Analysis of antigenic determinants on human monocytes and macrophages

Mo1, 2, 3, and 4, and Plt-1 are a series of five distinct antigens detected on the surface of human peripheral blood monocytes by mouse monoclonal antibodies. Mo2 and 3 are restricted to the monocyte- macrophage series, while Mo1, as previously reported, is also expressed by human granulocytes and null cells. Mo3, as distinguished from Mo1 and Mo2, is weakly expressed by virgin peripheral blood monocytes but becomes well expressed if monocytes are cultured overnight at 37 degrees C. Mo4 is coexpressed by monocytes and platelets, while Plt-1 appears to be a platelet-specific antigen whose detection on monocytes reflects adherence of platelets to monocyte membranes. That Mo2-4 are true monocyte antigens is demonstrated by their resynthesis following protease treatment of monocytes (Mol expression is resistant to proteolytic digestion). During myeloid-monocyte differentiation, the Mo antigens are infrequently expressed by immature myeloid cells but are found at higher frequency on leukemic monocytic forms. Macrophages from cultured peripheral blood monocytes and HL-60 cells exposed to lymphokines or phorbol diester express Mo1-4, but noncirculating peritoneal macrophages lack Mo3. The Mo antigens are differentiation markers whose expression reflects membrane heterogeneity during myeloid- monocyte-macrophage maturation.     

Isolation of myeloid progenitor cells from peripheral blood of chronic myelogenous leukemia patients

Myeloid progenitor cells (colony- and cluster-forming cells in semisolid medium, CFU-GM) were purified from the peripheral blood of chronic myelogenous leukemia (CML) patients. Lymphocytes, monocytes, and most immature myeloid cells were simultaneously depleted with specific monoclonal antibodies using an erythrocyte rosette technique for cell separation. Cells expressing Ia-like antigen were then selected from the residual cell population. Day 7 CFU-GM were enriched 44--116-fold in the IA+ cell fraction, when compared to the unseparated cells, and up to 47% of the cells could form a myeloid colony or cluster in culture. This cell fraction contained up to 92% undifferentiated blasts, with the remainder mostly promyelocytes. The enriched CFU-GM cells were dependent on an exogenous supply of colony- stimulating factor for growth, and colony formation was linear with cell concentration over a large range (10(4)-10(1) cells/ml). This technique of rosette depletion and enrichment with specific monoclonal antibodies provides a unique method for purifying a homogenous population of myeloid precursor cells with defined surface antigen characteristics.     

Occult hepatitis B virus infection: diagnosis, implications and management?

Abstract   Occult hepatitis B virus (HBV) infection is generally defined as the detection of HBV-DNA in the serum or liver tissue of patients who test negative for hepatitis B surface antigen. In most cases, occult HBV infection is related to low level HBV infection with subdetectable levels of HBsAg and not infection with HBV variants that cannot express S proteins or produce S proteins with aberrant epitopes that are not detected by conventional serological assays. Prevalence of occult HBV infection is related to the overall prevalence of HBV infection in that country, being more common in persons with prior exposure to HBV. Occult HBV infection has been found in a substantial proportion of patients with cirrhosis and hepatocellular carcinoma but other causes of liver disease are frequently present. Future studies should focus on delineating the pathogenic role of occult HBV infection and the basis for failure to detect circulating hepatitis B surface antigen.     

A carboxyl terminal truncation mutant of CD36 is secreted and binds thrombospondin: evidence for a single transmembrane domain

CD36 has been implicated in several intracellular signalling events, including platelet and monocyte activation, and receptor-mediated internalization of bound ligands such as oxidized low-density lipoprotein and apoptotic neutrophils. These processes are presumably mediated by the intracytoplasmic domain(s) of the molecule. By analysis of hydrophobicity plots and by analogy to rat LIMPII, which has a 60% homology to CD36, a two-transmembrane domain model has been proposed. To characterize the structure-function relationships of CD36 involved in transducing the signal, we have defined the number of transmembrane and intracellular domains experimentally using a mutagenesis approach. A truncated CD36 cDNA was constructed that encodes a protein that terminates just proximal to the putative C-terminal transmembrane domain. This mutant was cloned into eukaryotic expression plasmid vectors to generate short-term and stable transfected cells. Our results indicate that the truncated mutant is secreted by the transfectants into the postculture medium, indicating that there is only one transmembrane domain in CD36, which is present at the C- terminal end. The soluble secreted protein from all of these cells is functional as indicated by its binding to thrombospondin.     

2009慢性乙型肝炎指南更新

美国肝病学会（AASLD）慢性乙型肝炎（CHB）2009年更新指南日前已在www．assld．org刊登。这是更新的第4个版本,上一版于2007年公布。     

A novel protein tyrosine phosphatase gene is mutated in progressive myoclonus epilepsy of the Lafora type (EPM2)

Progressive myoclonus epilepsy of the Lafora type or Lafora disease (EPM2; McKusick no. 254780) is an autosomal recessive disorder characterized by epilepsy, myoclonus, progressive neurological deterioration and glycogen-like intracellular inclusion bodies (Lafora bodies). A gene for EPM2 previously has been mapped to chromosome 6q23- q25 using linkage analysis and homozygosity mapping. Here we report the positional cloning of the 6q EPM2 gene. A microdeletion within the EPM2 critical region, present inhomozygosis in an affected individual, was found to disrupt a novel gene encoding a putative protein tyrosine phosphatase (PTPase). The gene, denoted EPM2, presents alternative splicing in the 5' and 3' end regions. Mutational analysis revealed that EPM2 patients are homozygous for loss-of-function mutations in EPM2. These findings suggest that Lafora disease results from the mutational inactivation of a PTPase activity that may be important in the control of glycogen metabolism.      

青少年型前葡萄膜炎42例

临床资料青少年前葡萄膜炎住院患者42(男23,女19)例,年龄7～16岁,双眼30例,单眼12例,就诊时间3 d～3 mo,急性发病29例,慢性迁徙性13例. 初诊15例,复发27例. 42例均有不同程度视力下降,光感～指数21例,0.04～0.1者15例,≥0.2者6例。     

In-vitro fertilization and embryo transfer in women aged 40 years and over

The decline of fertility with age and its possible causes arediscussed; in particular the effect of ageing of oocytes andthe uterus, and the effect of the ageing processes on the resultsof in-vitro fertilization (IVF) and embryo transfer in womenaged <40 years. The role of prestimulation testing in olderwomen is considered together with the importance of screeningand counselling these patients about the likelihood of achievinga live birth. The potential problems that they may face shouldthey become pregnant are reviewed, together with the role ofoocyte donation as an alternative treatment for patients withreduced ovarian reserve. Possible ways of improving the chancesof achieving a live birth in older women using their own oocytesare reviewed, including the use of more effective stimulationprotocols, assisted embryo hatching and co-culture and highorder embryo transfer. The outcome of pregnancies in older womenand some of the ethical problems relating to their treatmentare also discussed.