QS Alex 755 nm激光对黑素细胞p16INK4a表达的影响

目的 了解激光对黑素细胞潜在恶变作用的可能性。方法 QS Alex 755nm激光体外照射HTB66、Sk-mel-24和G361 3种黑素瘤细胞株,照射剂量为0．85～2 J／cm^2,24h后收集细胞。应用流式细胞仪和RT-PCR方法分别测定p16INK4a蛋白和p16INK4a mRNA在激光照射前后和不同剂量照射后的表达水平。结果激光照射后,HTB 66细胞株(p16INK4a蛋白阳性株)的p16INK4a蛋白表达明显增加：而低水平表达的Sk-mel-24和G361细胞株无明显变化。在HTB66细胞株中虽然p16INK4a蛋白的表达上调,但对其功能的测定发现它并不能阻止细胞周期从G0/G1向S／G2M转变。HTB66细胞株的p16INK4a mRNA的表达也增加。结论经研究剂量的激光照射后DNA有损伤。具有黑素瘤家族史或个人史的患者可能有p16INK4a基因的突变或丢失,不提倡用激光治疗此类患者的色素性疾病。     

CTLA-4 is required for the induction of high dose oral tolerance

Mucosal and systemic administrations of high dose antigens induce long- lasting peripheral T cell tolerance. We and others have shown that high dose peripheral T cell tolerance is mediated by anergy or deletion and is preceded by T cell activation. Co-stimulatory molecules B7-1 (CD80)/B7-2 (CD86) and their counter-receptors CD28/CTLA-4 play pivotal roles in T cell activation and immune regulation. In the present study, we examined the roles of the B7 co-stimulation pathway in the generation of high dose peripheral T cell tolerance. We found that blocking B7:CD28/CTLA-4 interaction at the time of tolerance induction partially prevented T cell tolerance, whereas selective blockade of B7:CTLA-4 interaction completely abrogated peripheral T cell tolerance induced by either oral or i.p. antigens. These results suggest that CTLA-4-mediated feedback regulation plays a crucial role in the induction of high dose peripheral T cell tolerance.      

Inhibition of experimental autoimmune encephalomyelitis in Lewis rats by nasal administration of encephalitogenic MBP peptides: synergistic effects of MBP 68-86 and 87-99

Induction of mucosal tolerance by inhalation of soluble peptides with defined T cell epitopes is receiving much attention as a means of specifically down-regulating pathogenic T cell reactivities in autoimmune and allergic disorders. Experimental autoimmune encephalomyelitis (EAE) induced in the Lewis rat by immunization with myelin basic protein (MBP) and Freund's adjuvant (CFA) is mediated by CD4+ T cells specific for the MBP amino acid sequences 68-86 and 87-99. To further define the principles of nasal tolerance induction, we generated three different MBP peptides (MBP 68-86, 87-99 and the non- encephalitogenic peptide 110-128), and evaluated whether their nasal administration on day -11, -10, -9, -8 and -7 prior to immunization with guinea pig MBP (gp-MBP) + CFA confers protection to Lewis rat EAE. Protection was achieved with the encephalitogenic peptides MBP 68-86 and 87-99, MBP 68-86 being more potent, but not with MBP 110-128. Neither MBP 68-86 nor 87-99 at doses used conferred complete protection to gp-MBP-induced EAE. In contrast, nasal administration of a mixture of MBP 68-86 and 87-99 completely blocked gp-MBP-induced EAE even at lower dosage compared to that being used for individual peptides. Rats tolerized with MBP 68-86 + 87-99 nasally showed decreased T cell responses to MBP reflected by lymphocyte proliferation and IFN-gamma ELISPOT assays. Rats tolerized with MBP 68-86 + 87-99 also had abrogated MBP-reactive IFN-gamma and tumor necrosis factor-alpha mRNA expression in lymph node cells compared to rats receiving MBP 110-128 nasally, while similar low levels of MBP-reactive transforming growth factor-beta and IL-4 mRNA expressing cells were observed in the two groups. Nasal administration of MBP 68-86 + 87-99 only slightly inhibited guinea pig spinal cord homogenate-induced EAE, and passive transfer of spleen mononuclear cells from MBP 68-86 + 87-99-tolerized rats did not protect naive rats from EAE. Finally, we show that nasal administration of MBP 68-86 + 87-99 can reverse ongoing EAE induced with gp-MBP, although higher doses are required compared to the dosage needed for prevention. In conclusion, nasal administration of encephalitogenic MBP peptides can induce antigen-specific T cell tolerance and confer incomplete protection to gp-MBP-induced EAE, and MBP 68-86 and 87-99 have synergistic effects. Non-regulatory mechanisms are proposed to be responsible for tolerance development after nasal peptide administration.      

2009年成都市水性疾病及哨点监测结果分析

目的了解成都市介水传染病流行状况和特征,做好水性疾病预警,同时掌握其分布规律和流行趋势,探讨水性疾病的控制策略。方法收集成都市2009年经水传播的肠道传染病及哨点医院症状监测结果,数据用χ^2检验进行统计学分析。结果成都市水性疾病构成主要以其他感染性腹泻和细菌性痢疾为主,两者占总发病数的93.01%,除1～3月发病率较低外,其他月份发病率均较高,但无统计学差异（5～12月发病率P〉0.05）;发病人群以5岁以下散居儿童为主,哨点医院进行症状监测年发生率与成都市水性疾病年发生率相比无显著性差异（P〉0.05）。结论 5岁以下散居儿童为水性疾病的高危人群,水性疾病的控制可以其他感染性腹泻和细菌性痢疾为主进行相关性研究,而选择合适的医院门诊作为监测水性疾病的哨点,是一种切实可行的监测模式。     

大剂量甘露醇治疗癌性颅内高压症1例

1 临床资料患者、女性、38岁、因右小细胞肺癌术后16 mo,间断性头痛10 mo,加重1 wk后于2003-01-01入院.在2002-02因枕部疼痛,行头颅CT示: 脑多发转移癌.行多次头颅局部X-刀、γ-刀加全脑预防性放疗和化疗,疗效达部分缓解.2002-12末头痛症状复发,约1.5 h发作1次,伴短暂意识丧失、喷射状呕吐和四肢抽搐.