Human Y-79 retinoblastoma cells express functional corticotropin-releasing hormone receptors

In human Y-79 retinoblastoma cells corticotropin-releasing hormone (CRH) produces a marked and rapid increase of adenylate cyclase activity. The concentration of the peptide producing half-maximal stimulation is 60 nM. The effect of CRH is significantly antagonized by the specific CRH receptor antagonist alpha-helical CHR 9-41 and is mimicked by sauvagine and urotensin I, two peptides displaying sequence homology with CRH. These results demonstrate the presence of functional CRH receptors in human Y-79 retinoblastoma cells and suggest that this cell line may be a suitable model in which to study the action of CRH on human retinal cell function.     

二氯胺基酚诱发的染色体畸变及染毒时间对畸变率的影响研究

２，４－二氯胺基酚（ＤＣＡＰ）是８３—１除草剂在哺乳动物体内的主要代谢产物。本研究以三种染毒计划观察了ＤＣＡＰ诱发Ｖ７９细胞的染色体畸变。结果表明：ＤＣＡＰ是一种染色体损伤剂，诱发的畸变主要为染色单体断裂和交换；３ｈ染毒和染毒后培养１７ｈ诱发的染色体畸变率最高，２０ｈ染毒观察不到染色体畸变，说明以高浓度短期染毒对高细胞毒性化合物的细胞遗传毒性研究可能是较好的染毒方案。     

The expression of the B-cell marker mb-1 (CD79a) in Hodgkin's disease

Recent evidence indicates that membrane-bound immunoglobulin on B lymphocytes is associated with a molecule which comprises the products of the mb-1 and B29 genes. This molecule is a highly specific marker for B-cells, presumably because of its central functional role in antigen triggering, and has recently been clustered as CD79a at the 5th Leucocyte Workshop. Recently there has been controversy surrounding reports of B-cell antigen expression by Reed–Sternberg and related cells, and we have therefore studied 108 cases of Hodgkin's disease immunohistochemically using a novel antibody which detects mb-1 protein in paraffin sections. The results were compared with those achieved using antibody L26 to detect CD20. The mb-1 protein was present in the neoplastic cells in all 14 cases of lymphocyte predominance Hodgkin's disease studied, and CD20 immunoreactivity was also found in seven of the eight cases of this subtype studied. Of the non-lymphocyte predominance cases, 20% (19/94) expressed mb-1 and 30% (20/67) CD20 in the Reed–Sternberg cells, but the cells positive for either of these two markers usually constituted only a very small proportion of the neoplastic population. However, in occasional cases (one of 94 for mb-1 and five of 67 for CD20), more than 50% of the neoplastic cells expressed one or both B-cell antigens. These results confirm the B-cell origin of the neoplastic cells in lymphocyte predominance Hodgkin's disease, but they also indicate that, contrary to our previous study, mb-1 expression may occasionally be found in what appears, on histological grounds, to be other types of Hodgkin's disease.     

Identification of a family with nonspecific mental retardation (MRX79) with the A140V mutation in the MECP2 gene: Is there a need for routine screening?

Mutations in the methyl-CpG-binding protein 2 (MECP2) cause Rett syndrome, a severe neurodevelopmental disorder occurring predominantly in females. Male patients with Rett syndrome are extremely rare, as the Rett-causing mutations in the MECP2 gene are usually lethal in hemizygous males. However, different mutations in the same gene were reported to cause mental retardation, both in sporadic non-syndromic males as well as in syndromic families with disease manifestation in carrier females. The majority of the reported MECP2 mutations in mentally retarded patients cause amino acid substitutions and, especially in isolated cases, discrimination between a disease-causing mutation and a rare polymorphism is not obvious and the significance of each individual variation should be verified. We mapped a new non-syndromic X-linked family (MRX79) to the chromosomal region Xq27.3-Xq28 and identified an A140V mutation in the MEPC2 gene in all patients with the disease haplotype. In addition to data published by others, this suggests that A140V is a recurrent mutation (and not a polymorphism) found in patients with X-linked mental retardation.     

紫杉醇诱导视网膜母细胞瘤细胞凋亡及对磷酸化Bcl-2的影响

目的：研究紫杉醇(Tax)抑制视网膜母细胞瘤(Rb)细胞生长并诱导其凋亡及磷酸化Bc-2在其中的作用。方法：应用^3H-胸腺嘧啶掺入分析法观察Tax对细胞生长的抑制作用，以DNA片段凝胶电泳分析细胞凋亡，用Western blot分析Tax对磷酸化Bcl-2的影响，用cDNA细胞转染法观察突变型Bcl-2阻断Tax的作用。结果：Tax可明显地抑制Y79细胞的生长，1μmoL／L Tax处理24小时，^3H-胸腺嘧啶掺入率下降达55．43％，Tax可诱导Y79细胞凋亡。在此过程中，Bcl-2被磷酸化。当Y79细胞被转染突变型Bcl-2后，Tax对Y79细胞的作用被阻断。结论：Tax可抑制Y79细胞生长并诱导其凋亡，磷酸化Bcl-2参与其过程。     

bcl-xs基因对卵巢癌的作用及其凋亡机制的研究

目的 :研究全反式维甲酸 (ATRA)抑制视网膜母细胞瘤 (Rb)细胞生长的作用及信号转导机制。方法 :应用3 H 胸腺嘧啶掺入分析法观察ATRA对细胞生长的抑制作用 ,用流式细胞仪分析ATRA对Y79细胞周期的影响 ,用Westernblot分析c jun氨基末端激酶 (JNK)的磷酸化。 结果 :ATRA可明显地抑制Y79细胞的生长 ,10 -6mol·L-1ATRA处理 36h时 ,3 H 胸腺嘧啶掺入率下降达 4 0 % ,此条件下 ,Y79细胞被阻滞于G0 /G1期 ,并出现Sub G1峰 ;此生长抑制过程可被JNK的阻断剂Curcumin阻断 ;在此过程中 ,JNK被激活 ,磷酸化。结论 :ATRA可抑制Y79细胞生长 ,其过程是由磷酸化的JNK介导。提示 ,ATRA可能是一种潜在的抗视网膜母细胞瘤治疗药物     

柴胡皂甙d通过磷酸化p38诱导视网膜母细胞瘤细胞凋亡

目的研究柴胡皂甙d(SSd)抑制视网膜母细胞瘤(Rb)细胞生长并诱导其凋亡的作用及信号转导机制。方法应用~3H-胸腺嘧啶掺入分析法观察SSd对细胞生长的抑制作用,用流式细胞仪分析SSd对Y79细胞周期的影响,以DNA片段凝胶电泳分析细胞凋亡,用Westem blot分析p38的磷酸化。结果SSd可明显地抑制Y79细胞的生长,10μg/ml SSd处理9h时,~3H-胸腺嘧啶掺入率下降达55．15%,此条件下,SSd可诱导Y79细胞凋亡。在此过程中,p38被激活,即磷酸化。结论SSd可抑制Y79细胞生长并诱导其凋亡,其过程是由磷酸化的p38介导。