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Biomedical subjects

T Katagiri

Publications and source records attributed to T Katagiri.

At least 289 records · Page 16Linked to original sources
PubMed1988

Neurofibrillary tangle formation in the nucleus basalis of Meynert ipsilateral to a massive cerebral infarct.

Two cases of massive cerebral infarct in the territory of the middle cerebral artery on one side of the brain are presented, in which many (Patient 1) or several (Patient 2) neurofibrillary tangle-bearing neurons were observed in the nucleus basalis of Meynert (nbM), ipsilateral to the infarcts. Tangles were absent or rare in the opposite nbM or in other areas of the brain. Considering the widespread projection of nbM axons to the ipsilateral cerebral cortex, this suggests that formation of neurofibrillary tangles can occur as a retrograde reaction in nbM neurons secondary to massive, old cerebral infarction.

Aged↗
PubMed1988

The mode of recognition of tumor antigens by noncytolytic-type antitumor T cells: role of antigen-presenting cells and their surface class I and class II H-2 molecules.

The present study investigated the role of antigen-presenting cells (APC) in the activation of noncytolytic T cells against tumor antigens. The noncytolytic-type T cells exerted their antitumor effect by producing gamma-interferon (IFN-gamma) and by activating macrophages as the ultimate effectors. The production of IFN-gamma by these noncytolytic T cells following the stimulation with tumor cells required the participation of Ia+ APC, since the depletion of APC from cultures of tumor-immunized spleen cells resulted in almost complete inhibition of the IFN-gamma production. Both L3T4+ and Lyt-2+ subsets of T cells were capable of producing IFN-gamma, and the requirement of APC for the production of IFN-gamma was the case irrespective of whether noncytolytic T cells were of L3T4+ or Lyt-2+ phenotype. More importantly, it was demonstrated that the production of IFN-gamma by L3T4+ and Lyt-2+ T cells was inhibited by addition of the respective anti-class II and anti-class I H-2 antibody to cultures. These results indicate that antitumor L3T4+ or Lyt-2+ noncytolytic T cells are activated for the IFN-gamma production by recognizing tumor antigens in the context of self-class II or -class I H-2 molecules on APC.

Animals↗
PubMed1988

Sporadic lower motor neuron disease with Lewy body-like inclusions: a new subgroup?

A sporadic case of lower motor neuron disease with Lewy body-like inclusions is presented. A woman of 69, 6 months before death, had a history of muscle weakness and atrophy of the four extremities. Neuropathological examination revealed neuronal loss and associated gliosis in the anterior horns of the whole spinal cord. The cytoplasm of some of the remaining neurons contained Lewy body-like inclusions. Bunina bodies, or both. Spheroids and cord-like thickenings of cell processes were also observed in the anterior horns. A few neurons showed argentophilia of the cytoplasm. No tract degeneration was detectable in the white matter of the spinal cord. The present case and two reported similar cases may constitute a new subgroup of motor neuron disease.

Aged↗
PubMed1988

Existence of a new type of sulfite oxidase which utilizes ferric ions as an electron acceptor in Thiobacillus ferrooxidans.

A new type of sulfite oxidase which utilizes ferric ion (Fe3+) as an electron acceptor was found in iron-grown Thiobacillus ferrooxidans. It was localized in the plasma membrane of the bacterium and had a pH optimum at 6.0. Under aerobic conditions, 1 mol of sulfite was oxidized by the enzyme to produce 1 mol of sulfate. Under anaerobic conditions in the presence of Fe3+, sulfite was oxidized by the enzyme as rapidly as it was under aerobic conditions. In the presence of o-phenanthroline or a chelator for Fe2+, the production of Fe2+ was observed during sulfite oxidation by this enzyme under not only anaerobic conditions but also aerobic conditions. No Fe2+ production was observed in the absence of o-phenanthroline, suggesting that the Fe2+ produced was rapidly reoxidized by molecular oxygen. Neither cytochrome c nor ferricyanide, both of which are electron acceptors for other sulfite oxidases, served as an electron acceptor for the sulfite oxidase of T. ferrooxidans. The enzyme was strongly inhibited by chelating agents for Fe3+. The physiological role of sulfite oxidase in sulfur oxidation of T. ferrooxidans is discussed.

Ferric Compounds↗
PubMed1988

Reduction of Mo6+ with elemental sulfur by Thiobacillus ferrooxidans.

