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S Onishi

Publications and source records attributed to S Onishi.

At least 19 recordsLinked to original sources
PubMed1992

Administration of interleukin-2 induces major histocompatibility complex class II expression on the biliary epithelial cells, possibly through endogenous interferon-gamma production.

In various organ-specific autoimmune diseases, aberrant expression of major histocompatibility complex class II antigens on each target epithelial cell has been reported. Some researchers have attempted to link this phenomenon to the antigen-presenting capacity and the induction of autoimmunity, whereas others think it might serve as a peripheral mechanism for the induction and the maintenance of self-tolerance in autoreactive T cells. In this study, we showed that intraperitoneal administration of interleukin-2 (1.2 x 10(6) IU/kg) to 4-wk-old male BALB/c mice for 35 consecutive days induced lymphocyte infiltration around bile ducts in the liver and major histocompatibility complex class II expression on biliary epithelial cells, which was immunoelectron microscopically confined to the luminal cell surface. Immunohistochemically, lymphocytes accumulating around bile ducts were mainly T cells, positive for CD3, L3T4 and H-2 class II molecules, and a few of them were positive for Lyt-2 and negative for immunoglobulin. Half of the infiltrates were positive for asialo GM1, and one-third was positive for interferon-gamma. Interferon-gamma-positive, L3T4-positive cells were detected in mirror sections. However, neither the destruction of biliary epithelial cells nor the presence of granulomas was observed. Autoantibodies were serologically undetectable. The existence of interferon-gamma-positive cells in the lesion and the fact that intravenous administration of anti-interferon-gamma twice a week completely inhibited the lymphocyte infiltration and the major histocompatibility complex class II expression on biliary epithelial cells suggested that these changes were induced through endogenous interferon-gamma production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

FK506-induced kidney tubular cell injury.

Some renal changes associated with cyclosporine, such as tubular vacuolization and glomerular thrombosis, have also been reported with FK506. Furthermore, FK506 therapy is associated with a decrease in glomerular filtration rate and renal plasma flow and an increase in renal vascular resistance. We studied the in vitro tubular cell sensitivity to FK506 in comparison with CsA, the ultrastructural changes induced by FK506 and CsA, and the effect of both drugs on tubular cell growth in vitro. We also investigated whether FK506 and CsA induced endothelin-1 (ET-1) secretion of cultured tubular cells and whether this stimulatory effect coincided with a change in the endothelin systemic synthesis. Exposure of tubular cells to high concentrations of FK506 or CsA (10, 50, 100 microM) induced a time- and dose-dependent cell injury in vitro. The damage induced by FK506 and CsA was characterized by a direct cytotoxic effect on tubular cells, as expressed by release of 3H thymidine from prelabeled cells, N-acetyl-beta-D-glucosaminidase release, and cell detachment. Ultrastructural changes (vacuolizations, swelling, and mitochondrial enlargement) and inhibition of the growth of cultured tubular cells were also observed at high concentrations of FK506 and CsA. Low concentrations of FK506 and CsA (1, 0.1, 0.01, 0.001 microM) were not cytotoxic and induced only a minimal inhibitory effect on the growth of tubular cells in vitro. We demonstrated that FK506 (1, 0.1, 0.01 microM) time-dependently stimulated the secretion of endothelin by cultured tubular cells. CsA 10, 1, 0.1, 0.01 also exerted an enhancing effect on ET-1 secretion in cultured tubular cells. We observed that the concentration of CsA that induced the most important enhancing effect was 10 or 100 times higher than that required for FK506 to observe the same effect. The concentrations of FK506 or CsA that induced ET-1 secretion were not cytolytic for tubular cells in vitro. FK506- or CsA-treated rats showed an increase in serum level of ET-1 in comparison with the control. Through the stimulatory effect on endothelin secretion by tubular cells, FK506 and CsA may induce a perturbation of renal hemodynamics. Concentrations of FK506 and CsA, higher than established serum levels but close to those reached in tissues, are cytotoxic for tubular cells and induced ultrastructural changes and a significant delayed regeneration.

Acetylglucosaminidase↗
PubMed1992

Molecular analysis of immunoglobulin heavy chain genes coding for idiotypic and anti-idiotypic antibodies involved in B-B cellular interaction.

