Search PubMed⌕ Search

Biomedical subjects

R Risser

Publications and source records attributed to R Risser.

At least 91 records · Page 5Linked to original sources
PubMed1982

Genetic interactions in induction of endogenous murine leukemia virus from low leukemic mice.

The frequency of ecotropic murine leukemia virus (MuLV) production in cells induced with halogenated pyrimidines has been investigated in several low leukemic strains of mice. Very few BALB/c or C57BL/6 (B6) induced embryo cells produce MuLV; this low frequency increases 10 to 50 fold in cells of the BALB/c x B6 F1 hybrid. Data from back-crosses of the F1 hybrid to each parent and from BALB/c x B6 recombinant inbred strains indicate that the phenotype of enhanced MuLV production results from interaction of two unlinked loci, dominant (+/+) alleles of which are carried by either parent. Genetic tests with BALB/c x B6 recombinant inbred strains confirm this two-locus model. The loci are designated Inc-1 and Inb-1 to signify their phenotypic detection by induction and the BALB/c or B6 strain of origin, respectively. Examination of hybrids of BALB/c and of B6 with other strains indicates that strains related in pedigree to BALB/c carry Inc-1, whereas those related to B6 carry Inb-1. Identification of genetic loci that specifically interact to enhance MuLV production after exposure to halogenated pyrimidines indicates the existence of mechanisms that regulate the induction or intracellular expression of endogenous MuLV.

Animals↗
PubMed1982

Loss of viral gene expression and retention of tumorigenicity by Abelson lymphoma cells.

Lymphomas induced by the Abelson murine leukemia virus (A-MuLV) were examined for the expression of biochemical and biological markers associated with A-MuLV transformation before and after in vivo growth in genetically distinguishable host mice. Although all tumors and clonal lines derived from them initially expressed the A-MuLV-encoded gag fusion protein p160, they ceased synthesis of this molecule after several weeks of growth in vivo as ascites tumors. Transplanted clonal lines continued to express the alloantigenic marker H-2b and the isoenzyme marker Gpi-1b of the donor tumor cells, indicating that the cells were of donor and not host origin. Examination of cellular DNA obtained from p160-positive and derivative p160-negative lines indicated that p160-negative clones had lost A-MuLV-specific proviral sequences as detected by hybridization with several probes. Although the clonal lines no longer expressed p160, they retained their malignant phenotype and continued to express the Abelson antigen, a cell surface marker associated with A-MuLV lymphomagenesis. Continued expression of the A-MuLV genome was not required for maintenance of oncogenic potential under these conditions of in vivo tumor growth.

Abelson murine leukemia virus↗
PubMed1982

A locus that enhances the induction of endogenous ecotropic murine leukemia viruses is distinct from genome-length ecotropic proviruses.

The segregation of genes that enhance the induction of ecotropic murine leukemia viruses (In loci) has been compared with the segregation of ecotropic-specific nucleotide sequences in 12 low-leukemic mouse strains and 18 recombinant inbred strains. Endogenous ecotropic viruses of these strains are of genome length and structurally similar to AKR ecotropic proviruses. Low-leukemic strains of related pedigree contain ecotropic proviruses at common integration sites. Loci previously identified which enhance induction of ecotropic viruses (In genes) were correlated with the inheritance of ecotropic viral sequences in inbred low-leukemic mouse strains and in CXB recombinant inbred mouse strains. However, four BXH recombinant inbred strains were observed to possess an In gene(s) yet lack the probed envelope gene region for the corresponding endogenous ecotropic virus. These observations indicate that at least one gene that enhances ecotropic virus expression in vitro is encoded by DNA sequences outside ecotropic proviruses or by subgenomic viral sequences.

AKR murine leukemia virus↗
PubMed1981

Production of anti-self H-2 antibodies by hybrid mice immune to a viral tumour.

During the course of immunization of hybrid mice (genotype H-2b/k) with a parental Abelson virus-induced lymphoma (genotype H-2b/b), antibodies were produced to the H-2Kb or H-2Db antigens of the immunizing cells. Such 'anti-self H-2' antibodies demonstrate the existence of autoreactive B-cell clones in hybrid mice, and pose intriguing questions for the nature of self-tolerance.

Abelson murine leukemia virus↗
PubMed1979

Friend erythroleukemia antigen. A viral antigen specified by spleen focus-forming virus and differentiation antigen controlled by the Fv-2 locus.

