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Biomedical subjects

T Uchida

Publications and source records attributed to T Uchida.

At least 991 records · Page 55Linked to original sources
PubMed1987

Changes in proton T1 in dog brains due to the administration of haloperidol.

Changes in proton T1 in dog brains due to the administration of haloperidol were determined by the intravenous administration of a single dose of 20 mg of haloperidol to mongrel dogs. The MRI used was the Aberdeen type with the static magnetic field of 0.1 T. A coil made exclusively for these animals (bore diameter 120 mm) was used. There was a significant increase in the T1 value in the striate body 30 minutes and more (within two hours) after the administration of haloperidol. Subtraction images were also obtained by subtracting the image of the pre-treatment (control) T1 values from the image of the post-treatment values (2 hours after the injection). The subtraction images also revealed increases in the T1 values of the striate body.

Animals↗
PubMed1987

A monoclonal antibody against the nucleus reveals the presence of a common protein in the nuclear envelope, the perichromosomal region, and cytoplasmic vesicles.

A monoclonal antibody that recognizes antigenic determinants on the nucleus of cultured mammalian cells was isolated. Immunofluorescence studies using this antibody showed that the recognized antigen was present not only on the nucleus but also in cytoplasmic vesicles of interphase cells and in the perichromosomal region of mitotic cells. Premature chromosome condensation analysis showed that the reactive site for this monoclonal antibody could be detected in the perichromosomal region during the G2 and M phases, but not during the G1 and S phases. Finally, immunoblot analysis showed that this monoclonal antibody prepared against the nucleus recognized a protein of approximately 40 kD both in the cytoplasm and in the perichromosomal regions.

Animals↗
PubMed1987

A rapid vapor-phase acid (hydrochloric acid and trifluoroacetic acid) hydrolysis of peptide and protein.

A new method for the acid hydrolysis of protein is presented. Peptide bonds are cleaved by the action of an HCl/trifluoroacetic acid (TFA) vapor mixture. Contamination for the hydrolysis mixture is reduced to low levels (1-3 pmol). Recovery of hydrophobic amino acid is improved. Short reaction times are achieved and rapid removal of acids is facilitated. The reaction temperature is 158 degrees C for reaction times of 22.5 and 45 min with 7 M HCl and 10% TFA containing 0.1% phenol.

Amino Acids↗
PubMed1987

The mode of entry of herpes simplex virus type 1 into Vero cells.

The mode of entry of herpes simplex virus type 1 (HSV-1) into Vero cells was investigated quantitatively with biological techniques. The entry of virus occurred rapidly when the virus-adsorbed cells were incubated at 37 C. The kinetics of virus entry was found to be similar to that of the process of uncoating, indicating that the uncoating of HSV-1 occurs simultaneously with the entry of virus into the cell. Experiments with ammonium chloride revealed that acidity in endosomes is not necessary for the entry or uncoating of HSV-1, in contrast with the cases of enveloped RNA viruses. In addition, endocytosis of the virus seems to be one of the processes of entry for HSV-1. However, the kinetics of endocytosis showed that the cell-bound virus is endocytosed gradually and suggested that the endocytosis of HSV-1 does not lead the virus to an uncoating process. These results are most consistent with a mechanism of entry for HSV-1 involving fusion of the viral envelope with the plasma membrane of the host cell.

Adsorption↗
PubMed1987

Histopathological analysis of chronic hepatitis B virus (HBV) infection in relation to HBV replication.

The interrelationship among expression patterns of hepatitis B surface and core antigens (HBsAg and HBcAg) in the liver, hepatitis B virus (HBV) DNA in sera, HBeAg/anti-HBe status and histological features was examined in 189 liver specimens and 106 sera from Japanese patients with chronic HBV infection, utilizing immunoperoxidase methods and a spot hybridization technique. HBsAg and HBcAg were distributed uniformly among the lobules in 8 viral carriers with "normal" liver (NVC) and 30 patients with persistent hepatitis (PB) seropositive for HBcAg. This uniform staining pattern was quite distinct from the non-uniform and irregular patterns in 137 patients with chronic active hepatitis (CAH) associated with or not associated with cirrhosis. HBcAg was often found to be stained strongly in the cytoplasm as well as in the nucleus of hepatocytes in HBeAg-positive CAH, in contrast to NVC/PH, in which cytoplasmic HBcAg was very weak. Serum HBV DNA was detected in all 22 cases with HBeAg-positive NVC/PH, 41 of 46 (89.1%) cases with HBeAg-positive CAH, 6 of 23 (26.1%) casew with anti-HBe-positive CAH and none of 3 cases with anti-HBe-positive NVC/PH. The level of serum HBV DNA and staining of HBcAg were in decreasing order in these groups. While the presence of serum HBV DNA and HBcAg staining was always associated with HBeAg seropositivity in NVC/PH, this was not always found in CAH. Moreover, necroinflammatory activity in the liver did not always parallel viral replication in CAH. These findings seem to confirm that NVC/PH and CAH have different biologic processes; viral replication is always concordant in the former, but is sometimes discordant in the latter with HBeAg/anti-HBe status. The immunologic response of the host seems to suppress and distort replication of the virus to a varying degree among patients and areas of the same liver in CAH differently to that in NVC/PH. The different life cycle of the virus, including integration of viral DNA into the cellular genome, may subsequently result in discordant states of various virus markers in CAH.

