Loss of heterozygosity at 18q21 region in gastric cancer involves a number of cancer-related genes and correlates with stage and histology,but lacks independent prognostic value

Identification of neuroendocrine differentiation in tumours has important implications for prognosis and therapy. The aim of the present study was to evaluate monoclonal antibodies against synaptic vesicle protein 2 (SV2) as histopathological markers for neuroendocrine differentiation in tumours of the gastrointestinal tract and pancreas. Paraffin blocks from 211 gastrointestinal tumours were examined by immunocytochemistry, using a monoclonal antibody against SV2. Virtually all endocrine tumours of the gastrointestinal tract (11/11 gastric, 53/53 ileal, 16/21 appendiceal, and 22/22 rectal) and pancreas (24/24) were positively labelled. SV2 labelling was also demonstrated in gastrointestinal pacemaker cell tumours (8/8), while adenocarcinomas of the gastrointestinal tract and pancreas were negative, with the exception of occasional adenocarcinomas demonstrating weak SV2 labelling (stomach 1/22, rectum 1/29, and pancreas 0/21). Western blotting of tumour biopsies confirmed expression of SV2 in endocrine tumours of the gastrointestinal tract and pancreas. No relationship was observed between SV2 expression in tumours and hormone production or malignant potential. In conclusion, SV2 is expressed in neuroendocrine tumours of the gastrointestinal tract and pancreas, but not in non-endocrine tumours. The SV2 monoclonal antibody can therefore be used as a general marker for neuroendocrine differentiation in gastrointestinal and pancreatic tumours.     

Neuropsychological Deficit and Academic Performance in Children and Adolescents Following Traumatic Brain Injury

Evaluated the utility of neuropsychological testing in predictingacademic outcome in children 1 year following traumatic braininjury (TBI). Fifty-one schoolage children who were admittedto hospital after TBI were assessed with a battery of neuropsychologicalmeasures at 3 months postinjury. Academic achievement was assessedat 3 and 12 months postinjury. The neuropsychological batteryincluded intelligence testing and measures of memory, learning,and speed of information processing. Academic outcome was assessedin terms of post-TBI changes in reading, spelling, and arithmetic;changes in teacher ratings of school performance; and changein school placement. According to logistic regression analysis,change in placement from regular to special education at 1-yearpost-TBI was predicted by injury severity and by neuropsychologicalperformance at 3 months post-TBI. Findings suggest that neuropsychologicaltesting is useful in identifying children with special educationalneeds subsequent to TBI.     

The relationship of VEGF and PGE2 expression to extracellular matrix remodelling of the tenosynovium in the carpal tunnel syndrome

Tenosynovial thickening within the confined space of the carpal tunnel is thought to be the cause of the carpal tunnel syndrome (CTS). However, little is known about the pathological mechanism of tenosynovial thickening. In this study, the role of prostaglandin E(2) (PGE(2)) and vascular endothelial growth factor (VEGF) (two representative molecules that can induce oedema by increasing vascular permeability) was analysed in CTS by using immunohistochemistry and enzyme-linked immunosorptive assay (ELISA). Expression of these molecules was compared with the patients' clinical histories and a temporary increase in production of these molecules was found in cells within the vessels and synovial lining during the intermediate phase of the syndrome when the histology of the tenosynovium changes from oedematous to fibrotic. Statistical analysis clearly demonstrated that there is a close correlation between the expression of PGE(2) and VEGF. Furthermore, immunohistochemical analysis with anti-proliferating cell nuclear antigen (PCNA) revealed that the area with distinct VEGF expression closely matched the area where endothelial cells, vascular smooth muscle cells, and synovial lining cells proliferate. In contrast, despite marked alteration in the extracellular matrix (ECM) component of the tenosynovium, the fibroblasts responsible for most ECM framework production do not proliferate during any phase of CTS. Histological analysis demonstrated that angiogenesis takes place only during the intermediate phase. Since clusters of capillaries and arterioles are often surrounded by type III collagen-rich, disorganized, degenerate connective tissue, which contains fewer fibroblasts than normal, angiogenesis appears to take place as a part of a regenerative reaction that results in fibrosis. These findings strongly indicate that both PGE(2) and VEGF are expressed in the tenosynovium in CTS during the intermediate phase and induce the histological changes seen in the tenosynovium.     