We recently reported that a unique B cell clone (B19-1d), specific for a cross-reactive idiotype (CRI) on MOPC104E myeloma protein (M104E), enhances Igh-restricted CRI+ antibody production. In this paper, we report the nucleotide sequences of immunoglobulin heavy chain variable regions (VH) of both M104E and B19-1d-derived hybridoma (HB19) antibodies. The sequence data revealed that both belong to the J558 germ line VH gene subfamily. Strikingly, not only the VH region, but also the leader sequences of M104E and HB19 are very similar to each other at 88% (VH) and 91% (leader) homology, but they use different D and J segments. The VH region sequence similarity is highest among the germ line VH gene sequences of the BALB/c J558 subfamily so far screened. Southern hybridization data, using 5'-noncoding regions of either M104E or HB19 genomic VH gene clones as probes, revealed that both VH genes are conserved in the M104E CRI producer strains of mice. Moreover, these probes show the restriction length polymorphism pattern of mouse VH genes in various strains. That the HB19 VH gene locates to the 5' upper arm of the M104E VH gene on the chromosome was suggested by Southern blot hybridization. Immunoglobulin VH gene restriction of idiotypic and antiidiotypic B-B cellular interaction is discussed from a molecular point of view.

Amino Acid Sequence↗
PubMed1992

Prolonged QT interval in alcoholic autonomic nervous dysfunction.

QT prolongation on electrocardiography is related to sudden cardiac death and is frequently found in alcoholics. We studied QT prolongation in relation to the function of cardiac autonomic nerves assessed by the coefficient of variation of the R-R interval (CVRR) in three age-matched groups of men: 32 alcoholics with autonomic nervous dysfunction (AN), 32 alcoholics without AN, and 32 healthy controls. The QTc interval and CVRR were measured at rest on the 30th day of abstinence, when electrolyte imbalance had disappeared. Subjects with arrhythmia, conduction abnormality, cardiomegaly, ischemic heart disease or diabetes mellitus were excluded. A CVRR of less than 80% of standard predicted value was judged to represent AN. In alcoholics, QTc correlated negatively with the ratio of CVRR to its standard value (r = -0.49, p < 0.0001). The incidence of QTc prolongation was higher in alcoholics with AN (46.9%) than in alcoholics without AN (21.9%, p < 0.05). QTc prolongation was not observed in healthy controls. The QTc interval was significantly (p < 0.01) longer in alcoholics with AN (444 +/- 20 msec) than in alcoholics without AN (426 +/- 17) and in healthy controls (398 +/- 18). These results suggest that alcoholism causes dysfunction of the autonomic nerves as well as worsening QT prolongation, and this may predispose such patients to sudden cardiac death.

Adult↗
PubMed1992

Arterial blood ketone body ratio as a possible indicator for predicting fulminant hepatitis in patients with acute hepatitis.

Encephalopathy and severe coagulopathy in patients with acute hepatitis (AH) are good markers for the diagnosis of fulminant hepatitis (FH), which occurs in only about 1% of AH patients. However, even if patients show severe coagulopathy, it is quite difficult to predict FH before the onset of encephalopathy. The ratio of acetoacetate/beta-hydroxybutyrate in arterial blood (KBR) has been reported to reflect the cellular energy charge level in hepatocytes. In our previous report, KBR was quite low in FH patients and was an excellent marker for predicting the prognosis. KBR of normal subjects is distributed in a range of 1.0-2.1 (1.54 +/- 0.26, mean +/- SD). In this study, we assessed KBR serially in 15 AH patients with severe coagulopathy (hepaplastin test (HPT) < 40%), including seven patients who developed FH, to see if we could predict FH by using KBR as a marker. Seven patients with KBR < 0.6 of long duration (4 days or more) were complicated with hepatic encephalopathy (HE) and it took 3 or more days of KBR below 0.6 before HE appeared. The other eight patients with KBR < 0.6 of short duration (less than 4 days) were not complicated with HE. These data suggest that AH patients with HPT < 40% and a 3-day duration of KBR < 0.6 are at serious risk of FH.

Acute Disease↗
PubMed1992

[Report of two cases of neonatal alloimmune thrombocytopenia caused by anti-HLA antibody, and their screening using umbilical cord blood].

