Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Light- and electron microscopic alterations of the liver and light microscopic findings in the gastro intestinal tract, the kidney and adrenal gland of 80 female Wistar-Rats under CDCA therapy are reported. CDCA was applied by means of an endopharnygeal tube over a period of 60 days in doses of 150, 250, 500 and 1000 mg/kg body weight. The organs were examined at different times. We compared the achieved findings to results obtained already beforehand by light- and electron microscopy after application of 20, 50 and 90 mg/kg body weight and day: Up to a dosage of 90 mg/kg morphological changes of the liver were only visible electron optically, from 150 mg/kg onward they could be seen light optically as well. After 60 days a cirrhosis-like picture had developed. The lethal dose was established at 1000 mg/kg. There were no pathological alterations in the gastrointestinal tract and no definite ones in the kidneys. The adrenal glands were unchanged.--Since there are in the rats, in spite of potent mechanisms of detoxication of CDCA and LCA, even at low doses morphological alterations to be seen, the existence of other toxic, at this moment still unknown metabolites is being discussed.
 ...
PMID:[Morphologic investigations on the toxicity of orally applied CDCA in the liver, gastro intestinal tract, kidney and adrenal gland of the rat (author's transl)]. 91 85

We examined serologically and immunohistochemically the new carbohydrate antigen CA-50 to clarify the mechanism of its high serum value and clinical significance in several liver diseases. The subjects included 145 patients with benign liver diseases and hepatocellular carcinoma (HCC). The serum CA-50 value was high in chronic active hepatitis with lobular disorganization, liver cirrhosis and HCC. It was not correlated with serum levels of GPT nor gamma-GTP. Immunohistochemical analysis revealed that proliferated bile ductules showed mainly positive staining in all subjects, whereas hepatoma cells were negative. The proliferated bile ductules with positive staining for CA-50 were quantified by an original method. The number of the proliferated bile ductules with positive staining for CA-50 was significantly correlated with the serum CA-50 value (r = 0.62, P less than 0.05). In the FPLC analysis, there was no significant difference between the expression pattern and molecular weight of CA-50 in liver diseases and pancreatic cancer. Also no difference in the carbohydrate structure that coexisted with CA-50 was detected in the ConA or LCA affinity column study. It was suggested that the increase of carbohydrate antigen CA-50 in several liver diseases might reflect the proliferation of bile ductules, and that the structure of CA-50 in benign liver diseases does not differ from that of CA-50 from patients with pancreatic cancer.
 ...
PMID:[Serological and immunohistochemical evaluation of new carbohydrate antigen CA-50 in several liver diseases]. 196 7

An antibody-lectin enzyme immunoassay (EIA) technique was developed for the analysis of sugar chains of serum alpha-fetoprotein in various liver diseases. The anti-'alpha-fetoprotein'-IgG was coated on a microtiter plate and then treated with periodic acid. A serum sample was added to the plate and then a 'peroxidase'-conjugated lectin was added. The amount of lectin bound to the sugar chain of the 'alpha-fetoprotein' was estimated from the 'peroxidase' activity. The 'peroxidase' activities of 4 different lectins, LCA, Con A, LCA and EPHA, were compared. The LCA/'wheat germ agglutinin' activity ratio and LCA/EPHA activity ratio were increased in liver diseases and LCA/'wheat germ agglutinin' ratio showed a statistically significant difference between the chronic hepatitis and the liver cirrhosis groups (p less than 0.05). Furthermore, when serum samples were pretreated with sialidase, a statistically significant difference was observed in the LCA/EPHA and LCA/Con A ratios between the chronic hepatitis and the hepatoma groups (p less than 0.05). These results indicated that low sialylation at the non-reduced end of the sugar chains of 'alpha-fetoprotein' occurs in liver cirrhosis and that high fucosylation at the reduced end of N-acetylglucosamine residue of 'alpha-fetoprotein' occurs in hepatomas.
 ...
PMID:Alpha-fetoprotein antibody-lectin enzyme immunoassay to characterize sugar chains for the study of liver diseases. 246 50

