Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Mouse”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1975

The expression on mouse lymphoid cells of Th-B, an antigen common to mouse B cells and thymus cells.

A new cell-surface antigen of mouse lymphocytes, which was found earlier on normal and malignant plasma cells and about half the normal thymus cell population, has been shown to be on mature B cells and on the least immunocompetent subpopulation of cells of the thymus. The antigen was first detected by the cytotoxic effect on relevant cells of an in vivo purified rabbit antiserum raised against cells of the mouse IgM-producing plasma cell tumor MOPC-104E. We have now used a cell-transfer method to examine the effect of this antiserum (RantiM104E) on immunocompetent lymphocytes of spleen, including separated splenic B and T cells and thymus and bone marrow cells. We have found the antigen on the immunocompetent B lymphocytes of the spleen, but not on any other of the immunocompetent cells examined. The method involves determining the effect of the antiserum on the development of plaque-forming cells in the spleens of irradiated mice that have received lymphocytes from immune or non-immune donors by treating the lymphocyyes with RantiM104E antiserum before transfer. Plaque-forming cells are suppressed when antiserum-treated spleen cells are transferred to the irradiated mice.This suppression was found to be due to action on only the splenic B cells. The helper activity of splenic T cells was not reduced significantly by antiserum treatment. Neither was the helper activity of thymus cells similarly treated reduced by the antiserum. We found, in fact, that the subpopulation of the thymus cells which is resistant to the antiserum was more immunocompetent than the total thymus cell population. In addition, the hydrocortisone-resistant thymus cells were also found to be resistant to the cytotoxic action of the antiserum. The antiserum had no effect on bone marrow cells in the cell-transfer procedure. The antigen involved, which we are designating "Th-B" appears to be a B cell line marker which appears relatively early during the differentiation of mouse B cells from precursor cells and is lost during maturation of T cells.

Animals↗
PubMed1975

[Experimental xenogenic immune pancreatitis. 1. Histological findings in the mouse exocrine pancreas after treatment with anti-mouse pancreas rabbit serum (author's transl)].

QUESTION: In the pathogenesis of some forms of chronic pancreatitis an immunological influence has been discussed. Therefore, experimental studies of the exocrine pancreas after immunological damage should be done. In this communication histological findings on the mouse exocrine pancreas are presented after treatment with anti-mouse pancreas rabbit serum. MATERIAL AND METHODS: a total of 71 adult male white mice was divided into 4 groups treated in the following way: 1. 35 animals with anti-mouse pancreas rabbit serum 2. 14 animals with normal rabbit serum 3. 16 animals with physiological saline 4. 6 animals remained untreated. The sera under study and the saline were, without exception, administered intraperitoneally with single doses of 0.3 ml once, resp. twice daily for 0 up to 16 days. Constantly, 3 hours before sacrifice, the animals received the last injection. For histological examination, the fresh pancreas was fixed in formaline. After embedding in paraffin, sections were stained by the following methods: hematoxyline-eosin, trichrome according to Goldner, Giemsa staining, PAS-reaction, and tryptophane demonstration according to ADAMS (1957).

Animals↗
PubMed2003

[The effect of a mouse IL-12 plasmid on airway inflammation and cytokine production in a mouse asthmatic model].

