目的 探讨不同条件下高浓度葡萄糖(高糖)对大鼠肾上腺嗜铬细胞瘤细胞系PC12 细胞的损伤作用,分析建立高糖损伤细胞模型的影响因素,并用确定的细胞模型观察梓醇的保护作用.方法 PC12 细胞种植密度为1×103、1×104、1×105 个/mL,高糖加入时间点分别为细胞种植后 24h 和 48 h,葡萄糖终浓度为 30、40、50 和75 mmol/L,据此分为HG30、HG40、HG50、HG75 组,另外对照组细胞加入等容积生理盐水.分别作用24、48、72 h,MTT法检测细胞存活率.用确定条件建立的细胞损伤模型观察梓醇的保护作用,细胞分为对照组、模型组、梓醇低剂量组(1×10-5mol/L)和梓醇高剂量组(1×10-4mol/L),ELISA法和荧光探针检测细胞活性氧(ROS)含量,ELISA测定乳酸脱氢酶(LDH)的释放量.结果 不同葡萄糖作用条件下,与对照组比较,HG30 组细胞存活率不变或降低(P>0.05 或P<0.05),HG40、HG50 和HG75 组细胞存活率降低(P<0.05 或P<0.01).与对照组比较,模型组的细胞ROS含量增加(P<0.01),LDH释放量升高(P<0.01);与模型组比较,梓醇低剂量组和梓醇高剂量组细胞存活率升高(P<0.01),细胞ROS含量和LDH释放量降低(P<0.01).结论 高糖诱导的PC12 细胞损伤受细胞种植密度、葡萄糖浓度和作用时间等因素影响;以 1×104 个/mL 密度种植细胞、种植后 24h 加入终浓度50 mmol/L葡萄糖作用时长 24 h,可成功建立PC12 细胞高糖损伤模型,梓醇对该细胞模型有保护作用.

Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by reduced differentiation of myeloid cells and uncontrolled cell proliferation. AML is prone to drug resistance and has a high recurrence rate during treatment with cytarabine-based chemotherapy. Our study aims to explore the cell differentiation effect of a potent histone deacetylase inhibitor (HDACi), I13, and its possible mechanism on AML cell lines (Kasumi-1, KG-1, MOLM-13 and NB4). It has been shown that I13 can significantly inhibit proliferation and colony formation of these AML cells by inducing cell differentiation coupled with cell-cycle exit at G0/G1. Mechanically, I13 presented the property of HDAC inhibition, as assessed by the acetylation of histone H3, which led to the differentiation of Kasumi-1 cells. In addition, the HDAC inhibition of I13 likely dictated the activation of the antigen processing and presentation pathway, which maybe has the potential to promote immune cells to recognize leukemic cells and respond directly against leukemic cells. These results indicated that I13 could induce differentiation of M3 and M5 subtypes of AML cells, M2 subtype AML cells with t(8;21) translocation and leukemic stem-like cells. Therefore, I13 could be an alternative compound which is able to overcome differentiation blocks in AML.

Acute leukemia (AL) is characterized by excessive proliferation and impaired differentiation of leukemic cells. AL includes acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). Previous studies have demonstrated that about 10% of AML and 22% of ALL are mixed lineage leukemia gene rearrangements (MLLr) leukemia. The prognosis of MLLr leukemia is poor and new therapeutics are urgently needed. Differentiation therapy with all-trans-retinoic acid (ATRA) has prolonged the 5-years disease-free survival rate in acute promyelocytic leukemia (APL), a subtype of AML. However, the differentiation therapy has not been effective in other acute leukemia. Here, we aim to explore the cell differentiation effect of the potent HDACs inhibitor, I1, and the possible mechanism on the MLLr-AML and MLLr-ALL cells (MOLM-13, THP-1, MV4-11 and SEM). It is shown that I1 can significantly inhibit the proliferation and the colony-forming ability of MOLM-13, THP-1, MV4-11 and SEM cells by promoting cell differentiation coupled with cell cycle block at G0/G1 phase. We show that the anti-proliferative effect of I1 attributed to cell differentiation is most likely associated with the HDAC inhibition activity, as assessed by the acetylation of histone H3 and H4, which may dictates the activation of hematopoietic cell lineage pathway in both MOLM-13 and THP-1 cell lines. Moreover, the activity of HDAC inhibition of I1 is stronger than that of SAHA in MOLM-13 and THP-1 cells. Our findings suggest that I1, as a chromatin-remodeling agent, could be a potent epigenetic drug to overcome differentiation block in MLLr-AL patients and would be promising for the treatment of AL.

