Search PubMed⌕ Search

Biomedical subjects

A Tamura

Publications and source records attributed to A Tamura.

At least 325 records · Page 18Linked to original sources
PubMed1992

Degeneration of the ipsilateral substantia nigra following cerebral infarction in the striatum.

BACKGROUND AND PURPOSE: In rats, degeneration of the ipsilateral substantia nigra occurs a few weeks after occlusion of the middle cerebral artery. The aim of this study was to clarify whether similar change is observed in stroke patients. METHODS: Eighteen patients with striatal infarction and six patients with cortical infarction in the territory of the middle cerebral artery were examined by means of sequential magnetic resonance imaging. RESULTS: In all patients with striatal infarction, T2-weighted images revealed a high-signal-intensity spot in the ipsilateral substantia nigra. Changes in the ipsilateral substantial nigra appeared at day 14 after stroke on average and then became less intense and smaller a few months after the stroke. By contrast, we observed no nigral changes in any patient with cortical infarction. CONCLUSIONS: The degenerative change in the ipsilateral substantia nigra initially found in the rat model similarly occurred in patients with striatal infarction. This remote change in the substantia nigra may represent magnetic resonance imaging detection of neuropathologic changes in this region through the striatonigral pathway.

Aged↗
PubMed1992

Seasonality of admissions in the psychoses: effect of diagnosis, sex, and age at onset.

A summer peak was found in first admissions to hospitals in England and Wales between 1976 and 1986 for both affective psychoses and schizophrenia, but not for neurotic conditions or personality disorders. There was no significant relationship between age at first admission and season of admission. The summer peak was most prominent for mania, where it was present in both sexes; for schizophrenia, it was present only in females. These findings suggest that schizophrenia in females, and mania in both sexes, have some aetiological or precipitating factor in common.

Adult↗
PubMed1992

Mechanism of antioxidant action of pueraria glycoside (PG)-1 (an isoflavonoid) and mangiferin (a xanthonoid).

The antioxidant activities of pueraria glycoside (PG)-1 (isoflavonoid) and mangiferin (xanthonoid) were studied and compared with PG-3 and daidzein (isoflavonoids) and with wogonin (flavonoid). PG-1 and mangiferin rapidly scavenged 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and inhibited lipid peroxidation which was initiated enzymatically by reduced nicotinamide adenine dinucleotide phosphate (NADPH) or non-enzymatically by ascorbic acid or Fenton's reagent (H2O2 + Fe2+) in rat liver microsomes. Wogonin inhibited the enzymatically induced lipid peroxidation but had no scavenging effect on DPPH radical or on the non-enzymatic peroxidation. PG-3 and daidzein did not show any of these effects. Formation of Fe2+ by NADPH-dependent cytochrome P-450 reductase was inhibited by wogonin, but not by PG-1 or mangiferin. PG-1 and mangiferin had no effect on terminating radical chain reaction during the lipid peroxidation in the enzymatic system of microsomes or in the linoleic acid hydroperoxide-induced peroxidation system. These results suggest that PG-1 and mangiferin have an antioxidant activity, probably due to their ability to scavenge free radicals involved in initiation of lipid peroxidation. In contrast, wogonin may affect NADPH-dependent cytochrome P-450 reductase action, since it inhibited only the enzymatically induced lipid peroxidation.

Animals↗
PubMed1992

Kawasaki disease complicated by acute myocardial infarction due to thrombotic occlusion of coronary aneurysms 19 years after onset.

A 25-year-old man with a history of Kawasaki disease from the age of 7 had acute inferior myocardial infarction. Emergency right coronary arteriogram showed successive coronary aneurysms at the proximal to middle portion of the right coronary artery, and total occlusion at the proximal segment. Intracoronary thrombolysis was performed and the right coronary artery was recanalized. On left coronary arteriography, coronary aneurysms and mild localized stenoses at the inlet and outlet of the aneurysms were found. It was suggested that the myocardial infarction was caused by thrombotic occlusion of coronary aneurysms complicated with Kawasaki disease.

