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Biomedical subjects

A Nakane

Publications and source records attributed to A Nakane.

103 records · Page 6Linked to original sources
PubMed1983

Alternative induction of alpha/beta interferons and gamma interferon by listeria monocytogenes in mouse spleen cell cultures.

Production of interferon (IFN) by Listeria monocytogenes (LM) in nonimmunized mouse spleen cell cultures was studied. IFN-gamma defined by virtue of its acid stability and antigenicity was produced in spleen cell cultures obtained from ddY mice, C57BL/6 mice, and BALB/c mice in response to heat-killed (HK) LM within 24 hr. On the other hand, production of IFN-alpha/beta was demonstrated in spleen cell cultures obtained from one of four nude mice (BALB/c, nu/nu). Therefore, it is important to know the reason why the spleen cells of mice other than nude mice did produce only IFN-gamma, but did not produce IFN-alpha/beta in response to HK-LM. Spleen cells obtained from ddY mice were fractionated, and the cellular source for IFN production of either IFN-alpha/beta or IFN-gamma induced by HK-LM was investigated. IFN-gamma was produced only by a mixture of T lymphocytes (nylon wool-nonadherent, Thy-1-positive cells) and macrophages by HK-LM. Neither T lymphocytes nor macrophages alone produced IFN by HK-LM. Macrophage-depleted spleen cells produced neither IFN-gamma nor IFN-alpha/beta, but these cells acquired the ability to produce IFN-alpha/beta, not IFN-gamma, only when they had been treated with IFN-alpha/beta. A possible mechanism of both IFN-gamma and IFN-alpha/beta induction by Listeria in mouse spleen cell cultures is discussed.

Animals↗
PubMed1983

Spontaneous production of gamma-interferon in cultures of T lymphocytes obtained from patients with Behçet's disease.

The spontaneous production of interferon (IFN) in the cultures of peripheral blood mononuclear leukocytes (PBML) obtained from 30 patients with Behçet's disease was investigated. PBML obtained from each of 26 patients in the convalescent stage and four patients in the exacerbation stage were cultured at least twice without stimulation, and IFN activity in the culture fluid 2 to 7 days after the cultivation was assayed. Twenty PBML of normal healthy donors were also cultured simultaneously. PBML of all patients in the convalescent stage spontaneously produced high-titered IFN (60.0 +/- 9.5 IU/ml), but IFN activity produced in PBML cultures of four patients in the exacerbation stage was very low or was undetectable. Similarly, IFN was always detectable in the circulation of the patients whose PBML spontaneously produced IFN. All IFN activity detected both in the circulation and in the fluid of PBML culture from these patients was gamma-IFN, defined by virtue of its acid lability and antigenicity neutralized with antiserum for gamma-IFN and not with antisera for alpha- and beta-IFN. The cellular source of this gamma-IFN in the patients' PMBL was T lymphocytes and not non-T cells or macrophages. T lymphocytes did not require the help of macrophages. It is suggested that T lymphocytes of these patients may be stimulated by unknown causative agents in vivo and may produce gamma-IFN in vivo as well as in in vitro culture of T lymphocytes.

Adult↗
PubMed1982

Induction of alpha and beta interferons during the hyporeactive state of gamma interferon by Mycobacterium bovis BCG cell wall fraction in Mycobacterium bovis BCG-sensitized mice.

Characterization of interferon (IFN) induced by a second challenge with specific antigen was investigated during the development of hyporeactivity established after challenge of Mycobacterium bovis BCG-sensitized mice with BCG cell wall fraction (BCG-CW). When BCG-sensitized mice were challenged with BCG-CW, IFN-gamma was detected in the circulation 4 h later and rapidly disappeared. After IFN-gamma disappeared from their blood, mice became completely hyporeactive to the second challenge with BCG-CW for 1 day, and thereafter they recovered from this hyporeactive state. However, we always observed that IFN induced at first by the second challenge with BCG-CW during the hyporeactive state was type I IFN-alpha/beta, but thereafter was entirely IFN-gamma. Induction of IFN-alpha/beta by the specific antigen during restoration from the hyporeactive state in BCG-sensitized mice is discussed.

Animals↗
PubMed1981

Percutaneous needle muscle biopsy in the diagnosis of neuromuscular disorders in children. Histological, histochemical and electron microscopic studies.

