Search PubMed⌕ Search

Biomedical subjects

F Tsuda

Publications and source records attributed to F Tsuda.

At least 163 records · Page 9Linked to original sources
PubMed1980

Diagnosis of type A hepatitis by fecal IgA antibody against hepatitis A antigen.

A method was developed for the early diagnosis of type A hepatitis. The method involved the detection of fecal antibody against hepatitis A antigen (HAAg). We followed 6 patients who contracted type A hepatitis in an outbreak for the fecal excretion of HAAg and antibody against HAAg (anti-HA) by immune electron microscopy. Fecal anti-HA appeared soon after the disappearance of HAAg, at around the zenith of serum transaminase, and persisted approximately 4 mo after the development of hepatitis. Fecal anti-HA was of IgA class, since it was completely absorbed by an anti-IgA column, but not affected by anti-IgG or anti IgM column. Owing to its early appearance and short duration, fecal anti-HA allows an early diagnosis of type A hepatitis by the test of a single specimen. Fecal anti-HA would be assumed to herald the termination of the period during which patients should be segregated from the community to prevent secondary infection.

Antibodies, Viral↗
PubMed1979

Application of microtiter solid-phase radioimmunoassay to the determination of hepatitis B e antigen.

Microtiter solid-phase radioimmunoassay (micro-SPRIA) was applied to the detection of hepatitis B e antigen (HBeAg) in the serum. Antibody against HBeAg to coat the microtiter plate and for radiolabeling was obtained from the serum of asymptomatic carriers of hepatitis B surface antigen by an affinity column of partially purified HBeAg. The micro-SPRIA was sensitive and could be performed without prior concentration of the test serum. HBeAg was detected in 21 (35%) out of 60 serum samples positive for hepatitis B surface antigen, all of which were negative by the conventional immunodiffusion method even after they had been concentrated threefold.

Binding Sites↗
PubMed1978

Studies on the outbreak of hepatitis A in an institute for mentally retarded children.

The authors encountered an outbreak of acute hepatitis in a public institute for mentally retarded children in Aomori Prefecture, Japan. Studies revealed that the probable vehicles of transmission of infection were contaminated water, contaminated meals, and close contact. From the clinical manifestations and epidemiological investigations of 41 affected children and staff members, an outbreak of hepatitis A was strongly suspected. Immune electron microscopy disclosed hepatitis A virus antigen particles in the stool specimens collected during the few days before and after peak transaminase elevation. Hepatitis A antigen was further extracted and purified. The antigen was the first reported recovery of the virus from a natural outbreak of hapatitis A in Asia. Subsequently, with the immune adherence hemagglutination test, using this extracted antigen, an increase in titer of antibody to hepatitis A antigen was demonstrated. Thus, this epidemic was serologically established as an outbreak of hepatitis A. Human immune serum globulin for the protection against hepatitis A was administrated to the 80 individuals concerned, and it was effective in preventing the clinical manifestation of hepatitis.

Adolescent↗
PubMed1977

Clinical significance of e-antigen/anti-e, with special reference to HBc-antigen in the liver.

e-antigen and anti-e were assayed in sera of asymptomatic HBs-Ag carriers and of patients with liver diseases. Thirteen out of 34 (38.2%) asymptomatic carriers were positive for e-antigen, which was in sharp contrast to the reports from USA and Europe. e-antigen was detected to a greater extent in patients with chronic active hepatitis, reversely anti-e in patients with chronic persistent hepatitis. However, e-antigen was found rarely in patients with cirrhosis and never in 23 cases with hepatoma positive for HBs-Ag. HBc-Ag in the liver was detected in 4 out of 8 e-antigen positive asymptomatic carriers and in 4 out of 5 patients with chronic liver diseases with e-antigen respectively, and moreover in 3 out of 14 anti-e positive cases, so that the presence of anti-e did not necessarily mean the negativity of HBc-Ag in the liver. Anti-HBc titer, however, was lower in anti-e positive sera than in e-antigen positive ones. This may implicate the decreased replication of HBV in cases with anti-e. These results emphasize that the investigation of e-antigen/anti-e is mandatory for the evaluation of the prognosis of asymptomatic carriers and of patients with chronic hepatitis.