Adult↗
PubMed1992

[Serum 7S collagen levels in diffuse interstitial lung diseases--an index of the destruction of alveolar structure].

To examine whether alteration of 7S collagen in the alveolar basement membrane is related to the condition and prognosis of diffuse interstitial lung diseases (idiopathic interstitial pneumonia: IIP, collagen vascular diseases, sarcoidosis, and hypersensitivity pneumonitis), we measured serum 7S collagen levels in 123 patients with diffuse interstitial lung disease and other lung diseases. Patients with diffuse lung diseases (diffuse interstitial lung disease, pulmonary emphysema, and diffuse panbronchiolitis: DPB) showed significantly higher serum levels of 7S collagen than healthy normal controls. Serum 7S collagen levels in IIP and collagen vascular diseases were significantly higher than those in pulmonary emphysema and DPB. In cases of IIP, serum 7S collagen levels in the active stage were significantly higher than those in the inactive stage. Furthermore, the prognosis of patients with higher serum 7S collagen levels was significantly poorer than those of patients with lower serum 7S collagen levels. In infectious pulmonary diseases, serum 7S collagen levels of patients with adult respiratory distress syndrome (ARDS) were significantly higher than those of patients without ARDS. Autopsy specimens obtained from patients with positive serum 7S collagen showed diffuse alveolar damage and/or diffuse pulmonary hemorrhage in the alveolar areas. Immunohistochemical staining for 7S collagen showed disruption and/or loss of the alveolar basement membrane. The authors conclude that serum level of 7S collagen is useful for estimating the activity of diffuse interstitial lung diseases as an index of the destruction of alveolar structure.

Basement Membrane↗
PubMed1992

[Measurement of busulfan concentration in plasma and spinal fluid from transplant patients pretreated with busulfan and cyclophosphamide].

Busulfan (BU) concentrations in the blood and spinal fluid of 7 patients pretreated with BU for bone marrow transplantation (BMT) were measured using gas chromatography. The data from these periodically obtained samples were used to study the relationship between the BU concentration and complications (e.g. vomiting), indicating that vomiting leads to a lower maximum BU level. The trough level of BU concentration at 6 hours after administration was stable at around 500 ng/ml, not showing little effect of vomiting. The BU concentrations in the spinal fluid were virtually the same as those in plasma collected at the same time and the spinal fluid/plasma ratio of the BU concentration averaged 1.06. No veno-occlusive disease (VOD) was noted. Failure of engraftment occurred in one case of myelofibrosis, however, as the plasma BU concentration in this case was not lower than the others, the graft failure was not considered to be due to the preconditioning regimen including BU.

Adolescent↗
PubMed1992

[Primary myelofibrosis successfully treated with allogeneic bone marrow transplantation].

A 31-year-old man with primary myelofibrosis initially received low dose Ara C. Splenomegaly decreased but pancytopenia continued. Allogeneic bone marrow transplantation from his sister was then performed. Busulfan and cyclophosphamide were used as a preconditioning regimen, which included neither irradiation nor splenectomy. As the bone marrow was hypoplastic after transplantation, G-CSF was given. It was useful for systemic infection. After transplantation, leukoerythroblastosis and tear drop poikilocytosis disappeared in peripheral blood. Finally, bone marrow fibrosis disappeared and hemopoiesis to normal limits recovered 17 months later. These results demonstrate that bone marrow transplantation is effective for primary myelofibrosis for which there is no otherwise curative therapy.

Adult↗
PubMed1992

[A 62-year-old survivor with Ebstein's anomaly without right ventricular failure].

A 62-year-old woman was admitted our hospital because of concussion of the brain. The level of consciousness improved within several days. Cardiac examination was performed because the patient had experienced feelings of fainting since one year previously, and heart murmur also was heard. The electrocardiogram showed WPW configuration. At the same time that she complained of feelings of fainting, the electrocardiogram showed supraventricular tachycardia. The echocardiogram showed displacement of the septal tricuspid leaflet and mild tricuspid valve, regurgitation. Cardiac catheterization was performed and, using the intracardiac electrocardiogram, we confirmed atrialized right ventricle. We diagnosed this patient as having Ebstein's anomaly with WPW syndrome. The clinical manifestations of this anomaly are quite variable, depending upon the spectrum of pathology and the presence of associated malformations. It is well documented that a considerable proportion of these patients are able to survive into adult life. However, the patient who survives into the sixth decade without a sign of heart failure is extremely rare. We speculate that this patient had not developed right ventricular failure until her 60's because she had a milder form of Ebstein's anomaly and did not have any other congenital heart disease.