Lectin affinities of AFP were analyzed using Con A sepharose chromatography and crossed immuno-affino-electrophoresis. With Con A, AFP was divided into three subfractions, nonbound, loosely-bound and tightly-bound by chromatography, or two subfractions, nonbound and bound by electrophoresis. Con A nonbound subfraction was small in percentage in hepatocellular carcinoma (HCC), neonatal hepatitis, congenital biliary atresia (CBA), liver cirrhosis (LC) and cord sera. In contrast with these, the increase of Con A non-bound AFP was observed in yolk sac tumor (YST) and metastatic liver cancer (Meta). With LCA, AFP was divided into three subfractions: nonbound, loosely bound and tightly bound. Loosely bound fraction was very small in every specimen. AFPs from cord sera and LC showed uniform LCA affinity pattern, but AFPs from HCC were not uniform. Our data suggest that the analyses of lectin affinity of AFP serve as a diagnostic tool in differentiating (1) HCC from YST, (2) HCC from Meta, (3) CBA or neonatal hepatitis from YST and (4) LC from some cases of HCC.
 ...
PMID:[Analysis of lectin-affinity of alpha fetoprotein-diagnostic approach]. 619 65

We investigated the affinity and special combination of anti-human AFP variant monoclonal antibody (AFP-R-LCA McAb) for cells of AFP positive hepatocellular carcinoma (HCC). AFP-R-LCA McAb was labeled by 131I radioisotope (131I-AFP-R-LCA McAb injected into the peripheral veins of patients with HCC or liver cirrhosis after hepatitis B. 131I-AFP-R-LCA McAb was gathered in tumor of HCC in 6 AFP positive patients, but there was no positive gathering in HCC in 6 AFP negative or 4 liver cirrhosis patients. AFP-R-LCA McAb has strong affinity and special combination to AFP positive cells of HCC and can be recognized as a carrier for radioimmunodetection and radiommunotherapy.
 ...
PMID:[Anti-human AFP variant McAb in radioimmunodetection for primary hepatocellular carcinoma]. 959 55

An autopsy case of systemic mast cell disease (SMCD) without primary skin lesions in a 57-year-old Japanese male is described. Initially the patient was suspected of having liver cirrhosis or malignant lymphoma because of hepatomegaly and lymph node enlargement on admission. However, a lymph node biopsy and bone marrow aspiration conducted on his third admission indicated a SMCD because of the existence of metachromatic cell aggregates stained with toluidine blue. At autopsy, the diagnosis was confirmed because the proliferating cells were histochemically proven to be mast cells by naphthol AS.D chloroacetate esterase, Giemsa and alcian blue, in addition to toluidine blue staining. The intra-abdominal and retroperitoneal lymph nodes were replaced by mast cell aggregates, which caused the splenic infarction and bilateral hydronephrosis, with infiltration of mast cells into the spleen and kidneys also being apparent. Mast cell infiltration was similarly found in the bone marrow, liver, ileum and ascending colon. Immunohistochemically, the mast cells were positive for antibodies of alpha 1-antichymotrypsin, CD45 (LCA), CD43 (MT-1), CD45R (MB-1) and the oncoprotein c-kit. Electron microscopic examination using formalin-fixed tissue gave supportive evidence of a mast cell origin for the lesions.
 ...
PMID:Systemic mast cell disease with splenic infarction: a case report. 970 48

Inappropriate activation of the mineralocorticoid receptor (MR) results in renal sodium retention and potassium loss in patients with liver cirrhosis. Recent evidence suggested that this MR activation is, at least in part, a result of bile acid-dependent reduction in 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD2) activity, an enzyme preventing cortisol-dependent activation of MR by converting cortisol to cortisone. Here, we investigated the molecular mechanisms underlying bile acid-mediated MR activation. Analysis of urinary bile acids from 12 patients with biliary obstruction revealed highly elevated concentrations of chenodeoxycholic acid (CDCA), cholic acid (CA), and deoxycholic acid (DCA), with average concentrations of 50-80 microm. Although CDCA and DCA both mediated nuclear translocation of MR in the absence of 11 beta HSD2 and steroids in transiently expressing HEK-293 cells, the transcriptional activity of MR was not stimulated. In contrast, CDCA and DCA both inhibited 11 beta HSD2 with IC(50) values of 22 and 38 microm, respectively and caused cortisol-dependent nuclear translocation and increased transcriptional activity of MR. LCA, the bile acid that most efficiently inhibited 11 beta HSD2, was present at very low concentrations in cholestatic patients, whereas the weak inhibitor CA did not cause MR activation. In conclusion, these findings indicate that CDCA, and to a lesser extent DCA, by inhibiting 11 beta HSD2, mediate cortisol-dependent nuclear translocation and transcriptional activation of MR and are responsible at least for a part of the sodium retention and potassium excretion observed in patients with biliary obstruction.
 ...
PMID:Chenodeoxycholic acid and deoxycholic acid inhibit 11 beta-hydroxysteroid dehydrogenase type 2 and cause cortisol-induced transcriptional activation of the mineralocorticoid receptor. 1201 12

Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. However, accurate diagnosis can be difficult as most of the patients who develop this tumor have symptoms similar to those caused by longstanding liver disease. Herein we developed an integrated platform to discover the glycoprotein biomarkers in early HCC. At first, lectin arrays were applied to investigate the differences in glycan structures on serum glycoproteins from HCC and cirrhosis patients. The intensity for AAL and LCA was significantly higher in HCC, indicating an elevation of fucosylation level. Then serum from 10 HCC samples and 10 cirrhosis samples were used to screen the altered fucosylated proteins by a combination of Exactag labeling, lectin extraction and LC-MS/MS. Finally, 27 HCC and 27 cirrhosis serum samples were used for lectin-antibody arrays to confirm the change of these fucosylated proteins. C3, CE, HRG, CD14 and HGF were found to be biomarker candidates for distinguishing early HCC from cirrhosis, with a sensitivity of 72% and specificity of 79%. Our work gives insight to the detection of early HCC, and the application of this comprehensive strategy has the potential to facilitate biomarker discovery on a large scale.
 ...
PMID:Identification and confirmation of biomarkers using an integrated platform for quantitative analysis of glycoproteins and their glycosylations. 1996 Dec 39

A group of disorders with disparate symptomatology, including congenital cerebellar ataxia, retinal blindness, liver fibrosis, polycystic kidney disease, and polydactyly, have recently been united under a single disease mechanism called 'ciliopathies'. The ciliopathies are due to defects of the cellular antenna known as the primary cilium, a microtubule-based extension of cellular membranes found in nearly all cell types. Key among these ciliopathies is Joubert syndrome, displaying ataxia, oculomotor apraxia, and mental retardation* with a pathognomonic 'molar tooth sign' on brain magnetic resonance imaging. The importance of ciliary function in neuronal development has been appreciated only in the last decade with the classification of Joubert syndrome as a ciliopathy. This, together with the identification of many of the clinical features of ciliopathies in individuals with Joubert syndrome and the localization of Joubert syndrome's causative gene products at or near the primary cilium, have defined a new class of neurological disease. Cilia are involved in diverse cellular processes including protein trafficking, photoreception, embryonic axis patterning, and cell cycle regulation. Ciliary dysfunction can affect a single tissue or manifest as multi-organ involvement. Ciliary defects have been described in retinopathies such as retinitis pigmentosa and Leber congenital amaurosis (defects in photoreceptor ciliary protein complexes), renal syndromes with nephronophthisis and cystic dysplastic kidneys, and liver conditions such as fibrosis and biliary cirrhosis. Recognizing the diverse presentations of the ciliopathies and screening strategies following diagnosis is an important part of the treatment plan of children with cilia-related disorders.
 ...
PMID:The ciliopathies in neuronal development: a clinical approach to investigation of Joubert syndrome and Joubert syndrome-related disorders. 2167 65

The behavior of littoral cell neoplasms ranges from benign (littoral cell angioma, LCA) to highly malignant (angiosarcoma). Two unusual cases of low-grade metastatic littoral cell angiosarcoma (LCAS) have been reported with late recurrence and bulky metastases. We present the third case of this rare neoplasm in a 38-year-old man with cirrhosis and a large splenic artery aneurysm, without extrasplenic masses. The spleen showed nodules resembling LCA, immunoreactive for CD31, factor VIII, CD68, and CD163 but not CD8 or CD34. Also present were solid areas of immunophenotypically identical bland spindle cells, although lighter CD31 immunostaining distinguished them from LCA-like angiomatous channels. Similar cells diffusely infiltrated the cirrhotic liver. After splenectomy, pancytopenia resolved, and he is asymptomatic 19 months later. Low-grade LCAS is a previously unreported cause of cirrhosis and may metastasize without forming masses. In cases of LCA, CD31 immunohistochemistry may facilitate detection of LCAS and indicate metastatic potential.
...
PMID:Low-grade, metastasizing splenic littoral cell angiosarcoma presenting with hepatic cirrhosis and splenic artery aneurysm. 2342 63


1 2 Next >>