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T Tamagawa

Publications and source records attributed to T Tamagawa.

At least 19 recordsLinked to original sources
PubMed2006

An optical spectrum of the afterglow of a gamma-ray burst at a redshift of z = 6.295.

The prompt gamma-ray emission from gamma-ray bursts (GRBs) should be detectable out to distances of z > 10 (ref. 1), and should therefore provide an excellent probe of the evolution of cosmic star formation, reionization of the intergalactic medium, and the metal enrichment history of the Universe. Hitherto, the highest measured redshift for a GRB has been z = 4.50 (ref. 5). Here we report the optical spectrum of the afterglow of GRB 050904 obtained 3.4 days after the burst; the spectrum shows a clear continuum at the long-wavelength end of the spectrum with a sharp cut-off at around 9,000 A due to Lyman alpha absorption at z approximately 6.3 (with a damping wing). A system of absorption lines of heavy elements at z = 6.295 +/- 0.002 was also detected, yielding the precise measurement of the redshift. The Si ii fine-structure lines suggest a dense, metal-enriched environment around the progenitor of the GRB.

Journal Article↗
PubMed2005

Discovery of the short gamma-ray burst GRB 050709.

Gamma-ray bursts (GRBs) fall into two classes: short-hard and long-soft bursts. The latter are now known to have X-ray and optical afterglows, to occur at cosmological distances in star-forming galaxies, and to be associated with the explosion of massive stars. In contrast, the distance scale, the energy scale and the progenitors of the short bursts have remained a mystery. Here we report the discovery of a short-hard burst whose accurate localization has led to follow-up observations that have identified the X-ray afterglow and (for the first time) the optical afterglow of a short-hard burst; this in turn led to the identification of the host galaxy of the burst as a late-type galaxy at z = 0.16 (ref. 10). These results show that at least some short-hard bursts occur at cosmological distances in the outskirts of galaxies, and are likely to be caused by the merging of compact binaries.

Journal Article↗
PubMed2001

Production of (4)(double Lambda)H hypernuclei.

An experiment demonstrating the production of double-Lambda hypernuclei in (K(-),K(+)) reactions on (9)Be was carried out at the D6 line in the BNL alternating-gradient synchrotron. The technique was the observation of pions produced in sequential mesonic weak decay, each pion associated with one unit of strangeness change. The results indicate the production of a significant number of the double hypernucleus (4)(double Lambda)H and the twin hypernuclei (4)(Lambda)H and (3)(Lambda)H. The relevant decay chains are discussed and a simple model of the production mechanism is presented. An implication of this experiment is that the existence of an S = -2 dibaryon more than a few MeV below the double Lambda mass is unlikely.

Journal Article↗
PubMed2001

Observation of spin-orbit splitting in lambda single-particle states.

The spin-orbit splitting of Lambda single-particle states in (13)(Lambda)C was measured. The 13C(K-,pi(-))(13)(Lambda)C reaction was used to excite both the 1/2(-) and 3/2(-) states simultaneously, which have predominantly 12C(0(+)) x p(Lambda) configuration. gamma rays from the states to the ground state were measured in coincidence with the pi(-)'s, by which ls splitting was found to be 152+/-54(stat)+/-36(syst) keV. The value is 20-30 times smaller than exhibited by the ls splitting in the nuclear shell model. This value gives us new insight into the YN interaction.

Journal Article↗
PubMed2001

Effects of lifestyle factors on ultrasonographically determined bone health in Japanese women.

The objective of this study was to determine by ultrasonographic measurements, an inexpensive and radiation-free technique, the association between bone health and lifestyle factors among a large population of Japanese women. Two hundred and fifty-six pre-menopausal women and 585 post-menopausal women who underwent a voluntary medical check-up for osteoporosis in 1996-1997 were analyzed. There were significant positive correlations between the bone density (designated as the stiffness value) vs the weight, the height and the body mass index of the subjects only in the post-menopausal group. Negative correlations were also found between the bone density vs the age and the years since menopause. Our data using ultrasonographic technique agree well with previous studies using other devices. In both groups, subjects with current or past exercise habits had higher stiffness values. Dietary habits had no effects on the stiffness value. Smoking habits had a trend towards negative effects and alcohol consumption seemed to have a trend towards positive effects on the stiffness value in post-menopausal women, but these effects did not reach statistical significance. Positive effects of current exercise on bone density were maintained after adjustment for past exercise habits. These results support the effectiveness of exercise begun in adulthood. Having a good exercise habit is one of the most effective ways of maintaining good bone health.

