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1.
Yana Suchy David S Kosson 《Journal of the International Neuropsychological Society》2006,12(4):538-548
Three hypotheses for cognitive deficits among psychopaths were tested: executive dysfunction, left hemisphere activation, and an interaction between the two. Twenty-one psychopathic and 23 nonpsychopathic criminal offenders identified with the Hare Psychopathy Checklist-Revised participated in verbal and visual-spatial tasks during which the level of executive processing demands was manipulated. Consistent with prior research, psychopathic offenders made more errors than controls, but only during the verbal task and only on trials with high executive demand. Within those trials, most errors occurred when set-maintenance demands were the highest. No response latency differences between groups were found. 相似文献
2.
V Vilgrain J Frija C Yana L J Couderc M David J P Clauvel M Laval-Jeantet 《Journal de radiologie》1989,70(3):167-173
Three patients with lymphoid interstitial pneumonia (two HIV 1+ patients with chronic lymphadenopathic syndromes and one with a not-characterized autoimmune disease) have been studied with high-resolution computed tomography (HR-CT). This technique reveals septal lines, small reticulonodular opacities, polyhedral micronodular opacities, "ground-glass" opacities and a dense, subpleural, curved broken line in one patient. The lesions dominate in the bases of the lungs. They are not characteristic for lymphoid interstitial pneumonia. If a patient present with a chronic lymphadenopathic syndrome, the diagnosis of an opportunistic infection should not be automatically made, since the syndrome can be caused by lymphoid interstitial pneumonia. 相似文献
3.
Mel'nikova NP Timoshin SS Murzina NB Sazonova EN Kuznetsov AV Yarova EP 《Bulletin of experimental biology and medicine》2000,130(12):1206-1208
Effect of intraperitoneal injection of tetrapeptide A10 (H-Tyr-D-Orn-Phe-Gly-OH), selective -opiate receptor agonist, synthetic analog of dermorphine, in a dose of 100 g/kg on DNA synthesis and protein content in the myocardium was studied in albino rats. Five injections of tetrapeptide on days 2-6 after birth caused no changes in DNA synthesis 17 days after the last injection, i. e. in 24-day rats. The number of nucleoli and their area increased. In adult males long-term (3-week) treatment with tetrapeptide A10 increased the number of nucleoli and the mean and integral optical density of isolated cardiomyocytes stained with amido black B, which probably attested to activation of protein synthesis in the myocardium. Simultaneously, the content of catecholamines in the heart increased. These data are comparable with delayed effects of k-opiate receptor agonist dinorphine A1-13 and indicate that morphogenetic properties of opioid peptides in rat myocardium are realized via the same routes. 相似文献
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BackgroundLINC00941 has been proved to be related to various tumors, but its relationship with laryngocarcinoma remains vague.MethodsLINC00941 expression in laryngocarcinoma tumor and laryngocarcinoma cells was determined by real time‐quantitative polymerase chain reaction (RT‐qPCR). Besides, the five‐year survival of laryngocarcinoma patients with different LINC00941 expression was analyzed with Kaplan–Meier survival analysis, and the clinical characteristics of laryngocarcinoma patients were also recorded. After transfection, cell viability, cell proliferation, apoptosis, cell cycle, migration, and invasion were detected by cell counting kit‐8 (CCK‐8), colony formation, flow cytometry, cell scratch, and Transwell assays, respectively. Glycolysis was assessed by the colorimetric method. Expressions of proliferation‐associated proteins, migration‐associated proteins, glycolysis‐associated proteins, and phosphatidylinositol 3‐kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signal pathway‐associated proteins were detected by Western blot.ResultsIn laryngocarcinoma tumor tissues and cells, LINC00941 was highly expressed. High expression of LINC00941 decreased the 5‐year survival of laryngocarcinoma patients, and it was positively related to lymph node metastasis and clinical stages. LINC00941 overexpression decreased apoptosis but promoted cell viability, proliferation, cell‐cycle progression, migration, and invasion, and glucose consumption and lactate production in laryngocarcinoma cells. Moreover, LINC00941 overexpression elevated expressions of Ki‐67, PCNA, MMP2, N‐Cadherin, HK2, PFKFB4, and PKM, activated the PI3K/AKT/mTOR signal pathway but reduced E‐Cadherin expression, while LINC00941 silencing had the opposite effects. PKM overexpression reversed the effects of LINC00941 silencing on cellular and glycolytic phenotypes.ConclusionLINC00941 promoted in vitro progression and glycolysis of laryngocarcinoma cells by upregulating PKM via activating the PI3K/AKT/mTOR signaling pathway. 相似文献
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目的:构建NOD背景免疫缺陷小鼠,作为新的人源肿瘤异种移植(patient?derived xenograft,PDX)模型。方法:利用 CRISPR/Cas9技术获得NOD背景Prkdc和Il2rg双基因敲除小鼠,通过正常繁育得到能够稳定遗传的纯合子后代(命名为NYG 小鼠),流式细胞术检测小鼠外周血免疫细胞比例,移植接种新鲜肿瘤组织,观察记录肿瘤生长状况及HE染色观察传代PDX 肿瘤形态学特点。结果:NYG小鼠外周血小鼠无成熟的T细胞、B细胞和NK细胞表达,对移植的患者肿瘤组织几乎没有排斥反应,组织病理学表型及免疫系统未见明显异常。结论:成功构建NYG小鼠免疫缺陷小鼠,为肿瘤学基础理论及应用研究提供了新的PDX动物模型。 相似文献
8.
