Reward association facilitates distractor suppression in human visual search

Although valuable objects are attractive in nature, people often encounter situations where they would prefer to avoid such distraction while focusing on the task goal. Contrary to the typical effect of attentional capture by a reward‐associated item, we provide evidence for a facilitation effect derived from the active suppression of a high reward‐associated stimulus when cuing its identity as distractor before the display of search arrays. Selection of the target is shown to be significantly faster when the distractors were in high reward‐associated colour than those in low reward‐associated or non‐rewarded colours. This behavioural reward effect was associated with two neural signatures before the onset of the search display: the increased frontal theta oscillation and the strengthened top‐down modulation from frontal to anterior temporal regions. The former suggests an enhanced working memory representation for the reward‐associated stimulus and the increased need for cognitive control to override Pavlovian bias, whereas the latter indicates that the boost of inhibitory control is realized through a frontal top‐down mechanism. These results suggest a mechanism in which the enhanced working memory representation of a reward‐associated feature is integrated with task demands to modify attentional priority during active distractor suppression and benefit behavioural performance.     

Does surprise enhancement or repetition suppression explain visual mismatch negativity?

A long tradition of electrophysiological studies, using oddball sequences, showed that the neural responses to a given stimulus differ when their presentation occurs frequently (standards) as compared to rare, infrequent presentations (deviants). This difference, originally described in acoustic perception, can also be detected in the visual modality and is termed as visual mismatch negativity (vMMN). Also, a large number of studies detected the reduction of the neuronal response after the repetition of a given stimulus (repetition suppression – RS) and it was suggested that RS is the major mechanism of MMN, an explanation currently also supported by animal studies. However, human studies have proposed that a surprise‐related response enhancement for the deviant stimuli might also underlie vMMN. Therefore, the aim of the current study was to disentangle which neural mechanism explains vMMN better: the surprise related response enhancement for the presentation of rare deviants or the RS related to the frequent presentation of the standards. Since the MMN depends strongly on the applied categories, we tested the neural mechanisms of vMMN for different stimulus categories (faces, chairs, real and false characters) using a visual oddball paradigm. We found significant vMMN for every stimulus category. Interestingly, the neural mechanisms behind vMMN were found to be category dependent (assuming no cross‐adaptation effects): for faces and chairs it was largely driven by RS, whereas for real and false characters it was mainly due to surprise‐related changes.     

Vpr对人结肠癌细胞的抑制作用及其机制

目的 探讨人类免疫缺陷病毒1型( HIV-1)病毒蛋白r(Vpr)对人结肠癌细胞HCT-8的抑制作用及其机制.方法 将细胞分为空白对照组、空载体转染组和Vpr转染组.空白对照组:细胞不予干预;空载体转染组:对数生长期的细胞加入不同感染复数(MOI)的空载体腺病毒;Vpr转染组:加入不同MOI的含有HIV1-Vpr基因的重组腺病毒(Adv-Vpr).应用MTT比色法检测细胞增殖活性,流式细胞仪检测细胞周期、细胞凋亡及线粒体膜电位,Western blot法检测细胞凋亡相关蛋白的表达.多组间均数比较采用单因素方差分析,两两比较采用q检验;或采用双因素方差分析,组内比较采用t检验.结果 Vpr显著抑制人结肠癌细胞HCT-8增殖,Adv-Vpr转染72 h后(MOI=200),Vpr转染组细胞MTT值为1.03±0.04,与空载体转染组(2.46 +0.15)及空白对照组(2.51±0.14)比较,差异有统计学意义(F=144.6,P＜0.05);Adv-Vpr转染48 h后(MOI=200),Vpr转染组处于G2/M期的细胞比例及线粒体膜电位下降的细胞比例增加,分别为37.31％±5.90％和32.07％±5.64％,与空载体转染组(18.30％±6.04％、3.32％±0.79％)及空白对照组916.66％±3.51％、2.76％±1.43％)比较,差异有统计学意义(F=10.08,64.45,P＜0.05).Adv-Vpr转染72 h后(MOI=200),Vpr转染组细胞凋亡率为37.62％±6.48％,与空载体转染组(3.44％±1.11％)及空白对照组(2.93％±1.07％)比较,差异有统计学意义(F=122.4,P＜0.05).Adv-Vpr处理48 h后(MOI=200),Westem blot检测发现Vpr导致了Caspase-9、Caspase-3剪切为活性片段,p-Chk1-S345磷酸化增加,而Fas、Fas-L、ERK1及ERK2表达未见上调.结论 Vpr在体外能够有效抑制结肠癌细胞株HCT-8增殖,并诱导其细胞周期G2期阻滞及凋亡,其机制分别与DNA损伤信号通路激活及线粒体凋亡通路启动有关.Vpr在结肠癌的治疗中具有潜在的应用前景.     