Adult↗
PubMed1977

Anti-HBc titer in relation to the etiological role of hepatitis B virus in primary hepatocellular carcinoma.

The antibody to hepatitis B core antigen (anti-HBc) is belived to be a marker for natural infection with hepatitis B virus (HBV). In order to study the etiological role of HBV in relation to primary hepatocellular carcinoma (PHC), the anti-HBc in sera of 31 PHC patients was surveyed by the immune adherence hemagglutination method which was about 10 times more sensitive than the complement fixation method. Twenty two out of 31 PHC cases were positive for anti-HBc (71.0%). The is a higher rate of incidence than that of HBs-Ag (51.6%). However, high anti-HBc titer above 2(10) which might reflect current infection with HBV was observed in 15 of these 22 cases. The remaining 7 cases had a titer lower than 2(8); 5 of these patients had neither HBs-Ag nor anti-HBs in their sera. As control, 37 anti-HBs positive blood donors with no definite liver disease were surveyed for anti-HBc titer. Thirty-four of them were positive, but in the majority of cases, the serum titer was less than 2(9), which might only reflect previous infection with HBV. These findings indicate that not only the prevalence of anti-HBc, but also the determination of its real titer is quite important for studying the relationship of HBV to PHC.

Carcinoma, Hepatocellular↗
PubMed1977

Correlation between titer of antibody to hepatitis B core antigen and presence of viral antigens in the liver.

Liver specimens of 31 autopsied cases of liver cirrhosis who had had detectable levels of antibody to hepatitis B core antigen (anti-HBc) inthe serum were stained for hepatitis B core antigen (HBcAg) and hepatitis B surface antigen (HBSAg) by the direct immunofluorescence method. Their premortem serum samples were tested for HBSAg, antibody to HBSAg (anti-HBS) and anti-HBC. Persistent hepatitis B virus (HBV) infection as judged by circulating and/or liver HB antigens was identified in 18 patients, and all of them revealed a high titer of anti-HBC ranging from 2(11) to 2(16) by the immune adherence hemagglutination method. In contrast, anti-HBC titer of the remaining 13 patients without detectable HB antigens was less than 2(9), and the geometric mean titer of anti-HBC of the patients with persistent HBV infection was significantly higher than that of the patients without (13.9+/-1.55 versus 7.23+/-1.30; t test, P less than 0.001). A combination of circulating anti-HBS and hepatic HB antigens was found in one patient, whose serum revealed an anti-HBC titer of 2(12). On the basis of these results, a high titer of anti-HBC in the serum (immune adherence hemagglutination titer of 2(11) or more) seems to be a reliable indicator of persistent HBV infection in the liver.

Antibodies↗
PubMed1976

Association of dane particles with e antigen in the serum of asymptomatic carriers of hepatitis B surface antigen.

Asymptomatic carriers of hepatitis B surface antigen (HBsAg) were surveyed for serum e antigen (e Ag) and antibody to e (anti-e) by immunodiffusion. Seventeen serum samples containing e Ag and 17 containing anti-e, but with similar HBsAg titers, were tested for the presence of hepatitis B core antigen (HBcAg) by means of immune adherence hemagglutination method. HBcAg activity was detected in all of the samples containing e Ag, and the titer of HBcAg paralleled that of HBsAg in each serum. In remarkable contrast, no HBcAg activity was found in any of the serum samples containing anti-e. Dane particles were demonstrated in 14 of 17 serum samples with e Ag by electron microscopy, but in none of 17 with anti-e. Although both e Ag and HBcAg were closely associated with each other, the non-identity of e Ag and HBcAg was clearly demonstrated by a two-dimensional immunodiffusion test.

Antibodies, Viral↗
PubMed1975

Determination of antibody to hepatitis B core antigen by means of immune adherence hemagglutination.

A simple and rapid method utilizing immune adherence hemagglutination has been developed for the detection of antibodies to hepatitis B core antigen (anti-HBc). Hepatitis B core antigen (HBcAG) was prepared from Dane particles that had been isolated from plasma of asymptomatic antigen carriers. The method was specific and about 10 times more sensitive than the conventional complement-fixation method. A total of 215 serum samples obtained from healthy blood donors were surveyed for HBsAG and anti-HEc, as well as for hepatitis B surface antigen (HBsAg) and antibody to HBsAG (anti-HBs). Anti-HBc was found in 36 serum samples, at a prevalence rate higher than that of anti-HBs (31/215)...

