气相色谱法检测麝珠明目滴眼液中冰片和麝香酮的含量

目的建立气相色谱法同时测定麝珠明目滴眼液中冰片及麝香酮含量。方法用HP-INNOWAX（30m×320μm×0.25μm）色谱柱,火焰离子化检测器（FID）进行分析检测。程序升温：140℃维持8min,再以30℃.min-1升温至200℃维持10min,采用外标法测定。结果冰片在0.41~10.26mg.mL-1范围内线性相关（r=0.9993）,回收率为101.0%,RSD=1.1%（n=6）;麝香酮在0.007~0.38mg.mL-1范围内线性相关（r=0.9999）,回收率为98.2%,RSD=0.8%（n=6）。结论该方法简便、准确,重现性好,可用于麝珠明目滴眼液的质量控制。     

气相色谱法同时测定祛伤消肿酊中樟脑、薄荷脑、龙脑的含量

目的 建立祛伤消肿酊中同时测定樟脑、薄荷脑及龙脑含量的方法.方法 采用气相色谱法,FID检测器.色谱柱:HP- INNOWAX(30m×0.32mm×0.25μm);柱温:130℃;进样口温度:250℃;检测器温度:300℃.结果 樟脑、龙脑、薄荷脑回归方程的相关系数均在0.999以上,平均回收率(n=6)分别为97....     

气相色谱法测定头孢孟多酯钠的残留溶剂

目的：建立GC测定头孢孟多酯钠残留溶剂含量的方法。方法：采用DB-FFAP毛细管柱,柱温：150℃,以氮气为载气,氢火焰离子化检测器,检测器温度：250℃,进样口温度：200℃。结果：2-乙基己酸在0.15～0.90 mg/ml浓度范围内峰面积与内标峰面积呈良好的线性关系,平均回收率为99.03%（n=9）,定量限为0.001 ng。结论：该方法可靠、准确,可作为头孢孟多酯钠残留溶剂（2-乙基己酸）的测定方法。     

窄带成像放大内镜下食管黏膜微血管形态观察的临床价值探析

目的对窄带成像放大内镜技术对食管黏膜微血管的形态分型和临床意义进行探讨。方法应用NBI—ME技术对在笔者医院诊治的104例食管病变的患者进行检查,观察其食管黏膜上皮乳头内的毛细血管袢（IPCL）的形态,并于各不同形态所在的部位取活组织进行病理检查。结果食管炎的IPCL主要为Ⅱ型,占88．00％,低级别黏膜内瘤变的IPCL主要为Ⅱ、Ⅲ型,其中Ⅱ型占43．75％,11I型占56．25％,高级别黏膜内瘤变的IPCL主要为Ⅲ型,占83．33％,而食管癌的IPCL主要表现为Ⅳ型,为100％。结论通过NBI—ME对食管黏膜上皮乳头内的毛细血管袢进行有效地形态观察可以推测患者的病理诊断,提高镜下早期食管病变的诊断准确率,以指导正确的治疗方法及镜下的随诊。     

毛细管胶束电动色谱法检测尿液肌酸和肌酐含量

目的 建立高效毛细管电泳技术（HPCE）测定尿液中肌酸（Cri）和肌酐（Cr）的方法。 方法 运用毛细管胶束电动色谱技术（MEKC）,以pH 5.5、20 mmol/L的Na₂HPO₄-H₃PO₄（含100 mmol/L SDS）作为电泳缓冲液,非涂层石英毛细管进行分离,样品经过20倍稀释后以1 psi压力进样4 s,15 kV电压下分离尿液中的Cri和Cr,二极管阵列检测器（DAD）（λ=200 nm）检测。 结果 Cri和Cr的线性范围为4.9~2 500 μmol/L和4.9~2 500 μmol/L（r值分别为0.999 8和1）; Cri回收率为97.8%~100.8%、平均99.2%,Cr回收率为99.5%~104%、平均101.8%;Cri迁移时间批内和批间差异（CV）平均值为3.2%和8.0%、Cr为2.3%和6.8%;Cri和Cr的最低检出限分别为1.4 μmol/L和3.31 μmol/L。 结论 本法标本用量小、干扰因素少、精密度和准确度高、线性范围宽、测定成本低廉,可满足临床常规检测要求。     

