Neurofilament M and calbindin D28k are present in mutually exclusive subpopulations of enteric neurons in the rat submucous plexus

Immunocytochemical methods have been used to examine the localisation of 3 neurofilament proteins and the calcium binding protein, calbindin D_28k, in whole mount preparations of the submucous plexus in the Wistar rat. Neurofilament-M (160 kDA protein) was present in 40% of the submucosal neurons, staining fine filaments in the soma and the axonal processes. Calbindin D_28k was present in 40% of the submucosal neurons staining both the soma and nerves within the plexus. The neurofilament proteins and calbindin D_28k were never observed within the same neurons. Neurofilament-M was co-localised with substance P and calcitonin gene-related peptide but not somatostatin or the other neuropeptides investigated. Calbindib D_28k was co-localised with vasoactive intestinal polypeptide and neuropeptide Y. Galanin- and somatostatin-immunoreactive neurons did not contain either the neurofilament proteins or calbindin D_28k. The results demonstrate the presence of subsets of submucosal neurons that can be distinguished by the presence of neurofilament-M or calbinsin D_28k.     

自制32P敷贴器治疗瘢痕疙瘩

目的：观察自制32P敷贴器局部敷贴治疗不同类型瘢痕疙瘩的临床疗效。 方法：105例瘢痕疙瘩患者中，39例病变厚度≤ 0.3 cm的行单纯敷贴治疗，病变厚度> 0.3 cm的66例随机分为2组，单纯敷贴组36例，手术+敷贴组30例。单纯敷贴根据病变表面积大小及形状剪取敷贴片，根据剂量率和衰变校正计算每天敷贴时间，直接贴于病变表面，每天4.0~5.0 Gy/(部位•次)，连续4 d为一疗程，每疗程间隔4周，总治疗4~6个疗程。幼儿单次剂量控制在每天4 Gy/(部位•次)以下。手术+敷贴组患者手术切除瘢痕疙瘩，待手术伤口无渗出后根据伤口形状剪取敷贴片对准伤口敷贴，剂量及疗程同单纯敷贴组。 结果：单纯敷贴治疗对病变厚度≤0.3 cm的39例瘢痕疙瘩治愈32例(82%)，总有效率98%；对病变厚度> 0.3 cm的瘢痕疙瘩单纯敷贴和手术+敷贴两组治疗总有效率分别为56%和93% ，两组差异有显著性意义(P < 0.01)，其中病程< 9个月的患者治疗有效率分别为25%和75%，病程较长患者治疗有效率分别为13%和77%。治疗过程中有26例在敷帖过程中出现局部皮肤烧灼和刺痛感，均以炉甘石洗剂局部外用处理后缓解；5例出现Ⅰ度放射性皮炎，2例出现Ⅱ度放射性皮炎，以百多邦软膏局部外用后缓解，无出现Ⅲ度以上放射性皮炎病例。治愈患者局部皮肤均有不同程度的色素沉着或皮肤颜色改变。 结论：32P敷贴治疗瘢痕疙瘩治疗安全有效，对病程较短或病变厚度小于0.3 cm的患者可单纯敷贴治疗，病程较长或病变厚度大于0.3 cm患者建议先手术后再敷贴治疗。     

葛根素对血管性痴呆患者认知功能和事件相关电位P300的影响

目的观察葛根素对血管性痴呆（VaD）患者认知功能和听觉事件相关电位P300的影响。方法将70例VaD患者随机分成两组各35例，葛根素治疗组和对照组。应用简易精神状态检查量表（MMSE）评定两组患者治疗前后认知功能状况，并进行治疗前后P300检查。同时记录药物不良反应。结果两组各35例进入结果分析。治疗前两组MMSE评分、P300的潜伏期及波幅差异无显著性（均P〉0．05）。治疗14d、30d时，两组MMSE评分显著提高（均P〈0．01），P300潜伏期均有缩短，波幅均有提高（葛根素组P〈0．01，对照组P〈0．05）；治疗后14d时认知功能改善葛根素组明显优于对照组（总有效率分别为91．4％，71．4％）（P〈0．05）。两组治疗期间无严重不良反应。结论葛根素能够改善VaD患者的认知功能，这可能与葛根素的扩血管、脑保护作用有关。     

The participation of adenosine receptors in the adenosine 5''-triphosphate-induced relaxation in the isolated rabbit corpus cavernosum penis