Here reported are two cases with neonatal alloimmune thrombocytopenia (NAITP). In our 2 cases, anti-HLA antibodies, i.e. anti-HLA-A24+B51 and anti-HLA-Bw61+Cw3, respectively, were detected in the mother's sera, which reacted to each patient's lymphocytes and were presumed to have been contribute to NAITP. The thrombocytopenia, found on routine laboratory examination, recovered within 1 to 3 weeks without any therapy in both cases. Further, the relationship of platelet count and PAIgG in neonatal babies (umbilical cord blood) to anti-HLA antibodies in their mothers were examined in 284 pairs. Thrombocytopenia less than 150,000/microliters was found in 16/284 babies (5.6%), 3 of the 16 (1.1% of the total) being positive for anti-HLA, and one positive for PAIgG. Four (1.4%) of the 284 babies were positive for PAIgG, one of whom was thrombocytopenic, and one positive for anti-HLA. Anti-HLA antibody was found in 25/284 mothers (8.8%). Nevertheless, none of the pairs showed positive reactions in all of three tests. It seems that passive transfer of maternal anti-HLA antibodies to the fetus is not itself sufficient to cause thrombocytopenia. On the other hand, some NAITP cases may have been overlooked because of their mildness.

Female↗
PubMed1992

Infantile multilocular renal cyst.

A case of a Japanese 14-month-old male infant with multilocular renal cyst is presented. He was admitted with a chief complaint of an abdominal mass. Although clinically and radiographically multilocular renal cyst in the right kidney was suspected, total nephrectomy was performed because of extreme difficulty of partial nephrectomy and impossibility of complete neglect of malignant cystic tumor. Microscopically, immature glomeruloid tissue, primitive tubules, rhabdomyocytes and nerve fibers were noted. The histological diagnosis of multilocular renal cyst with partially differentiated dysplasia was made. Since the first report by Edmunds in 1892, the etiology of multilocular renal cyst has been discussed for years. In our present case, the pathologic findings suggest that multilocular cystic formation in the right kidney might be the result of developmental disturbances.

Humans↗
PubMed1991

Interleukin-6 positive follicular hyperplasia in the lymph node of a patient with rheumatoid arthritis.

We examined interleukin-6 production in the hyperplastic lymph node of a 77-year-old male rheumatoid arthritis patient with lymphadenopathy. The interleukin-6 production of the lymph node was observed by both immunohistological staining and in vitro culture. The results suggest that interleukin-6 plays a significant pathogenic role in the etiology of the lymphadenopathy seen in many rheumatoid arthritis patients.

Aged↗
PubMed1991

Immunoelectron microscopic identification of asialo GM1-positive cells in adult rat liver.

For the electron microscopic identification of asialo GM1-positive cells, fresh-frozen sections fixed with cold acetone and PLP-fixed vibratome sections of adult rat livers were prepared immunocytochemically using the avidin-biotin-peroxidase complex method. Asialo GM1-positive cells were located mainly in the sinusoids, and rarely in Glisson's sheath and portal veins. In the sinusoids, most pit cells, showing the ultrastructural characteristics of large granular lymphocytes (LGL), were positive for asialo GM1 but a few pit cells were asialo GM1-negative. There were several, morphological differences between asialo GM1-positive and -negative pit cells. The asialo GM1-negative pit cells were smaller and had less-developed cell organelles and fewer dense granules, suggesting a more immature stage of development. Almost all the monocytes, segmented neutrophils and eosinophils, and small or large lymphocytes in the sinusoids also showed positive reaction for asialo GM1. In Glisson's sheath, in addition to pit cells and lymphocytes, mast cells were also positive for asialo GM1. In contrast, fixed cells such as liver parenchymal cells, endothelial cells, Kupffer cells and Ito cells within the liver lobules, as well as biliary epithelial cells, smooth muscle cells, fibroblasts, endothelial cells and pericytes in Glisson's sheath were all negative for asialo GM1. Thus, cell surface asialo GM1 expression is not specific for pit cells (LGL) in the rat liver.

Animals↗
PubMed1991

Beta 2-microglobulin deposition in bone in chronic renal failure.

