体外培养下氢醌诱导淋巴细胞凋亡及对DNA损伤的影响

目的:研究氢醌对人淋巴细胞的细胞周期阻滞与凋亡、遗传毒性和氧化损伤作用。方法:离体培养淋巴细胞24 h后加S9液,设置氢醌低、中、高浓度(50,150,450μmol/L)组,另设空白对照组,经染毒处理后分别采用MTT比色法检测各组PBL相对存活率,FCM检测细胞周期和凋亡,DCFH-DA法检测ROS含量,FT-IR-ATR检测细胞损伤,SCGE检测DNA链断裂,微核实验检测染色体畸变。结果:氢醌能降低细胞存活度,诱导S+G2/M期周期阻滞,有明显促凋亡作用。细胞内ROS含量剂量依赖性增加,DNA/RNA的光谱区域(1 000～1 490 cm-1)峰型改变明显,高浓度氢醌(450μmol/L)诱导细胞DNA断裂与染色体畸变。结论:氢醌诱导人淋巴细胞结构和功能改变,与DNA氧化应激及DNA-蛋白质损伤有关。     

Effects of quinolinic acid-induced lesions of the nucleus accumbens core on inter-temporal choice: a quantitative analysis

Rationale There is evidence that lesions of the nucleus accumbens core (AcbC) promote preference for smaller earlier reinforcers over larger delayed reinforcers in inter-temporal choice paradigms. It is not known whether this reflects an effect of the lesion on the rate of delay discounting, on sensitivity to reinforcer magnitude, or both. Aim We examined the effect of AcbC lesions on inter-temporal choice using a quantitative method that allows effects on delay discounting to be distinguished from effects on sensitivity to reinforcer size. Materials and methods Sixteen rats received bilateral quinolinic acid-induced lesions of the AcbC; 14 received sham lesions. They were trained under a discrete-trials progressive delay schedule to press two levers (A and B) for a sucrose solution. Responses on A delivered 50 μl of the solution after a delay d _A; responses on B delivered 100 μl after d _B. d _B increased across blocks of trials, while d _A was manipulated across phases of the experiment. Indifference delay d _B(50) (value of d _B corresponding to 50% choice of B) was estimated in each phase, and linear indifference functions (d _B(50) vs d _A) derived. Results d _B(50) increased linearly with d _A (r ² > 0.95 in each group). The intercept of the indifference function was lower in the lesioned than the sham-lesioned group; slope did not differ between groups. The lesioned rats had extensive neuronal loss in the AcbC. Conclusions The results confirm that lesions of the AcbC promote preference for smaller, earlier reinforcers and suggest that this reflects an effect of the lesion on the rate of delay discounting.     

Mapping the brain pathways of declarative verbal memory: Evidence from white matter lesions in the living human brain

Understanding the contribution of the brain white matter pathways to declarative verbal memory processes has been hindered by the lack of an adequate model in humans. An attractive and underexplored approach to study white matter region functionality in the living human brain is through the use of non-aprioristic models which specifically search disrupted white matter pathways. For this purpose, we employed voxel-based lesion–function mapping to correlate white matter lesions on the magnetic resonance images of 46 multiple sclerosis patients with their performance on declarative verbal memory storage and retrieval. White matter correlating with storage was in the temporal lobe–particularly lateral to the hippocampus and in the anterior temporal stem–, in the thalamic region and in the anterior limb of the internal capsule, all on the left hemisphere, and also in the right anterior temporal stem. The same volumes were relevant for retrieval, but to them were added temporo-parieto-frontal paramedian bundles, particularly the cingulum and the fronto-occipital fasciculus. These 3D maps indicate the white matter regions most critically involved in declarative verbal memory in humans.     