Serum from C57BL/6 (B6) mice hyperimmunized with NB-tropic Friend virus complex (FV) was cytotoxic for FV-induced erythroleukemic spleen cells and B6 Friend-murine leukemia virus (F-MuLV) lymphoma cells. Cytotoxic activity for erythroleukemia cells remained after repeated absorption of B6 anti-FV antiserum with Friend-Moloney-Rauscher MuLV lymphoma cells but was removed by absorption with erythroleukemia cells induced by FV or Rauscher Vrus. This serologic test system identified a previously unrecognized cell-surface antigen of mouse leukemia, designated Friend Erythroleukemia (FE) antigen to signify its appearance as a determinant of virally induced erythroleukemic differentiation. FE antigen was not detected on 15 transplanted or primary hematopoietic neoplasms, nor was it detected on cells infected with ecotropic, xenotropic, or dualtropic MuLV isolates in tissue culture. Two spleen focus-forming virus (SFFV) nonproducer cells of rats and one of mice express FE antigen in amounts comparable to primary erythroleukemia cells. Absorption tests with FE typing serum indicated that FE antigen was expressed on bone marrow and spleen but not thymus, lymph node, or peripheral blood of uninfected AKR, BALB/c, DBA, and SWR mice; all five tissues from B6 and C57L were negative. Quantitiative absorption tests indicated that the expression of FE antigen, though much lower than on erythroleukemic cells, was greatest on fetal liver, less on bone marrow, and lowest on spleen from BALB and SWR mice. Treatment of BALB/c or SWR fetal liver, bone marrow, spleen, thymus, or lymph node cells with FE typing serum did not result in significant lysis. These observations are consistent with the interpretation that FE antigen is expressed by a minor cell population present in fetal liver, bone marrow, and spleen. Expression of FE antigen, determined by absorption with bone marrow cells, cosegregated with inheritance of the Fv-2s allele in the 17 inbred, 7 recombinant inbred, and 4 congenic mouse strains tested. In summary, the FE antigenic system identifies a cell-surface determinant that has the properties of a SFFV-specified antigen and hematopoietic differentiation alloantigen controlled by the Fv-2 locus. The similarity of FE antigen to Abelson antigen may provide insight into the pathogenic properties of defective transforming MuLV.

Animals↗
PubMed1979

Abelson antigen is expressed on hematopoietic spleen colony-forming cells from mice carrying the Av-2S virus sensitivity gene.

Abelson antigen is a cell-surface determinant specifically induced by the Abelson murine leukemia virus (A-MuLV); this antigen is also expressed on uninfected bone marrow of BALB/c mice. Antisera that contained antibody to Abelson antigen were cytotoxic for the spleen colony-forming cells (CFU-S) of adult bone marrow from BALB/c mice. Absorption tests with appropriate tissues and direct cytotoxic tests with bone marrow CFU-S from several mouse strains confirmed that the sensitivity of BALB/c CFU-S to lysis by anti-Abelson-antigen antisera was due to expression of Abelson antigen. Spleen or bone marrow from BALB/c mice undergoing hematopoietic regeneration amplified Abelson antigen expression, although no expression of Abelson antigen was observed on regenerating C57BL/B6 bone marrow or spleen. The presence of Abelson antigen on bone marrow cells of seven recombinant inbred strains coincided with the inheritance of sensitivity alleles at the Av-2 locus, a gene that determines susceptibility to A-MuLV lymphoma induction. These results indicate that expression of Ableson antigen may have a physiologic function in hematopoietic differentiation and a pathologic role in A-MuLV lymphomagenesis.

Abelson murine leukemia virus↗
PubMed1978

Abelson virus-induced lymphomagenesis in mice.

The salient facts which have emerged from our study of Abelson virus (MuLV-A)lymphomagenesis in mice are that lymphoma induction is (a) age dependent, (b) virus dose dependent, and (c) under the control of host genes unrelated to other genes known to control murine leukemia (e.g., Fv-1 on Fv-2). Of 16 strains tested, only BALB/c and some of its derivative strains showed high sensitivity. Studies from CXB recombinant inbred strains and hybrids between them are interpreted to indicate that BALB/c carries dominant sensitivity alleles at two loci, tentatively designated Av-1 and Av-2, which conferon these mice partial susceptibility to MuLV-A lymphoma induction. In addition, H-2 may play a minor role in determining the susceptibility of mice to MuLV-A, its effect being seen only in mice homozygous for resistance at both Av-1 and Av-2. Virologic studies indicate that the resistance of adult B6 mice is not related to restriction on the helper virus replication, but is specific for the defective transforming virus genome.

Age Factors↗
PubMed1978

Abelson antigen: a viral tumor antigen that is also a differentiation antigen of BALB/c mice.

