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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Young male crossbred chicks were fed crystalline amino acid diets containing excess L-methionine or DL-homocysteine to evaluate factors causing methionine toxicity. Chicks were fed diets containing graded levels of excess methionine from 0% to 2.0%. Rate of gain was reduced at all levels of excess methionine, but the magnitude of depression was greater between 1% and 2% than between 0% and 1% excess methionine. Methionine accumulated in plasma of birds fed excess methionine, but plasma levels of homocysteine, cystathionine and cystine remained essentially unchanged. Spleen iron levels increased linearly and blood hemoglobin decreased linearly when chicks were fed diets containing greater than 1% excess methionine, a level equivalent to about 3 times the chicks' requirement. Chicks fed 1.36% homocysteine had reduced gain and gain:feed values, but spleen iron and hemoglobin levels were unchanged. 3-Methylthiopropionate, a possible metabolite in a proposed alternate pathway, caused a precipitous increase in spleen iron levels. Various methyl sources (betaine, choline, methyl acetate) when fed in excess failed to increase spleen iron levels. Methyl mercaptan and methyl mercaptoacetate likewise did not result in an increase in spleen iron deposition. Both the hemosiderosis condition and the reduced food utilization caused by excess methionine were reversed by supplemental glycine plus threonine.
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PMID:Factors affecting methionine toxicity and its alleviation in the chick. 66 Feb 99

The influence of lead on iron absorption was investigated at various stages of development in rat pups exposed to lead first through mothers' milk and later in their solid diet. Hematocrit, hemoglobin, iron absorption, and tissue iron concentration were measured on d 14, 20, 23, 29, 35, 42, and 63 after birth. Both hematocrit and hemoglobin in the lead-exposed group were significantly below control levels at all periods earlier than d 42 and 63, respectively. Absorption of iron ([59Fe]-ferrous citrate in 10(-4)M FeSO4) from intestinal loops measured over 1/2 h remained at preweaning levels (10-12% of total activity added to the loop) for at least 1 wk after weaning in the lead-exposed rats, whereas in control animals iron absorption fell to adult levels (3-4%) at weaning. Spleen weight was significantly elevated in lead-exposed rats compared with control rats at all ages beyond d 14. However, spleen iron content (micrograms of Fe per gram of tissue) was not significantly elevated in the lead-exposed group before d 42. The results indicate that exposure to lead does not reduce iron absorption from the intestinal tract; thus alteration of intestinal iron absorption does not contribute to lead-induced anemia. Indeed, lead-exposed rats demonstrated increased iron uptake.
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PMID:Effect of exposure to lead on maturation of intestinal iron absorption of rats. 68 5

Spleen cell suspensions of methylcholanthrene-induced tumor-bearing mice were tested for their ability to inhibit tumor growth in vitro. The level of cytostasis was correlated with tumor growth and disappeared rapidly after surgical removal of the tumor. Pretreatment by anti-Thy 1-2 antiserum and complement, or by carbonyl iron and a magnet, showed that adherent, non-T-cells were the main effector cells of the cytostatic antitumor effect. Thymus cells suspensions from tubor-bearing mice were not effective in inhibiting tumor growth. This cytostatic effect was not tumor specific, inasmuch as the same spleen cell suspension inhibited growth of tumor cells of different origin.
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PMID:Cytostatic effect of spleen cells of tumor-bearing mice on syngenetic tumor cells. 87 Jan 85

Spleen cells collected from mice bearing transplanted chemically induced syngeneic fibrosarcomas non-specifically inhibited DNA synthesis of sarcoma and lymphoma target cells in vitro. Splenocytes from mice hyper-immunized against a syngeneic sarcoma specifically inhibited DNA synthesis of the tumour used for immunization. The impairment of tumour-cell DNA synthesis was associated in vitro with cytostasis, and lysis of the target cells was not seen. Since treatment with anti-theta serum and complement did not impair cytostatic action of the spleen cells, and since thymus-deprived animals showed similar activity to normal mice, T lymphocytes were not involved in non-specific cytostasis. Removal of phagocytic adherent cells by carbonyl iron markedly inhibited the cytostatic activity of the spleen cells, suggesting a role in this reaction for cells of the monocyte-macrophage series. The presence of an actively growing sarcoma was a prerequisite for the expression of non-specific cytostasis, since surgical excision resulted in complete disappearance of this activity of spleen cells.
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PMID:Non-specific cytotoxicity of spleen cells in mice bearing transplanted chemically induced fibrosarcomas. 88 83

