骨髓间充质干细胞体外诱导为神经细胞的研究

本实验观察了大鼠MSCs向神经细胞方向的诱导分化情况,以期为MSCs在神经移植领域的临床应用提供理论基础。用含10 ng／ml bFGF+20％FBS的DMEM对MSCs进行预诱导24 h后,以含200μmol／L的BHA+2％DMSO的无血清DMEM对MSCs进行诱导,观察诱导后细胞的光、电镜形态学变化,通过免疫组织化学法对诱导后细胞进行神经细胞表型及神经递质合成酶鉴定。结果显示:MSCs经BHA和DMSO诱导后,80％以上的细胞表现出神经元样形态,胞浆内可见较多Nissl体,并表达nestin、NSE、NF、MAP、SYN,部分诱导后的细胞表达ChAT、TH、GAD;电镜下观察,诱导后细胞核大而圆,核仁明显,胞浆内细胞器发达,可见大量粗面内质网和游离核糖体。提示,MSCs体外可被诱导分化为神经元样细胞,诱导后的细胞有合成某些神经递质的能力并具有发育早期神经元的超微结构特点。     

Vascular Endothelial Growth Pattern During Demineralized Bone Matrix Induced Osteogenesis

The purpose of the current study was to determine the timely ingrowth of blood vessels associated with demineralized bone matrix (DMB) induced osteogenesis. Critical-size (10 × 5mm), full thickness bony defects in rabbit parietal bone were implanted with DBM. Histological and ultrastructural changes were examined 1, 2, 3, 4, 5, 6, 7 and 14 days later. Neovascularization was assessed by immunohistochemical staining for factor VIII antigen (marker for vascular endothelium) and also confirmed by staining using pan-endothelial antibody (CD31) (a marker for endothelium). Immunohistochemical evaluation revealed a positive staining for CD31 and Factor VIII expressed by endothelial cells by day 3 post grafting. By day 4, small blood vessels were first seen budding from host bed towards the grafted DBM. Ultrastructural identification of cells in the early stages of healing revealed the presence of macrophages. The monocyte-derived macrophage appears to play a central role in the repair process using DBM. Results of this study demonstrated a rapid vascularization during the DBM induced osteogenesis. This rapid vascularization is vital to the healing and bone induction ability of the DBM.     

Effects of Lactobacillus rhamnosus GG and Lactobacillus reuteri R2LC on Acetic Acid-Induced Colitis in Rats

Background: Certain lactobacilli reduce the severity of experimental colitis. The aim of this study was to compare the effects of a human strain Lactobacillus rhamnosus GG and a rat strain Lactobacillus reuteri R2LC on acetic acid-induced colitis in rats. Methods:Lactobacillus rhamnosus GG, Lactobacillus reuteri R2LC or sulphasalazine were given orally to the rats. Colitis was assessed 72 h after induction with acetic acid. Results:Lactobacillus reuteri R2LC significantly antagonized body weight loss caused by inflammation compared with Lactobacillus rhamnosus GG and sulphasalazine, and oedema formation in the colon compared with sulphasalazine. Lactobacillus reuteri R2LC reduced the median value of macroscopic ulceration and the protein content of inducible nitric oxide synthase by 50% and the median of the protein content of inducible cyclooxygenase by 30% compared with that of the colitis control group, and Lactobacillus rhamnosus GG reduced the median of inducible nitric oxide protein content by 40% and increased the median of inducible cyclooxygenase protein content by 30% compared with the median value of the colitis control group, but these differences were not statistically significant. Conclusions: The rat strain Lactobacillus reuteri R2LC, but not the human strain Lactobacillus rhamnosus GG, is of benefit in reducing the severity of acetic acid-induced colitis in rats. These results suggest that it is not the total amount of Lactobacillus but the particular species or strain of Lactobacillus that is important in attenuating experimental colitis.     

Galacto-oligosaccharides Stimulate the Growth of Bifidobacteria but Fail to Attenuate Inflammation in Experimental Colitis in Rats

Background: Galacto-oligosaccharides potentially attenuate colonic inflammation by two mechanisms: through beneficial effects on intestinal microflora and by increasing the colonic short-chain fatty acid concentration. The purpose of this study was to investigate the effects of galacto-oligosaccharides on the development of inflammation and on the growth of bifidobacteria in trinitrobenzene sulphonic acid (TNBS)-induced colitis, a model that has been shown to benefit from short-chain fatty acid administration and to be associated with alterations in the colonic microflora. Methods: Rats were given daily either whey-derived or lactose-derived galacto-oligosaccharides (4 g kg -1 day -1 , p.o.), starting 10 days before colitis induction, or dexamethasone (2 mg kg -1 day -1 , s.c., a positive control), starting at colitis induction. Colon wet weight, macroscopic damage and myeloperoxidase activity were assessed 72 h after the induction of colitis. Faecal bifidobacteria were counted at the beginning of the study, and immediately before and 72 h after colitis induction. Results: Galacto-oligosaccharides increased the colonic levels of bifidobacteria but also the levels of other bacterial species. Neither whey-derived nor lactose-derived galacto-oligosaccharides reduced the severity of inflammation. Conclusions: Galacto-oligosaccharides are able to modify gut microflora in severe TNBS-induced colitis, but unable to attenuate the inflammation.     

