弥漫性轴索损伤病人的护理

弥漫性轴索损伤 (DAI) ,在脑损伤中发生率高 ,病死率高 ,占脑外伤死亡病人总数的 3 5 %。全部DAI病人中植物生存率为 15 % ,重残 14 % [1] 。为了降低病死率 ,提高病人的生存质量 ,现将 1999年 1月— 2 0 0 2年 1月我院收治的 5 5例DAI昏迷病人的护理体会总结如下。1　临床资料　　本组 5 5例 ,男 3 8例 ,女 17例 ,年龄 6岁～ 68岁 ,平均 40 .9岁。格拉斯哥 (GLS)计分均 <8分 ,其中评分为 3分～ 5分的特重型病人 3 2例。致伤原因 :车祸 44例 ,高处坠落 8例 ,打击伤 3例。 5 5例病人中有 17例因合并颅内血肿而行开颅手术 ,其他病人为保…     

不同临床和病理分型对肝门部胆管癌切除术预后的影响

目的 研究临床和病理分型与肝门部胆管癌切除术疗效的关系。方法总结1993年至2004年在解放军总医院肝胆外科手术切除的肝门部胆管癌198例病例资料。结果临床分型Ⅰ型34例，Ⅱ型60例，Ⅲa型27例，Ⅲb型33例，Ⅳ型19例，Ⅴa型6例。Ⅴb型19例。病理高分化腺癌35例，中分化腺癌52例，低分化腺癌54例，三者的中位生存期分别为29．5、11、5．5个月；病理切缘阴性者与切缘阳性者生存率有显著性差异（P 〈0．05）。手术并发症出现率41．4％，围手术期死亡1例。结论肝门部胆管癌根据临床分型进行相应的手术治疗；病理切缘阴性是影响预后的主要因素之一；围手术期正确处理，是减少手术并发症，提高患者生活质量和延长生存期的关键。     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

乳头溢液的外科治疗（附207例分析）

目的探讨乳头溢液的渗断和治疗方法，为合理的治疗提供科学依据。方法回顾分析手术治疗的207例乳头溢液病例资料。结果（1）在非哺乳期间发生乳头溢液多属病理性溢液；（2）通过美蓝法或平针头指示法行区段切除术，安全准确。结论（1）乳头溢液特别足血性溢液应手术治疗．对早期发现和早期治疗乳腺癌有鼋要的临床意义。（2）乳头溢液伴肿块者，不沧年龄大小、溢液性质均应手术治疗。     

老年人急性阑尾炎的腹腔镜手术治疗

目的 探讨老年人急性阑尾炎的临床特点，更好地把握腹腔镜阑尾切除（LA）术的方法和特点。方法 回顾分析50例老年人急性阑尾炎LA的临床资料。结果 LA均获成功，患者全部治愈，无严重的并发症发生，肠功能恢复时间及住院时间均缩短。结论 老年人反应迟钝，阑尾炎进展快，易发生坏疽及穿孔，合并症多，手术风险较高，LA是安全、可行的，除个别腹膜后阑尾炎外，其余均可施行LA。     

TNF-α和低氧对胰腺癌细胞表达VEGF-A、C的调节

目的:探讨细胞活素肿瘤坏死因子-α(TNF-α)、SNAP(S-Nitroso-Nacetyl-penicillamine)对胰腺癌细胞产生血管内皮生长因子A、C(VEGF-A、C)的调节.方法:用Northern杂交和Western杂交法分析6种人胰腺癌细胞株中VEGF-A、C基因和蛋白的表达;以TNF-α或SNAP刺激其中两个细胞株后用逆转录-聚合酶链式反应技术(RT-PCR)分析其VEGF-A、C基因的表达.结果:Northern杂交法显示这6种胰腺癌细胞株均有4.1kb VEGF-A基因和2.4kb VEGF-C基因的表达;Western杂交法显示它们均有分子量为43kD的VEGF-A蛋白质和分子量为55kD的VEGF-C蛋白质的表达.RT-PCR分析法显示:TNF-α使细胞株COLO-357产生VEGF-A、VEGF-C mRNA分别减少约1～2.5倍、1～2倍,使细胞株CAPAN-1产生VEGF-A、VEGF-C mRNA分别减少约1倍、1.6～2.5倍;而SNAP刺激细胞株COLO-357产生VEGF-A mRNA增加约5倍,刺激细胞株CAPAN-1产生VEGF-A mRNA增加约4倍,但对这两种细胞株产生VEGF-C mRNA均无明显刺激作用.结论:细胞活素TNF-α和低氧通过调节血管内皮生长因子A、C的表达而影响胰腺癌细胞的生物学特性,抑制癌细胞的增殖,促进其凋亡、死亡或进展、恶化.     