Recently, there have been reports of beta 2-microglobulin (beta 2 m) related amyloid deposition in perineural and periarticular tissues in patients receiving long-term hemodialysis, but it has been rarely described in bone. We, therefore, examined previously obtained bone biopsy specimens in patients receiving long-term hemodialysis to determine the prevalence of beta 2 m deposition in bone and to assess the relationship between beta 2 m deposits and bone histomorphometry. We found beta 2 m deposits in bone in 8% of 224 patients examined. Bone deposition of beta 2 m was absent in patients who were on dialysis for less than six years, but was present in 19% who dialyzed longer than 10 years. beta 2 m deposits were found in specimens from the iliac crest, femoral bone, tibia, vertebra and rib. In the iliac crest beta 2 m deposition was localized predominantly to the periosteum. Among these patients with beta 2 m in iliac crest periosteum, 62% had suffered a femoral neck fracture compared to only 4% of matched patients who had negative staining for beta 2 m in the iliac crest (P less than 0.001). Histologically, osteitis fibrosa seemed more common in patients positive for beta 2m than in patients negative for beta 2m deposition. We conclude that beta 2m deposition in bone is common in uremic patients who have received hemodialysis longer than 10 years. The high prevalence of femoral neck fracture in patients with beta 2m localized to the periosteum of the iliac crest suggests that this involvement may be useful to predict susceptibility to femoral fracture.

Adolescent↗
PubMed1991

Arterial ketone body ratio as a possible indicator for liver transplantation in fulminant hepatic failure.

Arterial ketone body ratio (AKBR [acetoacetate/beta-hydroxybutyrate]) was measured in nineteen patients under medical supportive therapy for fulminant hepatic failure (FHF), in order to evaluate its predictive value relative to liver transplantation. Of the 19 patients 8 (42%) were salvaged and 11 (58%) died. Seven of 8 survivors showed an increased AKBR over 0.6 at 24-hr after admission, and all of them showed AKBR over 0.8 at 48-hr with subsequent maintenance of the value over 1.0. By contrast, all 11 nonsurvivors demonstrated sustained suppression of AKBR below 0.4 from 24 to 72 hr after admission. AKBR values at 24 and 48 hr showed statistically significant differences between survivors and nonsurvivors. Neither the grade of portal systemic encephalopathy (PSE) nor other conventional laboratory parameters--such as AST, bilirubin, ammonia, prothrombin time, hepaplastin test, fibrinogen, and platelet count--could discriminate between survivors and nonsurvivors by univariate analysis. These results indicate that AKBR can accurately predict the prognosis of FHF at the initial 24-48 hr after admission, and that it can play an important role in setting the indication of FHF for liver transplantation.

Adult↗
PubMed1991

A biliary protein identified by immunoblotting stimulates proliferation of peripheral blood T lymphocytes in primary biliary cirrhosis.

The source of activation of T lymphocytes in primary biliary cirrhosis (PBC) is undefined. Hence, T-cell-mediated reactivity against a biliary tract antigenic protein from human bile was studied. The bile protein was fractionated by 30-50% saturated ammonium sulphate and gel-chromatography, and analysed by SDS-PAGE and Western immunoblotting using rabbit antisera to the bile protein. The antisera reacted specifically with human bile duct epithelium. Western blotting of bile proteins showed two major bands, the B1 and B2 antigens. B1 stained for sialoglycoprotein but not lipid, but B2 was negative for both. Cell-mediated reactivity was tested by proliferation of peripheral lymphocytes against B1. Taking the upper limit of the normal range for stimulation indices (S.I.) as less than 1.89 (= mean + 2 SD), a mitogenic response was detected in 14 of 16 patients with PBC (S.I.: 11.7 to 2.3), and in 4 of 15 patients with chronic active hepatitis, but in none of 12 patients with drug-induced intrahepatic cholestasis or obstructive jaundice. The B2 protein was non-stimulatory. Lymphocyte proliferation to B1 in PBC was confined to T cell fractions of peripheral blood leucocytes. There was no cross-antigenicity between B1 and the M2 antigens, according to Western blotting using the rabbit antisera and PBC sera with anti-M2 reactivity. Thus, the B1 biliary protein is a possible source of T cell activation in PBC and hence could be an immunological co-factor in the pathogenesis of this disease.

Aged↗
PubMed1991

Spatial distribution of late potentials assessed by signal-averaged body surface mapping.

