Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radiation-induced L8313 leukemia bearing mice (L8313 mice) had marked granulocytosis with splenomegaly. Hemopoietic stem cells and progenitors increased in the spleen but not in the bone marrow. Spleen conditioned-medium and serum from L8313 mice induced the formation of granulocyte-macrophage colonies (CFU-GM), erythroid bursts (BFU-E) and mixed colonies (CFU-Mix). Bone marrow conditioned medium did not show such activity. A cell line (STIL-3) was established from the spleen cells of L8313 mice. Surface marker analysis showed that the established cells were suppressor T cell. The cells produced IL-3 and GM-CSF in vitro, and induce essentially the same "leukemic" response in recipient mice. Inoculation of STIL-3 in diffusion chamber also induced leukemoid reaction, i.e. a marked granulocytosis with splenomegaly. Therefore, L8313 leukemia may be linked to an abnormality of growth and production of hemopoietic factors in hemopoietic regulatory cells.
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PMID:Physiopathological studies on granulocyte-macrophage colony stimulating factor and multi colony stimulating factor producing leukemia, L8313, induced by irradiation of C3H mice. 287 75

A new kind of myeloproliferative disorder (L-8313) has been discovered. It was transplantable into syngeneic mice with spleen cells. The mice showed hepato-splenomegaly with a marked leukocytosis and anemia 3 weeks after transplantation of L-8313 cells. The number of GM-CFU and CFU-S per spleen increased to more than 40 times normal. The results of chromosomal and PGK analysis demonstrated that these increased stem cells were of host origin. Both the culture medium of the spleen cells and the serum from L-8313 bearing mice showed high levels of IL-3, BPA and CSF. Consequently, hematopoietic cells of the host mice underwent remarkable proliferation in response to these stimulating factors when L-8313 cells were transplanted. We also have been successful in establishing an in-vitro cell line and have maintained it for over one year. The phenotype of L-8313 cells was Thy 1.2 positive. Some L-8313 cells showed a positive acid phosphatase reaction but the cytochemical character of myeloid lineage was not observed. Therefore, L-8313 is considered to be a T-cell derived hematopoietic regulatory cell neoplasm with the ability to produce several hematopoietic stimulating factors.
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PMID:Myeloproliferative disorder due to abnormal production of hematopoietic stimulators. 288 2

From December 1982 to June 1985, we diagnosed LAV/HTLV-III infection in 16 children of African origin living in Belgium or referred to one of the hospitals participating in this study. Diagnosis was proven in seven of them by isolation of virus of the LAV/HTLV-III group. In the nine others, LAV/HTLV-III infection was highly probable because of the presence of antibodies against the virus (seven subjects) or clinical and immunological evidence of immune deficiency associated with a parental history of LAV/HTLV-III infection (two subjects). Five of these children had a severe illness starting in the first months of life (range 20 days--4 months) and died within 4 months (range 19 days--10 months). Eight children presented later in life (mean age 35 months, range 2-66 months) with a milder and more chronic disease characterized by the presence of generalized lymphadenopathy (6/8), hepatomegaly (5/8), splenomegaly (5/8), interstitial pulmonary infiltration (4/8), parotid swelling (3/8), CSF lymphocytosis (3/5), diarrhoea without pathogen isolated (1/8) and fever (1/8). At least one of the parents of each child was of African origin. At the time of birth of their child two mothers and one father had an AIDS-related complex. After a mean period of 34 months (range 3-87 months) five fathers and six mothers had a symptomatic LAV/HTLV-III infection (AIDS or AIDS-related complex).
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PMID:LAV/HTLV-III infection in children of African origin: experience in Belgium. 294 77

