基于近红外光谱技术快速定性鉴别广陈皮模型的建立

目的采用近红外光谱技术(NIRS)建立广陈皮的定性分析模型,以建立快速鉴别广陈皮药材的方法。方法采集广陈皮与川陈皮的NIRS图,通过标准正交变量变换(SNV)预处理后采用聚类分析方法建立广陈皮与川陈皮鉴别模型,并进行模型内验证和模型外验证,建立了广陈皮定性分析模型。结果在4 000~10 000 cm-1广陈皮和川陈皮能够较好地区分,内部验证的准确率高达100%,外部验证准确率达到90.91%。结论采用近红外光谱技术对广陈皮样品进行鉴别是可行的。     

单纯鼻腔表面麻醉在电子喉镜检查中的应用效果观察

摘要：目的??探讨盐酸丁卡因行咽腔表面麻醉对电子喉镜检查的影响。方法?用双盲法随机将200例电子喉镜检查患者分成两组,每组各100例,一组患者咽腔用1.0%盐酸丁卡因表面麻醉（对照组）,另一组用0.9%氯化钠喷雾（实验组）,两组患者鼻腔均用呋嘛和1.0%盐酸丁卡因行表面麻醉,检查前均用盐酸达克罗宁胶浆涂抹镜身。根据自设评估标准对患者表面麻醉开始至检查结束期间的反应进行评估。结果?两组患者电子喉镜检查均顺利完成,检查时间差异有统计意义（P <0.05）,对照组咽部不适阳性率较实验组高,程度较实验组重,差异有统计学意义（P <0.05）。结论?单纯鼻腔表面麻醉不使用咽腔丁卡因表面麻醉,不会影响电子喉镜检查的顺利完成;不行咽腔表面麻醉的患者,咽部不良反应更少,患者检查后恢复进食快,患者检查全过程的舒适度体验大幅度提高;不使用咽腔麻醉缩短了患者的表面麻醉和等候时间,提高了检查效率,值得推广应用。     

普瑞巴林剂量对腹腔镜子宫全切术患者术后疼痛的影响

目的探讨不同剂量(75、150和300 mg)普瑞巴林预先给药在腹腔镜子宫切除术患者中的术后镇痛效果。方法该研究为前瞻性、随机、安慰剂对照和双盲研究。共纳入82例美国麻醉医师协会(ASA)分级为Ⅰ～Ⅱ级并择期行腹腔镜子宫切除术的患者。患者随机分成4组,其中第1、2和3组(每组20例)术前1晚、术前30 min和术后6 h分别口服浓度为75、150和300 mg的普瑞巴林,而对照组(n=22)按照相同方案接受安慰剂治疗。主要临床结局是术后24 h静息和运动时的疼痛视觉模拟评分(VAS)。药物相关副作用评估作为次要观察指标。嗜睡采用Ramsay镇静评分评估,而恶心和呕吐用数值评分评估。结果不同浓度预先普瑞巴林给药的镇痛效果优于安慰剂。事后检验显示,4组间AVS评分差异有统计学意义,表明浓度下降,疼痛评分作为时间自变量而下降。普瑞巴林浓度达到最高(300 mg)时,镇静评分高于其他组。结论预先服用75、150和300 mg普瑞巴林对减轻腹腔镜子宫切除术后疼痛具有重要作用。比较不同浓度与副作用表明,口服150 mg普瑞巴林是减轻腹腔镜子宫切除术后疼痛的安全有效方法。     

探讨STEPTY P与TR Band两种压迫止血器对经桡动脉介入术后止血效果的影响

目的 比较STEPTY P和TR Band两种压迫止血器对冠状动脉介入术后止血情况以及局部并发症的影响。方法 收集我院经桡动脉行冠状动脉造影的患者370例,随机分成A、B两组,其中A组200例患者采用STEPTY P桡动脉压迫止血器,B组170例患者采用TR Band桡动脉压迫止血器。观察比较两组术后止血效果、局部并发症及患者舒适度情况。结果 两种方法术后均能成功止血,在渗血、皮肤破损、二次包扎、血肿发生率方面差异均无统计学意义( P＞0.05),且均未发生桡动脉闭塞及血管迷走神经反射;A 组肢体远端肿胀、压迫止血时间、患者主观不适情况发生率均低于B 组( P<=0.001),具有统计学意义。结论 STEPTY P压迫止血器不但可以有效压迫止血,而且可以减少相关并发症的发生,缩短术后压迫时间,患者感觉更为舒适、满意,同时还能降低医护人员工作量、减少工作负担。可以将STEPTY P新型压迫止血器在临床应用中广泛推广。     