Age Factors↗
PubMed1991

Structure of the active 27-residue fragment of human calpastatin.

A synthetic 27-residue peptide corresponding to exon 1B of the endogenous inhibitor calpastatin contains a well-conserved region and has an ability to inhibit the cysteine endopeptidase calpain specifically. We examined the solution structure of this peptide in DMSO-d6 by two-dimensional 1H NMR spectroscopy. Although regular secondary structures such as alpha-helix and beta-sheet were not found, the region from Ile18 to Arg23 formed a well-defined structure with a type I beta-turn. This region coincided well with the highly conserved region of calpastatin. The result strongly suggests that this turn structure is essential for the inhibitory activity of calpastatin.

Amino Acid Sequence↗
PubMed1991

Cold denaturation and heat denaturation of Streptomyces subtilisin inhibitor. 1. CD and DSC studies.

Cold denaturation and heat denaturation of the protein Streptomyces subtilisin inhibitor (SSI) were studied in the pH range 1.84-3.21 and in the temperature range -3-70 degrees C by circular dichroism and scanning microcalorimetry. The native structure of the protein was apparently most stabilized at about 20 degrees C and was denatured upon heating and cooling from this temperature. Each denaturation was reversible and cooperative, proceeding in two-state transitions, that is, from the native state to the cold-denatured state or from the native state to the heat-denatured state. The two denatured states, however, were not perfect random-coiled structures, and they differed from each other, indicating that there exist three states in this temperature range, i.e., cold denatured, native, and heat denatured. The difference between the cold and heat denaturations was indicated first by circular dichroism. The isodichroic point for the transition from the native state to the cold-denatured state was different from that from the native state to the heat-denatured state in the pH range between 3.21 and 2.45. Moreover, molar ellipticity for the cold-denatured state was different from that of the heat-denatured state, and the transition from the former to the latter was observed at pH values below 2. Values of van't Hoff enthalpies from the native state to the heat-denatured state at pH values between 3.21 and 2.45 were obtained by curve fitting of the CD data, and delta Cp = 1.82 (+/- 0.11) [kcal/(mol.K)] was obtained from the linear plot of the enthalpies against temperature. The parameters obtained from the heat denaturation studies gave curves for delta G zero which were not in agreement with the experimental data in the cold denaturation region when extrapolated to the low temperature. Moreover, the value of the apparent delta Cp for the cold denaturation in the pH range 3.03-2.45 was estimated to be different from that for the heat denaturation, indicating that the mechanism of the cold denaturation of SSI is different from a simple cold denaturation.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Proteins↗
PubMed1991

Cold denaturation and heat denaturation of Streptomyces subtilisin inhibitor. 2. 1H NMR studies.

Structural transitions of the protein Streptomyces subtilisin inhibitor (SSI) from the native state to the cold-denatured and heat-denatured states were studied by 1H NMR spectroscopy in the temperature range from -10 to 60 degrees C in the acidic pH range. Assignments of some of the 1H NMR signals of SSI in the cold-denatured and heat-denatured states were performed by a combined use of selective deuteration and site-directed mutagenesis. Throughout the pH range from 2.1 to 3.1, both transitions were cooperative and basically only three distinct spectra corresponding to structures in the cold-denatured, native, and heat-denatured states were detected. In the cold-denatured state, the side-chain signals of Met73, His106, at least one Val, and two Leu were observed at distinctly shifted positions from those for a random-coiled structure, suggesting the formation of a tertiary structure, while those of Met70, His43, and Ala2 were observed at positions for a random-coiled structure. This tertiary structure in the cold-denatured state is entirely different from that in the native state, as some amino acid residues exposed to the solvent in the native state (e.g., Met73, His106) are buried while those sequestered in the native state (e.g., His43) are exposed. In the heat-denatured state, however, most 1H NMR signals were observed at random-coiled positions, indicating that there is much less tertiary structure in the heat-denatured state than in the cold-denatured state. At pH values below 2.09, a structural transition was observed from the cold-denatured state to the heat-denatured state without passing through the native state.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1991

Lipid peroxide makes rabbit platelet hyperaggregable to agonists through phospholipase A2 activation.