Mouse C127I cells were transformed with a chimeric plasmid consisting of bovine papillomavirus DNA and human granulocyte-colony-stimulating factor (G-CSF) cDNA placed under the control of the SV40 early promoter. The transformed cells secreted constitutively a high level of human G-CSF, 10-20 micrograms/ml in a low-serum medium. The secreted G-CSF has been purified to homogeneity by a two-step procedure including gel filtration and hydrophobic column chromatography. The purified recombinant G-CSF runs as a single band with an apparent Mr of 19,000 on a polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. This value corresponds to that of the native human G-CSF purified from the medium conditioned by human carcinoma CHU-2 cells. The recombinant human G-CSF was as active as native G-CSF in vitro in supporting proliferation of mouse NFS-60 cells and stimulating colony formation from human as well as mouse bone marrow cells. When the recombinant human G-CSF was subcutaneously administrated into mice, a remarkable stimulation of granulopoiesis and splenomegaly was observed.
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PMID:Characterization of recombinant human granulocyte-colony-stimulating factor produced in mouse cells. 303 99

The antileukemic activity of murine recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) and a combination of rGM-CSF and recombinant interleukin-3 (rIL-3) was examined by using a murine model of spontaneous B-cell leukemia (BCL1) in BALB/c mice. All untreated mice inoculated with 2 x 10(2) BCL1 cells developed leukemia within 4 weeks, with extreme lymphocytosis and a massive increase in both spleen weight and cell number while the number of myeloid progenitors (CFU-C) per spleen was decreased. In contrast, rGM-CSF-or rGM-CSF- and rIL-3-treated recipients did not show any evidence of leukemia or splenomegaly at 4 weeks and showed a significant increase in CFU-C per spleen. Hematologic parameters in the peripheral blood of untreated mice showed anemia and thrombocytopenia. Significant elevations in these parameters were recorded in mice treated with either protocol of CSF. Treatment of recipient mice with either rGM-CSF or rGM-CSF and rIL-3 prolonged their median survival from 6 weeks in untreated controls (range, 5 to 9 weeks) up to the time they were killed at 105 days. Adoptive transfer of spleen cells obtained from mice treated with rGM-CSF, mice treated with a combination of rGM-CSF and rIL-3, and untreated controls, into normal secondary recipients indicated improved survival in recipients inoculated with rGM-CSF. These data indicate that CSFs may inhibit in vivo expansion of leukemic cells of lymphoid origin.
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PMID:Therapeutic potential of recombinant granulocyte-macrophage colony-stimulating factor and interleukin-3 in murine B-cell leukemia. 304 86

Human recombinant macrophage CSF (CSF-1) was administered i.v. to mice. After four daily injections there was a dose-dependent increase in the responsiveness of bone marrow cells from the treated animals to CSF-1 in vitro. At the highest dose tested (20,000 U/day) there was a selective 10-fold increase in the circulating population of mature monocytes. CSF-1 treatment also increased the macrophage content of the liver and peritoneal cavity and caused splenomegaly. The macrophages isolated from the peritoneum of CSF-1-treated animals were larger and expressed higher levels of the macrophage-specific F4/80 Ag. These data demonstrate that CSF-1 can act as a circulating regulator of the mononuclear phagocyte system.
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PMID:The effect of human recombinant macrophage colony-stimulating factor (CSF-1) on the murine mononuclear phagocyte system in vivo. 305 99

