B12 deficiency in alpha-thalassemia.
Explore the source record for details and available documents.
Child↗
Biomedical subjects
M Bennett
Publications and source records attributed to M Bennett.
Lysis of FLD-3 Friend erythroleukemia cells in vitro and in vivo: effect of 89Sr treatment and Friend virus infection.
The effector cells from non-immunized mice capable of lysing 51Cr-labelled FLD-3 BALB/c Friend virus-induced erythroleukemia cells in vitro and cells capable of clearing FLD-3 cells labelled with 5-iodo-2'-deoxyuridine-125I (125IdUrd) from the lungs in vivo were characterized and compared with natural killer (NK) cells reactive against YAC-I lymphoma cells. Unlike NK cells, the cells capable of lysing FLD-3 cells in vitro were insensitive to antibodies directed against NK-2.1 or Thy-1.2 antigens (plus complement) and to pretreatment of mice in vivo with silica particles, 89Sr or estradiol. Heat-killed C. parvum organism stimulated anti-FLD-3 effector cells without changing the slow rate (24 h) of lysis in vitro. The ability to clear FLD-3 and YAC-1 cells from the lung was normal and defective, respectively, in C57BL/6-bg/bg(beige) mice and in mice pretreated with 89Sr or estradiol. We conclude that natural cytotoxic (NC) cells lyse FLD-3 cells, Fv-2, which regulates resistance to leukemia induction by Friend virus, does not regulate NC(FLD-3) activity, and the virus does not affect NC(FLD-3) activity during the first several days of infection of normal genetically susceptible mice. However, infection of 89Sr-treated mice inhibits NC(FLD-3) function owing to the activation of suppressor cells. These data suggest (but do not prove) that effector cells similar or identical to NC(FLD-3) cells may function in vivo to resist the proliferation/survival of certain leukemia cells.
Animals↗
Cutaneous mast cell maturation does not depend on an intact bone marrow microenvironment.
We sought to determine whether the maturation of murine cutaneous mast cells from stem cells depends on an intact bone marrow microenvironment. Normal bone marrow cells (+/+) were infused into 2 groups of mast cell-deficient mice: WBB6F1-W/Wv mice and 89Sr-pretreated W/Wv mice. 89Sr is a long-lived bone-seeking radioisotope which provides continuous irradiation of the marrow and thereby ablates the marrow microenvironment. Skin biopsies revealed that the 89Sr-pretreated mice and the controls had repopulated their skin with mast cells equally well. Natural killer cell function was significantly depressed in the 89Sr-treated mice, confirming that the marrow microenvironment had been functionally altered. We conclude that, although the precursors for cutaneous mast cells are marrow derived, they do not need an intact marrow microenvironment for maturation.
Animals↗
Bacterial interference with coliform colony sheen production on membrane filters.
The membrane filter (MF) method for detection and enumeration of coliform bacteria in drinking water requires that the coliforms both grow and produce a green metallic sheen when the filter is incubated on modified Endo medium at 35 degrees C for 22 h. Large numbers of noncoliform bacteria, which are enumerated by the standard plate count (SPC) technique, can interfere with the detection of coliforms on MF. This paper presents quantitative evidence from laboratory experiments on the interference of specific SPC bacteria on coliform colony sheen production on MF. Pseudomonas aeruginosa and Aeromonas hydrophila caused significant reductions in Escherichia coli sheen colony counts when present at 3,000 and 220 per filter, respectively. The Flavobacterium sp. and Bacillus sp. selected for this study from SPC did not interfere with coliform colony sheen production. Excessive crowding of E. coli and Enterobacter cloacae colonies on MF also caused a reduction in the number of colonies that produced sheen. Even when there was no crowding (14 colonies per filter), only a fraction of the E. cloacae colonies produced sheen colonies on modified Endo medium.
Bacteria↗
Suppression of tumor cell growth in vitro by a bone marrow factor.
