人脑外伤后皮层核因子-κB的表达

目的 探讨核因子-κB（nuclear factor—κB，NF—κB）在人创伤性脑损伤（traumatic brain injury，TBI）后挫伤皮层中的表达情况，包括表达位置、表达强度和表达时相。方法 挫伤区皮层的标本来自24例TBI患者，取样时间为伤后5h-5d，利用凝胶电泳迁移分析法（electrophoretic mobility shift assay，EMSA）和免疫组化技术测定NF—κB的活性和表达强度。结果 在人TBI后的挫伤区皮层中，NF—κB表达明显上调，表达高峰为伤后48—72h，NF—κBP65主要在血管内皮细胞和神经胶质细胞中表达，NF—κBP50主要在神经胶质细胞和少量神经元中表达，NF—κBP65的表达强度高于NF—κBP50。结论 NF—κB在人TBI后的挫伤区皮层中表达上调，提示其可能在TBI后的病理生理过程中起着重要作用。     

谷氨酸诱导体外培养的鸡胚脊髓神经细胞释放NO

用鸡胚脊髓神经细胞的原代培养,测定细胞中亚硝酸盐的含量,研究了谷氨酸(Glu)对原代培养神经细胞中NO的影响。结果表明,谷氨酸作用于原代培养的鸡胚脊髓神经细胞,在诱导神经细胞释放乳酸脱氢酶(LDH)的同时,还可诱导细胞释放一氧化氮(NO)。如先用NO合成酶抑制剂L-NOARG作用细胞,再加入Glu,则发现L-NOARG能降低Glu导致的培养液中LDH活性升高。提示NO可能参与介导Glu的神经毒性作用。     

Potential contribution of nuclear factor-kappaB to cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.

Nuclear factor-kappaB (NF-kappaB) plays a key role in inflammation, which is involved in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). In the present study, we assessed the potential role of NF-kappaB in regulation of cerebral vasospasm. Nuclear factor-kappaB DNA-binding activity was measured in cultured vascular smooth muscle cells (VSMCs) treated with hemolysate and pyrrolidine dithiocarbamate (PDTC, 80 micromol/L), an inhibitor of NF-kappaB. Forty-two rabbits were divided into three groups: control, SAH, and PDTC groups (n=14 for each group). The caliber of the basilar artery was evaluated. Nuclear factor-kappaB DNA-binding activity and the gene expression levels of cytokines and adhesion molecules in the basilar artery were measured. Immunohistochemical study was performed to assess the expression and localization of tumor necrosis factor (TNF)-alpha, intercellular adhesion molecule (ICAM)-1, and myeloperoxidase (MPO). It was observed that NF-kappaB DNA-binding activity was significantly increased by treatment with hemolysate in cultured VSCMs, but this increase was suppressed by pretreatment with PDTC. Severe vasospasm was observed in the SAH group, which was attenuated in the PDTC group. Subarachnoid hemorrhage could induce increases of NF-kappaB DNA-binding activity and the gene expression levels of TNF-alpha, interleukin (IL)-1 beta, ICAM-1, and vascular cell adhesion molecule (VCAM)-1, which were reduced in the PDTC group. Immunohistochemical study demonstrated that the expression levels of TNF-alpha, ICAM-1, and MPO were all increased in the SAH group, but these increases were attenuated in the PDTC group. Our results suggest that NF-kappaB is activated in the arterial wall after SAH, which potentially leads to vasospasm development through induction of inflammatory response.     

IL-2R 在急性细胞性排异反应的同种异体尸体移植肾组织中的检测及意义

为探讨白介素－２受体（ＩＬ－２Ｒ，即ＣＤ２５）在同种异体肾移植急性细胞性排异（ＡＣＲ）临床诊断的作用，着重观察移植肾发生（ＡＣＲ）和无ＡＣＲ时，其间质浸润细胞中ＩＬ－２Ｒ阳性细胞数的变化，及其与间质浸润的淋巴细胞的关系。作者选择同期行异体肾移植，且无并发症患者１７例，采用ＰＡＰ四层免疫酶标法，检测移植肾组织中间质浸润细胞中ＩＬ－２Ｒ阳性细胞数的变化。结果显示：无ＡＣＲ的肾组织中，ＩＬ－２Ｒ阳性细胞仅轻度增加，当移植肾出现ＡＣＲ时，ＩＬ－２Ｒ阳性细胞数的增加十分显著，并与间质浸润的ＣＤ８密切相关。作者认为ＩＬ－２Ｒ对于ＡＣＲ的诊断及鉴别诊断具有一定的临床应用价值。     