In order to evaluate the spatial location of late potentials (LPs), we designed a new system for the body surface mapping of signal-averaged, filtered ECG using 45 thoracic unipolar leads (5 X 9 array). Signals from patients with old myocardial infarction (MI, N = 8), arrhythmogenic right ventricular dysplasia (N = 1) and dilated cardiomyopathy (N = 2) were amplified and passed through a digital bandpass filter (60-300Hz). Departure maps, LP isopotential maps, and LP30 area maps were generated and superimposed. The LP30 duration was determined as the section between the filtered QRS endpoints and points 30 msec before. Isopotential maps of the LPs showed distinct positive and negative regions. In 8 cases with MI, the extreme was related to the zones indicated by departure maps, and LP30 area maps also corresponded to the departure areas. Most importantly, the spatial distribution for the LP30 area map was different for each type of disease. In conclusion, body surface LP isopotential maps and LP30 area maps may provide useful information concerning the spatial distribution of LPs.

Arrhythmias, Cardiac↗
PubMed1991

[Establishment and characterization of new cell lines from human renal cell carcinoma].

We have characterized seven human renal cell carcinoma cell lines established from primary sites of five patients between 1987 and 1989. Two lines, OUR-20P and OUR-20S, were derived from the OUR-20 cells by cloning with a dilution method 3 months after the primary culture. These three cell lines were tumorigenic in athymic nude mice when inoculated subcutaneously. Examined by a dye uptake method, OUR-20 was highly sensitive to interferon-alpha (IFN-alpha); OUR-20P, OUR-20S and OUR-30 showed slight sensitivities, while the other three cell lines were insensitive. All seven cell lines have been maintained for more than 2 years and over 50 passages in vitro. Cytogenetic analyses performed 1.5 to 3 years after the starts of primary cultures indicated that all seven cell lines, which exhibited different morphologies in phase-contrast micrographs, were aneuploid with modal chromosome numbers 41 to 89.

Carcinoma, Renal Cell↗
PubMed1990

Assessment of bilirubin clearance capacity of a newly developed ion-exchange adsorption column and its possible use as a supportive therapy in hepatorenal syndrome.

We assessed the bilirubin reduction capacity of three different types of devices in vitro: a high-permeable membrane column for double-filtration plasmapheresis (DFP) (Evaflux 2A, Kuraray, Japan), and non-coated charcoal column for hemoperfusion (HP) (N-180, Asahi Medical, Japan), and ion-exchange columns for plasma adsorption (PA) (BR-350, Asahi Medical, Japan, and B-001, Kuraray, Japan). A column for DFP reduced the concentration of low-molecular proteins effectively such as plasma bilirubin and bile acids in an albumin-dependent manner. A charcoal column adsorbed low-molecular substances preferentially. But in these two columns, the loss of fibrinogen is a limiting factor for determining the processing plasma volume. Ion-exchange columns for PA adsorbed bile acids, disconjugated bilirubin, and monoconjugated bilirubin more efficiently compared with delta-bilirubin and unconjugated bilirubin. Pretreatment of the column with heparin reduced the loss of fibrinogen to less than 10%. We applied the BR-350 ion-exchange column in vivo for treatment of three patients with hyperbilirubinemia. After treatment, an alcoholic hepatitis patient with the hepatorenal syndrome (HRS) recovered from acute renal failure. However, in a patient with primary biliary cirrhosis and in a patient with fulminant hepatitis, the decrease of serum bilirubin was transient and no obvious beneficial responses were noted. The capacity and ability of the BR-350 column to adsorb plasma bilirubin was shown sufficient to treat deeply jaundiced patients, because 4 liters of the plasma of a patient with 108 mg/dl of initial total bilirubin concentration was able to be processed continuously without an obvious decrease in bilirubin adsorption capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adsorption↗
PubMed1990

Long-term renal preservation after brain death maintained with vasopressin and epinephrine.

In order to examine renal function after brain death, twenty-eight patients were randomly separated into two groups. The systemic blood pressure of ten patients was maintained with epinephrine alone (group 1). Eight of the ten patients experienced cardiac arrest within 48 h (range 6-87 h) despite the rather large dosage of epinephrine. Urine output was uncontrollable and renal function deteriorated progressively in this group. Eighteen patients were maintained with arginine vasopressin and epinephrine (group 2). Circulation was maintained with a smaller dosage of epinephrine than that given group 1 for at least 4 days (mean +/- SD 16.5 +/- 12.2 days). Urine output was controlled within the normal range and serum levels of blood urea nitrogen (BUN) and creatinine were normal for 14 days. Daily creatinine clearance was more than 80 ml/min. The combined administration of arginine vasopressin and epinephrine preserved the kidneys after brain death for more than a week. This method will be of great value in renal transplantation from brain-dead organ donors.

Adolescent↗