Spleen and bone marrow patterns of response differ in mice subjected to erythropoietic depressors. Radioiron injected a few hours after a high dose of cyclophosphamide or x-irradiation is retained in the bone marrow. The magnitude of medullary retention is closely related to the number of cells able to synthesize hemoglobin at the moment of iron administration, and to the rate of cell death provoked by the cytotoxic agent. Depressors such as Actinomycin and transfusion, that block the differentiation of stem cells while allowing normal maturation of the erythroid cohort, do not induce marrow entrapment of iron. By contrast, retention is never observed in the spleen, where the 59-Fe turnover is not influenced by the mechanism and magnitude of aplasia. A functional lack of homogeneity of splenic and bone marrow erythropoiesis, hemoglobin metabolism and/or handling of iron stores is proposed. These results would be in agreement with other data from the literature reporting physiological differences among the various sectors of the reticuloendothelial system.
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PMID:Some aspects of iron metabolism during erythropoietic depression in the mouse. 89 66

Spleen cells from 2- to 3-month-old normal mice of some strains having a low incidence of spontaneous leukemia were found to lyse cells of the spontaneous AKR leukemia K36 in the 51Cr release assay. Incubation of 51Cr-labeled ADR K36 cells with spleen cells from normal C57BL/6, C57L, C57BL/10, and RF mice resulted in the release of significantly more 51Cr than that released in the presence of medium alone. In contrast, 51Cr released from AKR K36 cells after incubation with spleen cells from mice of the high leukemic strains AKR and C58 was less than that released spontaneously. The results of competitive inhibition tests when C57BL/6 spleen cells were incubated simultaneously with 51Cr-labeled AKR K36 target cells and varying numbers of nonlabeled cells demonstrated that the cytotoxic activity of normal C57BL/6 spleen cells was directed against an antigen(s) associated with several leukemias, but that was undetectable on normal thymocytes. Pretreatment of C57BL/6 spleen cells with carbonyl iron and a magnet, which removed phagocytic macrophages, did not decrease the cytotoxic acitivity for AKR K36 cells.
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PMID:Lysis of leukemia cells by spleen cells of normal mice. 105 93

Friend leukemia virus (FV) suppressed the proliferative responses of spleen, lymph node, marrow, and thymus cell populations to various T- and B-cell mitogens. Cells taken from mice, e.g. BALB/c genetically susceptible to leukemogenesis in vivo were much more susceptible to suppression of mitogenesis in vitro than similar cells from genetically resistant mice, e.g., C57BL/6. Nylon wool-purified splenic T cells from BALB/c and C3H mice lost susceptibility to FV-induced suppression of mitogenesis but became suppressible by addition of 10% unfiltered spleen cell. Thus, FV mediates in vitro suppression of lymphocyte proliferation indirectly by "activating" a suppressor cell. The suppressor cell adhered to nylon wool but not to glass wool or rayon wool columns. Pretreatment of spleen cells with carbonyl iron and a magnet did not abrogate the suppressor cell function. Suppressor cells were not eliminated by treatment with rabbit antimouse immunoglobulin (7S) and complement (C). However, high concentrations of anti-Thy-1 plus C destroyed suppressor cells of the spleen; thymic suppressor cells were much more susceptible to anti-Thy-1 serum. Nude athymic mice were devoid of suppressor cells and their B-cell proliferation was relatively resistant to FV-induced suppression in vitro. The suppressor cells in the thymus (but not in the spleen) were eliminated by treatment of mice with cortisol. Thus, FV appears to mediate its suppressive effect on mitogen-responsive lymphocytes by affecting "T-suppressor cells." Spleen cells from C57BL/6 mice treated with 89Sr to destroy marrow-dependent (M) cells were much more suppressible by FV in virto than normal C57BL/6 spleen cells. However, nylon-filtered spleen cells of 89Sr-treated C57BL/6 mice were resistant to FV-induced suppression in vitro, indicating that the susceptibility of spleen cells from 89Sr-treated B6 mice is also mediated by suppressor cells. Normal B6 splenic T cells were rendered susceptible to FV-induced suppression of mitogenesis by addition of 10% spleen cells from 89Sr-treated B6 mice. Thus, M cells appear to regulate the numbers and/or functions of T-suppressor cells which in turn mediate the immunosuppressive effects of FV in vitro. Neither mitogen-responsive lymphocytes nor T-suppressor cells are genetically resistant or susceptible to FV. The genetic resistance to FV is apparently a function of M cells, both in vitro as well as in vivo.
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PMID:Mechanisms of genetic resistance to Friend virus leukemia. III. Susceptibility of mitogen-responsive lymphocytes mediated by T cells. 108 14

