人血浆中氧氟沙星的HPLC测定及药代动力学研究

建立了人血浆中氧氟沙星含量的HPLC测定方法,以Spherisorb C18柱分离,流动相组成为甲醇-0.01mol/L磷酸盐缓冲液-0.5mol/L四丁基溴化铵(35:65:4,pH 2.5),流速为1.0 ml/min,在UV 294nm处测定。样品采用甲醇沉淀蛋白后,混旋、离心,吸取上清液在75℃下用氮气流吹干后,以0.4ml流动相稀释进样。采用内标法定量,在0.5～4.0μg/ml的浓度范围内呈线性关系,r=0.9999。最小检测浓度为20ng/ml。用本法对10名分别服用进口和国产氧氟沙星片剂的健康志愿者进行了血药浓度测定,取得了满意的结果,并对其药代动力学参数及生物利用度进行了研究。     

Effect of Ziziphus jujube Fruit Infusion on Lipid Profiles,Glycaemic Index and Antioxidant Status in Type 2 Diabetic Patients: A Randomized Controlled Clinical Trial

This study was designed to assess the effects of Ziziphus jujube fruit (ZJF) infusion on lipid profiles, glycaemic control and antioxidant status in patients with type 2 diabetes mellitus (T2DM). In this randomized controlled clinical trial, 116 participants with T2DM (older than 30 years) were assigned to consume a balanced diet or diet plus ZJF infusion (10 g/100 mL boiling water) three times/day before main meals for 12 weeks. Diet was designed to be energy restricted (500 kcal/day deficit from estimated energy requirements), and macronutrient content was similar in both groups (55% carbohydrate, 15% protein and 30% fat). The consumption of ZJF infusion compared with the control group was associated with significant improvement in glycosylated haemoglobin (?0.68 ± 0.65 vs. ?0.44 ± 0.55%; p  = 0.03), total cholesterol (?24.29 ± 28.89 vs. ?11.21 ± 29.98 mg/dL; p  = 0.02), triglycerides (?43.3 ± 39.26 vs. ?27.16 ± 46.84 mg/dL; p  = 0.05), low‐density lipoprotein cholesterol (?19.85 ± 27.62 vs. ?6.55 ± 27.82 mg/dL; p  = 0.01), low‐density lipoprotein cholesterol/high‐density lipoprotein cholesterol (?0.56 ± 0.80 vs. ?0.2 ± 0.72; p  = 0.01) and total cholesterol to high‐density lipoprotein cholesterol ratios (?0.73 ± 0.94 vs. ?0.35 ± 0.77; p  = 0.02). ZJF had beneficial effects on glycosylated haemoglobin and lipid profile in T2DM patients. Further research is needed to identify the mechanism of ZJF action on glucose and lipid metabolism. Copyright © 2017 John Wiley & Sons, Ltd.     

紫外分光光度法测定盐酸林可霉素乳膏的含量

目的：测定盐酸林可霉素乳膏的含量。方法：依据氯化钯与盐酸林可霉素形成稳定络合物，用紫外分光光度法于３８０ｎｍ处测定其吸收度，并计算含量。结果：回收率为９９．６３％，ＲＳＤ为０．１８％，线性范围为３６．５６￣８２．２６μｇ／ｍｌ。结论：该方法适合该制剂的含量测定。     

2,4-二氨基-5-氯-6-取代苄氨基喹唑啉类化合物的合成及其抗疟、抗肿瘤和抗菌活性

本文报道标题化合物的合成及其抗疟、抗肿瘤和抗菌活性,该类化合物是以5-氯-2,4, 6-三氨基喹唑啉与各种取代苯甲醛缩合成相应的Schiff碱,然后经NaBH₄还原,再甲酰化或亚硝化制得.经对感染伯氏疟原虫(P.berghei)的鼠抑制性治疗筛选,有八个化合物剂量20mg/kg×4d时抑制率100%,Ⅰ₃,Ⅰ₄,Ⅲ₄三个化合物剂量5mg/kg×4d时抑制率在90%以上;体外抗肿瘤试验有4个化合物的活性优于MTX和SIPl759,以Ⅰ₄最佳。对L1210白血病细胞株的IC₅₀为2.20×10^-9 m mol/L;经对18种常用菌株进行体外筛选,发现对肺炎双球菌(D.pneumoniae)有较好的活性。     

Neuroimaging findings of Zika virus infection: a review article

Zika virus (ZIKV) is an arbovirus from the Flaviviridae family. It is usually transmitted by mosquito bite. There have been no reports of severe symptoms caused by ZIKV infection up until the last few years. In October 2013 an outbreak was reported in French Polynesia with severe neurological complications in some affected cases. In November 2015, the Ministry of Health of Brazil attributed the increased number of neonatal microcephaly cases in northeastern Brazil to congenital ZIKV infection. The rapid spread of the virus convinced the World Health Organization to announce ZIKV infection as a “Public Health Emergency of International Concern” in February 2016. The main neuroimaging findings in congenital ZIKV infection include microcephaly which is the hallmark of the disease, other malformations of cortical development (e.g., lissencephaly, heterotopia, etc.), parenchymal calcifications, unilateral or bilateral ventriculomegaly, enlarged extra-axial CSF spaces, dysgenesis of the corpus callosum, agenesis of the cavum septum pellucidum, cerebellar and brainstem hypoplasia, and ocular abnormalities. ZIKV infection may also cause Guillain-Barré syndrome and acute disseminated encephalomyelitis in adults. Familiarity with neuroimaging findings of congenital and acquired ZIKV infection is crucial to suspect this disease in residents of endemic regions and travelers to these areas.     

Pontocerebellar hypoplasia due to bi-allelic variants in MINPP1

Pontocerebellar hypoplasia (PCH) describes a group of rare heterogeneous neurodegenerative diseases with prenatal onset. Here we describe eight children with PCH from four unrelated families harboring the homozygous MINPP1 (NM_004897.4) variants; c.75_94del, p.(Leu27Argfs*39), c.851 C > A, p.(Ala284Asp), c.1210 C > T, p.(Arg404*), and c.992 T > G, p.(Ile331Ser). The homozygous p.(Leu27Argfs*39) change is predicted to result in a complete absence of MINPP1. The p.(Arg404*) would likely lead to a nonsense mediated decay, or alternatively, a loss of several secondary structure elements impairing protein folding. The missense p.(Ala284Asp) affects a buried, hydrophobic residue within the globular domain. The introduction of aspartic acid is energetically highly unfavorable and therefore predicted to cause a significant reduction in protein stability. The missense p.(Ile331Ser) affects the tight hydrophobic interactions of the isoleucine by the disruption of the polar side chain of serine, destabilizing the structure of MINPP1. The overlap of the above-mentioned genotypes and phenotypes is highly improbable by chance. MINPP1 is the only enzyme that hydrolyses inositol phosphates in the endoplasmic reticulum lumen and several studies support its role in stress induced apoptosis. The pathomechanism explaining the disease mechanism remains unknown, however several others genes of the inositol phosphatase metabolism (e.g., INPP5K, FIG4, INPP5E, ITPR1) are correlated with phenotypes of neurodevelopmental disorders. Taken together, we present MINPP1 as a novel autosomal recessive pontocerebellar hypoplasia gene.Subject terms: Neurodevelopmental disorders, Mutation