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)

In contrast to the traditional belief that the popliteal lymph node (PLN) assay of graft-versus-host (GVH) reactivity is a local phenomenon, this study describes significant systemic components of both donor and host lymphoid cell activity. Not only are host radiosensitive lymphocytes of systemic origin necessary for the manifestation of normal PLN hypertrophy, but as few as 2.5 X 10(6) parental lymph node cells (LNCs) injected into the hind footpad of adult F1 hybrid rats disseminate widely, provoking significant systemic GVH reactions, as measured by splenomegaly, and distant lymphadenopathy. Futhermore, locally injected donor LNCs ultimately engender three forms of attenuated GVH reactivity: (1) the dissipation of potentially unlimited GVH reactivity, (2) refractoriness of the host to subsequent rechallenge by GVH-inducing cells, and (3) progressive loss of GVH reactivity in donor LNCs when serially transferred to secondary F1 recipients. Whether this modulation of the cell-mediated immune response is the expression of an anti-recognition structure response by the host or the activation of some other immunoregulatory protein, it is absent or reduced in splenectomized recipients. The data suggest that the spleen provides an immunoregulatory microenvironment in which cell-mediated immune responses, such as the GVH reaction, are modulated.
Transplantation 1976 Sep
PMID:Disseminated systemic expression of the "local" popliteal lymph node assay in rats. 0 14

The spleen cells transfer from mice CBA at the 25th day of the carcinogenesis latent period induced by adenovirus SA7(S8) to newborn syngeneic animals caused the graft versus host reaction in them. There was splenomegaly and progressive decrease in weight of the recipients' thymus. Analogous alterations of lymphoid organs were noted in the animals infected during the neonatal period by oncogenic adenovirus SA7(C8). Results showed that adenoviral carcinogenesis had some manifestations of autoimmune disease.
Biull Eksp Biol Med 1978 Sep
PMID:[Mechanisms of changes in the mass of the organs central to immunity during adenovirus carcinogenesis]. 2 79

The potential of cells from the Peyer's patches (PP) of normal adult DBA/2 Tru mice (DBA/2) to induce a graft-versus-host reaction when injected into (C57BL/6 Tru x DBA/2 Tru)F1 hybrid (B6D2F1) mice was studied. The injection of 10(6) to 10(7) DBA/2 PP or spleen cells i.p. into neonatal F1 mice produced a striking splenomegaly. Comparable doses of parental PP or spleen cells injected into a rear footpad of adult F1 mice also induced a marked enlargement of the draining popliteal lymph node. In addition, PP cells were also capable of producing a lethal runting syndrome when injected i.v. into sublethally irradiated adult F1 recipients. In all assays, injection of syngeneic B6D2F1 cells had little or no effect. Treatment of the DBA/2 PP cells with anti-theta serum and complement abolished their capacity to induce splenomegaly in neonatal F1 mice. The graft-versus-host reaction activity of the PP cells could also be eliminated by thymus deprivation of the donor DBA/2 mice. These data are contradictory to previous findings in which it was observed that mouse PP cells were unable to induce graft-versus-host reaction.
Transplantation 1978 Sep
PMID:Mouse Peyer's patches contain T cells capable of inducing the graft-versus-host reaction (GVHR). 3 Jan 92

Serum-IgM is always abnormally high in tropical splenomegaly syndrome. It is postulated that patients with this disease have an abnormal immunoglobulin response to malaria because they lack effective T suppressor cells. This defect may be genetically determined, thus explaining the tribal and familial aggregation of the disease. Hypermacroglobulinaemia is associated with the formation of large amounts of high-molecular-weight immune complexes. These complexes are important in the pathogenesis of the clinical features of the syndrome.
Lancet 1976 Sep 18
PMID:A suppressor T-cell defect in tropical splenomegaly syndrome. 6 46

Splenomegaly characterised by myeloid metaplasia was induced in BALB/c mice by the injection of antigens and immunostimulants. In difference from leukemoid reaction, this syndrome was transmissible both by the plasma and by the splenic cells. Small virus-like particles (30--50 nm) were revealed in the plasma, and RNA-containing viruses of type C--in the splenic cells.
Biull Eksp Biol Med 1977 Sep
PMID:[Induction of transplantable leukemia-like syndromes in mice by administration of antigens and immunostimulants]. 7 28