Background: Dioscin, a steroidal saponin natural product, has various pharmacological activities, such as antiinflammatory, antioxidant, lipid-lowering. However, little is known about its effects on myocardial infarction (MI) injury. Thus, the study aimed to investigate the protective effects and possible mechanisms of dioscin.Methods: We evaluated protective effects of Dioscin on HL-1 cells after hypoxia based on MTT and ROS in vitro. In vivo, we ligated left anterior descending (LAD) of C57BL/6 mice to establish MI model and assess serum levels of LDH, CK-MB, cTnI, SOD, MDA and CAT treated by dioscin. In addition, myocardial damages were reflected by H&E, masson and ultrastructural examination and Electrocardiograph (ECG) was detected in MI mice. And the BMP4/NOX1 pathway was measured by western blotting, immunofluorescence assay and Real-time PCR. Furthermore, to investigate cardio-protective effects of dioscin via targeting BMP4, we transfected siBMP4 into HL-1 cells in vitro and injected BMP4 siRNA though tail veins in vivo.Results: In vitro, dioscin significantly increased the viability of HL-1 cells and inhibited ROS level under hypoxia. In vivo, dioscin markedly reduced the elevation of ST segment and alleviated myocardial infarct area in mice. In terms of serology, dioscin evidently decreased LDH, CK-MB, cTnI, MDA levels, and increased SOD level. In addition, dioscin improved the pathological status of myocardial tissue and restrained the production of collagen fibers. Mechanism study proved that dioscin notablely regulated the levels of Nrf2, Keap1, HO-1, p-NF-Kappa B, nNF Kappa B, TNF-alpha, IL-1 beta and IL-6 by down-regulating the protein levels of BMP4 and NOX1 against oxidative stress and inflammation. Further investigation showed that siBMP4 transfection diminished hypoxia and MI-induced oxidative and inflammation injury. The transfection decreased LDH, CK-MB and cTnI levels, improved ischemia T-wave inversion and reduced striated muscle necrosis, nucleus dissolution, collagen fibrosis and mitochondrial swelling in mice. In addition, siBMP4 decreased ROS and MDA levels, increased SOD and CAT levels and down-regulated mRNA levels of TNF-alpha, IL-1 beta and IL-6. Moreover, BMP4, NOX1 and nNF-Kappa B protein levels were decreased and Nrf2 levels were increased by siBMP4.Conclusion: Our study confirmed that dioscin showed an outstanding anti-myocardial infarction effect via regulating BMP4/NOX1-mediated oxidative stress and inflammation, which has a promising application value and development prospect against MI injury in the future.

Dioscin presents extents of pharmacological activities on several diseases, but its effect and mechanism on diabetes cognitive dysfunction (DCD) remains unclear. Herein, we conducted a series of pharmacological evaluation assays of purinergic receptor P2X7 (P2X7R) with dioscin. We uncovered that dioscin presented a clearly protective effect on diabetes cognitive dysfunction via a methylglyoxal-treated PC12 cell model and streptozocin (STZ)-induced rat models. Additionally, it found that P2X7R and NLRP3 inflammasome signals were activated in diabetes cognitive dysfunction via in vivo and in vitro detection. Moreover, it was demonstrated that P2X7R regulated NLRP3 inflammasome signals in methylglyoxal-treated PC12 cells. Meanwhile, it was showed that dioscin-induced anti-diabetes cognitive dysfunction effect was accompanied with an inhibition of P2X7R/NLRP3 signal. A deeper mechanical study indicated that an overexpression of P2X7R further enhanced the protective effect of dioscin. Whilst, an inhibition of P2X7R abolished the protective effect of dioscin. These results suggested that dioscin protected type 2 diabetes cognitive dysfunction through, at least partially, regulating the P2X7R/NLRP3 signal pathway. Our findings further indicate the great value of dioscin on preventing type 2 diabetes cognitive dysfunction.

