Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat pups maintained on copper (Cu)-adequate (6ppm), Cu-deficient (2 ppm) or Cu-depleted (0 ppm) diets from parturition were killed at 8-wk. Liver Cu and serum-ceruloplasmin levels confirmed that on the 0- and 2-ppm diets, a Cu-deficient state was induced. Although body weight was unaffected by the deficiency, the liver, heart, and thymus weights (% body weight) were altered. Hepatomegaly occurred in females fed 0-ppm Cu and males fed 2-ppm Cu. Heart weights increased in both sexes fed 0-ppm Cu. Thymus weights decreased in male rats fed 0-ppm Cu. Antibody titers and natural killer-cell cytotoxicity were markedly suppressed in the animals fed 0-ppm Cu. Male rats given 2-ppm Cu showed reduced antibody titer. Delayed-type hypersensitivity and prostaglandin E2 levels were not significantly affected. These studies suggest that certain components of the immune system are Cu dependent.
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PMID:Immune dysfunction in rats fed a diet deficient in copper. 347 55

Two- to three-week-old mice homozygous for the recessive oc gene had negligible numbers of marrow cells but possessed no significant spleno- and hepatomegaly. They also maintained normal numbers of blood cells except for monocytes, which were significantly lower. Additionally, they had reduced numbers of total cells and resident macrophages in the peritoneum, as determined by cell counts in the peritoneal lavage fluid. The frequency of spleen colony-forming units (CFU-S) in the spleens of oc/oc mice was the same as that in the spleens of normal littermate control mice. These oc/oc CFU-S showed essentially similar differentiation patterns as CFU-S of control mice. Also, a few CFU-S could be detected in livers of oc/oc mice. On the other hand, the frequency of cells that formed macrophage colonies in a four-day liquid-culture system in the presence of colony-stimulating activity was significantly reduced in oc/oc mice and abnormalities were observed in the formation of the adherent (stromal) layers by oc/oc spleen cells in liquid cultures. Numbers of fibroblastoid cell colonies in these layers were reduced and, moreover, cultures demonstrated a marked decrease in the number of macrophages both within and outside the fibroblastoid cell colonies. Transplants of spleen and thymus cells of oc/oc mice into lethally irradiated +/? recipients induced oc/oc-like lesions. They included peritoneal macrophage deficiency, marrow deficiency, as well as hepatosplenomegaly. This suggests a hemopoietic stem cell and not microenvironmental defect in this particular type of osteopetrosis. The murine mutant characterized in this study may be useful in studies of cellular interactions during blood and bone formation and in studies of the mononuclear phagocyte system.
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PMID:Congenital murine osteopetrosis inherited with osteosclerotic (oc) gene: hematological characterization. 375 33

A low dose of nitrendipine (a calcium antagonist) ameliorated the percentage incidence and severity of cardiac and renal lesions induced by deoxycorticosterone (DOC) despite maintenance of the systolic blood pressure of the DOC plus nitrendipine group in the hypertensive range. The percentage mortality in the DOC-calcium antagonist group was slightly lower than that in the DOC-vehicle injected group. Nitrendipine did not reduce the DOC-induced renal hypertrophy, cardiomegaly, splenomegaly, or hepatomegaly as reflected in the absolute or relative weights of these organs. The absolute and relative weights of the thymus of the nitrendipine-DOC group did not differ significantly from those of controls although these weights decreased significantly in the group receiving DOC. No changes in relative weights of the adrenal gland were observed. The level of calcium in the serum of groups receiving DOC with or without nitrendipine was reduced significantly as compared to the comparable controls. Nitrendipine at the low dose employed separates at least in part the changes exerted by elevated blood pressure in animals receiving DOC from cardiac and renal lesions.
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PMID:A low dose of a calcium antagonist (nitrendipine) ameliorates cardiac and renal lesions induced by DOC in the rat. 651 May 6

This study evaluated the subchronic (14-day) toxicity of selected (0.2, 1.0, and 4.0 mg/kg) daily subcutaneous injections of diethylstilbestrol (DES) in female (C57B1/6 X C3H)F1 mice. Parameters observed included body and organ weights, gross organ morphology, histopathology, clinical chemistry, and hepatic microsomal enzyme activities. The liver, bone marrow, and thymus are major target organs for DES. Liver enlargement, with associated histopathological changes consistent with mild hepatitis, centrolobular necrosis, and sinusoidal changes were observed. Supporting the histological changes were alterations in serum enzyme levels and microsomal enzyme activity. Bone marrow changes included decreases in the number of cells as well as the number of colony forming units per gram stem cells. Toxicity to the thymus was evidenced by decreased thymic weights and lymphocyte depletion. The hepatic and thymic effects were observed at the lowest (0.2 mg/kg) dose. Although all parameters were not assessed for recovery, those that were evaluated returned to control levels by thirty days after treatment.
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PMID:Subchronic toxicology of diethystilbestrol in the mouse. 662 66

