EFNA1 is a potential key gene that correlates with immune infiltration in low-grade glioma

EFNA1 is a key gene that is associated with the pathogenesis of several human cancers. However, the prognostic role of EFNA1 in many cancers and the relationship between EFNA1 and tumor-infiltrating lymphocytes in different cancers remain unclear.The expression levels of EFNA1 in 33 types of cancer in the TCGA (The Cancer Genome Atlas) database were collected via the UCSC Xena browser. The clinical data of LGG (low grade glioma) patients were downloaded from the TCGA database. The glioma data from the CGGA (Chinese Glioma Genome Atlas) database were also downloaded to verify the results. Kaplan–Meier and Cox regression analyses were used to investigate the prognostic value of EFNA1 in different cancers using R software. We verified the differential expression of EFNA1 in glioma and normal brain tissue via gene expression profiling interactive analysis. We evaluated the relationship between the expression level of EFNA1 and the clinicopathological features of LGG patients via the Wilcoxon signed-rank test. The immune infiltration levels were evaluated via tumor immune estimation resource (TIMER) and CIBERSORT, and the correlations between EFNA1 and immune cell levels were investigated via TIMER. Finally, we conducted gene set enrichment analysis (GSEA) to explore the potential mechanisms.Data from the TCGA database showed that EFNA1 was differentially expressed in many kinds of cancers when compared with normal tissues. Upregulated EFNA1 expression in esophageal carcinoma (ESCA), cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), and LGG correlated with shorter patient overall survival (OS) times. The Cox regression analysis revealed that the expression of EFNA1 was also a risk factor for the disease-specific survival (DSS) and progression-free interval (PFI) of LGG patients. The multiple Cox regression analysis revealed that EFNA1 was an independent prognostic factor for LGG patients. In addition, EFNA1 expression was increased in the WHO grade III group and the 1p19q non-codeletion group. Moreover, EFNA1 expression was positively correlated with the levels of infiltrating CD4+ T cells, myeloid dendritic cells and neutrophils in LGG. GSEA suggested that several GO and kyoto encyclopedia of genes and genomes (KEGG) items associated with nervous system function and apoptotic pathway were significantly enriched in the EFNA1-low and EFNA1-high expression phenotypes.EFNA1 may play a pivotal role in the development of LGG and may serve as a potential marker for LGG prognosis and therapy.     

分离亲水气单胞菌外毒素的聚丙烯酰胺凝胶色谱填料

由丙烯酰胺和甲叉丙烯酰胺在水油悬浮液中共聚得到聚丙烯酰胺凝胶 (ZSP)系列 ,并用红外、溶剂吸收实验等对合成的ZSP的结构进行了研究。以商品葡聚糖凝胶SephadexG 10 0为对照 ,研究了ZSP 10对使中华鳖致病的亲水气单胞菌外毒素的分离性能。结果表明 :ZSP 10对毒素分离效率高 ,洗脱峰不拖尾 ,且结构和膨胀度可调 ,成本低廉 ,不易染菌霉变。经SephadexG 10 0和ZSP 10提纯的外毒素蛋白均保留了生物活性。根据SDS -PAGE的分析 ,确认经提纯的毒素蛋白的分子量为 3.2× 10 4     

经直肠超声引导下重复穿刺活检在前列腺癌高危人群中的诊断价值(附45例分析)

目的探讨经直肠超声（TRUS）引导下重复穿刺活检在前列腺特异性抗原（PSA）升高或直肠指检阳性的前列腺癌（PCa）可疑人群中的诊断价值。方法在首次穿刺活检诊断为前列腺良性病变的45例Pca高危人群中开展TRUS引导下10点重复穿刺活检。平均年龄78（58-92）岁；45例患者PSA均大于2．6ng／ml，其中12例直肠指检异常。结果在45例前列腺重复穿刺的患者中，34例穿刺2次，8例穿刺3次，3例穿刺4次；确诊Pca 10例（22．2％），良性前列腺增生32例，慢性前列腺炎3例。结论在Pca高危人群中开展TRUS引导下重复穿刺可以提高Pca的诊断率。     