In the presence of phosphate ions, molybdic ions (Mo6+) were reduced enzymatically with elemental sulfur by washed intact cells of Thiobacillus ferrooxidans to give molybdenum blue. The whole-cell activity that reduced Mo6+ was totally due to cellular sulfur:ferric ion oxidoreductase (SFORase) (T. Sugio, W. Mizunashi, K. Inagaki, and T. Tano, J. Bacteriol. 169:4916-4922, 1987). The activity of M06+ reduction with elemental sulfur was competitively inhibited by Fe3+, Cu2+, and Co2+. The Michaelis constant of SFORase for Mo6+ was 7.6 mM, and the inhibition constants for Fe3+, Cu2+, and Co2+ were 0.084, 0.015, and 0.17 mM, respectively, suggesting that SFORase can reduce not only Fe3+ and Mo6+ but also Cu2+ and Co2+ with elemental sulfur.

Acidithiobacillus thiooxidans↗
PubMed1988

Impairment of mitochondrial respiratory activity in the early ischemic myocardium--with special reference to electron transport system.

Impairment of mitochondrial respiration in early myocardial ischemia was studied with special reference to myocellular irreversible injury. The technique used was total ligation of the left anterior descending coronary artery, followed by reconstruction of coronary blood flow, in the dog. State 3 respiratory activity reduced significantly to 76% of that of the non-ischemic myocardium in subendocardial muscle (Endo) as early as 30 min after occlusion, and at 60 min to 84% in the subepicardium (Epi). The activity was not recovered by reperfusion. The activity of complex I of sonicated submitochondrial particles decreased at 30 min to 67% in Endo and at 60 min to 71% in Epi, and was not recovered by reperfusion. Complex II and IV activities were kept in the control level until 60 min of ischemia. DNP-stimulated ATPase activity reduced to 79% in Endo at 15 min and to 70% in Epi at 30 min, but recovered significantly by reperfusion until 30 min of ischemia. Mitochondrial respiratory activity was impaired irreversibly in ischemia for 30 min in Endo and this spread to Epi later. Degradation of complex I is considered to be one of the causes of myocardial irreversibility in early ischemia.

Adenosine Triphosphatases↗
PubMed1988

Degrading process of acute ischemic myocardial cells.

1. Development of acute ischemic myocardial injury was studied in mongrel dogs, induced by ligation of left anterior descending coronary artery (LAD), by biochemical analysis of myocardial fractions such as sarcoplasmic reticulum (SR) and mitochondria (Mt) and by electron microscopic observation of ischemic myocardial cells with lanthanum probe method. 2. Irreversible injury of ischemic myocardium initiated in subendocardial muscle as early as 20 min after occlusion of LAD as expressed degradation of major ATPase protein and phosphatidylcholine and phosphatidylethanolamine of SR and irreversible impairment of state III respiratory and dinitrophenol (DNP)-ATPase activities of Mt, and these necrotic changes advanced to subepicardial layer at about 60 min. 3. Ultrastructural irreversible findings appeared later at about 60 min following inflow of lanthanum ions in ischemia for 30 min. 4. Activation of cathepsin B inside of SR under ischemic acidic metabolism and abnormal inflow of Ca++ into ischemic cardiac myocytes are suspective of very important factors for the initiation of myocardial ischemic injury in early myocardial ischemia.

Animals↗
PubMed1988

Immunocytochemical study of Onuf's nucleus in amyotrophic lateral sclerosis.

The sacral segments of the spinal cord in 15 cases of amyotrophic lateral sclerosis and 7 control cases were investigated using peptides immunocytochemistry. A rich supply of somatostatin-, enkephalin- and substance P-immunoreactive fibers and terminals were found in common with the intermediolateral cell column in Onuf's nucleus, but not with the motor neurons in ventral horn. Furthermore, there was no significant difference with peptides innervation between ALS and control cases. Onuf's nucleus, though located in the ventral horn of the upper sacral segment, has a rich supply of peptidergic innervation which suggests that this nucleus does not represent merely somatic motor neurons, but also represents autonomic neurons. This may be related to sparing of Onuf's nucleus along with the autonomic sacral intermediolateral nucleus in ALS.

Adult↗
PubMed1988

Southern blot analysis of major histocompatibility genes of lpr mice.

Several recent functional and immunofluorescent studies have suggested that abnormal major histocompatibility genes may be expressed in mice homozygous for the autoimmune disease-accelerating lpr (lymphoproliferation) gene. In an effort to establish the molecular basis of the expression of abnormal MHC molecules in these mice, we used MHC class I- and class II-specific cDNAs to probe endonuclease-digested genomic DNA from strains expressing lpr to look for restriction fragment length polymorphisms (RFLPs). The RFLP pattern of MRL/Mp-lpr/lpr (MRL/lpr) DNA, as determined using five restriction enzymes, was identical to that of MRL/MP-+/+ and typical of the H-2k haplotype exhibited by C3H/HeSnJ and AKR/J, which are the two H-2k haplotype strains from which MRL was derived. DNA from C57BL/6-lpr/lpr (B6/lpr) exhibited a pattern similar to C57BL/6, again indicating that the lpr gene did not alter MHC genes, within the limitations of this approach. Because macrophages derived from lpr mice had been specifically reported to express altered MHC haplotypes, DNA was prepared from MRL/lpr peritoneal macrophages and Southern blotting was performed using probes for I-A beta and I-E beta. The patterns observed were typical of H-2k DNA. The data thus indicate that the abnormalities of MHC genes previously observed in lpr mice may be due to the influence of other genes on MHC gene products, but are probably not due to alterations in MHC genes themselves.