A supernatant factor derived from monodispersed bone marrow cells was tested for its ability to inhibit the growth of tumor cell lines and freshly dispersed hemopoietic cells in vitro. The supernatant fluid from bone marrow cells was capable of inhibiting the mitogenic response of rat thymocytes to concanavalin A. It also was capable of inhibiting growth of HeLa cells, Sarcoma 180, EL-4, and BALB/c K3T3 tumor cell lines as measured by thymidine incorporation. The factor did not inhibit the growth of normal thymus cells, marrow cells, or WI-38-SV40, and F-46 tumor cell lines. From data derived from 51Cr release assays, the factor appears to be selectively cytoreductive. Bone marrow supernatant factor is stable to heat (100 degrees for 10 min) and trypsin digestion, but is sensitive to carboxypeptidase B digestion. Molecular weight estimation by gel filtration chromatography on a Sephadex G-75 column indicates its apparent molecular weight to be less than 12,000. Bone marrow supernatant factor appears to function across species and strain barriers.
Animals↗
Correlation between a learning disorder and elevated brain-reactive antibodies in aged C57BL/6 and young NZB mice.
Previous studies have indicated an increase in brain-reactive antibodies (BRA) in sera of aging mammals and an autoimmune disorder underlying senescence has been suggested. Since New Zealand Black (NZB) mice have a shorter lifespan and greater propensity for autoimmune diseases than C57BL/6 mice, various age groups from both strains of mice were investigated for simultaneous occurrence of BRA serum titer and deficits in learning. NZB mice exhibited a marked learning deficit as well as higher BRA levels at all ages. C57BL/6 mice showed increased BRA and a learning deficit only at advanced ages. The findings of "precocious" BRA titers along with marked learning deficits, both occurring at young ages in NZB mice and both similar to defects seen in the normal mice at senescence and in patients with senile-dementia, suggest that NZB mice may serve as a useful animal model of pre-senile dementia.
Aging↗
A multifocal extra-abdominal desmoid tumour.
The literature on multifocal aggressive fibromatosis is reviewed and the fifth case recorded is reported. It conforms with the histopathological criteria for aggressive fibromatosis. Conservative local excision and radiotherapy have controlled the disease with preservation of a functioning limb.
Axilla↗
Lack of correlation between mycoplasma induced IFN-gamma production in vitro and natural killer cell activity against FLD-3 cells.
Interferon (IFN) stimulates natural killer (NK) cell-mediated lysis of tumor cells. However, it is not clear whether IFN production is essential for NK cells to lyse their target cells in vitro, especially in long-term (greater than 18 hrs) assays. To investigate this, 0.5 X 10(6) normal mouse spleen cells were cocultured in RPMI 1640 medium with Friend erythroleukemia cells (FLD-3) (1 X 10(4] for 24 hours under conditions which cause lysis of FLD-3 cells. Supernatant fluid from such cultures demonstrated antiviral activity (100-200 units) which could be identified as IFN-gamma. Prior filtration of spleen cells over nylon wool, and pretreatment with anti-Thy-1.2 + C' abrogated their ability to generate IFN-gamma without affecting their NK (FLD-3) activity. The IFN-gamma producing cell which could also be detected in spleens of nu/nu BALB/c mice lacked cell surface, Lyt-1, Lyt-2, and NK-1.2 antigens. The stimulus for IFN-gamma induction appeared to be Mycoplasma arginini carried in the FLD-3 tumor cells. Although mycoplasma-free FLD-3 cells failed to induce IFN in vitro, they retained their susceptibility to NK cell-mediated lysis. We conclude that IFN induction is not essential for NK(FLD-3) cell-mediated lysis; indeed IFN detected in NK cell assays may be produced in response to mycoplasma infection of the tumor cells. The Thy-1.2 positive cells stimulated by mycoplasma to produce IFN-gamma lack several characteristics of T-cells or NK cells.
Animals↗
Immunological studies of transplantation tolerance in irradiated rats repopulated with syngeneic hemopoietic cells.