Only few published autopsy studies exist on AIDS in Indians and they concentrate upon AIDS in adults. The authors report findings from the first autopsy study of a child with AIDS in India: a 2-year old female who presented with failure to thrive and pneumonia, and ultimately died in the hospital. The patient was stunted, emaciated, apathetic, and tested seropositive for antibodies to HIV. Investigators found precocious involution of the thymus, splenic atrophy, lymphoid interstitial pneumonia (LIP), and cryptosporidiosis of the colon in the body. No evidence was found of mycobacterial, fungal, or cytomegalovirus infection, and the heart, kidneys, endocrine organs, and brain were all normal. The lymph nodes were of normal size and showed unremarkable histological appearances, without apparent lymphocyte depletion. An enlarged liver revealed fatty change and mild portal lymphocytic infiltration. The presence of profound growth retardation and the finding of LIP suggest that HIV infection was acquired perinatally. The authors suggest in closing that all infants presenting with unexplained failure to thrive, growth retardation, and signs of pulmonary disease be screened for HIV infection.
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PMID:Paediatric AIDS: first autopsy report from India. 768 18

Administration of a single i.p. dose of 115 microg/kg of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to homozygous and heterozygous c-src deficient mice (i.e. c-src -/- and -/+ mice) and their wild-type littermates (c-src +/+ mice) induced differential toxic responses. In c-src +/+ mice, there were clear-cut signs of the toxicity of TCDD, such as the loss of weight in the body, thymus and adipose tissue, whereas in c-src -/+ mice these effects were modest and were not statistically significant. Yet, hepatomegaly, a characteristic effect of TCDD, took place in all three strains of mice. Histological examination of liver samples from control mice and from mice treated with TCDD for 10 days showed that there are qualitative differences in the expression of the effects of TCDD between control and treated mice as well as between c-src -/+ and +/+ mice. In the case of c-src +/+ mice, the predominant lesions were lipid accumulation, glycogen depletion, edema formation and necrosis, as shown by the presence of large areas of ballooning degeneration, and cellular influx of fluid. These changes were demonstrated only marginally in c-src -/+ mice. The predominant effect in -/+ mice was edema formation. At a high dose of TCDD (345 microg/kg), all of the +/+ mice died within 34 days, whereas none of the c-src -/+ mice died. Together these results clearly indicate that some of the toxic effects of TCDD are not fully expressed in c-src deficient mice.
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PMID:Altered in vivo toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in C-SRC deficient mice. 926 Aug 65

The SCID mouse represents a valuable tool for assessing growth characteristics and drug sensitivity of human leukemic cells. We have examined differences in the engraftment patterns in SCID mice of primary human leukemic cells isolated from children (< 21 years old) with either t(1;19)+/E2A-PBX1+ or t(9;22)+/BCR-ABL+ acute lymphoblastic leukemia. Leukemic cells from 13/24 t(1;19)+/E2A-PBX1+ patients caused overt leukemia in SCID mice. Macroscopic lesions were evident in 6/13 cases, with multiple sites involved in some mice: hepatomegaly,(3) splenomegaly(4), thymic enlargement; liver tumors(1), kidney tumors(1), abdominal tumors(1). Microscopic lesions in SCID mouse organs were present in all 13 cases and involved the bone marrow, brain, heart, gut, liver, kidney, lung, ovary, pancreas, skeletal muscle, spleen, and thymus. Leukemic cells from 5/20 t(9;22)+/BCR-ABL+ patients caused overt leukemia in SCID mice. Notably, macroscopic lesions (splenomegaly; leukemic bones; hepatic tumors) were observed in only 1 case. In all 5 cases, microscopic lesions were found in the mouse bone marrow. Additional microscopic lesions were restricted to skeletal muscle, spleen, and mesentery (1 case) or thymus (1 case). These findings differ markedly from those of t(1;19)+/E2A-PBX1+ leukemic cells due to the lack of involvement of major organs such as liver, pancreas, kidney, skin, or brain. These data illustrate the biological heterogeneity of childhood ALL and suggest that the differential risks associated with t(1;19)+/E2A-PBX1+ and t(9;22)+/BCR-ABL ALL might arise from unique engraftment and proliferation capabilities of the respective leukemic cell populations.
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PMID:Distinct in vivo engraftment and growth patterns of t(1;19)+/E2A-PBX1+ and t(9;22)+/BCR-ABL+ human leukemia cells in SCID mice. 1003 3