AIM: To investigate the participation of adenosine receptors in the adenosine 5'-triphosphate (ATP)-induced relaxation in the corpus cavernosum penis (CCP) of rabbits. METHODS: The ATP-induced relaxation was assessed on the noradrenaline precontracted CCP of rabbits in the presence and absence of 8-(3-chlorostyryl)caffeine (CSC); an adenosine A(2A) receptor antagonist; alloxazine and MRS1754; adenosine A(2B) receptor antagonists; and ARL67156, an inhibitor of ecto-nucleoside triphosphate diphosphohydrolases. RESULTS: Adenosine and ATP relaxed the noradrenaline precontracted CCP of rabbits in a concentration-dependent manner. The adenosine- and ATP-induced relaxations were suppressed by alloxazine and MRS1754, but not by 8-(3-chlorostyryl)caffeine. ARL67156 potentiated the ATP-induced relaxation but not the adenosine-induced one. MRS1754 suppressed the ATP-induced relaxation potentiated by ARL67156. CONCLUSIONS: The above results suggest that, in the CCP of rabbits, the adenosine receptor mediating adenosine-induced relaxation is of the A(2B) receptor and the ATP directly causes relaxation through the A(2B) receptor on the CCP.     

周围神经65KD蛋白单克隆抗体的制备

神经化学诱向生长的研究是神经科学中的一个重要方向。本文以自然系统聚丙酰胺凝胶电泳,分离提取坐骨神经损伤后的远侧端中具有诱神经生长作用的65KD蛋白。以该蛋白作为抗原免疫BALB/C小鼠,通过杂交瘤技术获得一株(VI5E)稳定分泌单克隆抗体的杂交瘤细胞株。免疫印迹法表明,该单克隆抗体特异性地与65KD区带结合。免疫组化法显示,在损伤后的坐骨神经远侧端组织中的雪旺氏细胞呈阳性反应。单克隆抗体的制备为进一步阐明该蛋白的生物学特性奠定了基础。     

Sources of P300 attenuation after head injury: Single-trial amplitude, latency jitter, and EEG power

Single trial amplitude, latency jitter, and electroencephalographic (EEG) power were examined as sources of the group difference in averaged P300 amplitude among 15 traumatically brain injured and 20 control individuals in an auditory oddball paradigm. Mean amplitude of the individual trials was highly correlated with the amplitude of the averaged P300, with little additional unique variance attributable to latency jitter or EEG power. The group difference in P300 amplitude was also explained by the mean amplitude of the single trials. These results support the robustness of the event-related potential averaging technique within the paradigm used.     

Immunohistochemical Study of Colorectal Polyps with Antibodies against CEA,CA19-9, CA125, CA15-3 (DF3), PCNA and p53

Abstract: We analyzed the expression of CEA, CA19-9, CA125, CA15-3 (DF3), PCNA and p53 immunohistochemically in 14 tissue specimens of mucosal cancers in adenoma, seven tubulovillous adenoma specimens, and 16 tubular adenoma specimens. The rates of positive staining for mucosal cancer in adenoma, tubulovillous adenoma and tubular adenoma specimens, respectively, were: for CEA: 100%, 85.7% and 75%; for CA19-9: 71.4%, 71.4% and 56.2%; for CA125:0%, 0% and 0%;for CA15-3 (DF3): 64.3 %, 0% and 0 %; for PCNA: 100%, 88.9% and 56.2%; and for p53: 35.7%, 0% and 0% . The results suggest that the expressions of CEA, CA19-9, CA15-3 (DF3), PCNA and p53 are related to colorectal tumorigenesis. None of the specimens studied showed staining for CA125, suggesting that CA125 is not involved in the early stages of colorectal carcinogenesis. There was no significant difference in the rates of positive staining for CEA and CA19-9 among mucosal cancer in adenoma, tubular adenoma and tubulovillous adenoma specimens. However, the rates of positive staining for PCNA and p53 were significantly higher in mucosal cancer in adenoma specimens than for tubular adenoma specimens (p<0.05), and the rate of CA15-3 (DF3) positive staining was significantly higher for mucosal cancer in adenoma than for tubulovillous adenoma (p<0.01) and tubular adenoma (p< 0.001) specimens. Therefore, the CA15-3 (DF3) antigen is an immunohistochemical marker for colorectal carcinomas. The present results suggest that CA15-3 (DF3), PCNA and p53 play important roles in the genesis of colorectal adenomas.