星形胶质细胞瘤伽玛刀治疗的疗效与影响因素

目的分析星形胶质细胞瘤伽玛刀(γ-刀)治疗的疗效与影响因素.方法回顾性分析48例星形胶质细胞瘤病人的γ-刀治疗结果.以性别、有无普通放疗经过、有无化疗经过、边缘剂量、病灶的平均直径、病变的病理等级、影像学上有无相对较清楚的边界为治疗结果影响因素,判定标准以病灶缩小为有效,采用logistic回归模型,确定多因素条件下治疗结果的影响因素.结果有效32例(66.7%),logistic回归模型分析表明:病理等级和病灶平均直径为与肿瘤控制有关的影响因素.结论γ-刀对星形胶质细胞瘤的治疗有一定的意义.     

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。     

儿童髓母细胞瘤显微手术治疗及术后并发症探讨

目的探讨儿童髓母细胞瘤显微手术及术后并发症问题。方法回顾性分析经小脑蚓部切开联合四脑室正中孔入路显微手术切除儿童髓母细胞瘤及术后并发症53例。全部经病理证实。结果全部病例术前均行MRI检查,46例同时行CT检查。手术全切除47例(88.7%)、次全切除6例(11.3%)。术后51例高颅压症状消失,临床体征改善,2例死亡。术后发生咸默症5例,其中合并下颏关节脱位1例。术后昏迷2例,呼吸机辅助人工呼吸2周1例,遗留一侧肢体轻瘫2例。中枢性面瘫2例。肿瘤位于小脑蚓部12例,四脑室内18例。小脑蚓部和四脑室内者23例。肿瘤血供来源于小脑后下动脉37例。全部病例均打通中脑导水管。术后37例患者随访6个月至5年3个月。35例接受放疗。其中30例未见复发和转移。4例原位复发,2例脊髓播种性转移。结论儿童髓母细胞瘤由于其临床特点诊断多无困难,但个性化深入了解肿瘤病理解剖及其与周围组织比邻有利于最大限度切除肿瘤。采用显微手术全切除肿瘤组织、解除导水管梗阻、妥善保护小脑后下动脉及其分支、避免伤及脑干及四脑室底是手术操作的关键。病程进展迅速,肿瘤巨大者术后生存质量及生存期更差,早期就诊尤为重要。     

成年大鼠神经元和星形胶质细胞细胞周期蛋白依赖性激酶抑制因子表达的差异研究

目的比较研究成年大鼠细胞周期蛋白依赖性激酶抑制因子在神经元和星形胶质细胞的表达差异。方法应用免疫荧光和激光扫描共聚焦显微镜观察成年大鼠生理状态下大脑皮层或海马CA1、CA3、DG区神经元和星形胶质细胞细胞周期蛋白依赖性激酶抑制因子(CDKI)p15Ink4b、p21cipl的表达。结果成年大鼠海马区和大脑皮层的神经元有p15Ink4b和p21cipl的表达,细胞核和细胞浆均有表达,且以胞核为主;星形胶质细胞也有上述细胞周期调控蛋白的表达,便细胞数目较少,并且表达这些指标的星形胶质细胞多聚集在海马区。结论成年大鼠大脑皮层和海马区的神经元和星形胶质细胞均表达p15Ink4b和p21cipl,而其在神经元的表达较星形胶质细胞更为普遍。     

丁酸钠促脑胶质瘤细胞分化作用研究进展

丁酸钠(NaB)是一种短链脂肪酸诱导分化剂,对脑胶质细胞瘤可通过抑制其组蛋白脱乙酰基转移酶,致细胞的基因表达、酶类和信号传导通路发生变化来遏制恶性瘤细胞的增殖,促进分化。同时,与化学疗法或温热疗法联合应用时,可产生协同效应。但由于其血浆中的半衰期较短,使其在临床上的应用受到了一定的影响。丁酸钠将会成为一种有潜力的治疗脑胶质细胞瘤药物。     

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.     

成人肾外型肾母细胞瘤1例报告

患者,女,27岁.因"左腹部阵发性疼痛7d"入院.查体:神志清,精神不振,营养发育正常,皮肤粘膜无黄染,浅表淋巴结无肿大.心肺无异常.腹平软,肝脾未及,左上腹可扪及一约7cm×5cm大小肿块,质硬,活动度差.     

儿童肾母细胞瘤的CT诊断

目的：探讨CT对儿童肾母细胞瘤的诊断价值。方法：回顾分析22例经手术病理证实为肾母细胞瘤的CT表现特点。结果：21例肾母细胞瘤位于单侧肾脏，位于上极14例，下极7例，表现为强化不明显的实质性肿块，瘤内常见坏死，出血与囊性病变，极少钙化，典型表现为残存肾实质呈“新月形”强化。结论：CT检查可清晰显示原发肿瘤及其侵犯,主时发现腹膜后淋巴结转移，对肾原发肿瘤与腹膜后肾外肿瘤的鉴别诊断有重要价值。     

巨大脊髓圆锥血管母细胞瘤一例并文献复习

目的 探讨脊髓血管母细胞瘤的诊断、治疗及预后.方法 对1例圆锥部位巨大血管母细胞瘤的诊治进行报告,并结合文献对脊髓血管母细胞瘤进行回顾分析.结果 脊髓血管母细胞瘤可以是单独发生,也可以是Von Hippel-Lindau病的系列疾病之一,临床发病率低,最常见症状是疼痛,MRI表现为瘤结节明显强化,周围可见异常血管流空影,多伴有空洞,DSA可显示染色的瘤结节、供血动脉及引流静脉,显微神经外科手术可完整全切.结论 显微神经外科手术是治疗脊髓血管母细胞瘤的最佳方法.对于有症状患者,应尽早手术,无症状患者可以定期复查MRI,如表现为肿物生长,可视为手术指证,患者预后较好.     

工频磁场对星形胶质细胞间隙连接通讯功能的影响

目的　探讨工频磁场 (PFMF)是否有促癌或协同促癌作用。方法　利用荧光光漂白后再恢复法观察漂白细胞荧光强度的恢复以判断经间隙连接的细胞间通讯 ,以相对荧光强度恢复速率(CFIRR)作为对细胞间隙连接通讯 (GJIC)作用的评价指标 ,研究不同磁场强度单独作用或协同佛波酯(TPA)对星形胶质细胞GJIC功能的影响。结果　 3ng/mlTPA作用 1h时CFIRR的中位数 (Md)值为4 .53 % /min ,空白对照组为 9.74% /min ,两组的差异有显著性 (H =1 2 .0 84,P <0 .0 0 5)。 0 .8或 1 .6mT磁场作用 2 4h时CFIRR的Md 分别 8.2 5、6 .68% /min ,与空白对照组比较 ,差异无显著性 (H =32 .61 7,P >0 .0 5)。 0 .8或 1 .6mT磁场作用 2 3h ,再与TPA共同作用 1h时CFIRR的Md 分别为 3 .32、2 .85% /min ,与TPA组比较 ,差异无显著性 (H =2 .589,P >0 .0 5)。结论　 0～ 1 .6mT的 50Hz磁场单独作用不能抑制星形胶质细胞GJIC功能 ;协同TPA ,不能增强TPA对星形胶质细胞GJIC的抑制作用 ;但是磁场对星形胶质细胞GJIC的抑制作用随着磁场强度增强呈递增趋势