Induced expression of c-fms in normal hematopoietic cells shows evidence for both conservation and lineage restriction of signal transduction in response to macrophage colony-stimulating factor

Retrovirus-mediated gene transfer was used to obtain expression of the macrophage colony-stimulating factor (MCSF) receptor, c-fms, on hematopoietic lineages that normally do not express this receptor. Cultures of murine fetal liver cells infected with the c-fms retrovirus developed erythroid colonies in cultures stimulated with M-CSF. However, these colonies were fewer and less hemoglobinized than colonies in parallel cultures stimulated by erythropoietin. Culture of isolated clones demonstrated a direct action of M-CSF on erythroid clones. Culture of c-fms retrovirus-infected adult murine bone marrow cells showed megakaryocyte and novel macrophage-megakaryocyte clones when stimulated by M-CSF. Culture of isolated clones again confirmed a direct action of M-CSF on megakaryocyte clones. In contrast, M-CSF stimulation of c-fms-infected granulocytes and granulocyte progenitor cells did not elicit proliferation, enhanced survival, or functional stimulation of granulocytes. These findings provide evidence for both conservation and lineage restriction of signal transduction in normal hematopoietic cells.     

Platelets express a membrane protein complex immunologically related to the fibroblast fibronectin receptor and distinct from GPIIb/IIIa

We have previously identified and characterized a membrane glycoprotein complex (GP150/135) that functions as fibronectin receptor (FN-R) in fibroblast adhesion. Here we report that an immunologically related protein complex is expressed at the surface of human platelets. Antibodies monospecific for the smaller subunit (GP135) of the fibroblast FN-R in fact specifically stained the platelet surface, as determined by FACS analysis, and reacted with a component of molecular weight (mol wt) 138,000 as shown in western blots of platelet membranes. Moreover, the same antibodies precipitated the 138,000 component together with a 160,000 protein, suggesting that the two molecules are associated in a supramolecular complex. A comparative analysis indicated that this protein complex is distinct from the GPIIb/IIIa complex, known to function as a receptor of wide specificity for fibrinogen, fibronectin, and von Willebrand factor. Differential extraction experiments revealed that the platelet 138,000 component is an integral membrane protein.     

缺血性脑卒中的A-S-C-O(表型)分类

背景和目的:国际5国脑血管病专家提出一种新的腩卒中亚型分类法,旨在介绍完整的"脑卒中表型"分类的新观念,该分类是包括脑卒中的病因和存在的所有病因相关的疾病,并将病因疾病按严重程度分成3级.     

高血压治疗的现代途径(MATH)

标　　题　硝苯地平胃肠治疗系统对老年患者的抗高血压治疗作用作　　者　ＢｒａｖｏＥＬ,ＫｒａｋｏｆｆＬＲ,ＴｕｃｋＭＬ,ｅｔａｌ.　　参考文献　ＡｍＪＨｙｐｅｒｔｅｎｓ,1990,3:326Ｓ目　　的　评估硝苯地平的新剂型胃肠治疗系统ＧＩＴＳ治疗高血压的疗效和安全性。研究疾病　高血压病。设　　计　多中心、开放性临床研究。病人资料　1155例ＤＢＰ在95～110ｍｍＨｇ的高血压患者。随　　访　至目标血压达到后12周。治疗方案　硝苯地平控释片30ｍｇ/ｄ,在6周内剂量逐渐增至最大量180ｍｇ/ｄ,每次增量为30ｍｇ,目标血压为舒张压降至90…     

Spectrum and origin of phenylketonuria mutations in Spain

In order to characterize the molecular heterogeneity of phenylalanine hydroxylase deficiencies in the Spanish population, 37 PKU patients were initially screened for 16 known European mutations. For the remaining unidentified alleles, we used a combined strategy based on single strand conformation polymorphism analysis and DNA sequencing. Overall, a total of 15 different mutations were found in our sample, which account for 62% of the total mutant alleles. We also investigated the association between the mutations, haplotypes and variable number of tandem repeats described on the phenylalanine hydroxylase gene. In addition, we analyzed the geographical distribution in Spain of the two most prevalent mutations in our population: IVS10 and I65T.     