Percutaneous needle biopsy was carried out in 75 patients with various neurological and muscle diseases (myopathies in 7, lower motor neuron diseases in 22, upper motor neuron diseases in 6, and unlocalized or miscellaneous diseases in 13) and its usefulness as a diagnostic procedure was evaluated. The ages of the subjects ranged from 2 months to 35 years, 77% were younger than 6 years. The materials were examined histologically, histochemically and electron microscopically with the following results. 1. The muscle volume obtained by needle biopsy was sufficient for studies in 64 cases (85%), insufficient in 8 (11%), while in 3 cases no muscle tissue was obtained. 2. Histological staining properties were excellent in all samples examined. In histochemical preparations, staining was judged as good in 61 cases, but poor in 11 due to an inappropriate freezing procedure. 3. In 33 cases, both needle and open biopsies were carried out simultaneously, and the morphological findings of the specimens were compared. There were no significant differences between them histologically as well as histochemically. Electron microscopic examinations also provided identical information in the seven cases studied so far. 4. The method of needle biopsy has many advantages over open biopsy as a routine diagnostic procedure for neuromuscular disorders in infants and young children, but there are a few disadvantages such as the requirement of technical skill and the inappropriateness for histogram construction in some cases.

Adolescent↗
PubMed1981

Alternative induction of IFN-alpha and IFN-gamma by Listeria monocytogenes in human peripheral blood mononuclear leukocyte cultures.

Production of interferon (IFN) by Listeria monocytogenes (LM) in human peripheral blood mononuclear leukocyte (PBML) cultures was studied. Acid-labile IFN-gamma was produced in Ficoll-Hypaque-purified mononuclear cell cultures in response to heat-killed LM (HK-LM). However, plastic dish (PD)-nonadherent cells produced acid-stable IFN-alpha, whereas the cells reconstituted with PD-adherent cells (M phi) and PD-nonadherent cells produced IFN-gamma by HK-LM, IFN-gamma was produced only in a mixture of SRBC rosette-forming (T) cells and M phi. Neither T cells nor M phi produced IFN by HK-LM. On the other hand, IFN-alpha was produced from non-T and nylon wool-nonadherent (non-T, non-B) cells by stimulation with HK-LM in the absence of M phi. A reciprocal type of IFN produced in human PBML was absolutely dependent on the presence or absence of M phi. A soluble fraction extracted from sonically disrupted LM had a high potential to induce IFN-gamma in human PBML. Possible mechanism of the alternative production of IFN-gamma or IFN-alpha in human PBML by Listeria are discussed.

Adult↗
PubMed1978

Proteases produced by a proteolytic mutant of Clostridium botulinum type E.

A proteolytic mutant from Clostridium botulinum type E produced extracellular proteases after the end of exponential growth coinciding with the period of sporulation. Proteases were separated into four fractions by chromatography on a DEAE-cellulose column. One was a sulphydryl-dependent protease that also apparently required a divalent cation for enzyme activity since it was inhibited by EDTA. This enzyme hydrolysed synthetic amide and ester compounds containing an arginine residue, and showed some activity towards L-lysine methyl ester. It appeared that two of the other proteases were serine proteases and the fourth was a metal protease. These last three proteases did not require a thiol agent and did not hydrolyse any of the synthetic amides or esters examined. Only the sulphydryl-dependent protease could activate C. botulinum type B, E and F toxins. The ability of this enzyme to activate type B and E toxins was markedly lower than that of trypsin. The susceptibility of type B toxin to this protease was lower than that of type E toxin. C2 toxin was not activated by this enzyme. It is suggested that the sulphydryl-dependent protease in this proteolytic mutant of C. botulinum type E has properties similar to those of proteases from C. botulinum types B and F.

Botulinum Toxins↗
PubMed1977

Proteolytic mutants obtained from Clostridium botulinum type E.

Proteolytic mutants were isolated from toxigenic strains of Clostridium botulinum type E after several transfers. When these cultures were plated on blood agar, almost all of the colonies obtained were proteolytic, and there were fewer toxigenic colonies than nontoxigenic colonies. The proteolytic mutants and nonproteolytic original strains were different in their biological properties.

Amidohydrolases↗
PubMedDate not supplied

Endogenous gamma interferon produced in central nervous system by systemic infection with Theiler's virus in mice.

Theiler's virus GD VII strain causes acute encephalomyelitis by intracerebral inoculation. We established acute encephalomyelitis in mice by the intravenous (i.v.) inoculation of Theiler's virus GD VII strain. Replication of Theiler's virus injected i.v. could be observed in both the brain and spinal cord of mice, and interferon (IFN)-gamma could be detected in the extracts of brain and spinal cord in parallel with viral replication. Furthermore, by the injection of anti-IFN-gamma monoclonal antibody (mAb) on Day 1 post-infection (p.i.), mortality and virus titres in the spinal cord increased compared with the control mice treated with normal rat globulin. The histological exacerbation of inflammation was observed in spinal cord of anti-IFN-gamma mAb-treated mice. These results indicate that endogenous IFN-gamma, produced locally in the brain and spinal cord of mice through both antiviral action and anti-inflammatory action of IFN-gamma in central nervous system, plays an important role in Theiler's virus infection.

Animals↗