目的:探究人参皂苷Rg3联合紫杉醇抑制人肝癌细胞HepG2的增殖,抑制裸鼠移植瘤体内肝脏肿瘤的增长及促进凋亡的作用.方法:体外实验,采用MTT法检测人参皂苷Rg3联合紫杉醇对人肝癌细胞HepG2增殖的抑制作用;体内实验,构建人肝癌HepG2细胞裸鼠移植瘤动物模型,随机分为人参皂苷Rg3组,GS-Rg3:10 mg/(kg·d)灌胃,紫杉醇组,Taxol:10 mg/kg腹腔注射,每周2次,联合组,GS-Rg3+Taxol,给药剂量和方法同上,对照组,灌胃给与等体积生理盐水,共4组,每组10只.连续给药3周,给药结束后颈椎脱臼处死,计算分析各实验组的肿瘤抑制率;WB法检测凋亡蛋白caspase-3、bac-2/bax的表达情况.结果:体外实验结果示,与24 h处理组比较,紫杉醇联合人参皂苷Rg3(30、60μg/mL)在48 h、72 h后对肝癌HepG2细胞增殖的抑制作用显著升高(P<0.05);与48 h处理组比较,紫杉醇联合人参皂苷Rg3(30、60、120μg/mL)在72 h后对肝癌HepG2细胞增殖的抑制作用显著升高(P<0.05).体内试验结果示,给药14 d后,人参皂苷Rg3联合紫杉醇组肿瘤抑制率(64.13±2.02)％较人参皂苷Rg3组(48.34±3.86)％和紫杉醇组(54.21±3.21)％显著升高(P<0.05);给药28 d后,联合组肿瘤抑制率(69.38±2.19)％较人参皂苷Rg3组(57.30±3.95)％和紫杉醇组(61.08±4.16)％显著升高(P<0.05).Western blot实验结果示,与对照组比较,联合用药组人肝癌细胞HepG2裸鼠移植瘤凋亡相关蛋白caspase-3表达显著升高(P<0.05);联合用药组和紫杉醇组bac-2/bax表达显著降低(P<0.05).结论:人参皂苷Rg3联合紫杉醇可通过抑制肝癌细胞的增殖、诱导其凋亡发挥协同抗肿瘤的作用.

目的 探讨恩替卡韦联合干扰素抗病毒治疗对慢性乙型肝炎肝纤维化患者炎症标志物IL-1β、IL-4、IL-12表达的影响.方法 72例慢性乙型肝炎肝纤维化患者随机分为观察组和对照组,各36例.对照组给予恩替卡韦片口服治疗,观察组在此基础上加用干扰素.对比两组患者治疗前、后细胞因子IL-1β、IL-4、IL-10的水平.结果 两组治疗前IL-1β、IL-4及IL-12水平比较无显著性差异(P>0.05).治疗后,两组肝穿刺活检肝纤维化评分及IL-1β、IL-4、IL-12水平均明显降低,其中观察组降低更为显著,差异有统计学意义(P<0.01).结论 恩替卡韦联合干扰素可显著降低患者肝纤维化评分,同时对IL-1β、IL-4及IL-12水平的升高具有明显的改善作用.