We have studied the clinical presentation and course of a chronic inflammatory disease occurring in childhood and observed in 30 patients. The first symptoms were generally present at birth, except in a few patients where they were first noticed in early infancy. All the patients had the association of three main symptoms: neurological, cutaneous and articular. The skin rash was the first symptom observed in all the patients and looked like a chronic non pruritic urticaria varying during the day. The articular manifestations involved knees, ankles and feet, elbows, wrists and hands unaffecting the other joints. They could be mild giving arthritis during flare-ups or severe with major radiological modifications affecting the epiphysis, metaphysis and growth cartilage. The neurological manifestations were characterized by a chronic meningitis and symptoms indicating meningeal irritation: headaches, seizures, spasticity of legs. Most patients had a cerebral atrophy and a low IQ. Sensory organ involvement occurred progressively during the follow-up: ocular inflammation with optic atrophy, deafness and hoarseness. Common morphological features characterized these patients with short stature, head enlargement, saddle back nose and short and thick extremities with clubbing of fingers. The course was that of a chronic inflammatory disease with numerous flare-ups associating fever, splenomegaly and adenomegaly. Except for a high level of eosinophils in blood, CSF and tissues, the biology was non specific and only exhibited features of inflammation. Except for two families, the disease was sporadic. A high frequency of prematurity with features resembling a foetal infection was observed but no proof of a possible causal virus has so far been found so that etiology remains unknown.
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PMID:A chronic, infantile, neurological, cutaneous and articular (CINCA) syndrome. A specific entity analysed in 30 patients. 348 35

The effects of an autologous transplanted mammary tumor (RIII-T3) on hemopoiesis in RIII mice are described. Tumor-bearing animals died 30 to 40 days after inoculation and displayed splenomegaly, extreme neutrophilia, and moderately increased monocyte levels in the spleen, peripheral blood, and bone marrow. The precursors of neutrophils and monocytes, granulocyte/macrophage colony-forming cells (GM-CFC) were elevated in the spleen, bone marrow, and peripheral blood. RIII-T3-conditioned medium stimulated bone marrow GM-CFC and caused the myelomonocytic cell line, WEHI-3B, to differentiate in vitro. The conditioned medium did not stimulate erythroid, megakaryocyte, or eosinophil colony formation. When conditioned medium was fractionated, two peaks of activity corresponding to GM-CSF and G-CSF were observed, suggesting that the extreme neutrophilia observed in tumor-bearing animals may result from chronic exposure of the hemopoietic system to these hemopoietic hormones.
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PMID:Effects of a murine mammary tumor on in vivo and in vitro hemopoiesis. 387 4

Inoculation of BMA1 cells into BALB/c nude mice formed tumors (BMA1 tumor) that were transplantable into ddY mice, and induced marked granulopoiesis in vivo. Histological study revealed that the tumor was a fibrosarcoma, some parts of which were calcified, and consisted of hemopoietic foci surrounded by adipose tissue. This tumor was regarded as producing CSF in vivo as well as in vitro, since CSF activity was detected in sera of the tumor-bearing mice and tumor extract. Granulopoiesis and splenomegaly developed, associated with an increase of stem cells in the spleen. The number of CFUc and CFUs in the spleen increased to about 91 times and 21 times those of control mice, respectively, whereas the number of stem cells in the tibia did not change significantly. The number of peripheral leukocytes increased to 15 times that of normal mice and amounted to 78% of matured granulocytes. After tumor resection these hematological changes were reversed. The findings suggest that the granulopoiesis in BMA1 tumor-bearing mice may be induced by CSF produced by BMA1 tumor and that the spleen may be a direct target organ of the excessive amount of CSF.
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PMID:Enhanced granulopoiesis in mice transplanted with colony-stimulating factor-producing BMA1 tumor. 392 8

Three unrelated children (one girl and two boys) have had since birth a syndrome characterized by a permanent skin rash which becomes more intense during flare-ups associated with fever, lymphadenopathy, splenomegaly, and arthritis symmetrically involving the large joints. In one boy, typical psoriasis was observed at age 3 years. In two patients, roentgenograms of the joints showed early patellar ossification and an abnormal epiphyseal appearance. The three children also had neurologic involvement, with mental retardation, enlarged head circumference, eye lesions, late closure of the anterior fontanel, and a chronic meningitis with infiltration by polymorphonuclear cells. No immunologic abnormalities were found, but polymorphonuclear cells infiltrated the skin, lymph nodes, synovial fluid, and CSF.
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PMID:Arthropathy with rash, chronic meningitis, eye lesions, and mental retardation. 725 69


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