Induction of Squamous Cell Carcinomas in the Salivary Glands of Rats by Potassium Iodide

In a 2-year carcinogenicity study of potassium iodide (KI) in F344/DuCrj rats, squamous cell carcinomas (SCCs) were observed in the salivary glands of 4/40 males and 3/40 females receiving 1000 ppm KI in the drinking water. Ductular proliferation with lobular atrophy was observed at high incidence in the submandibular glands of the high-dose animals, and squamous metaplasia was frequently evident within the proliferative ductules and the larger interlobular ducts. A transition from metaplasia to SCC was apparent. The results suggest that squamous metaplasia in proliferative ductules, occurring secondarily to lobular impairment induced by KI, may develop into SCCs via a non-genotoxic, proliferation-dependent mechanism.     

Directed sampling for electrolyte analysis and water content of micro-punch samples shows large differences between normal and ischemic rat brain cortex

Changes in sodium, potassium, and water content in brain tissue are important in the progression of pathology that follows ischemic stroke. Determining these parameters regionally in rodent models of experimental ischemia has been limited because typical tissue weights of more than 35 mg are too large. Identifying ischemic tissue to direct tissue sampling towards ischemic cortex is also represents a difficult generally unresolved area. We suggest that larger differences between normal and ischemic cortex of sodium, potassium, and water content than previously observed can be obtained from directed sampling of 2-mg brain tissue in a model of focal cerebral ischemia. In five rats, the middle cerebral artery and both common carotid arteries were occluded for 4.9+/-0.13 h (mean+/-SEM). Punch-sampling of 1-mm diameter tissue cores for water content (H(2)O%) by the wet-dry method, and [Na(+)] and [K(+)] by flame photometry, was guided by the observation of a subtle change in the surface reflectivity of ischemic cortex of quickly dried, 20-microm frozen brain sections, that was confirmed by MAP2 immunohistochemistry. The ratio of the lesion areas as determined by the reflective change and MAP2 immunoreactivity was 0.96+/-0.03 (n=5). In ischemic cortex H(2)O% was 79.9%+/-0.8%, [Na(+)] was 550+/-25 mEq/kg dry-weight, and [K(+)] 94.2+/-19.2 mEq/kg dry-weight (n=5), all significantly different from the values in border zone cortex, and in cortex contralateral to ischemic cortex and border zone (for all samples n=60, mean wet weight 2.037+/-0.046 mg). Differences between ischemic and normal cortex were 5.4+/-1.1%, 317+/-21 mEq/kg dry-weight, -304+/-27 mEq/kg dry-weight (n=5) for H(2)O%, [Na(+)], and [K(+)]. These differences between ischemic and normal cortex are 1.4-2.5, 1-3.11, and 1.4-3.5 times greater, respectively, than previous results obtained using samples weighing 35 mg or more. These results extend the association of sodium and potassium with ischemic brain edema in the rodent model, and show that these classical measurements can keep pace with the regionality of histochemical and morphological methods.     

氢化物发生--原子荧光光谱法测定铅的研究(Ⅰ)铁氰化钾试剂的影响

〔目的〕研究HCl -K3[Fe(CN) 6 ] -KBH4 体系氢化物发生———原子荧光光谱法测定铅时 ,铁氰化钾试剂质量对分析性能的影响。〔方法〕观察铁氰化钾空白溶液荧光信号的变化 ,研究空白荧光信号产生的原因及降低的方法。〔结果〕证实铁氰化钾试剂中杂质铅是导致试剂空白溶液荧光信号产生的原因之一。〔结论〕分析纯铁氰化钾中含有杂质铅 ,给分析过程中带入的偶然误差是产生噪声的离散源 ,影响检出限。活性碳可有效吸附分离铁氰化钾试液中的铅 ,降低空白溶液的荧光信号 ,改善分析方法检出限     

穿琥宁注射液的处方筛选及稳定性实验研究

目的考察辅料和温度对穿琥宁注射液的影响,预测其在室温下的贮存期。方法建立HPLC法测定穿琥宁注射液含量,采用经典恒温加速实验方法考察注射液不同处方的稳定性,筛选最佳处方,并预测其在室温下的贮存期。结果与结论筛选出含0.05?TA-2Na的最佳处方,其室温下的贮存期为3.45年。     

炎琥宁与利巴韦林联用治疗麻疹临床效果分析

目的：探讨针对麻疹患者，观察临床选择炎琥宁+利巴韦林完成治疗后获得的临床效果。方法选择我院2013年1月～2015年1月麻疹患者110例。通过随机数表法完成麻疹患者的随机分组。C2组（对照组55例）：临床选择利巴韦林进行治疗。C1组（观察组55例）：临床选择炎琥宁+利巴韦林进行治疗。对比两组麻疹患者在临床治愈率、患者退热时间以及皮疹消退时间等方面表现出的差异。结果两组麻疹患者分别完成临床治疗后，C1组患者疾病治愈率为81.82%，C2组为61.82%，C1组高于C2组麻疹患者（P＜0.05）结论针对麻疹患者，临床选择炎琥宁+利巴韦林进行治疗，最终显著提高麻疹患者的生活质量。     

沃诺拉赞富马酸盐与传统质子泵抑制药临床疗效对比研究进展

摘 要沃诺拉赞富马酸盐是一种新型的钾离子竞争性抑酸药，主要用于胃酸相关性疾病的治疗和预防，2014年在日本批准上市。与传统质子泵抑制药相比，具有众多优势，自上市后引起了广泛的关注并成为研究热点。本文从沃诺拉赞富马酸盐的临床疗效及不良反应等方面进行总结，以期为医护人员及患者提供最新信息。     

Toxicologic Myocardial Sensitization

Drug-induced polymorphic ventricular tachycardia (torsades de pointes) may lead to syncope or sudden cardiac death. One mechanism by which drugs and toxins may predispose to the development of this malignant dysrhythmia is through their ability to produce myocardial sensitization. The concept of myocardial sensitization actually represents a series of events involving altered cellular repolarization produced by blockade of myocardial potassium channels. Altered potassium ion flow raises the likelihood that an ectopic beat will occur via an early afterdepolarization and simultaneously alters the myocardial tissue to make it favorable for reentrant dysrhythmias, such as torsades de pointes, to propagate. Alternatively, calcium overload of the myocyte produces ectopy by causing delayed afterdepolarizations, which if the substrate for reentry is present, will result in ventricular tachycardia. This paper discusses the mechanisms underlying the production of both the altered myocardial substrate and the afterdepolarizations.