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Biomedical subjects

B Ando

Publications and source records attributed to B Ando.

16 recordsLinked to original sources
PubMed1999

A case of Graves' disease associated with autoimmune hepatitis and mixed connective tissue disease.

The patient was a woman of forty-eight. Liver dysfunction was pointed out at the age of forty-five. She was admitted to hospital because of her hyperthyroidism. Her palmar skin was wet and her fingers were swollen like sausages. She had a diffuse and elastic hard goiter with a rough surface. The serum levels of free T3 (9.6 pg/mL) and free T4 (3.76 ng/dL) were high and that of TSH (0.11 microU/mL) was low. The activity of TSH-binding inhibitory immunoglobulin (TBII) was 89%. The uptake rate of 123I to the thyroid was 55.1% and the uptake pattern was nearly diffuse. The goiter was proved to contain several nodules by ultrasonography, but aspiration cytology showed no malignant cells. She was diagnosed to have Graves' disease with adenomatous goiter. She also had high ALT (34 IU/L) and gamma-globulin (1.97 g/dL). She had positive antinuclear antibody (speckled type), positive anti-ribosomal nuclear protein antibody, and positive LE cell phenomenon. The liver biopsy revealed mononuclear cell infiltration with fibrosis in the portal area. These data indicated that she also had autoimmune hepatitis (AIH) and mixed connective tissue disease (MCTD). The analysis of human leukocyte antigen (HLA) showed positive A11 which had been reported to relate to Graves' disease, and positive DR4 which had been reported to relate to AIH and MCTD. These results suggested that HLA would determine susceptibility to three distinct autoimmune diseases in this case.

Alanine Transaminase↗
PubMed1996

Thermolabile beta-2 macroglycoprotein (Hakata antigen) in liver disease: biochemical and immunohistochemical study.

Thermolabile beta-2 macroglycoprotein is a novel serum protein that was detected by an autoantibody in sera of a Japanese woman with systemic lupus erythematosus. We developed an enzyme-linked immunosorbent assay for this glycoprotein and measured its serum levels in patients with chronic liver disease. There were significant correlations between serum levels of this glycoprotein and those of albumin and cholinesterase. The serum levels of TL beta 2MG decreased with increasing severity of cirrhosis. Immunohistochemical staining using monoclonal anti-thermolabile beta-2 macroglycoprotein antibody revealed positive staining in the cytoplasm of the hepatocytes. These data strongly suggested that hepatocyte may be one of the production sites of this glycoprotein. Measurement of serum levels of this glycoprotein was useful for evaluation of hepatic function in chronic liver disease.

Adult↗
PubMed1995

[Chronic pancreatitis and pancreatic dysfunction associated with Sjögren's syndrome].

Some pancreatic involvement was observed in Sjögren's syndrome (SS). Episodes of abdominal pain occurred infrequently in the course of SS, but there were some abnormal findings of the pancreatic functions and/or morphologic examinations. The level of serum amylase was affected by the destruction of both the pancreas and the salivary gland. Hyposecretion of bicarbonate in secretin test seemed to be characteristic in SS. ERP showed mild or moderate changes of the pancreatic duct, but their severities did not correlate with those of the salivary gland. Imaging of the pancreas tended to reveal definite abnormalities only in cases with an attack of pancreatitis. The roles of autoimmune mechanisms have been reported in pancreatitis associated with SS.

Amylases↗
PubMed1992

[A case of simple hepatic cyst accompanied with dilatation of the intrahepatic bile duct].

Here we report a rare case of simple hepatic cysts causing dilatation of the intrahepatic bile duct. A 75-year old female was admitted to Kyushu University Hospital because of liver dysfunction. Ultrasonogram and CT scan showed two neighboring cysts in the liver (S2, S4), and dilatation of the peripheral bile duct in left lateral segment of the liver. Echo-guided percutaneous aspiration of cyst fluid showed the elevated levels of CA19-9, but malignant cell were not seen. These findings suggested that the compression by these neighboring simple hepatic cysts caused the stenosis of the bile duct. The dilatation of the bile duct disappeared after the percutaneous ethanol sclerosing therapy for cyst.

Aged↗
PubMed1989

The secretory release reaction initiated by complement proteins C5b-9 occurs without platelet aggregation through glycoprotein IIb-IIIa.

The secretory and aggregation responses of stirred platelets exposed to complement proteins C5b-9 was investigated. C5b-9 assembly on the platelet surface resulted in the release of dense granule adenosine triphosphate (ATP) accompanied by a decrease in sample turbidity, but no detectable cell lysis. Inhibition of cellular protein kinase C completely blocked the C5b-9 initiated release of ATP, confirming the secretory nature of this response. Addition of fibrinogen (up to 1 mg/mL) had no effect on either the release of ATP or the decreased turbidity observed for C5b-9 cells. Addition of the peptides Arg-Gly-Asp-Ser (RGDS) and fibrinogen gamma-chain carboxyl-terminal (gamma 397-411) at concentrations sufficient to completely block fibrinogen binding to GP IIb-IIIa had no effect on either C5b-9 induced dense granule secretion or the associated turbidity change. Microscopic examination and electronic particle counting of the stirred platelet suspensions confirmed that no aggregation of C5b-9 platelets occurred even when these cells were stirred in the presence of fibrinogen. The capacity of the C5b-9 proteins to initiate platelet secretion without activation of cell surface glycoprotein (GP) IIb-IIIa suggests a mechanism for intravascular dissemination of activated platelets during complement activation in vivo.