OBJECTIVE: To investigate the effect of a mouse IL-12 gene expressive plasmid (mIL-12 plasmid) on the airway inflammation and the cytokine production in asthmatic mice and to study the possible mechanisms. METHODS: A mouse model of asthma was established by sensitization with ovalbumin (OVA). Forty-one BALB/c mice were divided into six groups including an asthmatic model group (group A, eight mice, sensitized with OVA plus challenging with OVA by aerosol), a model control group (group B, six mice, sensitized with OVA plus aerosolizing with normal saline), a mIL-12 plasmid prevention group (group C, eight mice, receiving intramuscularly mIL-12 plasmid 100 micro g on day 1, day 3, and day 5), a mIL-12 plasmid treatment group (group D, eight mice, receiving intramuscularly mIL-12 plasmid 100 micro g on day 14, day 16, and day 18), an empty plasmid prevention group (group E, five mice, receiving intramuscularly empty plasmid 100 micro g on day 1, day 3, and day 5), and an empty plasmid treatment group (group F, six mice, receiving intramuscularly empty plasmid 100 micro g on day 14, day 16 and day 18). The number of EOS and the concentration of IL-4, IL-5 and IFN-gamma in the mouse bronchoalveolar lavage fluids (BALF) were detected. RESULTS: The number of EOS and the concentration of IL-4, IL-5 and IFN-gamma from group B were (0.01 +/- 0.03) x 10(8)/L, (24 +/- 4) pg/ml, (33 +/- 6) pg/ml, (725 +/- 59) pg/ml,respectively; those from group C were (0.06 +/- 0.04) x 10(8)/L, (43 +/- 13) pg/ml, (63 +/- 10) pg/ml, (626 +/- 60) pg/ml, respectively, and those from group D were (0.11 +/- 0.12) x 10(8)/L, (38 +/- 14) pg/ml, (66 +/- 14) pg/ml, (661 +/- 40) pg/ml, respectively; the difference was significant as compared with those from group A [(2.97 +/- 1.20) x 10(8)/L, (122 +/- 45) pg/ml, (126 +/- 34) pg/ml, and (435 +/- 49) pg/ml] (P < 0.001). The number of EOS and the concentration of IL-4, IL-5 and IFN-gamma from group C and group D also showed significant difference in comparison with those from group E [(1.96 +/- 0.93) x 10(8)/L, (110 +/- 24) pg/ml, (112 +/- 11) pg/ml and (464 +/- 51) pg/ml], and group F [(2.11 +/- 0.90) x 10(8)/L, (88 +/- 17) pg/ml, (107 +/- 6) pg/ml and (481 +/- 64) pg/ml] (P < 0.01). CONCLUSION: The mIL-12 plasmid can significantly inhibit airway inflammation. Its regulatory effect on the balancing of Th1/Th2 cytokines may be a possible mechanism.

Animals↗
PubMed1992

Cloning of two mouse genes encoding alpha 2-adrenergic receptor subtypes and identification of a single amino acid in the mouse alpha 2-C10 homolog responsible for an interspecies variation in antagonist binding.

Molecular cloning and ligand binding studies have shown the alpha 2 class of adrenergic receptor (alpha 2-AR) to be a family of at least three related subtypes in humans. These studies have not, however, identified distinct subtype-specific functions for these receptors in vivo. It should be possible to extend the analysis of alpha 2-AR subtype function to the animal level through the use of experimental mammalian embryology in mice. To begin this process, we have isolated two mouse genomic clones encoding alpha 2-AR subtypes and expressed these genes in COS-7 cells for binding studies. Sequence homology and ligand binding data allow the assignment of one clone (M alpha 2-4H) as the mouse homolog of the human alpha 2-C4 subtype. The other clone (M alpha 2-10H) closely resembles the human alpha 2-C10 subtype in sequence but binds with significantly lower affinity to yohimbine and rauwolscine, members of a distinct class of bulky alpha 2-selective antagonists commonly used to evaluate alpha 2-AR function in vivo. To define the domain(s) responsible for this unusual binding property, we constructed a series of M alpha 2-10H/human alpha 2-C10 chimeric receptors. Analysis of these receptors identified a conservative Cys201 to Ser201 change in the fifth transmembrane domain of M alpha 2-10H as being responsible for the low affinity of the mouse receptor for yohimbine.

Adrenergic alpha-Antagonists↗
PubMed2004

The inhibitory effects of mouse ICOS-Ig gene-modified mouse dendritic cells on T cells.

