Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.     

原发性前列腺印戒细胞癌(1例报告并文献复习)

目的探讨原发性前列腺印戒细胞癌的临床特征。方法回顾性分析1例原发性前列腺印戒细胞癌患者的临床资料,并结合文献进行复习讨论。结果患者前列腺穿刺活检病理报告为前列腺印戒细胞癌,免疫组织化学检查示PSA( ),PAS、CEA、LCA、CKH(-),行双侧睾丸切除术和氟他胺治疗,术后1月死于肺部转移。结论原发性前列腺印戒细胞癌来自前列腺腺泡上皮,确诊依靠病理组织学和免疫组化检查。临床罕见,恶性程度高,预后较差。     

磁场对荷瘤小鼠TNF及TNFR水平的影响

目的　观察磁场对荷瘤鼠瘤组织内肿瘤坏死因子 (TNF)及肿瘤坏死因子受体 (TNFR)的影响。方法　采用磁场照射荷瘤小鼠瘤区。结果　磁疗组小鼠体内TNF活性明显增强 ,TNFR表达量增多 ,与非磁疗组相比 ,差异有高度显著性 (P <0 .0 1)。结论　磁场具有增强荷瘤小鼠TNF活性并促进TNFR表达的作用。     

脑创伤致迟发性脑梗死临床分析

目的探讨脑创伤后迟发脑梗死的发生机制,临床诊断及救治措施。方法对32例经影像学证实为颅脑创伤后迟发脑梗死患者的临床资料进行回顾分析。结果出院时按GOS标准评价:恢复良好12例、中残5例、重残4例、植物生存3例,死亡8例,其中非手术治疗20例,存活14例,死亡6例,死亡率30%;手术治疗12例,存活10例,死亡2例,死亡率17%。结论及时诊断与合理有效的治疗是提高脑创伤后迟发性脑梗死的治愈率及提高患者生存质量的关键。     

重睑术后继发上睑下垂的成因及防治

重睑术为最常见的、操作简单的门诊手术,但若想术后取得满意的效果却并非易事[1],术后并发症相对较多,其中继发上睑下垂是较严重的并发症之一,我们复习相关文献发现,关于如何在重睑术中、术后早期发现、早治疗,避免医疗纠纷及并发症发生的报道不多见。本文就重睑术后继发上睑下     

重症急性胰腺炎大鼠肺组织中LIF的表达变化及意义

目的:观察重症急性胰腺炎(SAP)大鼠白血病抑制因子(LIF)在肺组织中表达的时相变化, 探讨LIF在SAP病程及肺损伤中的意义．方法:36只♂SD大鼠随机分为正常对照组(N 组,n=6)、假手术组(Sham组,n=6)和重症急性胰腺炎组(SAP组,n=24)．采用胰管逆行灌注50 g/L牛磺胆酸钠的方法复制大鼠SAP模型．用RT-PCR法检测肺组织中LIF mRNA的表达水平,免疫组织化学方法检测NLIF在肺组织中的表达变化．结果:SAP组3 h后肺组织LIF mRNA的表达量明显高于对照组和假手术组(灰度值:1．018± 0．065 vs 1．451±0．067,1．322±0．072,P<0,05), 并且6,12,24 h持续升高(0．853±0．058,0．635 ±0．064,0．582±0．089)(P<0．01)．同样,SAP组 LIF蛋白表达在3和6 h后明显高于对照组和假手术(127．36±2．76,122．53±2．43 vs 159．46 ±2．78,156．35±3．12,P<0．05),并且12,24 h后也维持在很高的水平(109．37±2．87,102．42± 2．27)．结论:LIF作为促炎症因子参与了SAP肺组织的炎症反应．     

兔局灶脑缺血后脑片[Ca~(2 )]i的变化

目的：研究脑缺血后脑片[Ca2＋]i变化。方法：采用新型Ca2＋荧光指示剂Fura－2双波长法测定兔大脑中动脉阻塞（MCAo）局灶脑缺血后脑片细胞内游离钙（[Ca2＋]i）。结果：脑缺血后脑组织[Ca2＋]i显著升高。结论：[Ca2＋]i在脑缺血损害中起重要作用。     

RNA-DNA杂交法研究乳酸脱氢酶-C基因在睾丸中特异性表达

用同位32~P标记乳酸脱氢酶-C(LDH-C)cDNA作为探针,与小鼠胸腺、脑、胰、心肌、骨骼肌、睾丸、肾、肺、肝的RNA以及人胰、皋丸、肝、骨骼肌、心肌及脑的RNA分别作点溃杂交(dot blot hybridization)及Northern印迹杂交,证实LDH-C基因只在睾丸中特异性表达。     

合理使用高张葡萄糖

临床护理工作中发现，高张葡萄糖的使用，在某些情况下存在一定的危险性，使用不当则加重病情的发展，甚至危及病人的生命。因此要掌握好高张葡萄糖对某些疾病所产生的不良影响，做到预防在先，合理使用。     

胎儿主要肢骨发育时间表──超声骨龄

用Ｂ超检测正常妊娠中的胎儿。选择受精龄为１２至３８整周（ｃｏｍｐｌｅｔｅｄｗｅｅｋ）的胎儿２９７例。测量其主要肢骨（干）长度。并将所测数据进行统计学处理。结果表明胎儿肢骨的生长发育与胎龄有显著的正相关关系。