The normal human lymphocyte population which exhibits "spontaneous" cytolysis of EB2 Burkitt's lymphoma cells has been characterized. The effector cell has EA and EAC' receptors but lacks E receptors and probably surface Ig. "Spontaneous" anti-EB2 cytotoxicity was not reduced by preincubation of the effector cells with plastic or iron carbonyl or by passage through cotton wool or agarose columns but was reduced by passage through nylon wool columns. Thymocytes were not cytotoxic to EB2 cells, and chronic lymphocytic leukaemia cells (of B cell characteristics) had reduced cytotoxicity compared with normal lymphocytes. Cells from various lymphoid organs of rats and guinea-pigs were also cytotoxic to EB2 cells with reactivity in spleen greater than or equal to blood greater than lymph nodes. Spleen cells from neonatally thymectomized rats had increased cytotoxicity compared with normal rat spleen cells, suggesting that T lymphocytes are not essential. The effector cell in rat spleen did not adhere to cotton wool or agarose columns, indicating some resemblance to its counterpart in human peripheral blood.
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PMID:Characterization of the normal lymphocyte population cytolytic to Burkitt's lymphoma cells of the EB2 cell line. 108 44

W/Fu rats were injected subcutaneously with low numbers of cells from the Gross leukemia virus-induced lymphoma, (C58NT)D, which induced transient tumor growth and regression (regressors), or with high numbers of tumor cells resulting in progressive tumor growth (progressors). Spleen cells from regressors had a significant reactivity in the mixed leukocyte tumor cell interation (MLTI), while spleen cells from progressors were unresponsive. Similarly, the responses to the non-specific mitogens, phytohemagglutinin and concanavalin A, were suppressed in spleen-cell cultures of progressors. Passage of spleen cells from progressors over rayon adherence columns or pretreatment with an iron/magnet technique resulted in almost complete restoration of MLTI and mitogen responses. Addition of spleen cells from progressors depressed the MLTI of spleen cells from regressors and the mitogen reactivity of normal spleen cells. Serum from progressors also suppressed MLTI and mitogen reactivity. These data indicate that, in spleens of rats bearing progressively growing tumors, suppressor cells can be demonstrated which inhibit specific reactivity to tumor-associated antigens and non-specific reactivity to mitogens. The presence of suppressor cells or of inhibitory factors in the serum may contribute to the immunosuppression frequently observed in tumor-bearing hosts.
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PMID:Inhibition of in vitro lymphoproliferative responses to tumor-associated antigens by suppressor cells from rats bearing progressively growing Gross leukemia virus-induced tumors. 117

A single dose of erythropoietin stimulates DNA synthesis in the spleen of the polycythemic mouse with the maximum effect occurring 48 h after the hormone is administered. The increase in DNA synthesis is accompanied by morphologic evidence of increased erythropoiesis and by increases in the activities per cell of both thymidine kinase and cytoplasmic high molecular weight DNA polymerase-alpha. The activity of low molecular weight DNA polymerase-beta does not change significantly. Spleen cells from mice which had received either erythropoietin or saline 48 h previously were separated into 7 density classes on discontinuous bovine serum albumin gradients. Following the administration of erythropoietin, thymidine incorporation and thymidine kinase activity showed the greatest relative increases per nucleated cell in layers 3, 4 and 5 of the gradient. DNA polymerase-alpha showed the greatest increase in cells of the denser layers 5, 6 and 7. Each layer contained normoblasts and lymphocytes. The less well differentiated erythroid elements constituted a larger proportion of cells in layers of lower density. Increases in the rates of thymidine incorporation were better correlated with increases in thymidine kinase activity than with increases in DNA polymerase activities. Measurement of iron incorporation into heme confirm the morphological impression that the cell type responsible for increased thymidine incorporation and increased DNA polymerase-alpha activity is the young normblast.
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PMID:DNA polymerase, thymidine kinase and DNA synthesis in erythropoietic mouse spleen cells separated on bovine serum albumin gradients. 125 82


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