超微粉体技术对穿心莲药材中穿心莲内酯及脱水穿心莲内酯溶出率的影响

目的:探讨超微粉碎对穿心莲药材中有效成分溶出率的影响.方法:用高效液相色谱法(high performance liquid chromatography,HPLC)测定穿心莲超微粉与药材120目细粉中穿心莲内酯及脱水穿心莲内酯的溶出率.结果:超微粉药材中穿心莲内酯及脱水穿心莲内酯的溶出率明显增加.结论:超微粉碎可显著提高穿心莲药材中有效成分的溶出率.     

Pretreatment with recombined human erythropoietin attenuates ischemia–reperfusion-induced lung injury in rats

Objective: Based on the findings that erythropoietin (EPO) has been proved to be a multiple functional cytokine to attenuate ischemia–reperfusion (I/R) injury in various organs such as brain, heart, and kidney in animals, this experiment was designed to evaluate the effect of pretreatment with recombined human erythropoietin (rhEPO) on I/R-induced lung injury. Methods: Left lungs of rats underwent 90 min of ischemia and then were reperfused for up to 2 h. Animals were randomly divided into three experimental groups as sham group, I/R group, and rhEPO + I/R group (a single dose of rhEPO was injected intraperitoneally 3000 U/kg 24 h prior to operation). Lung injury was evaluated according to semi-quantitive analysis of microscopic changes, tissue polymorphonuclear neutrophils (PMNs) accumulation (myeloperoxidase (MPO) activity), and pulmonary microvascular permeability (Evan's blue dying method). Peripheral arterial and venous blood samples were obtained for blood–gas analysis after 5 min occlusion of right lung hilus at the end of reperfusion. The serum concentration of tumor necrosis factor (TNF)- was also measured by the method of enzyme-linked immunosorbent assay. Results: Histological injury scoring revealed significantly lessened lung alveolus edema and neutrophils infiltration in the rhEPO pretreated group compared with I/R group (p < 0.05). The rhEPO pretreated animals exhibited markedly decreased lung microvascular permeability (p < 0.05) and myeloperoxidase activity (p < 0.05). Blood–gas analysis demonstrated that the pretreated animals had significantly ameliorated pulmonary oxygenation function (p < 0.05). The serum concentration of tumor necrosis factor- in rhEPO pretreated group was markedly decreased compared with that of I/R group (p < 0.05). Conclusions: Pretreatment with rhEPO appears to attenuate I/R-induced lung injury. This function is partly related with the capacity that rhEPO inhibits the accumulation of polymorphonuclear neutrophils in lung tissue and decreases the systematic expression of tumor necrosis factor-.     

Toward a revision of criteria for the dementias

This article critically considers current diagnostic criteria for dementia and reports recommendations approved by at least 80% of experts attending the Third Canadian Consensus Conference on the Diagnosis and Treatment of Dementia (CCCDTD3). There was consensus that many of the features proposed as essential to a diagnosis of dementia in the 1980s no longer are relevant (for example, the requirements for memory impairment, electroencephalogram and cerebrospinal fluid studies, age-specific exclusions). In addition, other syndromes such as frontotemporal dementia have been recognized and need to inform new dementia criteria. It is also recognized that a diagnosis of depression need not exclude a dementia diagnosis. Other proposals, such as neuropathology should be considered as additional evidence and not as a gold standard or that some people with dementia have prolonged plateaus so that progressive decline need not be a criterion for Alzheimer’s disease (AD), were more controversial and did not receive similar support. Given the evidence of the last three decades, there is merit in reconsidering the criteria by which dementia and AD are diagnosed.