Animals↗
PubMed1987

The expression and regulation of c-myb transcription in B6/lpr Lyt-2-, L3T4-T lymphocytes.

Mice homozygous for the lpr gene spontaneously develop massive lymphoproliferation and an associated lupus-like autoimmune disease. In addition, the total lymphoid organs from these mice express high levels of mRNA for the c-myb proto-oncogene. Since enhanced c-myb mRNA is normally observed in immature thymic lymphocytes but not normal peripheral T cells, this may be indicative of the abnormal maturation state of lpr T lymphocytes. To determine whether the abnormal Lyt-2-, L3T4- (double negative) T lymphocytes in lpr mice express high c-myb, we purified this population by complement-mediated lysis with anti-L3T4 and Lyt-2 antibody from B6/lpr lymph nodes. We found that increased c-myb mRNA is expressed by this double-negative subset. To assess whether the high level of c-myb correlated with the aberrant undifferentiated state of these cells, we examined the effects of T cell differentiation inducers, phorbol ester and calcium ionophore, on c-myb expression. We found that c-myb levels were depressed after phorbol ester and calcium ionophore treatment. Concomitantly, transcriptional activation of the interleukin 2 receptor gene and progression of these cells through the cell cycle were observed. Thus, in B6/lpr double-negative T cells, the regulation of c-myb, interleukin 2 receptor, and cell proliferation may be interrelated. A combination of Northern hybridization and nuclear run-on transcription assays revealed two levels at which c-myb can be regulated in the double-negative T cell subset. The gene is transcriptionally regulated in untreated cells, but on induction with phorbol ester and calcium ionophore, the gene is negatively regulated via post-transcriptional mechanisms.

Animals↗
PubMed1987

Interleukin 2 responses of lpr and normal L3T4-/Lyt-2- T cells induced by TPA plus A23187.

The major population of cells that accumulate abnormally in MRL/Mp-lpr/lpr lymphoid tissue is Thy-1+, L3T4-, and Lyt-2-. To clarify the functional potential of these cells, we examined their proliferation, interleukin 2 (IL 2) receptor expression, and IL 2 secretion by using as stimulants the combination of 12-O-tetradecanoylphorbol-2-acetate and A23187 (a calcium ionophore). Although the lpr T cells were capable of responding to these stimulants, the nature of the response and of the concentrations of ligand required differed sharply from the responses of normal adult T cells, and of adult L3T4-Lyt-2- thymocytes. There was a strong similarity but not identity when responses of 16 day fetal thymocytes were compared with those of lpr L3T4-Lyt-2- cells. The unusual functional properties of the lpr cells, such as high A23187 dose requirement for maximal proliferation, low percentage of IL 2 receptor-expressing cells, and low levels of IL 2 secretion, suggested that these cells are arrested at a stage of development similar to that of 16-day fetal thymocytes and before adult L3T4-/Lyt-2- thymocytes.

Animals↗
PubMed1987

Establishment of murine macrophage hybridoma clones capable of acquiring tumoricidal activity upon activation with recombinant interferon-gamma and lipopolysaccharide.

Murine macrophage hybridoma clones were established by fusing glycogen-elicited peritoneal exudate cells (glycogen-PEC) derived from C3H/HeN mice and the hypoxanthine-aminopterin-thymidine-sensitive murine macrophage cell line, J774.3-2. The macrophage hybridomas were further screened for the capacity to acquire tumoricidal activity upon stimulation with lipopolysaccharide (LPS) and recombinant interferon-gamma (IFN-gamma) using murine mammary adenocarcinoma MM48 cells as targets, and three macrophage hybridoma clones, KM-1, KM-2, and KM-3, were established. With concomitant stimulation with LPS, IFN-gamma activated these hybridomas dose dependently to exhibit high tumoricidal activity, whereas single stimulation with either INF-gamma or LPS, even with higher concentrations, did not activate the macrophage hybridomas. This contrasted with the activation of glycogen-PEC for eliciting tumoricidal activity with a single stimulation with LPS (greater than 1 ng/ml) or IFN-gamma (greater than 10 IU/ml). Thus, the macrophage hybridoma clones established here represent inflammatory macrophages which require both IFN-gamma and LPS for their activation.