The main approach to reduce graft rejection has been focused on the development of immunosuppressive agents at present. Although these strategies have reportedly reduced graft rejection, there has been a reciprocal increase in more severe immunosuppression and lethal infections, as well as severe side effects. Blockade of costimulatory T cell response has been proved as one of useful strategies to reduce graft rejection. Furthermore, it has been shown that infusion of dendritic cells (DCs) with a potent negative regulatory ability for T cells could prolong allograft survival. In this study mouse DCs (mDCs) were transfected with the recombinant plasmid pcDNA3.0 containing mouse inducible costimulator-Ig (mICOS-Ig) cDNA by electroporation. The transient expression of mICOS-Ig in mDC could be detected by ELISA and SDS-PAGE. Mouse ICOS-Ig fusion protein expressed in mDC and mICOS-Ig gene-modified mDC could inhibit lymphocyte proliferation in mixed lymphocyte culture (MLC) in vitro. Furthermore, mICOS-Ig gene-modified mDC could inhibit lymphocyte proliferation in recipient mice. These results suggested that mICOS-Ig gene-modified mDC exerted inhibitory effects on T cells, and might be suitable for treatment or prevention of graft rejection and immunopathologic diseases.

Animals↗
PubMed1990

In vitro bone marrow purging of multidrug-resistant cells with a mouse monoclonal antibody directed against Mr 170,000 glycoprotein and a saporin-conjugated anti-mouse antibody.

Selective elimination of multidrug resistance-positive cells (LoVo/Dx) was obtained by using the monoclonal antibody MRK 16, which recognizes a surface epitope of the Mr 170,000 glycoprotein, and a sheep anti-mouse immunoglobulin antibody, conjugated to the ribosome-inactivating protein saporin 6. The killing was greatly decreased or even abolished by adding the monoclonal antibody at a 100-fold concentration. Both the MRK 16 and anti-mouse saporin 6 conjugate did not show any killing activity when they were used separately. In cell suspensions composed of 90% normal bone marrow cells and 10% multidrug resistance-positive cells, the monoclonal antibody MRK 16 followed by the anti-mouse immunotoxin caused the elimination of 99% multidrug resistance-positive cells, as revealed by immunofluorescence and immunocytochemistry as well as by a clonal assay. Human normal hematopoietic precursors (granulomonocytic colony-forming units, erythroid burst-forming units, and multipotent granulomonocytic, erythroid, and megakaryocytic-forming units) were not affected by the MRK 16 plus immunotoxin treatment. This technique might be suitable for ex vivo bone purging in an appropriate clinical setting, such as autologous bone marrow transplantation.

Antibodies, Monoclonal↗
PubMed1976

Carrier state of antibody and viruses in a mouse breeding colony persistently infected with Sendai and mouse hepatitis viruses.

In a large-scale mouse breeder colony persistently infected with Sendai and mouse hepatitis viruses, most adult breeders 8 wk or more of age were shown to have antibodies to both viruses when monitored over a periof of 20 mo. Antibody to Sendai virus, apparently transmitted from the dam, was detected in 76% and 2% of mice aged 3 and 4 wk. respectively, and 64% and 100% of mice aged 6 and 8 wk, respectively. By seroconversion of sentinel cage-mates, a Sendai virus-carrier state was demonstrated with 6-wk-old mice but not with those either 4 wk or 10 wk of age, suggesting that breeder candidates about 6 wk of age may play an important role in establishing and perpetuating Sendai infection in this breeding colony. With mouse hepatitis virus, however, mice aged 4 wk or older seem to be effective transmitters of the virus, while some of these mice were found to have antibody to the virus.

Age Factors↗
PubMed1990

Genomic sequencing of the 5'-flanking region of the mouse beta-globin major gene in expressing and nonexpressing mouse cells.

Genomic sequencing of two CG sites located in the 5'-flanking promoter region of the mouse beta-globin major gene shows these sites to be heavily methylated in the DNA from L929 mouse fibroblasts, a cell line that does not express the beta-globin gene. By contrast, the same CG sites in the DNA obtained from murine erythroleukemia cells, which can express the beta-globin gene, are unmethylated. The results suggest that either differentiation of progenitor cells to form the erythroid precursor murine erythroleukemia cell and/or transformation by the Friend virus group leads to demethylation of these CG sites. Final activation of the transcription process for the mouse beta-globin gene does not require demethylation in the 5'-promoter region of the DNA.

5-Methylcytosine↗
PubMed1985

Keratin gene expression in mouse skin tumors and in mouse skin treated with 12-O-tetradecanoylphorbol-13-acetate.