大鼠脊髓损伤后NGF及其受体TrkA在运动神经元及神经胶质细胞表达的变化

为探讨脊髓损伤后运动神经元及神经胶质细胞内神经生长因子(NGF)及其高亲和力受体(TrkA)表达的变化,用改良Allen重击法损伤SCI组动物T12脊髓,按伤后存活时间再将动物分为脊髓损1 d组、2 d组和5 d组。各组动物的脊髓切片经ABC法免疫组织化学染色,用光镜观察TrkA及NGF在脊髓前角运动神经元表达的变化和胶质纤维酸性蛋白(GFAP)及NGF免疫反应阳性胶质细胞的反应性增生程度,并进行图像分析。结果显示:脊髓损伤后前角运动神经元TrkA及NGF的表达随脊髓损伤后动物存活时间的延长逐渐上调;脊髓白质和灰质内尤其是皮质脊髓束内GFAP及NGF阳性胶质细胞明显增生;与此同时,室管膜细胞内亦可见明显的NGF免疫反应产物。上述结果表明,脊髓损伤可刺激脊髓前角运动神经元表达TrkA及NGF,通过自分泌维持受损神经元的存活;损伤部位反应性增生的胶质细胞亦可产生NGF,通过旁分泌作用于脊髓前角运动神经元或皮质脊髓束的轴突末梢,以维持运动神经元的存活及促进皮质脊髓束的再生;适时补充外源性神经营养素或改变损伤局部的微环境将有利于受损脊髓的修复和再生。     

Neural Correlates of the Results-of-Action Acceptor in a Functional Biotechnical Complex

This report presents data illustrating the neurophysiological features of efferent-afferent convergence on cortical neurons. During combination of stimulus of pyramidal tract axons with electrocutaneous reinforcement, some of the study neurons were found to change the parameters of their activity evoked by stimulation of this tract: evoked responses started to reproduce the structure of responses to the reinforcement. The most dynamic rearrangements of pyramidal tract responses were obtained in experiments in which the study neurons were included in a biotechnical complex with feedback, the complex consisting of neuron-computer-stimulator-animal and actually being an analog of a natural functional system. The role of efferent-afferent convergence on CNS neurons in the development of the results-of-action acceptor of a functional system for a voluntary behavioral act is discussed.     

Fas蛋白在糖尿病大鼠局灶性脑缺血再灌注损伤后海马区的表达及意义

目的探讨Fas蛋白在糖尿病大鼠脑缺血再灌注海马区神经元损伤中的表达及意义。方法健康雄性Wister大鼠60只,随机分为4组:①正常对照组,②假手术组,③脑缺血再灌注组(NIR),④糖尿病脑缺血再灌注组(DIR组);采用STZ诱导糖尿病和线栓法建立大脑中动脉闭塞(MCAO)模型,HE法观察海马CA1神经元缺失,用免疫组化方法检测Fas在糖尿病大鼠脑缺血再灌注海马神经元损伤中的表达。结果HE染色:正常对照与假手术组未见神经元缺失和细胞凋亡,DIR组与脑缺血再灌注组均见神经元缺失和神经细胞凋亡,而DIR组比脑缺血再灌注组神经元缺失严重(P<0.05)。正常对照与假手术组极少见Fas免疫染色阳性细胞,DIR组与脑缺血再灌注组明显见Fas免疫染色阳性细胞,且DIR组比脑缺血再灌注组多(P<0.05)。结论Fas介导的细胞凋亡可能是糖尿病脑缺血再灌注损伤后海马区神经元损伤的机制之一。     

Clinical epidemiology of ciprofloxacin-resistant Proteus mirabilis isolated from urine samples of hospitalised patients