Animals↗
PubMed1987

Interleukin-2 responses of MRL/lpr mouse splenocytes and lymph node cells induced by TPA and A23187.

Treatment of splenocytes and lymph node cells of 5 month-old MRL/lpr mice with TPA induced IL-2-dependent proliferation of the cells in the presence of CA++. The induced response was inhibited completely by a monoclonal antibody to IL-2 receptor. The combination of TPA and A23187 in the lpr cells induced both proliferation and production of IL-2 in a Ca++-dependent fashion. The proliferative response of the lpr cells was equivalent to that of congenic (MRL/+/+) or normal cells, but the quantity of IL-2 secreted from the lpr cells was significantly less than that of the controls. Actinomycin D, but not mitomycin C, blocked IL-2 secretion from the treated lpr cells indicating de novo synthesis of IL-2 mRNA in the cells. Thus the lpr lymphocytes can be activated to proliferate in response to IL-2, yet they do not secrete IL-2 at a normal level even if activation signals are transmitted into the cells.

Animals↗
PubMed1987

Studies on ultrastructure and cytochemical ATPase activity in human cardiac myocytes from biopsies from patients with various heart diseases.

Ultrastructural localization and intensity of ATPase activity were studied in myocardial cells from biopsies with reference to fine-structural alterations and cardiac functions in patients with various heart diseases. ATPase activity was found to be intense in the sarcoplasmic reticulum (SR), the matrices of the mitochondria (Mt), on the myofilaments (Mf) and along the gap-junctions of intercalated discs in the control myocardial cells. ATPase activity was more intense in cardiac myocytes from well-functioning or ultrastructurally well preserved hearts. In failing and degenerating hearts, ATPase activity was decreased. ATPase activity was more intense in clinically-improving than in clinically-worsening patients. However, the localized pattern of ATPase activity was similar in each heart disease. These results suggest that cytochemical observation of ATPase activity can reflect not only fine structural changes in cardiac myocytes, but also the metabolic state in the diseased heart, and is valuable therefore from the standpoint of clinical medicine.

Adenosine Triphosphatases↗
PubMed1987

Alterations in phospholipids in acute ischemic myocardium.

Alterations in the phospholipid component of membranes were studied in acute myocardial ischemia with respect to sarcoplasmic reticulum (SR) and mitochondria (Mt) in the canine heart and compared with changes in the phospholipid composition of intact membrane treated with exogenous phospholipases (PLases) A2 and C, in order to examine the mechanism of ischemic degradation. As early as 30 min after coronary ligation, the total phospholipid content of SR and Mt decreased significantly, 16.0% and 5.6%, respectively. The patterns of SR and Mt phospholipids from the ischemic myocardia did not differ on the chromatograms from those of the non-ischemic myocardia, and no significant increases in lysophospholipids were found for up to 3 hrs. Among the components of phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE) decreased mainly during ischemia, and depletion of PC exceeded that of PE in SR. PLase C hydrolysed phospholipids yielded no lysophospholipids, compared to the production of a large amount of lysophospholipids by PLase A2. It was concluded that degradation of membrane phospholipids occurs in the early stage of myocardial ischemia mainly in PC and PE, which are the major components of membrane phospholipids. This may be an expression of irreversible changes, and the activation of PLase C was considered to play an important role in their degradation.

Animals↗
PubMed1987

Degradation of the cardiac sarcoplasmic reticulum in acute myocardial ischemia.

The degradation of the sarcoplasmic reticulum (SR) in acute myocardial ischemia was studied with references to the regional irreversibility and to the mechanism of ischemic degradation by the measurements of Ca++-stimulated ATPase activity and composition of the major ATPase protein of the SR and activity of cathepsin B of the SR and lysosome (Ly) fractions. Ca++-stimulated ATPase activity decreased to 66% of that of the nonischemic portion at 20 min after coronary ligation in the subendocardium (Endo) and to 44% at 30 min in the subepicardium (Epi). Composition of the major ATPase protein decreased to 55% and 73% at 30 min in Endo and Epi, respectively. In both SR and Ly fractions cathepsin B exhibited the maximal activity at 6.0-6.5, and pH dependent. And incubation of the SR at pH 6.0 induced the degradation of the ATPase protein quite similarly to that in vivo ischemia. These results suggest that the degradation of the SR membrane of ischemic myocardial cells begins earlier in Endo 20 to 30 min after the cease of the coronary blood flow, and extends to Epi later. Cathepsin B is strongly conceivable to play an initial role of necrotic process of the ischemic myocardial cells by activation inside of the SR in ischemic acidic state.

Acute Disease↗