Treatment of rabbit platelets with tert-butyl hydroperoxide and Fe2+ caused increasing arachidonic acid release, lysophosphatidylcholine formation, and aggregation with increasing concentrations of Fe2+. A combination of tert-butyl hydroperoxide and a low concentration of Fe2+, which by itself causes slight or no such activation, elicited synergistic release of arachidonic acid and aggregation under stimulation with a suboptimal concentration of collagen or arachidonic acid as an agonist. These responses were inhibited by pretreatment of the platelets with vitamin E or mepacrine in a concentration-dependent manner, but not by uric acid. The arachidonic acid release was dependent on the presence of Ca2+ in the medium. Synergistic formation of lysophosphatidylcholine, but not diacylglycerol, was also observed under this condition. The aggregation was also inhibited by indomethacin, a cyclooxygenase inhibitor. Cyclooxygenase activity was not affected by the oxidative treatment. These results suggest that lipid peroxide formed in membranes causes phospholipase A2 to become hypersusceptible to the agonist used, making the platelets hyperaggregable.

Animals↗
PubMed1991

Mechanisms of temporary inhibition in Streptomyces subtilisin inhibitor induced by an amino acid substitution, tryptophan 86 replaced by histidine.

Just one amino acid substitution (Trp86 replaced by His), which is more than 30 A away from the reactive site, changed the inhibitor, Streptomyces subtilisin inhibitor (SSI), into a temporary inhibitor without a change in the inhibition constant. When the inhibitor was in excess of subtilisin BPN', the wild-type SSI was stable under protease attack, while the mutant inhibitor was hydrolyzed to peptide fragments in an all-or-none manner. The mechanism of this temporary inhibition induced by the amino acid substitution was studied on the basis of structural, thermodynamic, and kinetic data obtained by a combined use of NMR, hydrogen-deuterium exchange, differential scanning calorimetry, and gel filtration HPLC. The mutation did not induce major structural changes, and in particular, the structure of the enzyme-binding region was virtually unaffected. The denaturation temperature of SSI, however, was decreased by 10 deg upon mutation, although it still remained a thermostable protein with a denaturation temperature of 73 degrees C. Furthermore, the activation enthalpy for denaturation was reduced dramatically, to half that of the wild type. When the mutated SSI is present in excess of the enzyme, the proteolysis followed first-order reaction kinetics with respect to the total concentration of the mutated SSI molecules present. From these combined results, we conclude that the proteolysis proceeds not through the native form of the inhibitor in the inhibitor-enzyme complex but through the denatured (unfolded) form of the inhibitor whose fraction is increased by the mutation. This conclusion states that the necessary condition for being a serine protease inhibitor lies not only in the design of the reactive site structure that is highly resistant to protease attack but also in the suppression of such structural fluctuation that brings about cooperative denaturation. In contrast, when the protease existed in excess of the mutated inhibitor, the proteolysis reaction was accelerated by more than 2 orders of magnitude. Furthermore, the reaction occurred even in the wild-type SSI at a comparable rate as in the mutated protein. This indicates that in the enzyme excess case another, more efficient digestion mechanism involving fluctuation within the native manifold of the inhibitor dominates.

Bacterial Proteins↗
PubMed1991

Effects of thyrotropin-releasing hormone on behavioral disturbances in middle cerebral artery-occluded rats.