DNA Replication↗
PubMed1987

The characteristics of alcoholic liver disease in Japan. Clinicopathologic comparison with alcoholic liver disease in the United States.

Alcoholic liver disease (ALD) in Japan was compared clinicopathologically with the occurrence in the U.S.A. ALD found in Japan was more frequently complicated by other hepatic diseases including non-A, non-B chronic hepatitis than ALD found in the U.S.A. (9.9% versus 21.9%). Patients with such complications were excluded from this study. The chief complaints of the total of 51 alcoholics studied in the U.S.A. were abdominal distension or jaundice and those of 98 alcoholics studied in Japan were non-specific: general fatigue, weakness or appetite loss. The U.S. patients exhibited more elevated levels of serum bilirubin (8.1 +/- 7.5 versus 1.9 +/- 2.4 mg/dl, mean +/- SD) and a higher incidence of leukocytosis (49.0% versus 5.1%). While the serum glutamic-oxalacetic transaminase (GOT) levels were not significantly different between the two groups (146.5 +/- 116.8 versus 140.8 +/- 147.7 IU/L), the serum glutamic-pyruvic transaminase (GPT) levels among Japanese alcoholics were higher (38.6 +/- 31.4 versus 87.4 +/- 99.1 IU/L) and in about one quarter of these patients, serum GPT was higher than serum GOT, a feature not seen in the patients in the U.S.A. Comparative histopathologic study of 337 U.S. patients and 210 Japanese patients disclosed a higher frequency of cirrhosis (46.9% versus 33.8%), the presence of Mallory bodies (58.5% versus 13.8%) and marked neutrophilic exudation (45.1% versus 6.2%). Thus, the majority of Japanese alcoholics exhibited progression of liver disease, eventually leading to cirrhosis, due to hepatocellular drop-out and fibrosis caused by a mechanism different from alcoholic hepatitis. In addition, ALD in the U.S.A. revealed more striking extension of fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

A case of acute myelogenous leukaemia associated with eosinophilia: cytogenetic study of eosinophilic colonies showing the origin of the normal clone.

We describe a case of acute myelogenous leukaemia presenting with remarkable eosinophilia in relapse. Since the patient had chromosomal abnormalities, haemopoietic as well as eosinophilic colonies grown in culture were cytogenetically analysed to determine the origin of the eosinophils. Eosinophilic colonies as well as erythroid bursts revealed a normal karyotype, while a short-term culture of peripheral blood cells in relapse revealed an abnormal karyotype which had been observed before treatment. These data clearly demonstrate that the eosinophilia in this case originated from a normal clone. The cytogenetic analysis of eosinophilic colonies is a useful technique for the definite diagnosis of eosinophilic leukaemia or reactive eosinophilia in patients having marker chromosomes.

Adult↗
PubMed1987

Evidence for infection caused by spotted fever group Rickettsia in Kyushu, Japan.

Of 50 cases that gave negative immunofluorescence reaction with Rickettsia tsutsugamushi among patients with suspected tsutsugamushi disease encountered in Miyazaki Prefecture during the last four years, three showed a significant rise in the antibody titer to Rickettsia montana, a species of spotted fever group. This paper reports evidence for the occurrence of the rickettsial infection of the spotted fever group in Kyushu, Japan.

Adult↗
PubMed1987

Immunosuppressive activity of serum from liver-grafted rats: in vitro specific inhibition of mixed lymphocyte reactivity by antibodies against class II RT1 alloantigens.

