MRI在膝关节损伤诊断中的应用价值

目的:通过膝关节损伤MRI影像的分析,确定其诊断价值及意义。材料和方法:本文收集了自1992年以来我院所检查的42例膝关节损伤患者,52个膝关节成像。其中男性34人;女性8人,各年龄组以30～40岁组最多。损伤以前交叉韧带和外侧半月板损伤者多见,分别占总损伤数的20％及30％。损伤又以左膝多见,占总数的61％。结果:MRI能较明确地显示膝关节的半月板、关节软骨、韧带、滑膜及骨质的改变,明显地比CT所能看到的层次多,对软组织的损伤显示清晰。结论:只要正确地应用不同序列及切层方向、厚度等技术,可清晰地显示其信号特征,从而能确定其损伤部位、程度。     

基于蒙特卡罗方法的脑转移瘤术中放疗施照器设计及剂量学评估

目的 设计适用脑转移瘤术中放疗的施照器并评估其剂量学特征。方法 施照器设计首先通过模拟计算电子束经过一系列不同厚度散射箔后的散射角和剂量率,确定散射箔厚度;其次,建立散射箔位于不同高度的位置评估模型,通过计算模型表面平均能量方差,确定散射箔位置;最后,建立调节层几何结构特征与施照器表面剂量之间的关系,确定调制器的内表面特征。使用蒙特卡罗（MC）EGSnrc/BEAMnrc和EGS4/DOSXYZ程序完成Mobetron加速器、位置评估模型、调节层、施照器建模和剂量学分析。结果 半球囊状施照器的限光筒直径为2.5 cm、筒壁厚0.5 cm,材料为0.2 cm厚水等效材料加0.3 cm厚不锈钢;散射箔厚度0.14 cm,材料为金属钨,位置高度为0.5 cm;调制器为月牙形,材料为水等效材料。该施照器能够使Mobetron 12 MeV的电子束产生半球面剂量分布,剂量率为160 cGy/min,治疗深度为0.85 cm。结论 采用MC模拟设计的适用于高能电子束的半球囊状施照器,能产生半球面剂量分布。     

DR E2基因参与酵母内质网应激调控机制的初步研究

目的：初步研究 DRE2基因在抗肿瘤药物衣霉素诱导的内质网应激中的作用机制。方法以质粒pRS306为模板,通过 PCR 扩增含有 URA3开放阅读框的 DRE2基因破坏元件 der2：URA3,然后利用基因重组原理,构建 DRE2基因杂合缺失酵母菌株,并进一步检测其对衣霉素的抗性和复制寿命。结果相对于野生型菌株,DRE2基因杂合缺失酵母菌株对衣霉素的抗性增高,复制寿命缩短（P＜0．05）。结论 DRE2基因可能参与了酵母内质网应激和衰老的调控。     

负性心理暗示对不同年级和专业医学生身心健康影响的比较研究

负性心理暗示对于医学生身心健康的影响可以通过症状自评量表进行分析研究。本文应用症状自评量表对甘肃省某医学院校学生进行调查,初步分析负性心理暗示对不同年级和专业医学生影响的差异,为有针对性地提出心理干预措施,降低或消除负性心理暗示对医学生身心健康的影响提供一定的参考依据。     

欧美GMP数据库在我国仿制药参比制剂遴选方面的应用

目的:通过调查参比制剂生产企业的GMP符合状态,判断确定其产品质量与可及性的影响.方法:概述美国和欧盟GMP的法律法规基础以及相关GMP数据库应用的情况,并以我国仿制药参比制剂目录(第一批)中收录的3个参比制剂拉米夫定片(0.1 g)、醋酸甲羟孕酮片(0.25 g)和佐匹克隆片(3.75 mg)为例,结合各品种药品说明...     

Osimertinib successfully combats EGFR-negative glioblastoma cells by inhibiting the MAPK pathway

