈.临床药师协助医师为患者制定个体化的治疗方案,并对患者进行全程的药学监护,使疥疮的治疗更加规范和合理,取得了较好的治疗效果.

乙型肝炎病毒(HBV)再激活(HBVr)是指在化疗和(或)免疫抑制治疗过程中发生的HBV-DNA水平突然快速增高至原水平100倍以上,或之前没有HBV感染的患者出现HBV感染[1].淋巴瘤合并HBV感染的患者在接受化疗或免疫抑制治疗时可能会诱发HBVr[2].HBVr不但会增加患者的肝炎发病率及相关病死率,还会影响淋巴瘤患者的生存及预后.

《中国新闻周刊》自创刊已经走过18载春秋,曾连续两届获得中国出版政府奖.2013年以来,其充分利用既有平台,深耕时政、党建、文化、生活、科技等垂直领域,并以视频、漫画等形式创新,成为名副其实的社交媒体内容供应商.在传统广告断崖下滑的今天,年收入逆势增长,超过了1.1亿元.2018年营收中新媒体占总收入的三分之一,2019年新媒体营收有望占总营收的二分之一.《中国新闻周刊》已经转型为一家依托新媒体引擎的融媒体.

Acute hypobaric hypoxia (HH) gives rise to persistent cognitive impairment, influencing memory function specifically. Echinacoside (ECH), one of the phenylethanoids isolated from the stems of Cistanche salsa, has been reported to prevent ischemia induced by neuronal injury traditionally. This study then tried to investigate whether ECH could alleviate HH‐induced memory deficit. Ten C57 mice were used as control, and 50 were exposed to HH equivalent to 6,100 m for 7 days in a decompression chamber and were given ECH daily (50, 75, or 100 mg/kg) through gavage during the period of exposure. Cognitive performance was evaluated by the Morris water maze test. ECH, especially at 100 mg/kg, significantly reduced HH‐induced memory decline. Furthermore, ECH increased the expression of nuclear factor E2 p45‐related factor 2, heme oxygenase‐1, NAD(P)H:quinone oxidoreductase 1, and γ‐glutamyl cysteine synthetase in mRNA and protein levels, suggesting that the Keap1–Nrf2–ARE signaling pathway might be involved in neuronal adaptation. The results indicate that ECH could prevent HH‐induced memory impairment, which is associated with antioxidant effect of ECH in the hippocampus.

目的:研究松果菊苷（ECH）对低压低氧环境下小鼠空间认知功能的改善作用及其作用机制。方法:将60只小鼠随机分为空白组（生理盐水）、模型组（生理盐水）、阳性组（银杏叶提取物片,100 mg/kg）和ECH低、中、高剂量组（50、75、100 mg/kg）,每组10只。除空白组外,其余各组小鼠均饲养于低压氧仓模拟低压低氧,各组小鼠每天灌胃给药1次,连续给药7 d（给药后立即放入低压氧仓内）;以2 min内小鼠水平与垂直活动次数为指标,评价其负面情绪与空间认知功能;苏木精-伊红染色后显微镜观察小鼠海马组织病理学变化;并检测小鼠海马组织中的超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）、丙二醛（MDA）的水平。结果:与空白组比较,模型组小鼠水平活动次数、MDA水平均显著增加/升高（P<0.05）;垂直活动次数,SOD、CAT、GSH-Px水平均显著减少/降低（P<0.05）;海马组织CA1区锥体细胞排列疏松,多数锥体细胞紧缩深染。与模型组比较,阳性组和ECH高剂量组小鼠水平活动次数、MDA水平显著减少/降低（P<0.05）;垂直活动次数,SOD、CAT、GSH-Px水平显著增加/升高（P<0.05）;海马组织CA1区锥体细胞数量丰富,排列紧密,少量锥体细胞紧缩深染。结论:ECH对低压低氧环境下小鼠空间认知功能障碍具有一定的改善作用,其机制可能与升高海马组织中SOD、CAT、GSH-Px水平及降低MDA水平有关。