This study investigated the clinical characteristics of ciprofloxacin-resistant Proteus mirabilis isolates from urine samples associated with nosocomial infection or colonisation, and identified the risk-factors for ciprofloxacin resistance. Data for patients with ciprofloxacin-resistant P. mirabilis isolates (n=13) were compared with those for randomly selected patients with ciprofloxacin-susceptible P. mirabilis isolates (n=40) who were matched by temporal occurrence as control patients. The majority of ciprofloxacin-resistant P. mirabilis isolates were multiresistant, and ciprofloxacin resistance was associated significantly with previous use of fluoroquinolones and production of extended-spectrum beta-lactamases.     

Long-term potentiation deficits and excitability changes following traumatic brain injury

The effects of traumatic brain injury (TBI) on hippocampal long-term potentiation (LTP) and cellular excitability were assessed at postinjury days 2, 7, and 15. TBI was induced using a well-characterized central fluid-percussion model. LTP of the Schaffer collateral/commissural system was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope was found only in controls, and no recovery to control levels was observed for any postinjury time point. Four measurement parameters reflecting pyramidal cell discharges (population spike) indicated that TBI significantly increased cellular excitability at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased population spike amplitudes to a greater degree in injured animals than in control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated EPSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on postinjury days 7 and 15. These results suggest that TBI-induced excitability changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic efficacy and mechanisms related to action potential generation     

Effect of maximal arm exercise on skin blood flux in the paralyzed lower limbs in persons with spinal cord injury

 The purpose of the present study was to examine the effect of maximal arm exercise on the skin blood circulation of the paralyzed lower limbs in persons with spinal cord injury (PSCI). Eight male PSCI with complete lesions located between T3 and L1 performed graded maximal arm-cranking exercise (MACE) to exhaustion. The skin blood flux at the thigh (SBFT) and that at the calf (SBFC) were monitored using laser-Doppler flowmeter at rest and for 15 s immediately after the MACE. The subject's mean peak oxygen uptake and peak heart rate was 1.41 ± 0.22 l · min^–1 and 171.6 ± 19.2 beats · min^–1, respectively. No PSCI showed any increase in either SBFT or SBFC after the MACE, when compared with the values at rest. These results suggest that the blood circulation of the skin in the paralyzed lower limbs in PSCI is unaffected by the MACE. Accepted: 12 September 1996     

Monocytes and lymphocytes as active participants in the pathogenesis of experimental shock

We investigated the role played by monocytes and lymphocytes in the pathogenesis of experimental shock. Splanchnic artery occlusion (SAO) shock was induced in anaesthetized rats by clamping splanchnic arteries for 45 min followed by reperfusion. Sham operated animals were used as controls. SAO shocked rats had a decreased survival time (80±11 min, while sham shocked rats survived more than 4 h), increased serum (248±21 U/ml) and macrophage (145±15 U/ml) levels of TNF-, enhanced myeloperoxidase (MPO) activity in the ileum (3.38±0.2 U×10^–3/g tissue), decreased number of monocytes, lymphocytes and neutrophils and a profound hypotension. In addition we found an increased expression of vascular cell adhesion molecule-1 (VCAM-1) on aortic endothelium and a reduced percentage of VLA-4 positive monocytes and lymphocytes. Inhibition of TNF- synthesis, reversed the increased endothelial expression of VCAM-1, increased the percentage of integrin VLA-4 positive leukocytes and improved monocyte, lymphocyte and neutrophil count. Furthermore a passive immunization with specific antibodies raised against VCAM-1 (2 mg/kg, i.v. 3 h before SAO) increased survival, reduced MPO activity in the ileum (0.034±0.04 U×10^–3/g tissue) and improved mean arterial blood pressure. Our data suggest that monocytes and lymphocytes participate in the pathogenesis of splanchnic ischaemia-reperfusion injury and may amplify the adhesion of neutrophils to peripheral tissues.by I. Ahnfelt Rønne