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Biomedical subjects

R Zeff

Publications and source records attributed to R Zeff.

8 recordsLinked to original sources
PubMed2000

Murine pro-B cells require IL-7 and its receptor complex to up-regulate IL-7R alpha, terminal deoxynucleotidyltransferase, and c mu expression.

Phenotypic analysis of bone marrow cells from IL-7 knockout (KO) mice revealed that B cell development is blocked precisely at the transition between pro-B cells and pre-B cells. In contrast, the generation of pre-pro-B cells and pro-B cells appeared to be normal, as judged by total cell numbers, proliferative indexes, D-JH and V-DJH gene rearrangements, and mRNA for recombinase-activating gene-1 (RAG-1), RAG-2, TdT, Ig mu, lambda 5, and VpreB. However, upon closer inspection, several abnormalities in pro-B cell development were identified that could be corrected by injection of rIL-7 in vivo. These included the absence of the subset of late pro-B cells that initiates cmu expression for pre-B cell Ag receptor (BCR) formation, and the failure of pro-B cells to up-regulate TdT and the IL-7R alpha (but not the common gamma-chain) chain. Similar defects were present in common gamma-chain and Jak3 KO mice, but not in lambda 5 or (excluding cytoplasmic Ig mu heavy chain (c mu)) RAG-1 KO mice, all of which also arrest at the late pro-B cell stage. Consequently, up-regulation of TdT and IL-7R alpha expression requires signaling through the high affinity IL-7R, but does not require cmu expression or a functional pre-BCR. Taken together, these results suggest that IL-7 and its receptor complex are essential for 1) up-regulating the expression of TdT and IL-7R alpha, 2) initiating the production of cmu and 3) promoting the formation of a functional pre-BCR in/on pro-B cells. These key events, in turn, appear to be prerequisite both for differentiation of pro-B cells to pre-B cells and for proliferation of these cell subsets upon continued stimulation with IL-7.

Animals↗
PubMed1997

Probing the stability of class I major histocompatibility complex (MHC) molecules on the surface of human cells.

We used binding of a fluorescent adduct of beta2-microglobulin, fluorescein beta2m, to probe the stability of class I HLA molecules on the surface of human cells. The weight of the literature suggests that this ligand binds to heavy chains that have lost beta2m and possibly peptide as well. Hence Fl-beta2m reports on the stability of the class I HLA trimer. A small fraction of HLA molecules, approximately 5%, binds Fl-beta2m on both resting and activated T cells. A larger fraction of all HLA molecules binds Fl-beta2m in FO-1 cells, beta2m-deficient cells, transfected with various B2m genes. HLA molecules of FO-1 cells are more stable when expressed with human beta2m, than when expressed with mouse beta2m. The non-covalent association of HLA heavy chains, beta2m and peptide implies that eventually every molecule of HLA trimer ought to dissociate and bind Fl-beta2m. In fact, the extent of exchange is limited by the lifetime of a given molecule at the cell surface. beta2m exchange decreases as cell concentration increases, suggesting that some density-dependent process acts to enhance degradation or denaturation of beta2m-free HLA heavy chains.

Animals↗
PubMed1996

Tissue factor expression in human leukemic cells.

Patients with acute leukemia are at increased risk for thrombotic and hemorrhagic complications, particularly those patients with acute promyelocytic leukemia (APL) undergoing induction chemotherapy. These serious complications have been attributed by some authors to the release of tissue factor (TF) procoagulant activity (PCA), particularly during cytotoxic chemotherapy. In previous studies of normal peripheral blood cells, only cells of the monocyte lineage have been found to express TF PCA. Therefore, several questions remain regarding the origin and characterization of the PCA in malignant leukemic cells, particularly those thought to be derived from granulocyte progenitor cells. We utilized a full-length cDNA probe, several monoclonal antibodies (MAbs) and a sensitive one-stage PCA assay to study the expression of TF in the human cell line, HL-60, in human peripheral blood monocytes/macrophages (Mo/Mø) and in highly purified populations of human polymorphonuclear leukocytes (PMN). In the HL-60 cells we detected low but significant levels of TF mRNA and TF antigen (TF:Ag). In unstimulated cells, coordinate increased levels of TF mRNA, TF:Ag and TF PCA expression were noted following phorbol-ester-induced macrophage differentiation of the cells, but a decreased level of TF mRNA with no change in the basal level of TF:Ag expression occurred following retinoic acid-induced granulocyte differentiation of this cell line. Long-term cultures of stimulated mature Mo/Mø demonstrated initial coordinate expression of TF mRNA, TF:Ag and TF PCA, but TF:Ag expression persisted even after 7 days (when TF PCA was undetectable). No TF PCA, TF:Ag or TF mRNA was demonstrated in highly purified populations of human PMN, regardless of culture conditions. Discordant expression of TF mRNA, TF:Ag and TF PCA in HL-60 cells suggests the possibility of novel, post-synthetic mechanisms for the regulation of TF PCA expression, which might be dependent on the phenotypic differentiation level of the cell. Such mechanisms (yet to be defined) might account for the ability of some leukemic cells, which frequently express characteristics of more than one cell line (e.g. monocytes and granulocytes), to express a TF gene product capable of activating blood coagulation.

Antibody Specificity↗
PubMed1988

Studies on recombination within the mouse H-2 complex: IV. Characterization of new recombinant haplotypes H-2t7, H-2t8, H-2as2, and H-2as3.

Four new intra-H-2 recombinants were characterized serologically and functionally. In two of these recombinants, B10.ASR1 and B10.ASR7, crossing over occurred between the A alpha and E alpha subregions, very probably in E beta since most intra-I region recombinants thus far investigated at the DNA level appear to involve recombination within the E beta gene. In the other two recombinants, B10.ASR2 and B10.ARS8, crossing over occurred between the S and D subregions. B10.ASR2 and B10.ASR8, crossing over occurred between the S and D subregions. B10.ASR7, which is serologically indistinguishable from B10.BASR1 and B10.S(8R), slightly stimulates and strongly responds to both of these strains in MLR. The probable location of the B10.S(8R) stimulatory product is E beta. The H-2 composition of B10.ASR1 is closest to that of B10.S(9R) and B10.HTT; therefore, precise definition of the cross-over point at the DNA level will be of particular interest.

Animals↗
PubMed1975

Influence of primary closure of the pericardium after open-heart surgery on the frequency of tamponade, postcardiotomy syndrome, and pulmonary complications.

Experiences with primary closure of the pericardium in a series of 100 patients undergoing open-heart operations are described. The pericardium was kept under tension during the operation to minimize shrinkage and permit closure at the end of the procedure. In 28 patients one pleural space was opened for drainage, whereas in 72 patients intra- and extrapericardial sumps alone were used for drainage. Measurements of sump drainage revealed that most postoperative bleeding originates from outside the pericardium. There were no instances of cardiac tamponade although 19 patients lost more than 1 L. of blood after operation and 5 required reoperation for hemorrhage. Transpleural drainage tubes were shown to be ineffective and in addition were associated with a fourfold increase in postcardiotomy syndrome and a significantly greater frequency of pleural effusion and atelectasis when compared to the use of mediastinal sump drainage alone. We have concluded that closing the pericardium and using mediastinal sump drainage minimizes the risk of cardiac tamponade and allows early localization of the site of postoperative bledding. Another advantage of pericardial closure and drainage is that postoperative adhesions and postcardiotomy syndrome will be less significant. As a consequence the danger of injuring the heart in a subsequent operation is lessened.

Adult↗