Alterations in the pattern of epidermal differentiation and proliferation occur during mouse skin carcinogenesis. We have used cDNA clones corresponding to the major keratin subunits synthesized in differentiating epidermal cells (Mr 67,000 and 59,000) and in proliferating epidermal cells (Mr 60,000, 55,000, and 50,000) to study changes in keratin gene transcript levels in mouse epidermis exposed to tumor promoters. The same probes were used to characterize the keratin expression patterns in benign and malignant skin tumors. A single topical treatment with 12-O-tetradecanoylphorbol-13-acetate caused a rapid initial decrease in the epidermal transcript levels corresponding to the Mr 67,000 and 59,000 keratin subunits. By 48 h the transcript level for the Mr 67,000 keratin subunit was restored to control values, whereas the transcript levels for the Mr 59,000 subunit returned to control at a slower rate. In contrast, the transcript level for the Mr 55,000 subunit was increased substantially 12- 48 h after treatment, the Mr 50,000 subunit transcript increased to a lesser extent, and the Mr 60,000 subunit message was transiently decreased at 12 h but returned to the level of solvent-treated skin by 24 h. Single exposure to the incomplete tumor promoters 4-O-methyl-12-O-tetradecanoylphorbol-13-acetate, the ionophore A23187, and mezerein induced changes in keratin gene transcripts similar to those of 12-O-tetradecanoylphorbol-13-acetate. The antipromoter fluocinolone acetonide, administered with 12-O-tetradecanoylphorbol-13-acetate, partially inhibited the decrease in the Mr 59,000 and 67,000 transcripts and completely inhibited the increase in the Mr 55,000 transcript. In skin papillomas produced by initiation and promotion, keratin gene expression was similar to normal skin, with the exception of a two-fold increase in the transcript levels for the Mr 55,000 keratin subunit. However, in carcinomas, the transcript levels for the Mr 67,000 and 59,000 subunits were only 1-3% of those observed in untreated mouse epidermis. In concert with other data, the rapid and selective loss of transcripts for differentiation-related keratins after exposure to both complete and incomplete tumor promoters is most consistent with an accelerated rate of maturation in differentiating keratinocytes, resulting in the rapid production of transcript-depleted fully mature squames. The enhanced level of Mr 55,000 transcripts suggests a concomitant increase in the number of all cells or a subset of cells in the proliferative compartment.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

The receptor for 2,3,7,8-tetrachlorodibenzo-p-dioxin in the mouse hepatoma cell line Hepa 1c1c7. A comparison with the glucocorticoid receptor and the mouse and rat hepatic dioxin receptors.

The molecular properties of the receptor for 2,3,7,8-tetrachlorodibenzo-p-dioxin in the mouse hepatoma cell line Hepa 1c1c7 were investigated. The receptor was found to represent a highly asymmetrical molecule with a sedimentation coefficient, s20,w, of approximately 8 S, a Stokes radius of 7-8 nm, and a calculated Mr approximately equal to 260,000-300,000. In comparison, the Hepa 1c1c7 glucocorticoid receptor in analogy to the glucocorticoid receptor in general as well as the C57BL/6 mouse and rat hepatic dioxin receptors are molecules with an s20,w value of 4-5 S, a Stokes radius of approximately 6 nm, and a calculated Mr approximately equal to 100,000. In the presence of 20 mM sodium molybdate, a large Mr approximately equal to 270,000-310,000 form of the Hepa 1c1c7 glucocorticoid receptor is stabilized which is hydrodynamically indistinguishable from the Mr approximately equal to 260,000-300,000 Hepa 1c1c7 dioxin receptor. Sodium molybdate does not have any effect on the molecular properties of the Hepa 1c1c7 dioxin receptor. In conclusion, the large form of dioxin receptor present in Hepa 1c1c7 mouse hepatoma cells in the absence of sodium molybdate is strikingly similar to molybdate-stabilized steroid hormone receptors as well as the molybdate-stabilized form of the dioxin receptor previously demonstrated in rat hepatic cytosol. Therefore, the Hepa 1c1c7 dioxin receptor might offer an interesting model for studies on the structure and function of Mr approximately equal to 300,000 forms of soluble receptors.

