超声引导经皮穿刺活检与CA19-9联合检测对胰腺占位性病变的诊断价值

目的 :探讨超声引导下经皮穿刺活检与CA19 9联合检测对胰腺占位性病变的诊断价值。　方法 :对 30例超声检查怀疑胰腺占位性病变者行血清学CA19 9检测 ,并在体表B超引导下 ,用 18G或 19G切割活检针和 2 2G抽吸活检针行组织学和细胞学检查。　结果 :CA19 9诊断的敏感性为 92 % ,特异性 5 0 % ,准确性 92 %。超声引导经皮穿刺活检 30例患者总穿刺成功率为 93.3% (2 8/ 30 ) ,2 6例胰腺癌患者穿刺成功率为 92 .3% (2 4 / 2 6 ) ,活检阳性者 2 3例 ,其诊断敏感性为 88.4 % ,特异性 10 0 % ,准确性 88.4 %。CA19 9与超声引导经皮穿刺活检联合检测对胰腺占位性病变诊断的敏感性为 92 .3%、特异性 10 0 %、准确性 92 .3% ,与单行超声引导经皮穿刺活检比较有显著差异 (P <0 .0 5 ) ,而且对患者的治疗及预后有指导意义。穿刺结束后除个别患者有轻微腹痛外 ,无一例出现出血、胰瘘及胃穿孔等并发症。　结论 :体表B超引导下经皮穿刺与CA19 9联合检测对胰腺占位性病变诊断的敏感性、特异性、准确性较单一检测高 ,而且对患者的治疗及预后有一定价值 ,是一种安全、可靠的方法。     

Estrogen receptor alpha pathway is involved in the regulation of Calbindin-D9k in the uterus of immature rats.

It has been demonstrated in our previous studies that Calbindin-D9k (CaBP-9k) is a potent biomarker for screening estrogen-like chemicals in the rat model. Although treatments with 17beta-estradiol (E2) and endocrine disrupting compounds resulted in the up-regulation of uterine CaBP-9k, the mechanism of CaBP-9k induction by these compounds through two subtypes of estrogen receptors (ERalpha and ERbeta) is unclear. Thus, in the present study, immature rats were treated with propyl pyrazole triol (PPT, an ERalpha-selective ligand), diarylpropionitrile (DPN, an ERbeta-selective ligand), E2, or dimethyl sulfoxide (DMSO, a vehicle control) for three days in order to clarify which subtype of ER is involved in the uterine CaBP-9k induction. Following injection with these ER ligands, uterine CaBP-9k expression was analyzed by Northern blot and immunoblot assays. Uterine CaBP-9k expression is mainly mediated by PPT in a dose- and time-dependent manner in immature rats, whereas no significant alteration of the uterine CaBP-9k gene was observed after DPN treatment. In addition, an estrogenicity of PPT in inducing CaBP-9k expression was completely blocked by the anti-estrogen ICI 182,780, implying that uterine CaBP-9k is solely induced by ERalpha. A single treatment with PPT rapidly increased the protein levels of ERalpha and PR, an E2-mediated gene, in these tissues. Taken together, these results indicate that uterine CaBP-9k is induced by E2 and endocrine disrupting chemicals via the ERalpha pathway, but not ERbeta, in the uterus of immature rats.     

Pinacidil抑制线粒体和死亡受体通路减少大鼠脑缺血再灌注后神经元凋亡(英文)