儿童脊肌萎缩症运动神经元生存基因缺失分析 总被引:1,自引:1,他引:1
目的评价聚合酶链反应-限制性片段长度多肽性(PCR-RFLP)分析技术在脊肌萎缩症(SMA)临床诊断中的价值,分析端粒侧运动神经元生存基因(SMNt)表达与SMA临床分型之间的关系。方法对临床拟诊为SMA的23例患儿同时采用临床诊断标准和PCR-RFLP分析技术进行诊断,两种结果对比,分析灵敏度、特异度、Kappa值及P值。结果(1)临床诊断与PCR-RFLP基因诊断结果比较:23例拟诊患儿中临床确诊为SMA者18例,非SMA者5例。PCR-RFLP技术检测结果:5例非SMA者,SMNt基因检测均无缺失;18例确诊SMA者,SMNt基因缺失者15例,无SMNt基因缺失者3例,缺失频率为83.3%。此方法的灵敏度为83.3%,特异度为100%,阳性预测值100%,阴性预测值62.5%,真实性为86.96%,Kappa值为0.685。(2)SMA不同临床分型中SMNt基因7、8号外显子缺失检测结果:Ⅰ型患者以7、8号外显子缺失为主,SMNt基因缺失频率100.0%;Ⅲ型患者以7号外显子缺失为主,SMNt基因缺失频率为66.7%;Ⅰ型患者7、8号外显子联合缺失频率较Ⅲ型高(P〈0.05)。结论(1)PCR-RFLP分析技术简便、快捷、特异性高,敏感性好,适用于临床儿童型SMA的基因诊断,尤其对于SMAI型患者。(2)SMNt基因7、8号外显子联合缺失常常提示病情严重,预后不良;单独缺失提示病情较轻,预后较好。 相似文献
9.
The hypergastrinemia and hyperacidity associated with Helicobacter pylori infection has been explained by either a primary excess of gastrin or a lack of inhibitory influence by somatostatin (SOM). The objective of the present study was to compare the concentrations of fundic and antral SOM- and antral progastrin-derived peptides in nonulcer dyspepsia (NUD) subjects with and without H. pylori infection. Antral and fundic mucosal biopsies were extracted and assayed for SOM and gastrin amide, glycine–extended gastrin (gastrin gly), progastrin, and total gastrin. There was a significant sixfold reduction in antral SOM but no change in fundic SOM content in H. pylori-infected subjects compared to uninfected subjects. Antral gastrin amide concentrations were significantly higher in infected subjects. However, the concentrations of the nonamidated gastrin forms (progastrin and glycine-extended gastrin) were significantly lower in the infected subjects, indicating an increased conversion of the precursor forms of gastrin to amidated gastrin, the type known to stimulate gastric acidity. The present study demonstrates that the elevated gastrin concentrations associated with H. pylori infection may be due to a reduction in the paracrine inhibitory effect of SOM on antral gastrin release. In addition, the posttranslational processing of gastrin to the amidated forms is increased in infected subjects, explaining why the elevation in antral gastrin is confined to the amidated form. 相似文献
10.
Few studies have compared the processing of endogenous human amyloid precursor protein (APP) in younger and older neurons. Here, we characterized LUHMES cells as a human model to study Alzheimer's disease-related processes during neuronal maturation and aging. Differentiated LUHMES expressed and spontaneously processed APP via the secretase pathways, and they secreted amyloid β (Aβ) peptide. This was inhibited by cholesterol depletion or secretase inhibition, but not by block of tau phosphorylation. In vitro aged cells increased Aβ secretion without upregulation of APP or secretases. We identified the medium constituent glial cell line-derived neurotrophic factor (GDNF) as responsible for this effect. GDNF-triggered Aβ release was associated with rapid upregulation of the GDNF coreceptor “rearranged during transfection” (RET). Other direct (neurturin) or indirect (nerve growth factor) RET activators also increased Aβ, whereas different neurotrophins were ineffective. Downstream of RET, we found activation of protein kinase B (AKT) to be involved. Accordingly, inhibitors of the AKT regulator phosphatidylinositol-3-kinase completely blocked GDNF-triggered AKT phosphorylation and Aβ increase. This suggests that RET signaling affects Aβ release from aging neurons. 相似文献