优化PCR体系结合毛细管电泳技术检测FMR1基因前突变与全突变

目的 通过优化PCR并结合毛细管电泳,建立高扩增效率、高分辨率的FMR1基因CGG重复序列异常扩增检测体系.方法 选择标准样本和经Southern印迹技术确定(CGG)n的正常、前突变、全突变男性和女性样本15例,进行PCR检测体系的优化.优化的PCR扩增产物经琼脂糖凝胶电泳、聚丙烯酰胺凝胶电泳和毛细管电泳等多种方法进行结果比较.结果 经优化的PCR体系可以检测出(CGG)n大于260个拷贝的全突变男性和(CGG)n达到183个拷贝的前突变女性.毛细管电泳能够清晰分辨出相差1个CGG的两个等位基因,结果具有良好的可重复性.结论 该PCR检测体系大幅度提高了普通PCR方法的扩增效率和分辨率,明显降低了对于Southern印迹技术的依赖,可以作为临床筛查FMR1基因突变的首选方法.     

放大内镜下胃食管反流病患者食管乳头内毛细血管环形态学观察

目的探讨胃食管反流病（GERD）患者食管乳头内毛细血管环（IPCL）形态学检查在GERD诊断中的临床价值及护理。方法对非糜烂性食管炎（NERD）患者20例、糜烂性食管炎（EE）患者20例和10例健康志愿者行24h食管pH监测,采用白光和放大内镜窄波成像（NBI）模式观察食管下段黏膜IPCL形态并进行分型,同时配合有效的护理措施。结果3组受检者顺利完成内镜检查。NERD组患者24h食管pH监测阳性率为55％,EE组为90％,健康对照组均为阴性,NERD组低于EE组;放大内镜NBI模式下健康对照组食管IPCL呈茶色规律排列的卷发状、小螺旋状;NERD组85％及EE组100％食管IPCL形态为Ⅱ型,但仍排列规律,与健康对照组比较差异均有统计学意义（P〈0．05）。结论食管ICPL形态特异性改变有助于GERD的内镜诊断;高质量的护理配合对顺利完成内镜检查起到了重要的作用。     

cGMP/PKG pathway mediates myocardial postconditioning protection in rat hearts by delaying normalization of intracellular acidosis during reperfusion

Ischemic postconditioning has been demonstrated to limit infarct size in patients, but its molecular mechanisms remain incompletely understood. Low intracellular pH (pHi) inhibits mitochondrial permeability transition, calpain activation and hypercontracture. Recently, delayed normalization of pHi during reperfusion has been shown to play an important role in postconditioning protection, but its relation with intracellular protective signaling cascades is unknown. The present study investigates the relation between the rate of pHi normalization and the cGMP/PKG pathway in postconditioned myocardium. In isolated Sprague-Dawley rat hearts submitted to transient ischemia both, postconditioning and acidic reperfusion protocols resulted in a similar delay in pHi recovery measured by ³¹P-NMR spectroscopy (3.6 ± 0.2 min and 3.5 ± 0.2 min respectively vs. 1.4 ± 0.2 min in control group, P < 0.01) and caused equivalent cardioprotection (48% and 41% of infarct reduction respectively, P < 0.01), but only postconditioning increased myocardial cGMP levels (P = 0.02) and activated PKG. Blockade of cGMP/PKG pathway by the addition of the guanylyl cyclase inhibitor ODQ or the PKG inhibitor KT5823 during reperfusion accelerated pHi recovery and abolished cardioprotection in postconditioned hearts, but had no effect in hearts subjected to acidic reperfusion suggesting that PKG signaling was upstream of delayed pHi normalization in postconditioned hearts. In isolated cardiomyocytes the cGMP analog 8-pCPT-cGMP delayed Na⁺/H⁺-exchange mediated pHi normalization after acidification induced by a NH₄Cl pulse. These results demonstrate that the cGMP/PKG pathway contributes to postconditioning protection at least in part by delaying normalization of pHi during reperfusion, probably via PKG-dependent inhibition of Na⁺/H⁺-exchanger.     

Wave drag on floating bodies

We measure the deceleration of liquid nitrogen drops floating at the surface of a liquid bath. On water, the friction force is found to be about 10 to 100 times larger than on a solid substrate, which is shown to arise from wave resistance. We investigate the influence of the bath viscosity and show that the dissipation decreases as the viscosity is increased, owing to wave damping. The measured resistance is well predicted by a model imposing a vertical force (i.e., the drop weight) on a finite area, as long as the wake can be considered stationary.