As a reductive gas, hydrogen plays an antioxidant role by selectively scavenging oxygen free radicals. It has been reported that hydrogen has protective effects against nerve damage caused by ischemia–reperfusion in stroke, but the specific mechanism is still unclear. Therefore, this study aims to investigate the protective effects of hydrogen on stroke-induced ischemia–reperfusion injury and its detailed mechanism. Two weeks after the inhalation of high concentrations (66.7%) of hydrogen, middle cerebral artery occlusion (MCAO) was induced in mice using the thread occlusion technique to establish an animal model of the focal cerebral ischemia–reperfusion. Then, a metabolomics analysis of mouse cerebral cortex tissues was first performed by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF/MS) to study the metabolic changes and protective mechanisms of hydrogen on stroke ischemia–reperfusion injury. According to the metabolomic profiling of cortex tissues, 29 different endogenous metabolites were screened, including palmitoyl-l-carnitine, citric acid, glutathione, taurine, acetyl-l-carnitine, N-acetylaspartylglutamic acid (NAAG), l-aspartic acid, lysophosphatidylcholine (LysoPC) and lysophosphatidylethanolamine (LysoPE). Through pathway analysis, the metabolic pathways were concentrate on the glutathione pathway and the taurine pathway, mitochondrial energy metabolism and phospholipid metabolism that related to the oxidative stress process. This result reveals that hydrogen may protect against ischemic stroke by reducing oxidative stress during ischemia–reperfusion, thereby protecting nerve cells from reactive oxygen species(ROS).

Background. Saponin from Aralia taibaiensis (sAT) showed excellent antioxidative effects in several models; however, its effects on brain cells were unknown to us. The present study was designed to evaluate the protective effects of sAT on ischemia/reperfusion- (I/R-) induced injury and clarify its mechanisms. Methods. In vitro, HT22 cells were pretreated with sAT and then subjected to I/R. Apoptosis rate, mitochondrial function, and antioxidant proteins were measured. To clarify the mechanisms, siRNA were used. In vivo, sAT was pretreated through intragastric administration for 7 days and the I/R model was induced. The neurobehavioral scores, infarction volumes, and some cytokines in the brain were measured. Protein levels were investigated by Western blotting. Results. The results showed that sAT treatment significantly protected cells from I/R-induced cell apoptosis and mitochondrial dysfunction. The antioxidant protein levels were increased in a dose-dependent manner. Further study revealed that sAT induced the deacetylation and phosphorylation of PGC-1α and FOXO3a. sAT treatment also induced the phosphorylation levels of Akt and the expression levels of SIRT1. Using the specific targeted siRNA transfection, the interplay relationship between Akt, SIRT1, PGC-1α, and FOXO3a was verified. Furthermore, the same protective effects were also observed in rats subjected to I/R. Conclusion. sAT protected brain cells from I/R-induced mitochondrial oxidative stress and dysfunction through regulating the Akt/SIRT1/FOXO3a/PGC-1α pathway.

Ultraviolet B (UVB) irradiation increases the risk of various skin disorders, resulting in apoptosis, autophagy and oxidative stress and thereby promoting the risk of skin photoaging and carcinogenesis. The use of photochemoprotectors including natural products with antioxidant properties represents an effective strategy for preventing UVB-induced skin injury. Isoorientin (Iso), as a flavonoid compound, could be extracted from several plant species and possesses multiple biological activities. However, its role in regulating UVB-induced skin damage is little to be reported. In the study, we found that Iso treatment could protect human dermal fibroblasts (HDFs) against the effects of UVB irradiation by improving cell viability, suppressing MMP1 and MMP3 expression, inhibiting oxidative stress and inducing autophagy. In addition, Iso reduced UVB-triggered apoptosis, as evidenced by the decreased Caspase-3 activity in vitro. Furthermore, Iso was functioned as reactive oxygen species (ROS) scavenger that markedly hindered c-Jun N-terminal kinases (JNK) signaling activation in UVB-treated HFDs. Importantly, promoting JNK activity restored matrix metalloproteinase (MMP)-1/3 expression in Iso-incubated cells with UVB stimulation. Meanwhile, UVB exposure to the skin of mice and subsequent topical application of Iso delayed the progression of skin damage, resulting in autophagy and blocking the JNK activation and ROS production. In conclusion, these results indicated the photoprotective role of Iso and demonstrated that Iso could also be potentially used as an agent against UVB-stimulated skin damage.

The study tried to investigate whether apple polysaccharide (AP) could prevent colitis associated colorectal cancer (CACC) through the regulation of intestinal microbiota disorders. 10 % AP (w/v) was administrated to ICR mice by gavage for 15 wk. It was found that AP treatment protected against CACC in mice effectively. The level of Lactobacillus in the intestine of AOM/DSS-treated mice was significantly decreased and that of Fusobacterium increased; while AP could reverse this trend and increase the intestinal microbiota diversity. The number of T cells and macrophages in the colon tissue of mice in AOM/DSS group elevated; while AP could reduce the number of these cells significantly. AP suppressed nuclear aggregation of β-catenin, inhibited the activation of Wnt pathway in colon tissues. These data suggest that AP prevented ICR mice from CACC at least in part through regulating intestinal flora disorder and Wnt pathway.