灯盏花素注射液治疗病毒性肝炎高胆红素血症的疗效

目的观察灯盏花素注射液治疗病毒性肝炎高胆红素血症的临床疗效。方法将79例病毒性肝炎高胆红素血症患者随机分成对照组和治疗组,两组均采用相同的基础治疗方法,治疗组加用灯盏花素注射液静滴,观察两组治疗前后甲襞微循环及肝功能（TBil、ALT、AST）的变化。结果两组患者治疗后甲襞微循环加权积分、血清总胆红素（TBil）及丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）均有显著下降;治疗组中甲襞微循环加权积分及TBil、AIJT、AST下降较对照组更明显,总有效率治疗组92．50％,对照组为74．36％,两组相比差异有统计学意义（P〈0．05,χ2=8．775）;治疗组在改善血液微循环、降酶、退黄方面优于对照组,差异有显著统计学意义（P〈0．01）。结论灯盏花素注射液治疗病毒性肝炎高胆红素血症具有良好的临床疗效,适合各基层医院推广应用。     

PICU重症病毒性脑炎儿童CT、MRI影像学特征分析

目的探讨重症监护病房(PICU)重症病毒性脑炎儿童CT、MRI影像学特征。方法选取2017年1月至2018年7月我院PICU收治的重症病毒性脑炎儿童60例为研究对象,均采用CT、MRI两种影像学方式进行检查,比较两种方式的检查结果,分析临床应用价值。结果 60例患者中有48例被确诊为病毒性脑炎,5例被误诊为其他疾病,7例因影像显示无异常漏诊,阳性检出率为80.00%;48例患儿中18例在额叶处,6例在颞叶处,18例病灶在基底节,6例在脑顶叶处MRI检查确诊为病毒性脑炎的有56例,其中漏诊3例,误诊1例,阳性检出率为93.33%;脑内异常病灶在基底节的有22例,5例在颞叶处,15例在额叶处,4例在枕叶处,7例在脑顶叶处,以及小脑和丘脑处各有1例,其中2例为多发患者。结论 CT、MRI检查在病毒性脑炎患儿中均具有一定的诊断价值,但MRI检查对病毒性脑炎的诊断误诊、漏诊率明显低于CT检查,具有更高的临床应用价值,值得在临床上推广。     

Identification of differentially expressed genes in omental adipose tissues of obese patients by suppression subtractive hybridization

To identify differentially expressed genes between obese individuals and normal control, we have undertaken suppression subtractive hybridization （SSH）. Omental adipose tissues were obtained via abdominal surgery for appendicitis in both 13 obese subjects[BMI （body mass index） 〉 30 kg/m（2）] and 13 normal subjects （BMI 〉 18 and 〈 25 kg/m（2））.     

重庆儿童急性呼吸道感染1731例病毒病原学分析

目的:了解重庆地区儿童急性呼吸道感染(Acute respiratory infection,ARI)的病毒病原学构成,指导临床诊断与治疗.方法:对1731例住院的ARI儿童抽取鼻咽分泌物,采用直接免疫荧光法检测7种病毒即呼吸道合胞病毒(RSV)、腺病毒、副流感病毒Ⅰ、Ⅱ、Ⅲ、流感病毒A、B.结果:儿童ARI病毒病原的总阳性率与年龄、季节及病种有关,与性别无关.7种病毒中RSV的阳性率最高,其次为副流感病毒Ⅲ.RSV在冬季、6～12月的婴儿及毛细支气管炎中感染率较高;副流感病毒Ⅲ多见于5岁以上、上感的儿童.结论:通过检测儿童ARI的病毒病原,不仅可为临床提供快速、准确的诊断依据,防止滥用抗生素,而且为长期的病毒病原监测和病毒相关性疾病的研究奠定了基础.     