HPLC法测定盐酸美沙酮含量

本文采用高效液相色谱法，以盐酸布比卡因为内标，检测波长220nm，在Symmetry-C18柱上，以己腈-磷酸二氢钾（pH2．5）（3862，V／V）为流动相，测定盐酸美沙酮及其口服液的含量。方法平均回收率为100．17％，日内及日间的RSD均＜1％。方法简便、快速、准确。     

碱性成纤维细胞生长因子（bFGF）加速猪背部创伤修复的实验研究

实验采用猪背部创伤模型，观察重组的碱性成纤维细胞生长因子（ｂＦＧＦ）对创伤修复的作用。在无菌条件下用特制打孔器在猪背部切割皮肤，形成２．５ｃｍ２的园型创面。将１５０个创面分成５组，分别以ｂＦＧＦ（６０ｕ／ｃｍ２创面），ｂＦＧＦ（（６０ｕ／ｃｍ２创面）加ＳＤ－Ａｇ、ＳＤ－Ａｇ、生理盐水以及不治疗等方法处理，每间隔一天换药一次。实验结果表明，ｂＦＧＦ具有显著促进肉芽组织生长、加速创面再上皮化率以及增加创面愈合组织抗张力强度等作用。ＦＧＦ显著促修复效应的确切机制尚不完全清楚，可能包括直接与间接效应两方面。     

Activity-dependent Decay of Early LTP Revealed by Dual EPSP Recording in Hippocampal Slices from Young Rats

The early maintenance of long-term potentiation (LTP) was studied in the CA1 region of hippocampal slices from 12- to 18-day-old rats in a low-magnesium solution (0.1 mM). The α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components of the field excitatory postsynaptic potential were estimated in parallel using early and late measurements of the composite potential. At the normal test stimulus frequency of 0.1 Hz, LTP was seen initially as a predominant increase in the AMPA component, but converted, via a substantial decay of this component and a gradual growth of the NMDA component, into nearly equal changes of the two components. Interrupting the test stimulation for 10 min, changing the test stimulus frequency to 1/60 Hz after LTP induction, or using a test stimulus frequency of 1/60 Hz during the entire experiment significantly reduced the decay of the potentiation of the AMPA component while enhancing the potentiation of the NMDA one. The ratio between the magnitudes of the two excitatory postsynaptic potential (EPSP) components showed a decaying time course that was independent of the manipulations used. Application of the NMDA antagonist D(-)-2-amino-5-phosphonopentanoic acid (50μM) after LTP induction stabilized the LTP of the AMPA component until washout was started. On the other hand, the phosphatase inhibitor okadaic acid (1 μM) resulted in decay of the potentiation of both EPSP components back to around baseline and altered the time course of the ratio between the components. Our results show that the early maintenance of LTP is controlled in an activity-dependent and NMDA-dependent manner. This process accelerates the decay of LTP of both AMPA and NMDA components in parallel, suggesting that it is similar to homosynaptic long-term depression, although it operates at the normal test stimulus frequency. The data support a scenario in which LTP ensues as a selective AMPA receptor modification and subsequently converts to another modification, possibly a presynaptic one.     

钙拮抗剂TMB-8抑制BHQ,NE和KCl引起的培养乳牛基底动脉单个平滑肌细胞内游离钙的升高

用AR CM MIC阳离子测定系统,测量单个细胞内游离钙浓度([Ca²⁺]i),研究8-(N,N-二乙胺)-n-辛基 3,4,5-三甲氧基苯甲酸酯(TMB-8)对培养乳牛基底动脉平滑肌[Ca²⁺]i的作用。在细胞外钙浓度为1.3mmol·L^-1时,TMB-8(30μmol·L^-1)可明显抑制BHQ,NE及KCl引起[Ca²⁺]i的升高。在细胞外钙为零+EGTA 0.1mmol·L^-1时,TMB-8(10,30及100μmol·L^-1)可浓度依赖性地降低静息[Ca²⁺]i,TMB-8(30μmol·L^-1)可几乎完全阻断BHQ及NE引起[Ca²⁺]i的增加。研究表明TMB-8降低培养乳牛基底动脉平滑肌[Ca²⁺]i的机制,主要是抑制肌浆网Ca²⁺的释放,或增加肌浆网对Ca²⁺的摄入,并由此间接地抑制细胞外钙的内流。