The effects of thyrotropin releasing hormone (TRH) on behavioral and histological changes were studied in rats subjected to left middle cerebral artery occlusion. The drug was given i.p. once or several times a day from 1 week after occlusion for 2 weeks. A single administration of TRH (1 and 10 mg/kg) did not affect the neurological deficits, but recovery of the deficits was accelerated by multiple administration (7 times a day) of TRH and single administration (once a day) of YM-14673 (N alpha-[[(S)-4-oxo-2-azetidinyl]carbonyl]-L-histidyl-L-prolinamide dihydrate), a new TRH analogue with a longer half-life. Both YM-14673 and single (1 and 10 mg/kg) and multiple administration of TRH ameliorated the disturbance of passive avoidance learning. Neuronal degeneration in the cerebral cortex and striatum was not influenced by the administration of TRH. Thus, we found that neurological deficits and disturbance of passive avoidance learning behavior in middle cerebral artery-occluded rats could be ameliorated by administration of TRH.

Animals↗
PubMed1991

A comparative view of Rickettsia tsutsugamushi and the other groups of rickettsiae.

Recent researches on the rickettsial group microorganisms are summarized in their comparative aspects of morphology, cultivation and multiplication, susceptibility to chemotherapeutics, chemical structure of envelopes, nucleic acid, protein constitution, and gene structures. From this overview, Rickettsia tsutsugamushi seems to have different properties from the others and should be reclassified into a new genus, and a new species name as Orientia tsutsugamushi is proposed.

Bacterial Proteins↗
PubMed1991

Induced tolerance to ischemia in gerbil hippocampal neurons.

Brief ischemia induced tolerance to subsequent ischemia in the hippocampal neurons. Male Mongolian gerbils were subjected to 2 min of ischemia in an awake condition. This ischemic insult only rarely produced neuronal damage in the gerbil brain. One day (n = 9), 2 days (n = 9), or 4 days (n = 10) following the first brief ischemia, the animals (double-ischemia group) were subjected to the second ischemia for 5 min. The single-ischemia group received a sham procedure instead of the first ischemia and was identically subjected to the second ischemia 1 day (n = 9), 2 days (n = 10), and 4 days (n = 13) following the sham procedure. One week following the second ischemia, all gerbils were perfusion fixed and the neuronal density in the hippocampal CA1 sector was measured. In double-ischemia groups, the neuronal density per 1-mm length of the pyramidal cell layer was 103.4 +/- 93.1 (SD) in the 1-day subgroup, 125.6 +/- 64.2 in the 2-day subgroup, and 176.2 +/- 93.7 in the 4-day subgroup, while the density in normal gerbils was 254.7 +/- 18.6. The average neuronal density in the single-ischemia group was much lower than that in the double-ischemia group (whole control group: 10.9 +/- 27.4). Immunostaining using monoclonal antibody raised against 70-kDa heat-shock protein revealed an increase in 70-kDa heat-shock protein in the CA1 area following 2 min of ischemia. Very brief ischemia induces heat-shock proteins and, presumably, thereby renders neurons more tolerant to subsequent metabolic stress.

Animals↗
PubMed1991

In-vitro and in-vivo antimicrobial activities of a novel cephalosporin derivative, CP6162, possessing a dihydroxypyridone moiety at the C-3 side chain.

The antibacterial activity of a novel cephalosporin derivative, CP6162, possessing a dihydroxypyridone moiety at the C-3 side chain, was evaluated in vitro and in vivo, with ceftazidime, aztreonam and cefoperazone as the reference antibiotics. CP6162 showed weak or little activity against Gram-positive bacteria, but potent activity against clinical isolates of the Gram-negative species including strains of Pseudomonas aeruginosa, Ps. cepacia, Acinetobacter sp., Xanthomonas maltophilia, Serratia marcescens, Enterobacter cloacae and Citrobacter freundii, which were resistant to the reference antibiotics. The MICs of CP6162 were only slightly affected by the high producers of beta-lactamases except for cephalosporinase-producing C. freundii. It was, however, affected by the presence of ferric ion. CP6162 showed in-vivo activity paralleling the in-vitro activity, and also showed pharmacokinetic parameters similar to those of ceftazidime in mice and rats.

Animals↗