局部应用血管紧张素Ⅱ1型受体反义寡核苷酸对大鼠颈动脉损伤后内膜增生的影响

目的　观察血管紧张素Ⅱ1型受体的反义寡脱氧核苷酸对氮气干燥后的大鼠颈动脉内膜增生的影响 ,以期为临床防治再狭窄提供一种新的基因治疗策略。方法　动物分为六组 :反义组、正义组、错配组、阳离子脂质体DOTAP组、对照组和假手术组 ,以压力为驱动系统 ,阳离子脂质体DOTAP为转染系统 ,局部、靶向将不同反义寡脱氧核苷酸转染于大鼠颈动脉内膜损伤段 ,阳离子脂质体DOTAP组仅应用DOTAP ,对照组剥脱内膜后不作任何处理 ,假手术组仅用 0 .9%生理盐水冲洗颈动脉。饲养 2周 ,处死动物 ,对所取的血管段进行组织切片和HE染色 ,在显微镜下进行观察和计算机彩色图像处理系统进行图像分析 ,计算血管腔面积、内膜面积、内膜 /中膜面积比值、最大内膜厚度、内膜 /中膜厚度比值和内膜覆盖率等指标并进行统计分析。结果　反义组管腔面积大于正义组、错配组、阳离子脂质体DOTAP组及对照组 ,小于假手术组 (P <0 .0 5) ;内膜面积、内膜 /中膜面积比值、最大内膜厚度、内膜 /中膜厚度比值和内膜覆盖率 :反义组小于正义组、错配组、阳离子脂质体DOTAP组及对照组 (P <0 .0 5) ;而正义组、错配组、阳离子脂质体DOTAP组与对照组两两相比上述指标无明显差异 (P >0 .0 5) ;结论　血管紧张素Ⅱ1型受体在内膜形成的机制中起重要作用     

Photo-induced lipid peroxidation of erythrocyte membranes by a bis-methanophosphonate fullerene

Using human erythrocyte membranes (EMs) as a model system, we have examined photo-induced lipid peroxidation by a bis-methanophosphonate fullerene (BMPF) and four other fullerene derivatives including a mono-methanophosphonic acid fullerene (MMPF), a dimalonic acid C₆₀ (DMA C₆₀), a trimalonic acid C₆₀ (TMA C₆₀) and a polyhydroxylated fullerene (fullerol). Lipid peroxidation was assessed as the malondialdehyde (MDA) level measured by the thiobarbituric acid assay. It was observed that BMPF increased the MDA level of EMs after irradiation in both time- and dose-dependent manners. The photo-induced activity became very significant (p < 0.01) under the conditions of either the concentration of 10 μM and irradiation time of 30 min or the concentration of 5 μM and irradiation time of 60 min. Involvement of reactive oxygen species (ROS) in the activity was also examined by specific inhibitors of singlet oxygen, superoxide anions and hydroxyl radicals, respectively. While all three kinds were found responsible for the activity, the former two might play more important roles than the last one. Furthermore, the activity of BMPF was the strongest among all tested fullerene derivatives. These results indicated BMPF was a potential photosensitizer that would find application in photodynamic therapy.     

Effects of prenatal nicotine exposure on primate brain development and attempted amelioration with supplemental choline or vitamin C: neurotransmitter receptors, cell signaling and cell development biomarkers in fetal brain regions of rhesus monkeys.

Studies in developing rodents indicate that nicotine is a neuroteratogen that disrupts brain development by stimulating nicotinic acetylcholine receptors (nAChRs) that control neural cell replication and differentiation. We administered nicotine to pregnant Rhesus monkeys from gestational day 30 through 160 by continuous infusion, achieving maternal plasma levels comparable to those in smokers (30 ng/ml). Fetal brain regions and peripheral tissues were examined for nAChR subtypes, other neurotransmitter receptors, and indices of cell signaling and cell damage. Nicotine evoked nAChR upregulation, but with distinct regional disparities indicative of selective stimulatory responses. Similarly, indices of cell loss (reduced DNA), cell size and neuritic outgrowth (protein/DNA and membrane/total protein ratios) were distinct for each region and did not necessarily follow the rank order of nAChR upregulation, suggesting the involvement of additional mechanisms such as oxidative stress. We then attempted to offset the adverse effects of nicotine with standard dietary supplements known to interact with nicotine. By itself, choline elicited nicotine-like actions commensurate with its promotion of cholinergic neurotransmission. When given in combination with nicotine, choline protected some regions from damage but worsened nicotine's effects in other regions. Similarly, Vitamin C supplementation had mixed effects, increasing nAChR responses while providing protection from cell damage in the caudate, the brain region most susceptible to oxidative stress. Our results indicate that nicotine elicits neurodevelopmental damage that is highly selective for different brain regions, and that dietary supplements ordinarily thought to be neuroprotectant may actually worsen some of the adverse effects of nicotine on the fetal brain.     