目的 观察梓醇对阿尔茨海默病(AD)大鼠模型大脑皮质的保护作用.方法 健康雄性Wistar大鼠36只,体质量范围为250～300 g,随机数字表法分为4组,每组9只:健康对照组、模型组、梓醇小剂量组、梓醇大剂量组.除健康对照组大鼠外,其余组大鼠均行右侧脑室定位注射β-淀粉样蛋白片段25-35(Aβ25-35)和腹腔注射D-半乳糖结合制备AD模型,然后梓醇小剂量组大鼠注射梓醇5 mg·kg-1·d-1,梓醇大剂量组大鼠注射梓醇10 mg·kg-1·d-1,健康对照组和模型组大鼠注射等容积0.9％氯化钠水溶液,连续腹腔注射给药7 d.Y-迷宫检测大鼠的学习指数,苏木精-伊红(HE)染色和透射电镜观察AD大鼠皮层结构,免疫组织化学染色观察大脑皮质胆碱能毒蕈碱受体M1亚型(M1受体)的表达,蛋白质印迹法(Western Blot)检测M1受体蛋白的含量.结果 实验过程中模型组大鼠死亡1只,最终模型组n=8,其余组均n=9.与模型组比较,从造模后第14天开始,梓醇显著提高了大鼠的学习指数(第14天:小剂量组t=3.267,P=0.0309,大剂量组t=4.648,P=0.0097;第21天:小剂量组t=5.010,P=0.0074,大剂量组t=4.614,P=0.0099),第14天4组大鼠的学习指数分别为(5.6±0.2),(2.6±0.3),(3.7±0.5),(4.4±0.6);第21天4组大鼠的学习指数各组分别为(6.3±0.8),(4.1±0.5),(5.3±0.4),(5.8±0.8).HE染色可见模型组大鼠大脑皮质结构有损伤性表现,透射电镜检查见大脑皮质神经元细胞内线粒体、粗面内质网、核染色质等异常改变,梓醇干预组神经元的结构显著改善.免疫组织化学染色可见模型组大鼠大脑皮质M1受体染色浅,神经元数目减少,M1受体蛋白表达下调,梓醇能够显著上调M1受体蛋白表达(与模型组比较,小剂量组t=3.983,P=0.0164;大剂量组t=6.694,P=0.0026),4组大鼠M1受体蛋白表达分别为100％,64.75％,74.63％,85.74％.结论 梓醇能够改善AD大鼠大脑皮质结构异常,升高M1受体表达.

临床药理学研究人体与药物相互作用及其规律,是药学专业研究生的主干课程之一.随着人才需求日益更新,课程教学过程中的问题更加凸显.对临床药理学教学内容、教学方法、教学结果评价等三个方面进行分析,为提高教学质量提供参考.