Animals↗
PubMedDate not supplied

Antibody to the receptor for polymerized human serum albumin in acute and persistent infection with hepatitis B virus.

The antibody against the receptor for polymerized human serum albumin was determined by radioimmunoassay. The method involved the inhibition by the test serum, absorbed with HBsAg particles without the receptor, on the binding of polymerized human serum albumin to HBsAg particles with the receptor fixed on a solid support. The amount of polymerized human serum albumin captured by the receptor on HBsAg was then determined by the radiolabeled monoclonal antibody directed to an epitope specific for polymerized human serum albumin. In acute infection, the antibody to the receptor for polymerized human serum albumin appeared in the early recovery phase while HBs antigenemia and elevated transaminase levels were still present, preceding the antibody to HBsAg (anti-HBs). The antibody was detected in 4 (1%) of 358 sera from asymptomatic carriers of HBsAg containing antibody to HBeAg, and in none of 67 sera containing HBeAg. Although the antibody was found in as many as 111 (74%) of 150 sera from blood donors who had presumably acquired anti-HBs after natural infection, it was not detected in any sera from 77 recipients of hepatitis B vaccine who had seroconverted for anti-HBs. On the basis of these observations, the determination of antibody to the receptor for polymerized human serum albumin helps in further understanding the immunity to hepatitis B virus.

Acute Disease↗
PubMedDate not supplied

Immunoglobulin A antibody against hepatitis B core antigen of polymeric and monomeric forms, as well as of IgA1 and IgA2 subclasses, in acute and chronic infection with hepatitis B virus.

Solid-phase radioimmunoassays using monoclonal antibodies were used to assay antibody to hepatitis B core antigen of immunoglobulin A class in terms of polymeric and monomeric forms, as well as of IgA1 and IgA2 subclasses, in the serum of persons infected with hepatitis B virus. The level of secretory immunoglobulin A antibody was significantly higher in patients with acute hepatitis (mean +/- S.E., sample per normal ratio = 29.2 +/- 1.9) than that in asymptomatic carriers (2.1 +/- 0.1), patients with chronic persistent hepatitis (3.5 +/- 0.5), patients with chronic active hepatitis (6.9 +/- 1.3) or patients with cirrhosis (5.8 +/- 1.1). In acute type B hepatitis, only polymeric immunoglobulin A antibody of either IgA1 or IgA2 subclass was detected. In contrast, in chronic infection, antibody to hepatitis B core antigen of IgA2 subclass was found in the polymeric form, but antibody of IgA1 subclass was detected in both polymeric and monomeric forms.

Antibodies, Monoclonal↗
PubMedDate not supplied

Antibodies to translation products of the pre-S1 and pre-S2 regions of the envelope gene of hepatitis B virus in fulminant hepatitis B.

Sera from 11 patients with fulminant hepatitis B were tested for antibodies to translation products of the pre-S1 and pre-S2 regions of hepatitis B virus of IgM, IgA and IgG classes, as well as of IgA1, IgA2 and SIgA, with solid-phase enzyme immunoassays using native viral polypeptides. Antibodies to pre-S1 region product of IgM and/or IgA class were detected invariably in six patients who still had detectable hepatitis B surface antigen in serum at the time of clinical presentation. The remaining five patients who had lost HBsAg at presentation had antibodies to pre-S region products of various immunoglobulin classes in higher titers. The five patients with fulminant hepatitis without HBsAg had higher levels of IgA antibodies to pre-S region products than the seven patients with nonfulminant acute hepatitis B who had lost HBsAg: IgA antibody to pre-S1 region product (75.6 +/- 63.8 vs. 2.9 +/- 3.2, p less than 0.01) and IgA antibody to pre-S2 region product (28.9 +/- 25.3 vs. 4.2 +/- 6.9, p less than 0.01). IgA antibodies to pre-S1 and pre-S2 region products were invariably polymeric in fulminant hepatitis B. These findings are compatible with the hypothesis that a heightened humoral antibody response to pre-S1 and pre-S2 region products occurs early during the course of fulminant hepatitis B, participating in severe hepatic injury and early clearance of virus characteristic of this disease.