Insulin-like growth factor II signaling through the insulin-like growth factor II/mannose-6-phosphate receptor promotes exocytosis in insulin-secreting cells

The insulin-like growth factor II (IGF-II)/mannose-6-phosphate (M-6-P) receptor is known to participate in endocytosis as well as sorting of lysosomal enzymes and is involved in membrane trafficking through rapid cycling between cytosolic membrane compartments and the plasma membrane. Here we demonstrate that IGF-II, acting through the IGF-II/M-6-P receptor, promotes exocytosis of insulin in the pancreatic β cell. The effect of IGF-II was evoked at nonstimulatory concentrations of glucose, was mediated by a pertussis toxin sensitive GTP-binding protein, was dependent on protein kinase C-induced phosphorylation, and was independent of changes in cytoplasmic free Ca²⁺ concentration. Since the applied concentration of IGF-II is within the range normally found free in circulation in humans, this novel signaling pathway for the IGF-II/M-6-P receptor is likely to be involved in modulation of insulin exocytosis under physiological conditions.     

结肠灌洗联合善宁治疗重症急性胰腺炎肝损伤的研究

目的探讨结肠灌洗治疗重症急性胰腺炎所致肝细胞损伤的保护性机制及其对肝细胞凋亡的影响。方法16只杂种犬随机分成4组:对照组、AP组、善宁治疗组和结肠灌洗加善宁治疗(联合治疗)组,每组4只。用牛磺胆酸钠+胰蛋白酶混合溶液诱导犬造成重症急性胰腺炎(SAP)模型。所有犬除术后禁食、水,常规补液外,善宁治疗为皮下每12h注射善宁0.1mg,结肠灌洗1次/d。所有犬分别于术前、12h、24h、48h、72h采取静脉血检测淀粉酶(AMY)、羟自由基OH·、丙二醛(MDA)、ALT、GST。72h后处死动物取胰腺及肝脏组织标本,用TUNEL检测肝细胞凋亡指数(AI)。结果SAP组的AMY、OH·、MDA、GST在术后12h后显著升高,ALT在术后24h显著升高,并持续至72h;联合治疗组OH·、MDA、GST和ALT均于术后24h达到高峰后开始下降,72h后下降明显,与SAP组、善宁治疗组有显著性差别(P<0.05),并且MDA值与ALT值呈正相关(模型组r=0.899,P=0.038;善宁治疗组r=0.901,P=0.037;联合治疗组r=0.83,P=0.084);联合治疗组的肝细胞凋亡指数(AI)明显低于SAP组、善宁治疗组,具有统计学差异(P<0.05),而与对照组无明显差异(P>0.05)。结论氧化应激参与了犬SAP时的肝损伤,而结肠灌洗治疗SAP肝损伤的机制之一可能是通过降低机体的自由基水平而减少氧化损伤,进而减少肝细胞的凋亡,达到保护肝脏的目的。     

质子泵抑制剂的研究进展

质子泵抑制剂(proton pump inhibitor,PPIs)为苯并咪唑类衍生物,特异性和非竞争性的作用于H /K -ATP酶,能抑制基础胃酸的分泌及组胺、进食等多种刺激引起的酸分泌,具有起效快、作用强和持续时间长的特点,是治疗酸相关性疾病的首选药物,在根除幽门螺杆菌(Helicobacter pylori,Hp     

Tissue Kallikrein Prevents Restenosis After Stenting of Severe Atherosclerotic Stenosis of the Middle Cerebral Artery: A Randomized Controlled Trial

