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MeSH Review

Mice, Inbred CBA

 
 
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Disease relevance of Mice, Inbred CBA

  • Blocking factors in the sera of inbred CBA mice bearing either Moloney murine sarcoma virus-induced tumors or transplanted 3-methylcholanthrene-induced tumors specifically blocked in the leukocyte adherence inhibition reaction between tumor-sensitized peritoneal cells and tumor antigens [1].
  • Ethidium bromide (2,3-diamino-5-ethyl-6-phenylphenanthridinium bromide) significantly inhibited the RNA-dependent DNA polymerase of types A and C particles isolated from transplanted adenovirus 12-induced tumors of CBA mice [2].
  • Cultures of resting macrophages were rendered nonspecifically tumoricidal for the two lymphoma sublines ESb and 721 (ESb-Cl 18.1), for the mastocytoma P815X, for LS lymphoma cells, and for proliferating lymphoblasts from DBA/2, C57BL/6J, and CBA mice by exposure to Bestatin at 50 micrograms/ml culture medium [3].
  • Pulmonary granulomas (GR) with type 1 or type 2 cytokine involvement were induced in presensitized CBA mice by embolization of beads coupled to purified protein derivative (PPD) of Mycobacterium tuberculosis or soluble Ags derived from Schistosoma mansoni eggs (SEA) [4].
  • Danshen extracts were then administered to adult CBA mice receiving concurrent treatment with kanamycin (700 mg/kg of body weight twice daily for 15 days) [5].
 

Psychiatry related information on Mice, Inbred CBA

 

High impact information on Mice, Inbred CBA

 

Chemical compound and disease context of Mice, Inbred CBA

  • Age-matched male CBA mice on a conventional or a vitamin A acetate (VAOAc)-rich diet were immunized with irradiated cloned 3-methylcholanthrene- or Harvey sarcoma virus-induced (McSa-1 or HT3-2.1) sarcoma cells and then challenged with viable corresponding or unrelated (non-crossreacting) syngeneic sarcoma cells [12].
  • A nonspecific stimulation of macrophage cells by muramyl dipeptide analogs may contribute to the protection because antiinfective activity against Listeria monocytogenes given intraperitoneally was achieved with CBA mice [13].
  • The ability of arginine supplementation to abrogate or potentiate Mycoplasma arthritidis-mediated cytotoxicity induction by normal CBA mouse lymphocytes was investigated [14].
  • It was previously reported that administration of cadmium (Cd) to CBA mice latently infected with herpes simplex virus (HSV) results in a high incidence of virus reactivation in vivo [15].
  • We demonstrate that a single, sublethal dose of cyclophosphamide (400 mg/kg body weight) profoundly inhibited the humoral immune response of CBA mice to sheep red blood cells (SRBC), as measured by the number of antibody forming cells (AFC) in the spleen after 5 weeks following CP treatment [16].
 

Biological context of Mice, Inbred CBA

 

Anatomical context of Mice, Inbred CBA

  • CBA mice were rendered tolerant of major histocompatibility antigens of A/J mice by neonatal injection of 100 x 10(6) lymphoid cells of (CBA X A/J)F1 followed by repeated injections of F1 cells at 2-week intervals throughout the study [22].
  • Bimodal circadian secretion of melatonin from the pineal gland in a living CBA mouse [6].
  • Injection of these spleen cells, together with bone marrow cells, in fully mismatched preirradiated CBA mice delayed GVHD by only 6 days [23].
  • Previous results from our group had shown that when CBA mice are primed to sheep red blood cells (SRBC) in the presence of various doses of placental extract (PE) (or liver extract [LE] as control), their spleen cells injected into normal syngeneic recipients have important immunoregulatory properties [24].
  • In this test, antigen-presenting cells (APC) from MRL / lpr mice were required; APC from naive CBA mice failed to stimulate CD4(+) cells from MRL / lpr mice [25].
 

Associations of Mice, Inbred CBA with chemical compounds

  • Treatment of inbred CBA mice with hydrazine sulfate, a liver carcinogen, plus [14C]formate or L-[methyl-14C]-methionine as a source of "C1" units, produced [14C]7-methylguanine (7-MG) in liver DNA and RNA [26].
  • Complete heavy (H) chain variable region (V region; amino acids 1-118) sequences have been determined for three phosphocholine (PCho)-binding monoclonal antibodies of CBA mouse strain origin [27].
  • Prostaglandin sensitivity of myeloid precursors from NZB and CBA mice was also different [28].
  • CBA mouse spleen cells were subjected to hapten affinity fractionation on thin layers of fluorescein (FLU)-gelatin [29].
  • In contrast, eight rat IgG2b, mouse IgG2a, and 2b anti-Thy-1 MoAbs with high affinity for C1q still remained strongly T-cell-depleting and prevented GVHD even in fully mismatched CBA mice depleted of C3 [30].
 

Gene context of Mice, Inbred CBA

  • While neutralization of TNF activity in vivo did not alter the course of infection in BALB/c mice, in CBA mice it led to an increase in lesion size and a delay in the healing process but did not interfere significantly with the outcome of infection [31].
  • However, this also occurred in vivo since CBA mice produced substantial amounts of IL-10 following infection with L. major [32].
  • To investigate the conditions under which autoimmune responses can be generated against self hsp60, groups of CBA mice were immunized with recombinant mouse hsp60, recombinant chlamydial hsp60, or both proteins [33].
  • In order to study the regulation of Aldh3a1 gene expression, we isolated two overlapping genomic sequences from a B6/CBA mouse genomic library that included the entire Aldh3a1 gene, along with considerable 5' and 3' flanking sequences [34].
  • The dorsal cortex, lateral nucleus, and NCO showed increases of 42.3, 49.0, and 61%, respectively, in the number of CR+ cells, but only in the old CBA mice [35].
 

Analytical, diagnostic and therapeutic context of Mice, Inbred CBA

  • Although splenocytes from inbred C3H and CBA mice exhibited much higher proliferative responses to MAM than did those from B10.TRG.E alpha+ or B10.E alpha TG +/+ mice, flow cytometry showed similar levels of E alpha expression [36].
  • METHODS: Islet allograft from BALB/C mice or islet isografts were transplanted into STZ-induced diabetic CBA mice and autoimmune nonobese diabetic (NOD) mice [37].
  • The present studies in Nramp1(-/-) BALB/c and Nramp1(+/+) CBA mice question the significance of this genotype as a determinant of the level of gut colonization following oral administration of naturally attenuated or highly virulent Salmonella strains [38].
  • METHODS: CBA mice were given donor splenocytes (1x107) or Kb peptide (100 microg) by ITD with or without antibody specific for mouse CD40 ligand (MR1, 200 microg) 7 days before transplantation of a C57BL/10 heart [39].
  • Adoptive transfer experiments demonstrated an ability of immune splenocytes from CBA mice intraperitoneally infected with the MOP/LAS reassortants to protect recipient mice against lethal disease after ic inoculation with LAS virus [40].

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