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)

Suspensions of Wellcome C. parvum strain 6134 produce splenomegaly in mice when injected i.p. in amounts as low as 20 microgram. This lymphoreticular stimulatory activity is extremely sensitive to cell breakage and is abolished by heating for 4 h at 100 degrees. Periodate oxidation of the bacteria destroys their capacity to produce splenomegaly and abrogates the agglutination of intact C. parvum by Con A. Mild HCl hydrolysis also abolished the splenomegaly but phenol:chloroform:ether and chloroform:methanol extractions did not. These results suggest that the relevant stimulatory principle in C. parvum is of carbohydrate nature, and most probably present on the surface of the bacterium.
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PMID:Chemical properties of the principle in C. parvum that produces splenomegaly in mice. 22 Jan 83

Splenomegaly induced in mice inoculated intraperitoneally (i.p.) with purified formalin-killed phase I and phase II Coxiella burnetii (C.b.) cells was dose-dependent. The phase I cells induced higher splenomegaly than phase II cells. The splenomegaly-inducing ability of phase I cells was reduced upon incubation with phase I but not with phase II antiserum, whereas the phase II cells preincubated with phase I or phase II immune sera induced higher splenomegaly than the phase II cells alone. Phase I cells caused lower splenomegaly in mice previously immunized with C.b. The splenomegaly-inducing ability of phase I cells was abolished by mild acid hydrolysis, by treatment either with phenol-chloroform-petroleum ether (PCP) or with a chloroform-methanol (CM) mixture. However, either the CM or the PCP-treated phase I cells retained their capacity to protect mice challenged with virulent phase I C.b.
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PMID:Induction of splenomegaly in mice by killed Coxiella burnetii cells. 613 32

The effects of several biochemically derived fractions of Corynebacterium parvum and chemically treated intact organisms on the generation of cytotoxic T-lymphocytes (CTL) were assessed in a tumor allograft model with the use of C57BL/6 and DBA/2 mice. The acid-modified, active and inactive fragmented preparations and pyridine extract and residue were all capable of inhibiting primary spleen cell allocytotoxicity. Only the active fragmented, pyridine residue and unfractionated preparations caused splenomegaly and prevented the secondary in vitro generation of CTL. Periodate treatment, acid modification, and pyridine extraction abrogated the ability of C. parvum to activate suppressor macrophages. Although incapable of activating suppressor macrophages, the phenol and pyridine extracts significantly enhanced suppressor T-cell activity. The effect of whole C. parvum organisms on T-cell-mediated cytotoxicity is thus extremely complex and due to the direct activation or inhibition of various cell types that interact with each other.
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PMID:Effects of different fractions of Corynebacterium parvum on the cytotoxic T-cell response to alloantigens in mice. 621 7

Bacterin of Propionibacterium acnes (Corynebacterium parvum), its cellular fractions (lipids, fractions obtained by mechanical disruption and differential centrifugation, by phenol-water and pyridine extractions), and a polysaccharide from culture filtrate were prepared and tested in mice. The activation of RES by splenomegaly and hepatomegaly, prevention of listerial infection, prevention of the lethal effect of sarcoma 180, and depression of liver microsomal cytochrome P-450 were employed. The bacterin was effective in all tests. Lipid-free cells were less active, in particular in the activation of RES and in the listerial infection model. Fractions prepared by the disruption and differential centrifugation lost their activity in all tests along with a decrease in molecular weight. Lipids extracted by ethanol caused pronounced splenomegaly and decreased the cytochrome P-450 content. The residue left after the phenol-water extraction was very active, its delipidation did not destroy the activity. Pyridine extraction provided a completely inactive extract, but a very active residue. The possibility of reducing the complexity of bacterin while preserving immunomodulatory effect is demonstrated.
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PMID:The influence of Propionibacterium acnes (Corynebacterium parvum) fractions on immune response in vivo. 772 4

Splenic sinuses in idiopathic portal hypertension (IPH; 8 patients), liver cirrhosis (LC; 14 patients) and in regenerating autotransplanted spleens from 25 rats were compared with each other by scanning electron microscopy (SEM) and immunohistochemistry using antibodies against proliferating cell nuclear antigen (PCNA). Spleens obtained from six patients with gastric carcinoma and from five untreated adult rats were examined as controls. SEM of the sinuses showed that in IPH endothelial cells became irregular in shape, and the interendothelial slits of sinuses were irregularly enlarged. Sinus endothelial processes traversing the sinusal lumen were also found. The same changes were observed in the proliferating sinuses during regeneration of splenic tissue after autotransplantation in rats, but disappeared when the regeneration was completed. Irregular endothelial cells were few in LC. PCNA-positive sinus endothelial cells were increased in number in IPH as compared with those in LC; the mean number of PCNA-positive ones per cm2 was 45.4 in IPH and 8.2 in LC. It was suggested that, from SEM observation of sinus endothelial cells and counting PCNA-positive sinus endothelial cells, the sinuses of the spleen in IPH consist of proliferating endothelial cells or are in the state of increased proliferation. In conclusion, splenomegaly in IPH was presumed to be caused by proliferation of sinus endothelial cells, and by the increased splenic blood flow in the irregularly widened interendothelial slits of the sinuses.
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PMID:Structural characteristic of splenic sinuses in idiopathic portal hypertension. 854 36

