Proteasome Inhibitors Sensitize Hepatocellular Carcinoma Cells to TRAIL

A poptosis, an evolutionarily conserved form of cell suicide, oc- curs in two physiological stages: commitment and execution.[1] It has been found that several Bcl-2 family proteins are located in the outer mitochondrial membrane, where they control relea…     

十二指肠溃疡患儿胃窦组织胃泌素与生长抑素、增殖与凋亡免疫组化研究

目的:分析十二指肠溃疡(DU)患儿胃窦组织中胃泌素(GAS)、生长抑素(SS)、增殖细胞核抗原(PCNA)、凋亡Fas基因配体(Fas-L)的免疫组化表达,探讨它们在小儿DU发病机制中的意义。方法:收集我院44例DU患儿胃镜活检胃窦黏膜标本。设3组实验对象:A组,DU,HP+;B组,DU,HP-;C组,正常对照组,正常胃窦黏膜组织未见明显病变,HP-。应用免疫组化EnVision法,对每例组织分别进行GAS、SS、PCNA、Fas-L染色,数阳性细胞数,比较各组差异。结果:GAS、SS的表达A组、B组均高于C组,PCNA、Fas-L的表达A组高于C组,但统计学上比较差异无显著性。结论:GAS、SS表达增高在小儿DU发病机制中起一定作用;HP感染可能促进胃窦黏膜上皮细胞增殖和凋亡。     

输卵管妊娠保守治疗适应证选择

目的　探讨彩色多普勒超声 (CDFI)筛选合适药物保守治疗异位妊娠的临床价值。方法　 5 0例生命体征平稳的异位妊娠患者 ,在行CDFI检查后接受甲氨蝶呤 (MTX) 5 0mg/m2 单次肌肉注射配合米非司酮 2 5mg ,Bid 3d口服 ,随访直至临床结局。分析成功与失败病例CDFI的特点和绒毛膜促性腺激素 (HCG)的水平 ,并制作CDFI评分。结果　CDFI能直接反映胚胎生命力 ,不同CD FI图像和血清HCG水平的病例 ,保守治疗成功率有很大差异。结论　CDFI评分可应用于适合保守治疗异位妊娠病例的筛选。对评分 >10者 ,因失败率高 ,不推荐药物保守治疗     

NO-1886对高糖高脂饲料喂养新西兰兔糖代谢的影响

合成药NO-1886是脂蛋白脂肪酶(LPL)的激动剂，能降低血浆甘油三酯(TG)并升高高密度脂蛋白胆固醇(HDL-c)水平。我们曾发现NO-1886还具有降低血糖的作用。本研究主要观察NO-1886对糖尿病兔胰岛素抵抗及β-细胞功能方面的影响。用高糖高脂饲料诱导，使新西兰兔血浆葡萄糖升高，发生胰岛素抵抗。在高糖高脂饲料中添加1％NO-1886进行治疗。结果：发现NO-1886可抑制血清葡萄糖升高，经糖耐量和胰岛素敏感性试验检测，NO-1886可保护胰岛素的急性相分泌，增强胰岛素对葡萄糖的清除能力。研究结果提示NO-1886具有改善胰岛素抵抗、降低血糖的作用。     

脊髓血管母细胞瘤的显微手术治疗(附11例分析)

目的探讨脊髓血管母细胞瘤的临床特点和外科治疗技巧。方法回顾性分析11例脊髓髓内血管母细胞瘤的诊治经验。本组临床表现主要为感觉和运动障碍、肌肉萎缩及大小便失禁。均经后正中入路切除肿瘤,术中及术后常规使用甲基强的松龙。结果肿瘤均获全切除。术后短时间内症状改善8例,无变化2例,加重1例,无手术死亡。结论本病根据术前典型的影像资料均可确诊。术中尽可能避免活检或分块切除肿瘤,以免引起难以控制的出血和盲目止血引起的脊髓损害。大剂量甲基强的松龙可减轻脊髓水肿。     

全雄激素阻断前后前列腺癌细胞中Bcl-2和Bcl-XL基因表达改变

全雄激素阻断是前列腺癌(PCa)治疗的重要手段。虽然已发现一些蛋白分子涉及雄激素的调节[1] ,但其分子机理尚不清楚。我们采用分子生物学方法检测人PCa全雄激素阻断前后Bcl 2和Bcl XL 蛋白的表达,探讨PCa发生发展的分子机理。材料与方法　4 2例局限性PCa患者。全雄激素阻断治疗采用抑那通或诺雷德皮下注射加口服Flutamide 3个月,然后患者接受PCa根治术。PCa标本分别经穿刺活检和根治术标本取得,10 %福尔马林固定后石蜡包埋,病理证实。Bcl 2和Bcl XL 蛋白单克隆抗体(1/ 2 0 0 )和试剂盒购于SantaCruzInc。显微镜下,细胞着色棕黄…     

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.