活血化瘀法和补益法协同在肿瘤化疗后骨髓抑制中的运用

骨髓抑制是恶性肿瘤化疗后的常见不良反应.化疗药物入血,损伤血络,致血脉空虚、气血瘀滞,加上化疗后元气虚衰,无力推动血液运行,致使血停而为瘀,影响新血生成,"瘀血不去,新血不生".因此,临证中在补益正气的前提下,同时因人制宜、辨证活血化瘀,使益气与行血并行,可祛瘀生新、推陈出新,促进骨髓造血,从而可有效改善骨髓抑制.     

乙型肝炎病毒在不同丙氨酸氨基转移酶状态下对Th17、Treg细胞及其比率的影响

目的: 探讨不同载量的乙型肝炎病毒 (hepatitis B virus, HBV)在不同丙氨酸氨基转移酶 (alanine aminetransferase, ALT) 状态下对慢性乙型肝炎患者辅助性T淋巴细胞17 (helper T lymphocytes 17, Th17)、调节性T淋巴细胞 (regulatory T lymphocyte, Treg)及其比率的影响。方法: 分析兰州大学第一医院确诊为慢性乙型肝炎的患者336例,采用化学发光免疫分析仪检测乙肝抗原抗体,采用生化分析仪检测肝功能,采用荧光定量PCR分析仪检测被测者的病毒载量,采用流式细胞分析仪检测Th17、Treg细胞及其比率,其中ALT正常的乙肝患者111例(ALT<40 U/L),ALT≥正常上限且<2倍增高的慢性乙肝患者108例(40 U/L≤ALT<80 U/L),ALT≥正常上限2倍增高的慢性乙肝患者117例(ALT≥80 U/L),并且按病毒载量分为低复制组(HBV DNA<4.0 lg copies/mL),中复制组(4.0 lg copies/mL≤HBV DNA<6.0 lg copies/mL),高复制组(HBV DNA≥6.0 lg copies/mL)。采用Dunnett T3方差分析在不同ALT状态下,不同载量的乙型肝炎病毒对慢性乙型肝炎患者Th17、Treg细胞及其比率的影响。对ALT≥正常上限2倍增高的乙型肝炎患者进行抗病毒治疗24周,观察治疗前后病毒学及Th17、Treg细胞及其比率的变化。结果: 在ALT正常组及ALT≥正常上限且<2倍增高的慢性乙肝组中不同载量的乙型肝炎病毒对Th17、Treg细胞及其比率的影响差异无统计学意义,而在ALT≥正常上限2倍增高的慢性乙肝患者组中,随着病毒载量的增加,Th17(低复制组 3.18%±0.79%、中复制组 3.78%±0.92%、高复制组4.57%±1.15%)、Treg细胞 (低复制组 5.52%±1.58%、中复制组 5.89%±1.84%、高复制组6.37%±2.35%) 及其比率Th17/Treg (低复制组0.57±0.25、中复制组 0.65±0.29、高复制组 0.73±0.36) 均明显增高(P<0.05)。恩替卡韦治疗24周后,患者HBV DNA明显下降,Th17(3.89%±1.02% vs.2.06%±0.46%)、Treg细胞(6.02%±2.03% vs.5.06%±1.25%)及其比率(0.65±0.28 vs.0.41±0.14)均明显下降(P<0.05)。结论: 在不同ALT状态下HBV对Th17、Treg细胞及其比率的影响不同,可以从免疫学的角度阐明HBV对机体的影响,进一步理解以ALT分组抗病毒治疗的意义,从而有助于临床治疗。     

免疫抑制基因研究进展

在感染性疾病、自身免疫疾病、肿瘤的发生发展过程中普遍存在着免疫抑制作用,本文概述了小鼠免疫抑制基因和人类免疫抑制基因研究进展情况及其背景知识。目前,已克隆到小鼠免疫抑制基因,人类免疫抑制基因的研究也正在进行,这对人类在疾病的防治、组织和器官移植等方面的深入研究将具有重要的理论意义和潜在的社会价值。