目的探讨ATP敏感性钾通道开放剂pinacidil对大鼠脑缺血再灌注后神经元凋亡的保护作用及信号转导机制。方法 100 只Wistar 雄性大鼠随机分为四组:A 组(假手术组)、B组 (缺血组)、C 组 (KATP开放剂处理组)及D组 (KATP开放剂和阻断剂处理组)。用线栓法制备大鼠大脑中动脉缺血(middle cerebral artery occlusion,MCAO)模型,用DNA断端末端标记法(terminal-deoxynucleotidytransferase-mediated dUTP-biotin nick end labeling,TUNEL)检测神经元凋亡,用原位杂交方法检测caspase-3、caspase-8及caspase-9 mRNA的表达。结果 (1) C组12 h、24 h、48 h、72 h 时间点的凋亡细胞数较 B、D 组显著减少(P<0.05 或 P<0.01) ;B 组和 D组之间无显著性差异(P>0.05)。(2) C 组 caspase-3 mRNA 和 caspase-8 mRNA 在各时间点及 caspase-9 mRNA 在 12 h、24 h、48 h、72h 时间点的表达显著少于B组和D组(P<0.01或P<0.05),B组和D组之间无显著性差异(P>0.05)。结论 KATP通道开放剂能显著减少大鼠脑缺血再灌注后的细胞凋亡及caspase-3、caspase-8及caspase-9 mRNA的表达。KATP通道开放剂可能通过抑制线粒体通路和死亡受体通路降低神经元凋亡,保护缺血再灌注损伤后的脑组织。     

雷公藤多甙对白细胞介素-1β诱导大鼠滑膜细胞株RSC-364基质金属蛋白酶-3、c-Jun基因表达的影响

目的 观察雷公藤多甙对白细胞介素(IL)-1β诱导大鼠滑膜细胞株RSC-364基质金属蛋白酶-3(MMP3)、c-Jun mRNA表达的影响.方法 选择不同浓度的雷公藤多甙作用IL-1β刺激的大鼠滑膜细胞株RSC-364,37℃,5%CO2的环境下培养48 h,运用酶联免疫吸附试验(ELISA)检测细胞上清的MMP3和实时聚合酶链反应(real-time PCR)检测分析细胞中的c-Jun mRNA表达.结果 不同浓度的雷公藤多甙(0、5、10、20 mg/L)对IL-1β刺激的大鼠滑膜细胞株RSC-364分泌MMP3的水平依次是198、176、140、115 μg/L,c-Jun mRNA表达分别是1.17×106、3.31×105、9.32 ×104、2.81 ×104copies/ml,即呈现明显地抑制.重要的是:c-Jun mRNA表达抑制呈现明显的剂量依赖性.结论 雷公藤多甙治疗类风湿性关节炎的有效的作用机制,可能与其抑制MMP3、c-Jun基因的表达相关.     

三级医院病人就诊流向探讨

研究通过对包括专科医院在内的多家三级医院住院病人资料的分析，将疾病种类按ICD－9编码分为19类，研究各类疾病应往低级别医院分流的比例。结果表明：各大类疾病的分流比例不同，分流比例较高的主要是常见病和多发病，总的分流比大约在60％左右。     

尿激酶溶栓对大鼠局灶性脑缺血基质金属蛋白酶-9表达的影响

目的研究大鼠局灶性脑缺血后应用尿激酶(urokinase,UK)溶栓对基质金属蛋白酶-9(Matrix metalloproteinase-9,MMP-9)表达的影响,探讨MMP-9在UK溶栓引起的再灌注损伤及出血性转化中的作用。方法将实验动物随机分成3组进行研究(1)UK溶栓组;(2)缺血对照组;(3)假手术组。分别用免疫组织化学方法分析3组缺血后24hMMP-9的表达,对比研究两组MMP-9表达的差异性。结果缺血后24h前两组均有MMP-9的表达,但是UK溶栓组表达的程度明显高于缺血对照组;假手术组无MMP-9的表达。结论(1)缺血能导致MMP- 9的表达。(2)UK溶栓引起MMP-9表达的上调。     

Sural nerve biopsies in Guillain-Barre syndrome: axonal degeneration and macrophage-associated demyelination and absence of cytomegalovirus genome.

T-cell infiltration was detected by immunohistochemistry in only 2 of 10 sural nerve biopsies from patients with Guillain-Barré syndrome (GBS). The number of endoneurial macrophages, identified by the monoclonal antibody MAC 387, was increased, compared with the number in 10 cases of axonal neuropathy. Macrophage-associated demyelination was identified in 7 and axonal degeneration in 8 cases. Cytomegalovirus (CMV) genome was not detected with the polymerase chain reaction.     