Adult Lewis (LEW) rats that are lethally irradiated, grafted with allogeneic Wistar Furth (WF) hearts and repopulated with syngeneic bone marrow (LEW) become specifically and permanently tolerant to the allografts. In vivo transfer of spleen cells from tolerant animals to sublethally irradiated LEW rats was capable of preventing the rejection of WF cardiac allografts in 16 of 25 animals, suggesting the possibility of suppressor cells. For further characterization of this putative suppressor cell, mixed lymphocyte reactions (MLR) and cell mediated lympholysis (CML) assays were performed with spleen cells from tolerant and normal LEW rats. In 24 of 52 cases, spleen cells from rats bearing intact WF grafts proliferated in response to the tolerated WF alloantigens, and in 27 of 49 cases they were unable to generate effector cells against WF targets, which indicates that many of these animals were competent to respond to donor antigens as represented in bulk MLR. No suppression was found when spleen cells from nonresponsive recipients were mixed with normal LEW spleen cells in vitro either at the sensitization (MLR) or at the effector (CML) phase of the assay. Neither was there consistent in vitro suppression at the sensitization or effector level, with serum from LEW rats bearing long-term WF cardiac allografts. We suggest that the unresponsiveness observed in vivo is mediated by suppressor cells that interfere with the generation of mature effector cells from immature precursors. It is conceivable that suppressor cells that are present in vivo cannot act on mature effector cells generated in vitro. Additionally, or alternatively, the failure to detect suppression in vitro may result from the presence of stimulator cells in vitro that are not representative of stimulator cells seen by the tolerant animals in vivo.
Animals↗
Potential use of an asparaginase-dextran conjugate in acute lymphoblastic leukaemia.
Explore the source record for details and available documents.
Amino Acids↗
Aging of natural and acquired immunity of mice. I. Decreased natural killer cell function and hybrid resistance.
Two "natural resistance" functions, natural killer (NK) cell activity against YAC-1 lymphoma cells and rejection by irradiated mice of parental-strain or H-2 allogeneic bone marrow cell grafts (hybrid or allogeneic resistance) were compared in mice at ages between 10 weeks and 26 months. NK cell numbers, as assessed by target-binding cells, decreased to one-half that of young mouse spleen cells, whereas NK lytic function was much more depressed. Hybrid, but not allogeneic, resistance to marrow grafts was weakened by 17 months of age. The immunogenicity of marrow stem cells of old Fl hybrid mice had not changed. The interferon inducer polyinosinic:polycytidylic acid (pI:pC) restored hybrid resistance to marrow grafts but only weakly boosted NK cell function in old mice. Incubation of spleen cells of old mice with beta interferon resulted in a weak boosting of NK cell activity. No cells capable of inhibiting NK cell function were detected in the spleens of old mice. These findings in old mice were similar to findings in young mice treated with 89Sr, with the exceptions that both hybrid and allogeneic resistance to marrow grafts are defective in 89Sr-treated mice and pI:pC failed to restore hybrid resistance in mice treated with 89Sr. This loss of "natural resistance" by aged mice, perhaps mediated by marrow-dependent effector cells, can partially explain the increased incidence of tumors in aging populations.
Aging↗
Aging of natural and acquired immunity of mice. II. Decreased T cell responses to syngeneic tumor cells and parental-strain spleen cells.
Cytolytic T lymphocyte (CTL) functions were compared in mice between the ages of 2 and 30 months. The stimulator cells were H-2 allogeneic spleen or tumor cells, parental-strain spleen cells, or syngeneic tumor cells. Effector cells capable of lysing syngeneic tumor cells were shown to be T cells and not NK cells. The cell-mediated lympholysis (CML) responses by spleen cells of aged mice were near normal against H-2 allogeneic spleen or tumor cells but were defective against syngeneic tumor cells or parental-strain spleen cells. The defective syngeneic tumor CML response was observed at various responder:stimulator ratios and at various days of incubation. The defect was in the nonadherent, and not in the adherent, fraction of spleen cells. Suppressor cells were detected in spleens of 30 month, but not of 18 month old mice. Aged mice were more susceptible than young mice to small inocula of syngeneic C57BL EL-4 lymphoma cells. The immunogenicity of irradiated spleen cells of old mice had not changed for the F1 antiparent CML response. Splenic CML responses of young mice treated with 89Sr demonstrated a similar pattern, i.e., good responses to H-2 allogeneic stimulator cells but poor responses to syngeneic tumor cells or to parental-strain spleen cells. This loss of certain CTL functions influenced by marrow dependent cells can partially explain the increased susceptibility of old animals to tumors.
Age Factors↗
Prevention of lethal, minor-determinate graft-host disease in mice by the in vivo administration of anti-asialo GM1.