Objective To observe the effect of catalpol on glycemic metabolism in hyperglycemic Alzheimer disease(AD) rat model.Methods Fifty Sprague Dawley rats were randomly divided into normal control group (n =10),hyperglycemia group (n =10),hyperglycemic AD model group (n =9),catalpol group (n =9) and pioglitazone group(n =6).Y-maze test was performed before injection and on the 7th,14th day after injection of β-amyloid fragment 25-35 (Aβ25-35).Body weight,blood glucose and serum insulin were detected before injection and on the 3rd,9th,15th day after injection of Aβ25-35.Contents of insulin and insulin-like growth factor(IGF-1)in brain homogenate were tested by enzyme-linked immunosorbent assay;expressions of insulin and IGF-1 were observed through immunohistochemical staining and western blotting.Results Learning index in hyperglycemic AD model group was significantly lower than that in normal control group on the 7th,14th day after injection of Aβ25-35(P ＜0.01).Iearning index in catalpol group and pioglitazone group was significantly higher than that in hyperglycemic AD model group(P ＜0.01).Blood glucose level in catalpol group was significantly lower than that in hyperglycemia AD model group on the 9th,15th day after injection of Aβ25-35 [(10.4 ± 2.1) mmol/L vs (17.4 ±0.9) mmol/L,(7.9 ± 0.5) mmol/L vs (19.2 ± 0.8) mmol/L] (P ＜ 0.05).Serum insulin level in catalpol group and pioglitazone group was significantly lower than that in hyperglycemic AD model group on the 15th day after injection of Aβ25-35 [(14.8 ± 1.7),(15.1 ± 1.7) mIU/L vs (17.2 ± 1.4) mIU/L] (P ＜ 0.05).Levels of insulin and IGF-1 in brain homogenate in hyperglycemic AD model group were significantly lower than those in normal control group;levels of insulin and IGF-1 in brain homogenate in catalpol group and pioglitazone group were significantly higher than those in hyperglycemic AD model group [(14.93 ± 0.37),(15.06 ±0.26)mIU/Lvs (13.70 ±0.54)mIU/L;(6.13 ±0.11) × 105,(6.42 ±0.15) × 105 ng/L vs (3.44 ±0.19) × 105 ng/L] (P ＜ 0.05).Pathological images showed positive staining of insulin and IGF-1 in cytoplasm of cortical neurons;hyperglycemic AD model group showed cell cytoplasmic reduction and positive staining reduction compared with normal control group;insulin and IGF-1 positive staining increased in catalpol group and pioglitazone group.Electrophoretic results showed that expressions of insulin and IGF-1 in hyperglycemic AD model group were significantly lower than those in normal control group;expressions of insulin and IGF-1 in catalpol group and pioglitazone group were significantly higher than those in hyperglycemic AD model group.Conclusion Catalpol regulates the glucose metabolism in hyperglycemic AD rats.

目的 探讨恩替卡韦联合干扰素抗病毒治疗对慢性乙型肝炎肝纤维化患者炎性细胞因子及氧化应激指标的影响.方法 72例慢性乙型肝炎肝纤维化患者随机分为观察组和对照组,各36例.对照组给予恩替卡韦片口服治疗,观察组在此基础上加用干扰素.对比两组患者治疗前、后肝功能指标丙氨酸氨基转移酶(ALT)、天冬氨酸转氨酶(AST)、谷氨酰转移酶(GGT),纤维化指标透明质酸(HA)、Ⅲ型前胶原(PCⅢ)、四型胶原(Ⅳ-C)、层粘连蛋白(LN),炎症细胞因子白介素(IL)-6、IL-17、肿瘤坏死因子(TNF)-α、转化生长因子(TGF)-β及氧化应激指标丙二醛(MDA)和超氧化物歧化酶(SOD)水平.结果 治疗结束后,两组患者炎症细胞因子、氧化应激指标、肝脏功能指标及纤维化指标均有明显改善,停药12周后无反弹.其中观察组改善效果更佳,各指标回复40％～65％不等,与对照组相比,差异具有统计学意义(P＜0.05).结论 恩替卡韦联合干扰素能有效抑制慢性乙型肝炎肝纤维化患者体内炎性细胞因子的表达,改善机体内环境,助其发挥抗纤维化、保护肝脏的治疗作用.

Objective: To study the protective mechanism of bellidifolin separated from LiuMao ZhangYaCai (Swertia pseudochinensis Hara) for the pancreas of diabetic rats. Methods: The male Wistar rats were randomized into the normal group, the model group and bellidifolin group (50 mg/kg), eight rats each group. The rats in the model group and bellidifolin group were established by STZ into diabetic models, bellidifolin group were intervened by bellidifolin. The protective effects of bellidifolin to the pancreas were analyzed by detecting the concentrations of oxidation metabolite malonaldehyde (MDA), the activity of serum antioxidant factor SOD and catalase (CAT) of the rats in different groups, studying the difference between the contents of damage related factors NF-κBp65 and IκBα protein expressions after HE staining of the pancreatic island by western blotting method. Results: Bellidifolin could improve the activity of SOD and CAT (P＜0.01), decrease the concentrations of MDA (P＜0.01); HE staining of the pancreatic island showed that bellidifolin could relieve the atrophy of pancreatic island of diabetic rats, Western blotting demonstrated that bellidifolin could increase the expressions of IκBα in pancreatic tissue and decrease the expressions of NF-κBp65 protein. Conclusion: Bellidifolin could alleviate STZ-induced damage to pancreatic island and protect pancreatic island, which might ease oxidative stress level through pancreatic island NF-κB signal channel.