The immunosuppressive activity of serum from PVG rats following orthotopic transplantation of DA liver has been examined in vitro. Liver grafts in this combination are never rejected, but induce a state of specific transplantation tolerance in the recipient. Serum from such tolerant animals was able to inhibit proliferation of normal PVG lymph node cells in response to DA stimulators in the mixed lymphocyte reaction (MLR); inhibition was specific for donor (DA) antigens. Interleukin-2 (IL-2) production during the MLR was also reduced. The production of anti-DA cytotoxic T cells developing in the MLR was not affected, but the total yield of such cells was reduced. Evidence was obtained that part of the inhibitory serum activity was due to IgG antibody against class II RT1a alloantigens. Thus, a purified IgG fraction retained much of the inhibitory activity which could be removed by an anti-IgG absorbent. Studies of MLR inhibition in different rat strains indicated the anti-class II specificity of the inhibitory IgG. Lymph node cells from DA-liver-grafted PVG rats responded normally against DA stimulators in vitro, and this MLR was also blocked by the inhibitory IgG. Our results suggest that anti-class II allo-antibody may play a role in immunosuppression and long-term graft survival following liver transplantation in this combination.

Animals↗
PubMed1987

Relationship of human cord blood mononuclear cell lines, established by the HTLV-I integration, to expression of T-cell phenotypes and the T-cell receptor gene rearrangement.

The HTLV-I integrated cell lines originated from human cord blood mononuclear cells were examined for the T-cell receptor beta chain gene rearrangement in conjunction with immunological phenotype analysis. Five of seven cell lines contained the rearranged T-cell receptor beta chain gene. Interestingly, most of the rearranged lines failed to express the T cell differentiation antigens, OKT 4 and 8, though their positive expression of Leu 1 antigen indicated the commitment to the T-cell lineage. On the other hand, two cell lines retained the germ-line configuration of the beta chain gene, while phenotypical examination revealed that the two cell lines have distinct T-cell antigens. Non-rearranged cell lines have proved to be nearly monoclonal from HTLV-I integration pattern and/or surface marker clonality. Thus, the relationship between the immunological phenotypes and the T-cell receptor gene rearrangement observed in the T-cell lineage is not strict and often dissociates. A possible involvement of HTLV-I infection on the dissociation between phenotype and genotype is discussed from the viewpoint of phenotypical modulation.

Antigens, Surface↗
PubMed1987

PFK inhibition test for cancer detection: clinical applications and mechanisms of PFK inhibition.

A newly established cancer marker, the PFK inhibition test, has been further examined for its capacity to detect malignant neoplasms irrespective of the organs in which cancer cells start proliferating. We tested 1,160 sera from cancer patients and compared them with 756 normal sera, using histograms and normal paper for analysis of accumulated frequency. PFK activity through the influence of normal sera showed normal distribution, and cancerous sera shifted to the inhibitory site with an irregular shape. From these analyses, the patients were classified into the following types: normal range: PFK greater than SD (standard deviation of PFK activity in normal sera); suspicious range: SD greater than PFK greater than 2SD, must be given the PFK test again; and dangerous range: PFK less than 2SD, further examination must be carried out to detect cancer. Fifty percent of the sera from all the cancer patients inhibited PFK beyond 2 SD of normal sera. We also analyzed organ-associated PFK distribution, eg, gastric, colorectal, and mammary cancer. In gastric cancer, PFK inhibition was stronger in accordance with how far a particular stage of cancer had progressed. However, 50% of sera from stage I gastric cancer patients was positive beyond the cut-off line of 2 SD. We examined 104 sera from patients diagnosed as benign prostatic hypertrophy and found malignant cells in 10 patients whose sera tended to be positive in PFK inhibition. The PFK inhibitory factor in the body fluids of cancer patients was fractionated by Sephadex G-75 gel filtration and DEAE ion exchange chromatography. The approximate molecular weight of this factor was 13,000 daltons. The factor was resistant to heat and acid (0.1 N HCl and H2SO4) and was sensitive to 0.1 N NaOH and phosphate buffer. Diluted sulfuric acid and ammonium sulfate made an inactive NaOH-treated sample active when lyophilized following dialysis against distilled water. PFK inhibition by cancerous sera was eliminated by fructose-2,6-bisphosphate (the strongest activator of PFK) in a dose-dependent manner. PFK attached to agarose beads was found to be reversible even after being inhibited by cancerous body fluids and ATP water solution. Although PFK is apt to decay in a low pH range, the established procedure did not destroy PFK, but induced a direct inhibition of PFK by ATP through the ATP inhibition site on the PFK molecule. The PFK inhibitor may possibly function as a proton carrier and release protons to activate the ATP inhibition site.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