Adenosine Diphosphate↗
PubMed1988

Complement proteins C5b-9 initiate secretion of platelet storage granules without increased binding of fibrinogen or von Willebrand factor to newly expressed cell surface GPIIb-IIIa.

The functional and conformational activation of cell surface glycoproteins IIb-IIIa (GPIIb-IIIa) was probed in platelets stimulated to secrete by complement proteins C5b-9. Gel-filtered human platelets exposed to the purified human C5b-9 proteins exhibited non-lytic secretory release of both alpha- and dense granule storage pools with only a small increase in total binding of 125I-fibrinogen (less than 3000 molecules/cell) to the cell surface. By contrast to ADP- or thrombin-activated platelets, increased 125I-fibrinogen bound to C5b-9 platelets was not inhibited by Arg-Gly-Asp-containing peptides, suggesting that the high affinity membrane receptor for fibrinogen is not expressed under these conditions. C5b-9-stimulated platelets also failed to bind 125I-von Willebrand factor (less than 1 ng/10(8) platelets), confirming that the adhesive protein receptor function of cell surface GPIIb-IIIa is not expressed in these cells. Although specific binding of 125I-fibrinogen or 125I-von Willebrand factor did not significantly increase after C5b-9 assembly, these proteins elicited de novo expression of the GPIIb-IIIa activation-associated epitope recognized by monoclonal antibody PAC-1, and binding of this antibody to C5b-9 platelets was fully competed by Arg-Gly-Asp-containing peptides. These data suggest that the metabolic events which trigger granule secretion after C5b-9 insertion into the plasma membrane cause cell surface GPIIb-IIIa to be expressed in an activation-associated but functionally incompetent conformation.

Adenosine Diphosphate↗
PubMed1987

Complement C5b-9-stimulated platelet secretion is associated with a Ca2+-initiated activation of cellular protein kinases.

Membrane assembly of the C5b-9 proteins on gel-filtered human platelets has been shown to initiate the nonlytic release of alpha-granule contents and expression of membrane prothrombinase sites, suggesting cellular activation by these ostensibly cytolytic plasma proteins (Wiedmer, T., Esmon, C. T., and Sims, P. J. (1986) J. Biol. Chem. 261, 14587-14592). We now examine the mechanism of the C5b-9-induced release reaction. The release of alpha-granule contents upon C5b-9 assembly is accompanied by expression of alpha-granule membrane glycoprotein 140 on the platelet surface, confirming that the complement-mediated release reaction occurs by secretory fusion of the alpha-granule with the plasma membrane. C5b-9 binding initiates the phosphorylation of both 40- and 20-kDa platelet proteins, indicative of activation of protein kinase C and myosin light chain kinase, respectively. Activation of cellular protein kinases under these conditions was not accompanied by the formation of inositol phosphates and was found to strictly depend upon extracellular Ca2+, suggesting that the platelet's secretory response to the C5b-9 proteins is triggered directly by the influx of Ca2+ across the plasma membrane. measurement of intracellular Ca2+ confirmed that elevation of this ion in the cytosol was strictly dependent upon increased plasma membrane permeability due to C5b-9 assembly and was not accompanied by mobilization of this ion from internal storage pools. The C5b-9-mediated secretory response was blocked by sphingosine, a potent inhibitor of protein kinase C, but was unaffected by the cyclooxygenase inhibitor indomethacin, suggesting that feedback (receptor-linked) by thromboxane is not required for platelet activation after C5b-9 insertion.

Adult↗
PubMed1986

Identification of anti-Lea by platelet complement fixation.

Two anti-Lea sera which were able to detect Lea antigen on platelets were identified in a screening for anti-platelet antibodies by means of a platelet complement fixation test. These two antisera hemolyzed erythrocytes without enzyme treatment. The anti-Lea activity could be completely absorbed by red cells, platelets and lymphocytes of Le(a+b-) donors but not by cells from Le(a-b+) or Le(a-b-) donors. The antibody activity against red cells was eliminated by treatment of the antisera with dithiothreitol, thereby suggesting that the activity resided in the IgM class of immunoglobulins. As the anti-Lea was more reactive at 37 degrees C than at room temperature against both red cells and platelets, we suggest that transfusion of platelets of Lea-negative donors should be considered for patients with this type of anti-Lea.

Blood Platelets↗
PubMed1986

[An unresectable case of hepatoma completely disappearing after oral administration of an anticancer drug (UFT)].

A 78-year-old man was admitted to our hospital complaining of hypochondralgia. Since he was diagnosed as having advanced and unresectable hepatoma. UFT was administered as an oral chemotherapy, resulting in reduction of the liver tumor, and a decrease in AFP (ng/ml) from 1,200 to 18. Twenty-six months have already passed since the tumor was detected and 21 months since the start of UFT administration. The patient is still enjoying a good general condition and is presently under follow-up at our out-patient clinic. By the standard for the efficacy of cancer chemotherapy proposed by Koyama and Saito, this case corresponds to the state of complete response. This case suggested the clinical usefulness of UFT as an oral chemotherapy for advanced hepatoma.

Administration, Oral↗