目的 研究二十二碳六烯酸-磷脂(docosahexaenoic acid-phosphatidylcholine,DHA-PC)对海马CA1区注射A＆5-35所致的阿尔茨海默病(Alzheimer's disease,AD)大鼠模型学习记忆能力改善作用,为DHA-PC的药用开发奠定理论基础.方法 SPF级雄性Wistar大鼠40只,250～300 g,随机分为正常对照组、AD组、多奈哌齐组、DHA-PC组.大鼠双侧海马CA1区注射Aβ25-35制作AD大鼠模型,水迷宫检测学习记忆能力改变,检测Tau(Ser 396)蛋白的含量,检测超氧化物歧化酶活性.结果 水迷宫结果显示:与AD组相比,定向航行实验DHA-PC组大鼠的潜伏期明显降低(P＜0.05);空间探索实验DHA-PC组大鼠在安全平台所在象限的活动时间明显增加(P＜0.05).与AD组相比,DHA-PC组和DHCI组大鼠皮层和海马的Tau(Ser396)蛋白含量明显降低(P＜0.05,P＜0.01),DHA-PC组和DHCI组皮层SOD活性增强(P＜0.01).结论 DHA-PC可通过降低皮层和海马396位点磷酸化Tau蛋白的表达和增强SOD活性,改善AD大鼠学习记忆能力,具有较好的药用开发前景.

Objective To analyze the treatment regimens and related factors of the hospitalized patients with type 2 diabetes mellitus( T2 DM) ,and provide references for clinical pharmacists. Methods A total of 250 inpatients with T2 DM were enrolled in the study. The body mass index( BMI) ,course of disease,complications and antihypergly-cemic agents use was recorded by cross-sectional study method. The 250 cases were divided into 3 groups according to the different medication. Patients in OAHA group ( n =109 ) received oral antihyperglycemic agents, patients in Ins group (n=46) accepted insulin treatment,and patients in OAHA+Ins group (n=95) received oral antihyperglycemic agents combined with insulin. The related factors and medication of the patients in 3 groups were compared. Results There was statistical difference in related factors,such as drinking,course of treatment,diabetic retinopathy and diabetic peripheral neuropathy,coronary heart disease among the three groups ( P<0. 05 ) . Metformin accounted for 58. 4% in the hypoglycemic agents used in the three groups,and α-glycosidase inhibitor 34. 4%,followed by sulfonylurea,nateg-linide,DPP-4 inhibitors and TZDs in sequence. Metformin+insulin and α-glycosidase inhibitor+insulin accounted for 66. 32% and 49. 47% in the combination use of hypoglycemic agents and insulin. The discharged FPG standardized rate in OAHA+Ins group was higher than that at the time of admission(58. 95% vs. 35. 79%,P<0. 05). The discharged 2hPG standardized rate in OAHA group,Ins group and OAHA+Ins group was higher than those at the time of admis-sion (71. 56% vs. 3. 67%,69. 57% vs. 0,76. 84% vs. 7. 37%,P<0. 05). Conclusion The oral antihyperglycemic a-gents-centered treatment regimen is suitable for the patients with short duration and high BMI,while most of the pa-tients with long duration and low BMI receive insulin treatment in our hospital. The drug use generally conforms to the standard of clinical diagnosis. The combination of oral antihyperglycemic agents with insulin can reduce the FPG and 2hPG more significantly than the single use.