Experimental muscle pain changes motor control strategies in dynamic contractions

This study investigated the effect of muscle pain on muscle activation strategies during dynamic exercises. Ten healthy volunteers performed cyclic elbow flexion/extension movements at maximum speed for 2 min after injection of (1) hypertonic (painful) saline in the biceps brachii, (2) hypertonic saline in both biceps brachii and triceps brachii, and (3) isotonic (nonpainful) saline in the biceps brachii muscle. Surface electromyographic (EMG) signals were collected from the upper trapezius, biceps brachii, triceps brachii, and brachioradialis muscles (to estimate EMG amplitude) and with an electrode arrays from biceps brachii (to estimate muscle fiber conduction velocity [CV]). In all conditions, the acceleration of the movement decreased throughout the exercise, and kinematic parameters were not altered by pain. With respect to the control condition, pain induced a decrease of the biceps brachii (mean ± SE, –23±4%) and brachioradialis (–10±0.4%) integrated EMG (IEMG) in the beginning of the exercise, and an increase (45±3.5%) of the upper trapezius IEMG at all time points during the exercise. The biceps brachii IEMG decreased over time during the nonpainful exercises (–11±0.6%) while it remained constant in the painful condition. Biceps brachii CV decreased during painful conditions (–12.8±2.2%) while it remained constant during the nonpainful condition. In conclusion, muscle pain changes the motor control strategy to sustain the required dynamic task both in the relative contribution between synergistic muscles and in the motor unit activation within the painful muscle. Such a changed motor strategy may be highly relevant in models of occupational musculoskeletal pain conditions.     

上下文效应对大学生面孔吸引力的影响

目的 研究上下文效应在大学生面孔吸引力的影响.方法 采用实验法对随机选取的唐山市3所高校的160名大学生单独进行实验处理,让被试对其所在组的照片上人物的面孔吸引力作出5维度等级评价,并用统计学方法对数据进行统计分析.结果 大学生实验组与对照组对一般吸引力的异性面孔照片评价存在显著性差异(x2=51.30,P＜0.01).不同性别的大学生在相貌评价过程中的影响存在显著差异(x2=11.06,P＜0.05).结论 大学生在评价面孔吸引力的过程中会受到上下文效应的影响.男性大学生在评价面孔吸引力的过程中比女性大学生更容易受到上下文效应的影响.     

非接触磁感应脑阻抗断层成像系统设计

针对脑组织电阻抗的研究，本文设计了工作频率在10MHz的单通道硬件电路和试验台，可以分辨电导率介于0．001s/m到6s/m的四种不同浓度的NaCl盐溶液，并对模拟正常人脑组织（0．375s/m）的0．195％NaCl盐溶液目标，给出了初步成像结果。     

大鼠实验性胃溃疡自愈期间胰岛胃泌素和生长抑素细胞的免疫组织化学研究

目的　探讨大鼠实验性胃溃疡自愈期间 ,胰岛胃泌素免疫反应细胞 (gastrin ,G)和生长抑素细胞(somatostatin ,SSorD)的变化。　方法　免疫组织化学ABC技术。　结果　大部分G细胞免疫反应深浅不一 ;溃疡术后 4、10d ,胰岛G细胞面数密度增高 ,与正常或盐水组相比P <0 0 5。D细胞面数密度于 4d增加 ,P <0 0 5。　结论　成年大鼠胰岛细胞呈胃泌素免疫反应阳性 ;胰岛G细胞和D细胞可能以内分泌或旁分泌调节的途径间接或直接参与大鼠实验性胃溃疡修复的过程。     

Cytokine shifts and tolerance in experimental autoimmune encephalomyelitis

Cytokines play an important role in the pathogenesis of both multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). Effective treatments for both diseases have been shown to alter cytokines in the central nervous system and in activated mononuclear cells. EAE is an animal model that mimics many aspects of multiple sclerosis, and has been widely used to study the mechanisms of disease and therapeutic approaches to multiple sclerosis. Cytokines play an important role in regulation of disease expression in EAE, and in tolerance to disease induction. In this review, we will summarize the current findings on the role of cytokine shifts in the induction of tolerance in EAE. In addition, we will discuss modulation of EAE by altered expression of members of the cytokine-regulated Jak/STAT intracellular signaling pathway.