The neural basis of perceptual bias and response bias in the Landmark task

Spatial neglect as a multifaceted syndrome may consist of perceptual/attentional as well as motor/intentional components. The present study investigated the lesion anatomy underlying perceptual and response bias using a manual response Landmark task (Bisiach, Ricci, Lualdi, & Colombo, 1998) in 68 patients with right-hemispheric stroke. The two differential aspects of the neglect syndrome were assessed by measuring response tendencies resulting from underestimations of the length of left line segments and from hypometric movement execution towards contralesional space, respectively. Perceptual and response bias were orthogonal components of task performance in the Landmark task. Perceptual as well as response bias both explained variance in the performance of standard paper-and-pencil neglect tests. While lesions within middle frontal, inferior parietal and parieto-occipital brain regions were related to perceptual bias, subcortical lesions within the caudate were related to response bias in the Landmark task. Our data suggest that perceptual/attentional and motor/intentional aspects of neglect are independent components of the syndrome with differential neural underpinnings in fronto-parietal and subcortical brain regions.     

伏核毁损对精神分裂症模型大鼠行为和学习记忆能力的影响

目的　探讨毁损伏核对调控精神分裂症行为的有效作用及对学习记忆能力的影响 ,为精神分裂症外科治疗提供参考。方法　给大鼠腹腔内注射苯环己哌啶 (PCP)制作精神分裂症动物模型。采用立体定位仪 ,电极毁损大鼠伏核 ,观察社会行为、刻板行为评分 ,并进行Morris水迷宫实验。结果　毁损伏核组能使精神分裂症模型大鼠刻板行为和运动失调有所减轻 ,与假毁损组比较差异具有显著性 (P <0 .0 5 )。水迷宫实验毁损组在初期空间记忆能力的建立上存在缺陷 ,与假毁损组比较差异具有显著性 (P <0 .0 5 )。结论　伏核毁损能改善精神分裂症症状 ,对大鼠初期学习记忆能力有一定影响     

Neurochemical identification of A13 dopaminergic neuronal projections from the medial zona incerta to the horizontal limb of the diagonal band of Broca and the central nucleus of the amygdala

Studies utilizing fluorescent histochemical techniques first revealed that A₁₃ dopaminergic (DA) perikarya located in medial zona incerta (MZI) project to various regions within the hypothalamus; accordingly, these DA neurons were designated the ‘incertohypothalamic’ DA neuronal system. More recently, it has been shown that the anterograde neuronal tract tracer Phaseolus vulgaris leucoagglutinin, after injection into MZI, is identified in nerve terminals outside of the hypothalamus: for example, in horizontal limb of the diagonal band of Broca (HDB) and central nucleus of the amygdala (cAMY). The purpose of the present study was to determine, using neurochemical techniques, if A₁₃ DA neurons project to the HDB and cAMY. Concentrations of dopamine and one of its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) were determined in HDB and cAMY following: (1) electrical stimulation of MZI, (2) electrolytic lesion or knife ablation of MZI, and (3) administration of gamma-hydroxybutyric acid (GHBA) into MZI. For comparison, similar measurements were made in nucleus accumbens (N. Acc.), a terminal region of A₁₀ DA neurons in the ventral tegmental area (VTA). Electrical stimulation of MZI increased DOPAC concentrations in HDB and cAMY, whereas electrolytic or ablative lesions of MZI decreased dopamine concentrations in both of these regions. By contrast, neither stimulation nor lesion of MZI had any effect on DOPAC or dopamine concentrations in N. Acc. Intracerebral injection of GHBA into MZI increased dopamine concentrations in MZI and HDB, but not in cAMY or N. Acc. Intracerebral administration of GHBA into VTA increased dopamine concentrations in HDB and N. Acc., but not in MZI or cAMY. These results suggest that A₁₃ DA neurons project to HDB and cAMY but not to N. Acc., and HDB receives projections from both A₁₀ and A₁₃ DA neurons.     