Acute Disease↗
PubMedDate not supplied

Relative risks of death due to liver disease among Japanese male adults having various statuses for hepatitis B s and e antigen/antibody in serum: a prospective study.

Taking advantage of the compulsory annual medical check-up at the Central Institute of Health, Japan National Railways, hepatitis B seromarkers were tested in male employees at work and their "dead and alive" status was followed for more than 6 years for their prognostic significance. Two prospective studies were carried out. In the first study, two groups (cohorts) of males age 40 to 55 years were tested in 1973 and 1978, respectively, for HBsAg and anti-HBs. The relative risk of dying from primary liver cancer in HBsAg-positive carriers (n = 126) as compared to the controls who were negative for both HBsAg and anti-HBs (n = 5,322) was 30.03 and significantly high, whereas those positive for anti-HBs (n = 1,470) had no increased risk of dying from primary liver cancer or from other liver diseases. The follow-up period ranged from 6.5 to 11.5 years, averaging 8.5 years. In the second study, three male cohorts of the same ages were tested for HBsAg and HBeAg/anti-HBe (micro-Ouchterlony method) in 1977, 1978 and 1979, respectively. There were 513 HBsAg-positive carriers among 25,547 examinees, who were followed for an average of 7.3 (6 to 8) years. Among these HBsAg carriers, those who were positive for HBeAg on entry had the highest risk of dying from primary liver cancer (relative risk, 50.25) and from other liver diseases (78.06), followed by those negative for both (28.95 and 21.78, respectively) and those positive for anti-HBe (9.47 and 6.43) when compared with 25,034 noncarriers.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatitis B Antibodies↗
PubMedDate not supplied

Infection with hepatitis delta and human immunodeficiency viruses among hemophiliacs in Japan.

Two hundred two patients with hemophilia, dependent solely on imported coagulation factor concentrates, were tested for markers of hepatitis B virus infection, antibody to hepatitis delta virus (anti-HD), and antibody to human immunodeficiency virus (anti-HIV). Nine carriers of hepatitis B surface antigen (HBsAg) were identified. Six (66.7%) of them were positive for anti-HD, a prevalence much higher than that in HBsAg carriers without hemophilia in Japan (1/113 or 0.9%, p less than 0.001). Anti-HIV was found in 96 (47.5%), in sharp contrast to the low prevalence (0/1205) in apparently healthy blood donors (p less than 0.001). These results implicated imported plasma products in the transmission of both delta and human immunodeficiency viruses to hemophiliacs. An efficient method for the sterilization of plasma products is warranted to prevent exposure of hemophiliacs to the accompanying pathogenic viruses.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Defects in the precore region of hepatitis B virus DNA in a plasma pool from carriers seropositive for antibody against e antigen and with infectivity in chimpanzees.

A plasma pool from 12 asymptomatic carriers seropositive for antibody against hepatitis B e antigen (anti-HBe) contained hepatitis B virus (HBV) with chimpanzee infectious doses of 1-100/mL, and another pool from 12 carriers positive for hepatitis B e antigen (HBeAg) contained 10(8)/mL doses or more. The HBeAg-positive pool contained 10(6)-fold more HBV DNA than the anti-HBe-positive pool, reflecting the difference in infectivity in chimpanzees. The precore region sequences of HBV DNA in the two plasma pools were amplified by polymerase chain reaction, and separate HBV DNA clones were propagated for determining the nucleotide sequence. Of 114 clones from the anti-HBe-positive pool, 113 displayed a point mutation from guanine to adenine at nucleotide 83 in the precore region, which converted codon 28 for tryptophan (TGG) to a stop codon (TAG), and the remaining clone had a point mutation from adenine to cytosine at the first letter of codon 1 (CTG) to inhibit the translation initiation of the precore region. Precore region defects, in contrast, were observed in only 10 (8%) of 119 clones from the HBeAg-positive pool. These results indicate the infectious capacity of HBV mutants, defective in the precore region and incapable of directing the synthesis and secretion of HBeAg, which prevail in the circulation of hosts after they seroconvert from HBeAg to anti-HBe.

Amino Acid Sequence↗