Nutrition et fonction immunitaireNutrition and immune function

A deficiency of total energy or of one or more essential nutrients, including vitamins A, B₆, B₁₂, C, and E, folic acid, zinc, iron, copper, selenium, essential amino acids and essential fatty acids, will impair immune function and increase susceptibility of the host to infectious pathogens. This is most likely because these nutrients are involved in the molecular and cellular responses to challenge of the immune system. Providing these nutrients to deficient individuals restores immune function and improves resistance to infection. Thus, appropriate nutrition is required in order for the host to maintain adequate immune defences towards bacteria, viruses, fungi, parasites and tumour celîs. Although the intakes of several nutrients which result in greatest enhancement of immune function appear to be greater than recommended intakes, excess intake of certain nutrients also impairs immune responses. Some nutrients (e.g. glutamine, arginine) may become limiting in critical illness and there is mounting evidence that provision of these will aid patient recovery.     

Treatment of diabetic polyneuropathy with the neurotrophic peptide ORG 2766

The efficacy of the neurotrophic peptide ORG 2766 in diabetic patients with polyneuropathy was evaluated in a double-blind, placebo-controlled, multicentre trial. One hundred and twenty four patients were randomised in five groups to receive 0.1, 0.4, 2 or 5 mg ORG 2766 or placebo, once daily, administered subcutaneously 52 weeks. Thermal discrimination thresholds (TDT) and vibration perception thresholds (VPT), motor and sensory nerve conduction velocity, Hoffmann reflex, heart rate variation during deep breathing and heart rate response after standing up, neurological examination score and neuropathic symptom score were determined at baseline and after 17, 34 and 52 weeks of treatment. Of the nerve function indices studied, at week 52 the TDT_warmth of the hand in the ORG 2766 0.1, 0.4 and 5 mg groups and the TDT_cold of the foot in the ORG 2766 0.1 and 0.4 mg groups significantly improved compared with placebo. Further significant improvement as compared with placebo was observed in the paraesthesia score at week 34 and week 52 in the ORG 2766 2 mg group. Only at week 34 had both the heartbeat variation during deep breathing and the VPT of the foot in the ORG 2766 0.1 mg group improved significantly, compared with placebo. No further statistically significant differences were observed at time for the other measures. No adverse reactions were observed. The only recorded drug-induced side effect was pain at the injection site. Taking all measures of efficacy into account, the statistically significant results observed did not show consistency within each measure. Therefore, it is concluded that ORG 2766, in contrast to earlier reports, is not effective in treating diabetic polyneuropathy.     

Mutagenicity of benzo(a)pyrenyl-1-sulfate in the Ames test.

Comparison of the mutagenicity of nine isomeric benzo(a)pyrenyl [B(a)P] phenols conjugated with either sulfate or glucuronide was carried out using strain Salmonella typhimurium TA98. Of the nine conjugates tested, only B(a)P-1-sulfate was mutagenic. Accordingly, the mutagenicity of B(a)P-1-sulfate was compared with that of B(a)P and 1-hydroxybenzo(a)pyrene [B(a)P-1-OH] in the presence and absence of rat lung S9 and Aroclor-induced liver S9 with and without an NADPH-generating system. B(a)P-1-sulfate was slightly mutagenic, whereas B(a)P and the 1-hydroxy derivative were nonmutagenic when S9 fractions and NADPH were omitted. Addition of induced liver S9 with NADPH caused mutagenicity with B(a) -1-OH greater than B(a)P greater than B(a)P-1-sulfate. B(a)P-1-sulfate was the only mutagenic species when lung S9 was added. This mutagenicity did not require NADPH. Sodium sulfite, an inhibitor of arylsulfatase, decreased the mutagenicity of B(a)P-1-sulfate. These data suggest that a unique mutagenic species is generated from B(a)P-1-sulfate via arylsulfatase in rat lung.