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Biomedical subjects

S Ikematsu

Publications and source records attributed to S Ikematsu.

At least 19 recordsLinked to original sources

Heterozygote for plasmin inhibitor deficiency developing hemorrhagic tendency with advancing age.

A heterozygote for congenital deficiency of plasma plasmin in inhibitor had hemorrhagic episodes repeatedly after the age of 79. Before the age of 79, he had not exhibited any hemorrhagic tendency and did not have abnormal bleeding even after surgical operations. Although heterozygotes for congenital deficiency of this inhibitor usually have no or only a mild hemorrhagic tendency, this case suggests that they may exhibit severe hemorrhagic tendency when they reach advanced ages because of age-related vascular changes producing hemostatic imbalance.

Aged

A transgenic mouse line with alpha-1,3/4-fucosyl-transferase cDNA: production and characteristics.

cDNA of human alpha-1,3/4-fucosyltransferase (Fuc-TIII) was placed under the control of the chicken beta-actin promoter and cytomegalovirus enhancer, then introduced into male pronuclei of fertilized mouse eggs. A transgenic mouse line thus obtained exhibited enhanced expression of Lex (4C9) antigen in endothelial cells located in the glomerulus, sinusoidal capillaries of the liver and capillaries of the heart. Furthermore, in the transgenic mice, sialyl dimeric Lex (FH6) and sialyl Lea (2D3) antigens were strongly expressed in the glomerular endothelial cells.

Animals

Transgenic mouse lines with ectopic expression of alpha-1,3-galactosyltransferase: production and characteristics.

The cDNA of murine alpha-1,3-galactosyltransferase was placed under the control of the beta-actin promoter and cytomegalovirus enhancer, then introduced into male pronuclei of fertilized mouse eggs. The three transgenic mouse lines obtained were analysed for the expression of the transferase by staining with Griffonia simplicifolia agglutinin I-B4 (GSI-B4), which is alpha-galactosyl specific. Compared with wild-type mice, all lines of transgenic mice expressed GSI-B4 binding sites more intensely in the renal tubular brush border and lung alveolar epithelium, and newly expressed them in the photoreceptor outer segments, goblet cells of the small intestine and around spermatogonia. GSI-B4 binding sites were also detected in the liver of some transgenic mice. Even though the introduced enzyme gene was expressed in embryos, it did not severely hinder embryogenesis. The transgenic mice tended to secrete more proteins in the urine than the wild type. Furthermore, low body weights, partial damage to hair growth and early death occurred more frequently in the transgenic mice.

Animals

Efficacy of recombinant human granulocyte colony-stimulating factor on neutropenia in patients with AIDS.

The efficacy of recombinant human granulocyte colony-stimulating factor (rhG-CSF) on neutropenia was evaluated in 14 patients with AIDS and AIDS-related complex (ARC). In all patients, including 11 neutropenic patients, 100 or 200 micrograms/m2 of rhG-CSF significantly increased the neutrophil counts. The response was greater in patients with higher neutrophil counts before the treatment, and was also dose-dependent. Although the effect seemed to be less potent, the agent also increased the neutrophil counts even when zidovudine (azidothymidine, AZT) and other myelosuppressive antiviral agents were administered simultaneously. These observations indicate that rhG-CSF may be beneficial in preventing and treating some secondary infections, and will make it easier to continue therapy with antiviral agents in patients with AIDS or ARC.

AIDS-Related Complex

Frequent infection with human T-cell lymphotropic virus type I in patients with AIDS but not in carriers of human immunodeficiency virus type 1.

Antibody to human T-cell lymphotropic virus type I (HTLV-I) was measured in 49 Japanese patients (48 with hemophilia) infected with human immunodeficiency virus type 1 (HIV-1) and in 18 hemophiliacs who were not infected with HIV-1, by use of an enzyme-linked immunosorbent assay (ELISA). The antigen used was a gag-env hybrid protein constructed in vitro and expressed in Escherichia coli. This assay detected a specific antibody against HTLV-I. Four of the 18 HIV-1-negative hemophiliacs (22%) were positive for anti-HTLV-I antibody; their geometric mean titer was 951 U/ml. Seven of the 12 patients (58%) with acquired immune deficiency syndrome (AIDS) were positive for anti-HTLV-I antibody, and 8 of 35 HIV-1 + AIDS-free carriers (23%) were positive. The difference between the prevalence of HTLV-I infection in the two groups was statistically significant (p less than 0.0297). The geometric mean titer of antibody in the patients with AIDS was 318 U/ml and that for the HIV-1 + AIDS-free carriers was 1,496 U/ml. These findings suggest that HTLV-I infection could be one of the factors in the development of AIDS in individuals infected with HIV-I.

AIDS-Related Complex

Anti-HTLV-III and anti-HTLV-I antibodies and T cell subsets in hemophiliacs living in HTLV-I endemic and nonendemic areas of Japan.

Sera from 154 hemophiliacs, including 132 with hemophilia A and 22 with hemophilia B, were examined for antibodies against human T cell lymphotropic virus type III (HTLV-III) and type I by strip radioimmunoassay based on the Western blotting technique. Sixty-two patients lived in Kyushu, a known endemic area of HTLV-I and 92 patients lived in Tokyo, a nonendemic area of HTLV-I. Results showed a prevalence of HTLV-III antibodies of 64.5% in Kyushu and of 57.6% in Tokyo. There were no significant differences between these two groups. Helper/suppressor (T4/T8) ratios of seropositive patients were 0.69 +/- 0.41 and those of seronegative patients were 1.05 +/- 0.56. Ratios of both groups were lower than those of normal healthy people (1.35 +/- 0.45). Our findings confirmed that hemophiliacs living in an HTLV-I endemic area and those living in a nonendemic area in Japan equally possessed antibodies to HTLV-III. Low T4/T8 ratios and increases of serum IgG and IgM levels were found even in seronegative hemophiliacs.

Antibodies, Viral

[Factor XIII].

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Factor XIII