Graft-vs-Host disease (GVHD) remains a devastating problem in human bone marrow transplantation (1, 2). Because removal of Thy-bearing cells from the donor inoculum has prevented GVHD in murine models (3, 4), it has been hoped that a similar cell surface antigen or combination of antigens could be found in humans. Unfortunately, treatment of human donor cells with various T cell antisera has not yet been successful in preventing GVHD (5). Encouraging results have been reported in five patients who received bone marrow depleted of T cells by the sequential use of soybean agglutinin and the differential sedimentation of cells forming rosettes with sheep red blood cells (6). Although donor T cells are thought to be necessary for initiating GVHD, the immunopathogenesis of GVHD is still not understood. Because donors and recipients are routinely major histocompatibility complex matched and chosen to be nonreactive in mixed lymphocyte cultures human GVHD is thought to result from minor histocompatibility antigen disparities. Lopez and coworkers (7, 8) found a strong association between the incidence of human GVHD and the pretransplant levels of natural killer (NK) activity of the recipients; when the recipient NK activity was low, GVHD rarely developed. They speculated that the NK cell lineage is serving as an important stimulator-inducer. We therefore examined the in vivo effects of anti-asialo GM1 on a murine model of GVHD based on minor antigen disparity. This antiserum has several immunologic effects, including a profound NK suppression. We found that the mice treated with this antibody have normal survival rates, even though they do develop histologic GVHD in the skin. This finding suggests the possibility of a new prophylactic approach to human GVHD and raises many questions regarding the function of asialo GM1-bearing cells in immune regulation.
Animals↗
Selecting students for training in health care. A practical guide to improving selection procedures.
Explore the source record for details and available documents.
College Admission Test↗
Natural killer cells in mouse lung: surface phenotype, target preference, and response to local influenza virus infection.
Natural killer (NK) and natural cytotoxic (NC) cells can be recovered from the spleens of mice. NK/NC cells are thought to serve as a first line of defense (before the development of immune responses) against tumor and virus infected cells; therefore organs such as the lung that are exposed to the environment may harbor NK/NC cells. Studies reported in this manuscript characterize a population of pulmonary cells (recovered from collagenase-treated lungs) that exhibited cytotoxic activity against 51Cr-labeled tumor targets in vitro. As with the spleen cell populations, the mononuclear cells from the lung lysed the NK-sensitive target YAC-1 as well as the NC-sensitive WEHI 164.1 tumor cells in vitro. By using flow cytometry, it was observed that 15 to 20% of nylon wool-passed (NWP) lung cells and 5 to 15% of NWP spleen cells from C57BL/6 mice could bind antibody for NK cell alloantigens (NK 1.2, defined by (CE X NZB)F1 anti-CBA sera). Treatment of lung and spleen cell populations with complement and antisera to NK 1.2, asialo GM1, and Ly-5 but not Thy-1 antigens significantly decreased lung and splenic NK (YAC-1) activity. Forty-eight hours after infection of mice by intratracheal inoculation of an infectious dose of influenza virus (PR/8/34) NK activity was stimulated in the lung and not the spleen. Therefore although NK cells in the lung and spleen are similar in antigenic phenotype and target preference there appears to be a pulmonary compartment of natural resistance cells the function of which can be modulated locally. These data are consistent with the hypothesis that the lung contains a separate compartment for NK/NC cells that may participate in the defense mechanisms of the lung.
Animals↗
89Sr-induced bone marrow aplasia: effects on seed (stem cells) and soil (inductive microenvironment).
Explore the source record for details and available documents.
Animals↗
Effect of combined antibiotic therapy on fertility in brood bitches infected with Brucella canis.
Bitches with naturally occurring Brucella canis infection were treated with combined antibiotic therapy consisting of tetracycline, dihydrostreptomycin, and trimethoprim-sulfadiazine. After treatment, all but 1 bitch became abacteremic, and serologic titers declined for a variable length of time (3 months to 1 years). Abortion did not occur while these bitches were abacteremic. Although sequential antibiotic therapy for 6 weeks did not eradicate Brucella canis from affected bitches, it did not prevent abortion. The number of live pups whelped and weaned by treated bitches was comparable with that in bitches before they became infected.
Abortion, Septic↗