Curcumin has anticancer functions in various tumors. It has been shown to induce apoptosis through p53-dependent pathways. p73 gene is a member of the p53 family which encodes both a tumor suppressor (transactivation-competent p73 (TAp73)) and a putative oncogene (dominant-negative p73 (DNp73)); the former shares similarity with the tumor suppressor p53, and the latter behaves as dominant-negative proteins that interfere with the activity of TAp73. To understand the p73-dependent mechanisms that are engaged during curcumin-induced apoptosis, we established a p73 overexpression cell models using p53-deficient Hep3B cells (Hep3BTAp73/DNp73). Our results demonstrated that curcumin at concentrations of 40 and 80 μM induced DNA damage, increased TAp73/DNp73 ratio, and also led to apoptosis in the Hep3BTAp73/DNp73 cells. The apoptotic cell death was concurrent with the loss of mitochondrial membrane potential; release of cytochrome c from mitochondria; and the cleavage of caspase 9, caspase 3, and poly(ADP-ribose) polymerase (PARP). These results demonstrated a p73-dependent mechanism for curcumin-induced apoptosis that involves the mitochondria-mediated pathway.

在医学本科生药理学实验中,不改变验证性实验学时安排,将科研培养贯穿于实验整个过程,增加实验课PBL教学,引导学习自主发现问题并分析解决,教师总结注重渗透人文和道德教育,全方位提升本科生科研素质.

OBJECTIVE To explore the clinical characteristics of hospital‐acquired pulmonary infections in the elder‐ly patients with diabetic mellitus and put forward corresponding prevention measures so as to reduce the infection rate .METHODS A total of 300 elderly patients with diabetic mellitus who were treated in the hospital from Jun 2011 to Jun 2013 were enrolled in the study ,then the related laboratory indicators for the hospital‐acquired pulmo‐nary infections were observed ,and the corresponding prevention measures were put forward .RESULTS The hospi‐tal‐acquired pulmonary infections occurred in 43 of 300 elderly patients with diabetic mellitus ,with the infection rate of 14 .3% .The age ,length of hospital stay ,invasive operation ,and level of glycated hemoglobin were the im‐portant influencing factors for the hospital‐acquired pulmonary infections in the elderly patients with diabetic melli‐tus (P<0 .05) .Of the 43 pulmonary infection patients with the length of hospital stay of 48 hours ,30 (69 .8% ) had cough and expectoration ,20 (46 .5% ) had fever ,33 (76 .7% ) had pulmonary consolidation signs and rales , 38 (88 .4% ) had oval lesions such as sheet ,porphyritic invasive shadow and increased lung markings ,and 23 (53 .5% ) had the white blood cell counts more than 10 × 109/L or the neutrophils more than 70 .0% .The sputum specimens were cultured positive in 23 of 43 patients with pulmonary infections ,with the positive rate of 53 .5% ;totally 29 strains of pathogens have been isolated from the 23 patients with positive culture of specimens ,including 19 (65 .52% ) strains of gram‐negative bacteria ,6 (20 .69% ) strains of gram‐positive bacteria ,and 4 (13 .79% ) strains of fungi .CONCLUSION There are a variety of influencing factors for the hospital‐acquired pulmonary infec‐tions in the elderly patients with diabetic mellitus .It is necessary for the hospital to conduct the diagnosis and&nbsp;treatment in a timely manner so as to effectively reduce the incidence of adverse reactions .

Objective To investigate the expression of the cutaneous T-cell lymphoma-associated antigen 5 (cTAGE5 ) in tumor cell lines and its biological role in the development of tumor preliminarily.Methods Expression of cTAGE5 in tumor cell lines was detected by immunofluorescence.Ovarian clear cell adenocarcinoma cell line ES-2,which was proved to be positive expression of cTAGE5 ,were divided into normal control group,liposome control group,siRNA transfection group and epirubicin control group(final concentration 1 ×10 -6 mol/L).The Proliferation and growth ability of ES-2 were detected by plate clone formation test and MTT test respectively,and migration ability was detected by cell scratch assay.Results cTAGE5 was expressed in cell lines got from human breast cancer,lung cancer and ovarian canc-er,but little in cell lines from human stomach and liver cancer.Compared with normal control group,growth and prolif-eration ability of tumor cells in siRNA transfection group decreased(P<0.01),migration ability reduced (P<0.01), and proliferation ability of tumor cells in epirubicin control group decreased(P<0.01 ),also migration ability reduced (P<0.01).Conclusion Expression of cTAGE5 in tumor cell lines from different tissue was different.Inhibition of cTAGE5 expression can depress the proliferation,growth and migration ability of tumor cells.