Animals↗
PubMed1986

Purification and characterization of a senile amyloid-related antigenic substance (apoSASSAM) from mouse serum. apoSASSAM is an apoA-II apolipoprotein of mouse high density lipoproteins.

Two putative serum precursors which cross-react with antiserum against murine senile amyloid protein (ASSAM) were isolated from the high density lipoprotein (HDL) of normal mouse serum. Apolipoproteins designated "apoSASSAM-1" and "apoSASSAM-2" have the same molecular weight as tissue amyloid fibril protein. ApoSASSAM-1 and apoSASSAM-2 migrate to an intermediate position between apoA-I and apoC on alkaline-urea polyacrylamide gel electrophoresis and are present mainly in HDL apoproteins and to a slight extent in very low density lipoprotein apoproteins when compared to apoC. ApoSASSAM-1 and apoSASSAM-2 are polymorphic; there are two apparent isoproteins of apoSASSAM-1 with isoelectric points of 4.72 and 4.79 and two major isoproteins of apo-SASSAM-2. Subunit bands of ASSAM separated by alkaline-urea polyacrylamide gel electrophoresis and that migrated to the same positions as apoSASSAM-1 and apoSASSAM-2 were labeled by anti-apoSASSAM-1 antiserum. The amino acid compositions of apoSASSAM-1 and apoSASSAM-2 were much the same and closely resembled those of ASSAM and mouse apoA-II. Sequence analysis of apoSASSAM and ASSAM revealed a blocked amino terminus. ApoSASSAM is considered to be a mouse apoA-II and probably transforms to amyloid fibril "ASSAM" in tissues through a process yet to be clarified.

Amino Acids↗
PubMed1979

Detection of thymosin 5 in calf and mouse thymus and in nude mouse dysgenetic thymus.

Thymosin 5 was traced in calf and mouse thymuses by fluorochrome-labelled rabbit anti-calf thymosin. The presence of thymosin 5 or its individual components was found 1. in groups of cortical epithelial cells in calf thymuses and in single cortical epithelial cells in mouse thymuses. 2. In some marginal (blastema) cells of the thymus cortex of calves and 14-day-old mice. 3. In perivascular epithelial cells of the calf thymus. 4. In occasional medullary epithelial cells of the calf and mouse thymus. In all cases there was a marked alternation of entirely negative and positive cell-containing thymic lobuli. In 4 of 13 cases comparatively strong positivity was found in tightyly arranged epithelial cells in an individual acinus in the dysgenetic thymus of nude mice, the positive cases being concentrated among the youngest mice studied.

Animals↗
PubMed1978

Detection of a cell surface antigen common to a mouse myeloma and a population of mouse thymocytes.

A new antigen termed PTA (plasmocytoma thymus antigen) is described which occurs on 70--80% of mouse thymocytes of all mouse strains tested and on an IgG 2b producing BALB/c plasma cell tumor. PTA is detectable on mouse spleen and lymph node cells. It is absent from liver, brain, bone marrow, and antibody plaque forming cells. PTA is not related to theta antigen and is not detectable on rat thymocytes.

Animals↗
PubMed1985

A human-mouse chimeric immunoglobulin gene with a human variable region is expressed in mouse myeloma cells.

We have constructed and obtained expression of a chimeric human-mouse immunoglobulin gene after transfection into mouse myeloma cells. A human VDJH gene segment was joined to a mouse C kappa gene in the plasmid vector pSV2-gpt, and the construct was transfected into J558L cells by protoplast fusion. Analyses of six transformants by RIA and SDS-PAGE indicated that the chimeric protein was synthesized in large amounts in five. A kappa-specific transcript was observed by Northern blot analysis. Four out of five clones were stable producers of this chimeric chain over a period of 10 mo.

Animals↗
PubMed1979

[In-vitro effect of X-irradation on respiration and glycolysis of Ehrlich-ascitic carcinoma cells of the mouse--an experimental comparison with the mouse tumour-tetanus assay (author's transl)].