Evidence for B cell participation in the in vitro and in vivo maintenance of in vivo staphylococcal enterotoxin B-induced T cell anergy

The mechanisms involved in the maintenance of staphylococcal enterotoxin B (SEB)-induced T cell anergy are poorly understood. Here, we demonstrate that CD4+ T cell anergy induced by SEB treatment is under partial B cell control. This effect is not mediated by anti-SEB antibodies or any in vitro B cell-produced suppresser factor. At day 13 after SEB immunization, T cells from B cell-deficient mice proliferate upon in vitro stimulation with SEB. These results suggest that SEB- induced T cell anergy is reversible and that B cells have an important function in anergy maintenance in CD4+ T cells, both in vivo and in vitro.      

A new spontaneous mouse mutation of Hoxd13 with a polyalanine expansion and phenotype similar to human synpolydactyly

Human synpolydactyly (SPD) is an inherited congenital limb malformation caused by mutations in the HOXD13 gene. Heterozygotes are typically characterized by 3/4 finger and 4/5 toe syndactyly with associated duplicated digits; hands and feet of homozygotes are very small because of a shortening of the phalanges, metacarpal and metatarsal bones. Here we describe the phenotype and molecular basis of a spontaneous mutation of Hoxd13 in mice that provides a phenotypically and molecularly accurate model for human SPD. The new mutation, named synpolydactyly homolog (spdh), is a 21 bp in-frame duplication within a polyalanine- encoding region at the 5'-end of the Hoxd13 coding sequence. The duplication expands the stretch of alanines from 15 to 22; the same type of expansion occurs in human SPD mutations. spdh/spdh homozygotes exhibit severe malformations of all four feet, including polydactyly, syndactyly and brachydactylia. The phenotype of spdh is much more severe than that exhibited by mice with a genetically engineered, presumably null, disruption of Hoxd13. Thus spdh probably acts in a dominant-negative manner and will be valuable for examining interactions with other Hox genes and their protein products during limb development. Homozygous mice of both sexes also lack preputial glands and males do not breed; therefore, spdh/spdh mice may also be valuable in studies of reproductive physiology and behavior.      

维生素C及E联合作用对体外大鼠胚胎中脑神经细胞分化和增殖的影响

目的:观察维生素C,维生素E和维生素C 维生素E联合后对胚胎中脑神经细胞生长发育的影响。方法:实验于2006-03/04在江苏大学医学院研究中心细胞培养室完成。采用16d大鼠胚胎中脑神经细胞体外培养方法,观察不同剂量的维生素C(5,10,25,50μmol/L),维生素E(10,25,50,100μmol/L)和维生素C、维生素E联合作用(维生素C25μmol/L 维生素E50μmol/L,维生素C50μmol/L 维生素E100μmol/L),培养10d后收集细胞,并利用图像分析细胞形态的变化、蛋白质、丙二醛含量及超氧化物歧化酶活性指标。结果:①维生素C、维生素E和维生素C 维生素E联合能促进体外培养中脑神经细胞突起生长,集落数增多。②与正常对照组比较,维生素C10,25μmol/L组、维生素E10,25,50μmol/L组、维生素C25μmol/L 维生素E50μmol/L组神经细胞总蛋白相对含量明显增加。③与正常对照组比较,维生素C10,25μmol/L组、维生素E25,50μmol/L组、维生素C25μmol/L 维生素E50μmol/L组神经细胞超氧化物酶活性增加,丙二醛含量降低。④维生素C50μmol/L组、维生素E100μmol/L组和维生素C50μmol/L 维生素E100μmol/L组超氧化物酶活性低于正常对照组,丙二醛含量高于正常对照组。结论:维生素C、维生素E和维生素C 维生素E联合剂量在一定范围内能够明显提高中脑神经细胞的抗氧化能力,同时能促进胚胎中脑神经细胞分化和增殖作用。