Glioblastoma(GBM)patients have extremely poor prognoses,and currently no effective treatment available including surgery,radiation,and chemotherapy.MAPK-interacting kinases(MNK1/2)as the downstream of the MAPK-signaling pathway regulate protein synthesis in normal and tumor cells.Research has shown that targeting MNKs may be an effective strategy to treat GBM.In this study we investigated the antitumor activity of osimertinib,an FDA-approved epidermal growth factor receptor(EGFR)inhibitor,against patient-derived primary GBM cells.Using high-throughput screening approach,we screened the entire panel of FDA-approved drugs against primary cancer cells derived from glioblastoma patients,found that osimertinib(3μM)suppressed the proliferation of a subset(10/22)of EGFR-negative GBM cells(>50%growth inhibition).We detected the gene expression difference between osimertinib-sensitive and-resistant cells,found that osimertinib-sensitive GBM cells displayed activated MAPK-signaling pathway.We further showed that osimertinib potently inhibited the MNK kinase activities with IC50 values of 324 nM and 48.6 nM,respectively,against MNK1 and MNK2 kinases;osimertinib(0.3–3μM)dose-dependently suppressed the phosphorylation of eukaryotic translation initiation factor 4E(eIF4E).In GBM patient-derived xenografts mice,oral administration of osimertinib(40 mg·kg^?1·d^?1,for 18 days)significantly suppressed the tumor growth(TGI=74.5%)and inhibited eIF4E phosphorylation in tumor cells.Given the fact that osimertinib could cross the blood–brain barrier and its toxicity was well tolerated in patients,our results suggest that osimertinib could be a new and effective drug candidate for the EGFR-negative GBM patients.     

六价铬经口摄入的动物慢性毒性实验研究

本文是“地面水六价铬卫生标准研制”课题中的实验研究报告之一。在本实验中观察到:实验动物——Wistar纯种大白鼠经口摄入含六价铬的饮水60天,低剂量组(0.37mgCr~(+6)/L),体重增长明显快于对照组(P<0.05);180天时,高剂量组(37.78mgCr~(+6)/L)SGPT、尿中溶菌酶含量显著增高,其中尿溶菌酶尚与剂量成明显正相关。但未发现血液常规、IgG、NPN,I~(131)-马尿酸血液廓清排泄试验及主要器官组织病理学检查等指标有明显的异常政变。     

妇卫康治疗慢性盆腔炎的临床观察

目的:探讨坐药丸(阴道后穹窿置中药丸)妇卫康治疗慢性盆腔炎的临床疗效及可能的作用机制.方法:将115例符合入选诊断标准的患者随机分为两组.治疗组58例,用自拟坐药丸妇卫康治疗盆腔炎:对照组57例,给予口服抗生素配合微波理疗;治疗1个月为1个疗程,连续治疗2个疗程,观察症状和体征变化情况.结果:治疗组总有效率98.27%,对照组总有效率82.46%,两组总有效率进行统计学χ2检验比较,差异有显著意义(P＜0.01).治疗组优于对照组.结论:以坐药丸妇卫康治疗慢性盆腔炎,可以显著提高疗效,并且减少副作用的发生.在慢性盆腔炎的综合治疗中,增加了更简便,副作用小,疗效好,患者易接受的治疗手段.     

Interaction of Hepatitis B Virus X Protein with the Pregnane X Receptor Enhances the Synergistic Effects of Aflatoxin B1 and Hepatitis B Virus on Promoting Hepatocarcinogenesis

Background and AimsHepatitis B virus (HBV) infection has been found to increase hepatocellular sensitivity to carcinogenic xenobiotics, by unknown mechanisms, in the generation of hepatocellular carcinoma. The pregnane X receptor (PXR) is a key regulator of the body’s defense against xenobiotics, including xenobiotic carcinogens and clinical drugs. In this study, we aimed to investigate the molecular mechanisms of HBV X protein (HBx)-PXR signaling in the synergistic effects of chemical carcinogens in HBV-associated hepatocarcinogenesis.MethodsThe expression profile of PXR-cytochrome p450 3A4 (CYP3A4) signaling was determined by PCR, western blotting, and tissue microarray. Cell viability and aflatoxin B1 (AFB1) cytotoxicity were measured using the cell counting kit-8 assay. Target gene expression was evaluated using transient transfection and real time-PCR. The genotoxicity of AFB1 was assessed in newborn mice with a single dose of AFB1.ResultsHBx enhanced the hepatotoxicity of AFB1 by activating CYP3A4 and reducing glutathione S-transferase Mu 1 (GSTM1) in cell lines. Activation of PXR by pregnenolone 16α-carbonitrile increased AFB1-induced liver tumor incidence by up-regulating oncogenic KRAS to enhance interleukin (IL)-11:IL-11 receptor subunit alpha-1 (IL11RA-1)-mediated inflammation in an HBx transgenic model.ConclusionsOur finding regarding AFB1 toxicity enhancement by an HBx-PXR-CYP3A4/ GSTM1-KRAS-IL11:IL11RA signaling axis provides a rational explanation for the synergistic effects of chemical carcinogens in HBV infection-associated hepatocarcinogenesis.