Depending on the dose of X-rays, in-vitro irradiation of Ehrlich-ascitic carcinoma cells of the mouse affected both respiration and glycolysis. 15,000 R irradiation suppressed the aerobic and anaerobic energy metabolism rather strongly followed by a reduction of the "take" and growth of the subcutaneously injected tumour cells, as opposed to the growth behaviour of non-irradiated cells. In analogy, tetanus mortality rates were reduced in the mouse tumour-tetanus assay with 15,000 R irradiated cells. On the other hand, irradiation with 2,000 R of Ehrlich carcinoma cells resulted in unchanged rates of respiration and glycolysis, in spite of the strongly limited growth capacity of the tumour cells. The tumour-tetanus assay of the mouse showed good correlation with subcutaneous tumour growth; no such correlation was found in the tetanus assay and the manometric values of respiration and glycolysis with 2,000 R irradiated tumour cells.--After subcutaneous injection of mixed cell suspensions consisting of 1 x 10(5) viable and 1 x 10(6) 15,000 R irradiated Ehrlich-ascitic carcinoma cells as well as of 3 x 10(2) tetanus spores per single dose, we observed similar rates of tumour growth, or tetanus mortality, respectively, if 1 x 10(5) viable tumour cells alone were administered together with 3 x 10(2) tetanus spores, without addition of irradiated tumour cells.

Animals↗
PubMed1982

Different susceptibilities of cultured mouse cell lines to mouse interferon.

Cultured mouse cells were treated with 3.3 approximately 10,000 units of mouse interferononon for 3 days and further cultivated in fresh medium for 2 days (recovery incubation). The IC50 (concentration of drug required for 50% inhibition) of interferon was not changed much after the recovery incubation. The most susceptible cell line to interferon was B16 melanoma; the IC50 was 10.5 units per ml of medium on day 3 after the start of treatment. P388 leukemic cells, Lewis lung carcinoma cells, and colon adenocarcinoma 38 cells were moderately susceptible to interferon and the IC50s of these cell lines were 200, 80, and 180 units per ml medium, respectively, on day 3. The cells least susceptible to interferon were those of colon adenocarcinoma 26; IC50 was greater than 10,000 units per ml. In the recovery incubation, the growth of B16 melanoma cells, P388 leukemic cells, Lewis lung carcinoma cells and colon adenocarcinoma 38 cells was considerably inhibited when these cells were treated with more than 100 approximately, 1,000 units of interferon per ml medium. The rate of multiplication was usually more than 1 for these cell lines, except for Lewis lung carcinoma cells where the rate of multiplication was less than 1. This indicates that interferon is not cytocidal towards B16 melanoma cells, P388 leukemic cells, or colon adenocarcinoma 38 cells, but mouse interfer is cytocidal towards Lewis lung carcinoma cells when the cells are treated with a relatively high concentration of interferon and then cultured in the medium without interferon.

Adenocarcinoma↗
PubMed1983

Growth of normal and neoplastic mouse mammary epithelial cells in primary culture: stimulation by conditioned medium from mouse mammary fibroblasts.

Conditioned medium obtained from mouse mammary fibroblasts markedly stimulated both DNA synthesis and cell proliferation in primary monolayer cultures of mouse mammary tumor cells. Growth of normal mammary epithelial cells from virgin female mice was likewise stimulated by the conditioned medium. The growth-stimulating activity was absent in conditioned media from 3T3 cells, 3T6 cells, mouse embryonic and lung fibroblasts, mammary tumor cells and normal mammary epithelial cells. Stimulation of DNA synthesis in mammary tumor cells was also observed with epidermal growth factor (EGF), although the effect was less than that observed with the conditioned medium. Receptor studies using 125I-labeled EGF further showed that the specific binding of EGF to mammary tumor cells was not inhibited by the conditioned medium. The molecular weight of the growth-stimulating activity in mammary fibroblast-conditioned medium was estimated to be approximately 100,000 daltons by Sephadex G-200 column chromatography. These observations suggest that mammary fibroblasts, which constitute the stroma of the mammary gland, produce a mammary epithelial cell growth factor(s) distinct from EGF.

Animals↗