Ethnopharmacological relevance: Saponins of many herbs could inhibit the growth of colorectal cancer cells. In the study, we investigated the effects of Paris saponin VII (PSVII), and elucidated its mechanism in colorectal carcinoma cells and a xenograft mouse model. Materials and methods: HT-29 and HCT-116 cells were treated with different concentrations of PSVII (0-100 mu M). The effects of PSVII on HCT-116 cells were assessed using a microarray. Then, apoptotic cells were detected by flow cytometric analysis and apoptosis related protein expression was evaluated by Western blot. A xenograft model of nude mice was used to assess the effect of PSVII in vivo. Results: MTT assay showed the IC50 values of PSVII for growth inhibition of HT-29 and HCT-116 cells were 1.02 +/- 0.05 mu M and 3.50 +/- 0.79 mu M respectively. Edu assay demonstrated that PSVII effectively suppressed the growth of HT-29 and HCT-116 cells. Treatment with 0-3 mu M PSVII not only triggered apoptosis, but also activated caspase-3 and caspase-9 of HT-29 and HCT-116 cells in a concentration dependent manner. In parallel to the alterations, Bax and Cyto-c expression increased while Bcl-2 decreased. In nude mice, PSVII reduced the tumor size and induced the apoptosis of tumor cells. PSVII could suppress IL-6-induced phosphorylation of STAT3 in vitro and blocked STAT3 phosphorylation in vivo. Conclusion: Our results suggest that PSVII suppressed the activation of IL-6/STAT3 pathway, consequently suppressed the growth and proliferation and triggered the apoptosis of CRC cells. These findings indicate that PSVII might be an effective tumouristatic agent for the treatment of colorectal cancer.

It is widely accepted that regulating microbiome could improve human health. We previously observed apple polysaccharide (AP) reversed high-fat-induced microbial dysbiosis, but the mechanism remains to be elucidated. In this study, the function of AP in vitro was evaluated in Bifidobacterium longum (B. longum) and Lactobacillus rhamnosus (L. rhamnosus). The effects of AP on the composition of fecal bacteria of normal SD rats were investigated by qPCR, TA cloning and 16S sequencing. 0.125-2% AP showed no significant effect on the growth of B. longum and L. rhamnosus. DNA concentration of fecal bacteria cultured with 1% AP was significantly higher than that of control group. qPCR revealed that the number of Bifidobacterium and Lactobacillus in fecal flora incubated by 1% AP was significantly higher than that of control group. Three strains of escherichia coli (E. coli) in fecal bacteria were screened out and analyzed. AP can be utilized by one E. coli and the metabolic products of AP could enhance the proliferation of B. longum. These data suggest that AP could promote the growth of B. longum indirectly, and provide another basis to understand the health care function of apple. (C) 2019 Elsevier B.V. All rights reserved.

目的:考察乌梅丸水提液中多糖含量,建立HPLC法分析乌梅丸多糖分子量及单糖组成方法,观察其对右旋葡聚糖硫酸钠(DSS)所致小鼠溃疡性结肠炎(UC)的预防作用,为乌梅丸临床用药及药理活性成分的研究提供依据.方法:采用水提醇沉法提取多糖;硫酸-苯酚法测定乌梅丸多糖含量;凝胶色谱法-龙智达分子量工作站测定多糖分子量;PMP柱前衍生化法HPLC分析单糖组成;DSS(3％)法建立UC小鼠模型.ICR小鼠50只随机分为5组:正常组,模型组,乌梅丸多糖2.5％,5％,10％剂量组,每组10只.造模前7天,在乌梅丸多糖治疗各组的小鼠饮水中添加乌梅丸多糖,一直给药维持至实验结束(第14天).结果:葡萄糖在0～0.08 mg·mL-1浓度范围内呈良好的线性关系(r=0.998);右旋葡聚糖酐标准品分子量在2500～2000000 Da范围内呈良好线性关系(r=0.998);乌梅丸水提液中多糖含量为40.3％,纯化的乌梅丸多糖糖含量为91.6％;分子量范围在171343～525009 Da之间,分布系数D=1.18;其多糖的单糖组成主要为甘露糖、葡萄糖醛酸、葡萄糖、半乳糖和木糖组成,其相对含量比为1.8∶1.0∶19.3∶32.8∶4.2;乌梅丸多糖能降低结肠组织损伤程度.结论:多糖可能是乌梅丸汤剂中有效的活性成分,对小鼠UC有一定的防治作用,其理化性质分析方法简便快速,结果准确,重复性好,可作为乌梅丸多糖的质量控制方法.