A 48-year-old women was admitted to our hospital because of gradually developed spastic gait. She showed spasticity of the lower extremities with mild weakness. Laboratory tests disclosed decreased WBC and platelet counts and mild increases of transaminase and total bilirubin. Blood manganese level was markedly increased (6.0 micrograms/dl). Abdominal ultrasound showed splenomegaly, and abdominal angiography showed a dilatation of the portal and paraumbilical veins. T1-weighted MR images showed high signal intensities at the bilateral globus pallidus and cerebral peducles, and T2-weighted images showed high signal intensities at the bilateral deep white matter, posterior limbs of the internal capsule and right upper cervical spinal cord. Following the diagnosis of IPH, splenectomy was performed. The blood level of manganese decreased thereafter and her neurological deficits gradually improved. Hepatic diseases often show high signal intensities at the basal ganglia on T1-weighted images, and this seemed to be due to accumulation of manganese in our case. Because demyelination or axonal injury of the spinal cord are found in hepatic disease, we speculate that the high signal intensities at the spinal cord on T2-weighted images of our case reflect hepatic myelopathy, which may also be caused by high blood levels of manganese.
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PMID:[A case of idiopathic portal hypertension (IPH) with hypermanganemia presenting as spastic gait]. 1271 91

We have isolated a substance with anti-retroviral activity from the freshly prepared crude extract of Chelidonium majus L. (greater celandine) by 9-aminoacridine precipitation method and ion exchange chromatography using Dowex-50W/H+ resin followed by the gel filtration on Sephadex-75 column. Elemental and phenol/sulfuric acid method analyses as well as the mass spectrometry of the purified substance indicated that it may represent a low-sulfated poly-glycosaminoglycan moiety with molecular weight of approximately 3800 Da. The substance prevented infection of human CD4+ T-cell lines AA2 and H9 with HIV-1 at concentration of 25 microg/mL as well as the cell-to-cell virus spread in H9 cells continuously infected with HIV-1, as determined by the measurement of reverse transcriptase activity and p24 content in cell cultures. Furthermore, we have shown in a murine AIDS model that the treatment with purified substance significantly prevented splenomegaly and the enlargement of cervical lymph nodes in C57Bl/6 mice chronically infected with the pool of murine leukemia retroviruses. The mechanism(s) of anti-retroviral activity of this substance have to be elucidated.
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PMID:In vitro and in vivo anti-retroviral activity of the substance purified from the aqueous extract of Chelidonium majus L. 1664 65

NCPH is a heterogeneous group of liver disorders of vascular origin, leading to PHT with near normal HVPG. NCPF/IPH is a disorder of young adults or middle aged women, whereas EHPVO is a disorder of childhood. Early age acute or recurrent infections in an individual with thrombotic predisposition constitute the likely pathogenesis. Both disorders present with clinically significant PHT with preserved liver functions. Diagnosis is easy and can often be made clinically with support from imaging modalities. Management centers on control and prophylaxis of variceal bleeding. In EHPVO, there are additional concerns of growth faltering, portal biliopathy, MHE and parenchymal dysfunction. Surgical shunts are indicated in patients with failure of endotherapy, bleeding from sites not amenable to endotherapy, symptomatic hypersplenism or symptomatic biliopathy. Persistent growth failure, symptomatic and recurrent hepatic encephalopathy, impaired quality of life or massive splenomegaly that interferes with daily activities are other surgical indications. Rex-shunt or MLPVB is the recommended shunt for EHPVO, but needs proper pre-operative radiological assessment and surgical expertise. Both disorders have otherwise a fairly good prognosis, but need regular and careful surveillance. Hepatic schistosomiasis, CHF and NRH have similar presentation and comparable prognosis.
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PMID:Non-cirrhotic portal hypertension - diagnosis and management. 2397 14

Non-cirrhotic portal hypertension (NCPH) encompasses a wide range of disorders, primarily vascular in origin, presenting with portal hypertension (PHT), but with preserved liver synthetic functions and near normal hepatic venous pressure gradient (HVPG). Non-cirrhotic portal fibrosis/Idiopathic PHT (NCPF/IPH) and extrahepatic portal venous obstruction (EHPVO) are two prototype disorders in the category. Etiopathogenesis in both of them centers on infections and prothrombotic states. Presentation and management strategies focus on repeated well tolerated episodes of variceal bleed and moderate to massive splenomegaly and other features of PHT. While the long-term prognosis is generally good in NCPF, portal biliopathy and parenchymal extinction after prolonged PHT makes outcome somewhat less favorable in EHPVO. While hepatic schistosomiasis, congenital hepatic fibrosis and nodular regenerative hyperplasia have their distinctive features, they often present with NCPH.
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PMID:Non-cirrhotic portal hypertension. 2467 6