残胃病变846例内镜及临床表现

目的：探讨胃部分切除术后残胃病变的发病学特点。方法：回顾性分析我院1980年至2001年20年间846例胃部分切除术后患的内镜资料及临床表现。结果：残胃病变中以残胃炎及吻合口炎最常见，占89．2％，其次为胆汁反流，占58．5％，再次为残胃及吻合口溃疡，占16．9％；残胃癌的发生率为4．8％。此外还有食管贲门炎，缝线残留等。残胃病变的临床表现主要为上腹部疼痛占60．3％，恶心、呕吐及／或纳差、消瘦占19．1％，呕血、黑便占11．3％。结论：为减少残胃病变，尤其是残胃癌的发生，要严格掌握胃切除的指征，而且手术后定期复查胃镜，早期发现残胃病变。     

内镜下门脉高压性胃病38例的特征分析

目的:观察门脉高压性胃病(PHG)的内镜下特点.方法:用Olympus GIF-XQ40胃镜对38例已确诊的门脉高压症和114例非门脉高压症对照组进行内镜下观察.结果:PHG发生率65.79%,Mosaic病变达96.00%,并且病变多位于胃底、胃体部.而114例对照组中无1例Mosaic病变.结论:门脉高压症并发胃粘膜病变非常普遍,Mosaic病变是其镜下特征.     

踝关节骨折伴距骨软骨损伤的实验及临床研究

目的　探讨踝关节骨折伴距骨软骨损伤的规律及治疗。方法　通过应用踝关节骨骼标本及距骨模型 ,观察在模拟踝关节骨折各种外力作用下距骨模型受力及关节面压缩情况 ,并对 42例踝关节骨折在关节镜辅助下手术所见及关节镜图像进行分析。结果　踝部骨折伴距骨软骨损伤的部位、程度与损伤时足位置及外力、关节类型密切相关 ,有一定的规律可循。结论　此规律有利于踝关节镜入路的选择和手术步骤的制定 ,遵循其规律可做到踝关节镜手术操作准确 ,避免漏诊 ,减少意外损伤 ,并提高临床治疗效果     

Monoaminergic system lesions increase post-sigh respiratory pattern disturbance during sleep in rats

Monoamines are important regulators of behavioral state and respiratory pattern, and the impact of monoaminergic control during sleep is of particular interest for the stability of breathing regulation. The aim of this study was to test the effects of systemically induced chemical lesions to noradrenergic and serotonergic efferent systems, on the expression of sleep-wake states, pontine wave activity, and sleep-related respiratory pattern and its variability. In chronically instrumented male adult Sprague-Dawley rats we lesioned noradrenergic terminal axonal branches by a single intraperitoneal dose of DSP-4 (N-(2-chloroethyl)-N-ethyl-2-brombenzilamine; 50 mg/kg, i.p.), and serotonergic axonal terminals by two intraperitoneal doses, 24 h apart, of PCA (p-chloroamphetamine; 6 mg/kg, i.p.). In each animal, we recorded sleep, pontine waves (P-waves) and breathing at baseline, following sham injection, and every week for 5 weeks following injection of either systemic neurotoxin. Distinct responses were observed to the two lesions. DSP-4 lesions were associated with a trend toward increased NREM sleep (p < 0.06), decreased wakefulness (p < 0.05) and increased respiratory tidal volume during NREM (p = 0.0002) and REM (p = 0.0001) sleep with respect to baseline. None of these effects, however, were observed during the first 14 days after injection. No significant changes were observed in the frequency of apneas or sighs, nor in the coupling between these two, at any time after DSP-4 injection. Conversely, selective serotonergic lesion by PCA produced no change in the baseline respiratory frequency or tidal volume during sleep or wakefulness, nor was the expression of Wake, NREM or REM sleep affected. Instead, PCA injection resulted in a sustained increase in the frequency and duration of post-sigh apneas (PS) during NREM sleep (p = 0.002). This reflected increased coupling between sighs and apneas, because neither the frequency nor the amplitude of spontaneous sighs was altered by PCA.