Objective: To explore the effect of catalpol on choline acetyl-transferase and M receptor affinity in a PC12 cell model and a rat model induced by beta-amyloid 25-35 (A beta(25-35)).Methods: In PC12 cells, catalpol (10 mu mol/l, 100 mu mol/) or saline was retained in the medium and A beta(25-35) (final concentration 20 mu mol/l) was added. Choline acetyl-transferase (ChAT) expression was determined by immunocytochemistry, ChAT activity measured by radioenzymatic assay, and M receptor (muscarinic receptor) affinity determined by H-3-QNB binding test. In Wistar rats, A beta(25-35) was injected intracerebroventricularly to establish AD model. After injection of A beta(25-35), the rats were injected catalpol at 5 and 10 mg/kg d(-1) intraperitoneally for the next 7 days, and saline for the control rats. ChAT expression, ChAT activity and M receptor affinity were tested. Cells and rats all were divided into four groups: Group A (control), Group B (model), Group C (catalpol low dose), and Group D (catalpol high dose).Results: Compared with control, both PC12 cell and rat AD models showed decreased expression and activity of ChAT (p < 0.01), but M receptor affinity remained the same (p > 0.05). Compared with model group, treatment of catalpol increased expression and activity of ChAT of PC12 cell and rat AD model induced by A beta(25-35), p < 0.05 or p < 0.01 respectively. But there was no difference of M receptor affinity among the four groups (p > 0.05). M receptor affinity remained the same as concentration of catalpol increased gradually in atropine competition experiments (p > 0.05).Conclusions: Catalpol could regulate the cholinergic nerve system function from its effect on ChAT and may have beneficial effect for treatment of AD, but had no effect on M receptor affinity. (C) 2014 Elsevier Masson SAS. All rights reserved.

AIMS To investigate the regulating effects of catalpol on the hypothalamic-pituitary- adrenocortical-axis (HPA) in an Alzheimer's disease (AD) rat model. METHODS Healthy male Wistar Rats were selected. The AD model was generated by orthotopic injection of beta-amyloid 25-35 (Abeta25-35) into the right lateral ventricle. The animals were divided into five study groups: Catalpol at low dose (5 mg/kg), Catalpol at high dose (10 mg/kg), model control group and sham surgery control group, n = 9 respectively. The serum concentration of hydrocortisone (HYD), adrenocorticotropin (ACTH) and corticotropin releasing hormone (CRH) determined by Enzyme-Linked Immunosorbent Assay (ELISA). Structural alterations of the hypothalamus were examined by H&E stain and electron microscope. The CRH receptor 1 (CRHR1) positive neurons were detected with immunohistochemistry. RESULTS Serum HYD level was significantly increased (p < 0.01), and both ACTH and CRH were dramatically decreased (p < 0.01) in the AD model group rats compared with normal control rats at day 7. Catalpol treatment was able to improve the hormone secretion disorder in AD model group rats compared with the model group (p < 0.01 or p < 0.05) in particular at 21 days. Structure damage of hypothalamus in the AD rat as evidenced less CRHR1 positive neurons, rough endoplasmic reticulum dilation and degranulation, and mitochondrial swelling under electron microscope. Catalpol treatment at both high and low doses was able to alleviate the structure damage of the hypothalamus in the AD rats. CONCLUSIONS Catalpol could improve the endocrine function of the HPA and alleviate the structural damage of hypothalamus in AD rats.