We report here the serologic detection of a cell surface antigen common to cells transformed by the Abelson murine leukemia virus (A-MuLV) and to normal hematopoietic cells from certain strains of mice. Serum from C57BL/6 mice hyperimmunized with syngeneic A-MuLV lymphoma cells was cytotoxic for the immunizing cells; this reaction was used as the serologic test system for recognition of A-MuLV antigens. Absorption analysis using 40 tumors and 21 cell lines revealed that two serologic specificities were detected by this test system: (i) FMR antigen(s) related to the Moloney MuLV helper (the virus from which A-MuLV was originally derived), and (ii) an antigen expressed on all cells transformed by A-MuLV. The A-MuLV-specific antigen was also present on uninfected cells from BALB/c bone marrow, spleen, and fetal liver but not from adult liver, thymus, lymph nodes, or peripheral blood. Abelson antigen was not expressed on bone marrow or spleen cells of 12 other mouse strains. In light of the original isolation of A-MuLV from a BALB/c mouse infected with Moloney virus, it is possible that Abelson antigen is a serologic marker for a gene of BALB/c mice, normally encoding a cell surface molecule, that was incorporated into the Moloney virus genome during the generation of A-MuLV.

Animals↗
PubMed1975

Tumorigenicity of virus-transformed cells in nude mice is correlated specifically with anchorage independent growth in vitro.

Clonal isolates of mouse 3T3 cells and primary rat embryo cells, recovered nonselectively after infection by simian virus 40 (SV40), have been tested for tumorigenicity in the immune-deficient nude mice in order to determine the cellular growth properties in vitro specifically correlated with neoplastic growth in vivo. In addition, mouse 3T3 cells transformed by murine sarcoma virus (MuSV, Kirsten strain), and revertants isolated from cells fully transformed by either SV40 or MuSV were also studied. Results suggest that the single cellular property consistently associated with tumorigenicity in nude mice is the acquisition by virus-transformed cells of the ability to proliferate in vitro in the absence of anchorage. Other cellular parameters of virus-induced transformation, such as lack of sensitivity to high cell density and the capacity to grow in low serum concentration, are dissociable from cellular tumorigeneicity. This conclusion is supported further by the demonstration that specific selection in vivo for tumorigenic cells from anchorage-dependent cells results in the isolation of anchorage-independent cells. Conversely, a single-step selection in vitro for anchorage-independent cells from nontumorigenic cells results in a simultaneous selection of highly tumorigenic subclones.

Animals↗
PubMed1974

Plasminogen activator production accompanies loss of anchorage regulation in transformation of primary rat embryo cells by simian virus 40.

We have isolated several lines of rat embryo cells transformed by simian virus 40. All these lines are fully transformed with regard to saturation density and serum sensitivity, but they differ greatly in their anchorage dependence, as assayed by efficiency of plating in methyl cellulose suspension. This set of lines reveals a consistent relation of plasminogen activator production to plating efficiency in methyl cellulose. T-antigen-positive transformed lines that synthesize activator grow in methyl cellulose suspension, while T-antigen-positive transformed lines that do not synthesize activator fail to form colonies in suspension. Normal rat embryo cells produce very little plasminogen activator and do not grow in methyl cellulose. Sera that permit high levels of plasmin formation and activity support growth in semi-solid medium better than sera whose plasminogen is activated poorly and/or sera that contain inhibitors to plasmin.

Animals↗
PubMedDate not supplied

Severe fetal acidemia: neonatal neurologic features and short-term outcome.

The objectives of this study were to determine if infants delivered with severe acidemia (cord umbilical arterial pH < 7.0) had short-term neurologic effects and whether infants with persistent bradycardia who received cardiopulmonary resuscitation (CPR) in the delivery room would be at greatest risk for subsequently developing neonatal seizures. Forty-seven infants (39 term, 8 preterm) delivered with severe fetal acidemia were studied. The mean (+/- S.D.) for pH, PaCO2, and base deficit for the 47 infants was 6.86 +/- 0.11, 97 +/- 22 mm Hg, and -17 +/- 4, respectively. Labor complications were common and included placental abruption in 8, ruptured uterus in 4, cord prolapse in 3, fetal heart rate decelerations in 12, and other (n = 14). Most infants were delivered via emergency cesarean section (n = 29). Delivery room interventions included oxygen and bag/mask ventilation only (n = 20) and intubation and ventilation (n = 22); 7 of 22 infants received CPR and epinephrine for persistent bradycardia (heart rate < 80 beats/min despite ventilatory support). Five infants required no intervention. Eight infants (17%) had seizures; 6 of these infants received CPR in the delivery room. Short-term outcomes were abnormal in 7 of 8 infants (i.e., death in 5, abnormal neurologic examination at discharge in 2). In 39 infants without seizures, 32 had transient neurologic abnormalities (i.e., irritability, hyperreflexia, proximal hypotonia) which resolved by discharge, and 2 had abnormal and 5 normal examinations.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