大鼠胆汁中酮洛芬Ⅱ相代谢物酮洛芬葡萄糖醛酸的测定方法

目的:建立 RP-HPLC 法测定胆汁中酮洛芬Ⅱ相代谢物酮洛芬葡萄糖醛酸(S-KPG、R-KPG)。方法:采用 ODS 柱(5μm,4.6 mm×250 mm);流动相为乙腈-水(35:65),内含0.05 mol·L~(-1)磷酸二氢钾和0.005 mol·L~(-1)的四丁基溴化胺,pH5.6;流速为1 mL·min~(-1);检测波长232 nm;柱温30℃;进样是20μL。内标为10 mg·L~(-1)的萘普生甲醇溶液。结果:在2～1000μmol·L~(-1)浓度范围内,胆汁中 S-KPG、R-KPG 回归方程分别为 Y=0.0039X-0.0256,r=0.9998和 Y=0.0039X-0.0229,r=0.9998;最低检测限分别为0.5 μmol·L~(-1)和1 μmol·L~(-1)。S-KPG 和 R-KPG 在室温和胆汁生理 pH 时不稳定,在 pH4时最稳定。结论:本文应用 RP-HPLC 检测胆汁 S-KPG、R-KPG,方法简便、易行、实用,可以作为肝脏葡萄糖醛酸转移酶活性和胆排泄实验研究的分析手段。     

中医发展百年史实回顾与思考

以西方医学传入我国、并逐步得到发展为切入点,系统回顾了近百年来中医发展的曲折历程,客观地分析了中医发展缓慢的诸多因素。明确提出了要正视现实,科学地、理性地认识中医,实事求是地评价中医,给予恰当定位,使传统中医按照自身学科的内在规律自然发展。     

ATP酶变化在1,2二氯乙烷致脑水肿过程中的作用研究

为探索Na+ K+ATP酶、Ca2 +、Mg2 +ATP酶在 1,2 -二氯乙烷 (1,2 DCE)致脑水肿过程中所起的作用 ,在复制脑水肿模型的基础上 ,检测受试动物脑组织中Na+ K+ATP酶、Ca2 +、Mg2 +ATP酶活力的变化。结果显示 ,随着染毒剂量的增加 ,Na+ K+ATP酶活力逐渐降低 ,最高剂量组与各组相比 ,具有显著性差异 ;Ca2 +、Mg2 +ATP酶活力显著下降 ,与其余各组相比 ,P <0 0 5。结果提示 :1,2 DCE引起了ATP酶活力的下降导致脑组织能量代谢障碍 ,从而可能引起“Ca2 +超载” ,ATP酶活力下降和“Ca2 +超载”可能是引起脑水肿的主要原因     

赖氨酸、钙、铁、锌强化食品的研究及其营养评价

本实验在面包中强化赖氨酸、钙、铁和锌进行动物实验,评价其营养价值。 实验动物为wistar种系大鼠,4～5周龄,体重相近。随机分为四组、第一组为对照组用普通面包饲养,其余各组分別饲以不同强化面包。 实验结果:对照组四周体重净增59g。单纯加锌组开始两周动物生长加快,以后渐趋抑制,四周后体重净增46g明显低于对照组。加赖氨酸、钙、铁的大鼠生长加快,四周后体重净增91g,饲料效价、蛋白质功效比值、净氮利用率、生物价及骨长和骨重量、铁营养状况均优于对照组。在强化赖氨酸、钙、铁的基础上再补充锌,可进一步促进动物生长,四周后体重净增120g,饲料效价,蛋白质功效比值不但高于对照组也高于赖氨酸、钙、铁强化组,该组饲料中锌对钙、铁生物利用无明显干扰,对血铜亦无显著影响。