This paper gives, in detail, the causes of either liver disease or hepatomegaly in 100 patients, mostly adults, admitted to the medical wards of Angau Memorial Hospital, Lae, during 1968 and 1969. The major findings included liver cell carcinoma, cirrhosis (often with chronic active hepatitis), tropical splenomegaly, pericholangitis and hepatitis. There were 27 with miscellaneous findings including ten with normal, or almost normal, livers despite the definite enlargement. Patients with liver cell carcinoma presented late in the course of their illness and had a poor prognosis. Others, with pericholangitis, had clinical features of portal hypertension indistinguishable from that complicated cirrhosis. There was an unexpected number with chronic active hepatitis and a liver biopsy is essential for such a diagnosis. Hepatic sinusoidal lymphocytosis is almost invariably found in patients with TS but may occasionally be found in those with a non-palpable spleen. Patients with right heart failure of chronic respiratory disease, and jaundice of acute pneumonia were excluded from the study.
P N G Med J 1976 Sep
PMID:Liver disease in Papua New Guinea. 19 19

The thymic region of neonatal Swiss mice was exposed to doses varying from 1000 R to 2000 R of X-irradiation. The animals did not show any signs of wasting syndrome up to 6 months after irradiation. At this time hyperplasia of the thymus with an associated lymphocytosis was evident in irradiated animals. Antibody production to sheep red blood cells (SRBC) was not affected. However, at 12 months post-irradiation the animals showed signs of wasting disease with a progressive increase in their numbers at 18 and 24 months of age. The percentage incidence of animals with wasting disease was dose dependent. At this stage in the majority of the animals with the disease the thymus showed varying degrees of atrophy along with splenomegaly. There were no significant differences in the number of lymphocytes but the number of granulocytes showed a substantial increase. This was more evident in animals exposed to 2000 R to the thymic region. Though one observed a lowered ability to form antibodies to bovine serum albumin (BSA) with advancing age, the thymic irradiation did not affect the immune response to BSA even in animals manifesting wasting disease. An interesting observation has been the development of a severe loss of muscle power and tone in the hind limbs in a large majority of animals.
Int J Radiat Biol Relat Stud Phys Chem Med 1979 Sep
PMID:Effects of neonatal thymic exposure to high doses of X-irradiation. 31 96

The clinical and laboratory features of 72 patients with Felty's syndrome described within the last ten years have been compared with Felty's five original patients. Felty's syndrome appears to be a variant of rheumatoid arthritis with extra-articular manifestations in which leukopenia (usually due to neutropenia) and splenomegaly occur, although not always at the same time. Both are manifestations of the underlying disease process and are not necessarily otherwise related. The mechanism of the leukopenia is complex and abnormalities in leukocyte function appear to be as important as the leukopenia in predisposing patients with Felty's syndrome to infection. Functional abnormalities of the leukocytes in this syndrome are due in part to immune complex formation. Hypocomplementemia associated with this process may be another cause for the increased susceptibility to infection. It is proposed, therefore, that therapy in Felty's syndrome be directed at the underlying disease process, and gold salts and penicillamine should be considered for this purpose. Splenectomy should be reserved for specific situations, such as hemolytic anemia, severe thrombocytopenia, leg ulcers, and infections associated with profound leukopenia that are not responsive to medical therapy.
Johns Hopkins Med J 1977 Sep
PMID:Felty's syndrome: an analytical review. 33 Sep 14

Portal hypertension and variceal hemorrhage may be found in the renal transplant patient with chronic liver disease. The development of portal hypertension was found to occur after long-term graft survival without significant rejection. The development of positive cytomegalic virus and negative hepatitis-associated antigen appeared to be common. Splenomegaly and prominent venous collateral were the most frequent physical findings, while ascites and hepatomegaly were less frequent. Portasystemic decompression can be performed successfully, however, the mortality and morbidity appear to be higher for this group than for other cirrhotic patients with comparable hepatic reserve.
Surgery 1978 Sep
PMID:Portal hypertension following renal transplantation. 35 15

Changes in the proportions and total numbers of splenic Thy-1.2+ cells, Ig+ cells and normoblasts were analysed during fatal Plasmodium berghei and non-fatal P. yoelii infections in mice. Thy-1.2+ and Ig+ cells were identified by rosetting techniques, and normoblasts by morphological criteria. The splenomegaly observed during these infections was found to be caused mainly by proliferation of normoblasts. An early increase in the numbers of Thy-1.2+ and Ig+ cells was detected in both infections, but in P. berghei infections these responses were subsequently suppressed. In P. yoelii infections Thy-1.2+ and Ig+ cell numbers were maintained at four to five-fold above normal levels until the mice had completely recovered. During the acute phase of P. yoelii infection it appeared that most splenic T-cells expressed surface immunoglobulin.
Immunology 1978 Sep
PMID:Spleen cell changes during fatal and self-limiting malarial infections of mice. 35 62


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