A series of studies was conducted to determine whether growth hormone (GH) exerts effects on adult female chickens. Recombinant chicken GH (rcGH) was administered continuously via osmotic minipumps. No consistent effects of rcGH treatment were observed on reproductive indices. Hens receiving rcGH treatment for 10 days exhibited hepatomegaly and showed a tendency (P < 0.1) for increased spleen and thymus weights. Moreover, there were increases in the circulating concentrations of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGF-BPs) (22-kDa IGF-BP after 2, 5, and 10 days; 28-kDa IGF-BP after 5 and 10 days; and 36-kDa IGF-BP after 10 days) with rcGH treatment. To determine whether the changes in IGF-BPs were due directly to GH or indirectly via IGF-I, the effects of the continuous administration of rcGH or recombinant human IGF-I (rhIGF-I) were compared. While rcGH again elevated the circulating levels of 28- and 36-kDa IGF-BPs, no such effect was observed with rhIGF-I treatment. However, both treatments exerted similar effects in depressing pituitary GH mRNA levels and elevating plasma concentrations of IGF-I. It is concluded that GH directly elevates circulating concentrations of IGF-I and IGF-BPs, but the negative feedback effect on GH synthesis is mediated via IGF-I.
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PMID:Influence of continuous growth hormone or insulin-like growth factor I administration in adult female chickens. 1033 19

The present study was carried out to establish a human chronic lymphocytic leukemia (CLL) mouse model by transplantation of a JOK-1 human CLL cell line into SCID (severe combined immunodeficient) mice and to examine anti-leukemic effects of fludarabine phosphate, a prodrug of 9-beta-D-arabinofuranosyl-2-fluoroadenine (2F-ara-A). In vitro cytotoxic screening pattern of 2F-ara-A differed from those of other anticancer agents. Intraperitoneal inoculation with JOK-1 cells in SCID mice allowed the cells to infiltrate into a variety of organs including the liver and thymus, and resulted in the death of the mice with a median survival time of 29.5 days, associated with hepatomegaly, splenomegaly and enlarged lymph nodes. The ascitic cells expressing the human B-lymphocytic cell surface antigen CD19 actually grew after a latent period of 15 days. In this model, twice daily administration of fludarabine phosphate at a dose of 135 mg/kg for 5 days prolonged the survival time of the mice for considerably longer period than once-a-day treatment. Fludarabine phosphate in the doubled course of twice daily increased life span of 32.9%, which was in a similar range to that of doxorubicin. Thus, intraperitoneal inoculation of the human JOK-1 CLL cells into SCID mice seems to serve as an animal model potentially for human leukemia, suggesting that transplantation and subsequent infiltration processes of human CLL cells is useful measures to explore mechanistic aspects for drug-induced modulation of the tumor progression.
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PMID:A human B-cell CLL model established by transplantation of JOK-1 cells into SCID mice and an anti-leukemia efficacy of fludarabine phosphate. 1060 87

We report on a neonate presenting with polyhydramnios; macrosomia; macrocephaly; visceromegaly including bilateral nephromegaly, hepatomegaly, cardiomegaly; thymus hyperplasia; cryptorchidism; generalized muscle hypotonia; and a distinctive facial appearance. The clinical course was marked by severe neurodevelopmental deficits combined with progressive respiratory decompensation leading to death at the age 6 months. Magnetic resonance imaging (MRI) disclosed a generalized cerebral atrophy with a marked deficit of the white matter. Renal ultrasound and MRI showed markedly enlarged kidneys with multiple small cystic lesions, a pattern indistinguishable from polycystic kidney disease. The postmortem kidney biopsy revealed dysplastic changes, microcysts, and a focal nephrogenic rest, characteristic features of the Perlman syndrome. In children with fetal gigantism, renal abnormalities, and neurological deficits, Perlman syndrome should be considered and may be confirmed by kidney biopsy.
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PMID:A case of Perlman syndrome: fetal gigantism, renal dysplasia, and severe neurological deficits. 1075 Oct 85


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