In-stent restenosis (ISR) following intracranial artery stenting affects long-term clinical outcome. This randomized controlled trial sought to identify the long-term efficacy of exogenous tissue kallikrein (TK) for preventing ISR after intracranial stenting of symptomatic middle cerebral artery (MCA) atherosclerotic stenosis.Sixty-one patients successfully treated with intracranial stenting for symptomatic MCA M1 segment stenosis (>70%) were enrolled and randomized into 2 groups: control group and TK group. Patients in the TK group received human urinary kallidinogenase for 7 days, followed by maintenance therapy of pancreatic kallikrein for 6 months. The primary end point was angiographically verified ISR at 6 months, and secondary end points included vascular events and death within 12 months. Endogenous TK plasma concentrations of patients were measured before stenting and at the 6-month follow-up time-point.Patients in the TK group had lower occurrence rates of ISR and vascular events than patients in the control group. There was no difference in endogenous TK levels in plasma at 6 months postoperatively between the TK and control groups. Further subgroup analysis revealed that patients without ISR had higher endogenous TK levels at baseline and lower concentrations at 6 months postoperatively compared with patients who underwent ISR.Exogenous TK is effective for the prevention of ISR after intracranial stenting.     

阿托伐他汀改善自发性高血压大鼠的心肌脂质代谢和抑制心肌肥厚

目的通过研究阿托伐他汀对自发性高血压大鼠(SHR)心肌中PPARα、CPTⅠ表达和心肌脂质代谢变化及心肌肥厚指标的影响,探讨阿托伐他汀对SHR心肌肥厚的改善作用及其机理。方法观察阿托伐他汀灌胃10周的SHR心肌肥厚指标、血清和心肌游离脂肪酸含量及心肌PPARα、CPTⅠmRNA表达的改变。结果与WKY(n=6)比较,SHR(n=6)心肌中PPARαmRNA(0.285±0.062比WKY:0.478±0.093,P<0.01)与CPTⅠmRNA(0.795±0.139比WKY:1.115±0.109,P<0.01)表达减少,血清及心肌中游离脂肪酸含量增加,分别为[(798.2±38.0比WKY:354.7±27.7)nmol/L,P<0.01]和[(635.0±77.4比WKY:245.3±47.3)nmol/L,P<0.01],心室质量指数增加(VWI)[(3.16±0.08比WKY:2.99±0.10)g/kg,P<0.05],心肌细胞直径增加(TDM)[(21.3±1.3比WKY:18.18±0.75)μm,P<0.01];阿托伐他汀50mg/kg·d治疗10周后(n=6),心肌中PPARα、CPTⅠmRNA表达增加,心肌中游离脂肪酸含量明显降低、VWI降低,TDM降低。结论阿托伐他汀能够增加心肌中PPARα、CPTⅠmRNA表达,降低心肌中游离脂肪酸含量,改善心肌脂质代谢障碍,可能是其抑制心肌肥厚发生与发展的机制之一。     

Activation of intracellular signaling by hepatitis B and C viruses: C-viral core is the most potent signal inducer

To clarify the effects of hepatitis C virus (HCV) infection on hepatocytes, we analyzed and compared the induction of intracellular signals by HCV and hepatitis B virus (HBV) proteins. We examined the influence of 7 HCV (core, NS2, NS3, NS4A, NS4B, NS5A, and NS5B) and 4 HBV (precore, core, polymerase, and X) proteins on 5 well-defined intracellular signaling pathways associated with cell proliferation, differentiation, and apoptosis by use of a reporter assay. Viral protein-expression vectors were cotransfected into mammalian cells with reporter vectors having a luciferase gene driven by the following inducible cis-enhancer elements: the cyclic adenosine monophosphate response element, the serum response element (SRE), and the binding sites for nuclear factor kappaB (NF-kappaB), activator protein 1 (AP-1), and serum response factor (SRF). In addition, the activation of signals by HCV proteins was examined in a reporter plasmid having a natural interleukin-8 (IL-8) promoter upstream of a luciferase gene. Of 11 HCV and HBV proteins, HCV core had the strongest influence on intracellular signals, especially NF-kappaB-, AP-1-, and SRE-associated pathways. HCV core's activation level exceeded that of HBV X protein, a well-characterized transactivator of these signals. Moreover, HCV core activated the IL-8 promoter through NF-kappaB and AP-1. For the other proteins, HCV NS4B showed signal activation, but signals were activated at a lesser extent. The luciferase reporter assay, a recently introduced technique, helped in the elucidation of molecular events underlying the inflammatory and proliferation process in the liver induced by HCV.