Adult↗
PubMed2001

Comparison of the effects of three sulfonylureas on in vivo insulin action.

To clarify the diversity in hypoglycemic actions of sulfonylureas, chronic effects of three sulfonylureas were compared on in vivo insulin-induced glucose uptake in peripheral tissues. After oral administration of glimepiride (CAS 93479-97-1), glibenclamide (CAS 10238-21-8), gliclazide (CAS 21187-98-4), or saline as control, two-step euglycemic clamp procedures were performed. During physiological hyperinsulinemia induced by 6 mU/kg/min insulin infusion, metabolic clearance rates (MCR) of glucose of the glimepiride-administered group (GP) significantly (p < 0.01) increased to 153% of the saline-administered group (SA). There was no significant statistical difference between the glibenclamide-administered group (GC), gliclazide-administered group (GZ) and SA. During 30 mU/kg/min clamps that lead to maximal insulin action, MCR of either GP or GC were significantly higher than those of SA (128% and 141%, p < 0.05 and p < 0.01, respectively). MCR of GZ were lower than those of GC (80%, p < 0.05), and showed no significant difference from those of SA. These data indicate that glimepiride activates insulin binding levels to a greater degree than the other two sulfonylureas, and that glibenclamide and glimepiride activate post-receptor binding mechanisms in peripheral tissues much more than gliclazide. These results suggest that hypoglycemic actions of sulfonylureas at the extra pancreatic levels vary with the nature of each reagent.

Animals↗
PubMed2000

Dietary fat-induced increase in blood pressure and insulin resistance in rats.

OBJECTIVES: To determine whether the dietary-fat-induced increase in blood pressure is caused by excess energy intake or the fat composition of the diet, what type of fat increases the blood pressure, and whether insulin resistance is involved in the dietary-fat-induced increase in blood pressure. METHODS: In a series of experiments, rats received: chow alone or chow supplemented with lard or sucrose to provide 33% of a total energy content increased by 50%; chow alone or chow in which 50% of the energy content was from substituted lard, safflower oil or medium-chain triglyceride oil; or chow alone or chow in which 50% of the energy content was from substituted lard, with or without troglitazone. Systolic blood pressure (SBP) was measured every week during each 8-week feeding period. A steady-state serum glucose method was used to determine the insulin sensitivity after the lard substitution with or without troglitazone. RESULTS: Both the lard and sucrose enrichment increased SBP and body weight compared with controls. Lard substitution significantly increased SBP and immunoreactive insulin, although body weight did not differ from control. Neither a diet substituted with safflower oil nor one substituted with medium-chain triglyceride oil influenced SBP. Troglitazone completely inhibited the increase in SBP and immunoreactive insulin induced by the lard. The steady-state serum glucose concentration was significantly greater after the lard substitution than after isoenergetic chow; this effect also was reversed by troglitazone. CONCLUSION: Chronic feeding with lard increased SBP in rats, independently of excess energy intake. Of the fats tested, lard exerted an intrinsic pressor effect. Troglitazone reversed the lard-induced increase in SBP.

Adipose Tissue↗
PubMed2000

Plasma endotoxin and serum cytokine levels in patients with alcoholic hepatitis: relation to severity of liver disturbance.

BACKGROUND: Endotoxin plays an important role in the initiation and aggravation of alcoholic liver disease. In this study, we evaluated plasma endotoxin levels and serum concentrations of cytokines and lipopolysaccharide binding protein (LBP) during the acute and recovery phase of patients with alcoholic hepatitis; we also explored the prognostic factors associated with a fatal outcome. METHODS: Fourteen patients, consisting of eight patients with alcoholic hepatitis (AH), five cirrhotics with superimposed AH (LC+AH), and one patient with severe alcoholic hepatitis (SAH), were studied. Among these, two with LC+AH died of hepatic failure. RESULTS: Plasma endotoxin levels in the acute phase were higher in patients with AH (184.4 +/- 159.4 pg/ml) and LC+AH (206.9 +/- 174.9 pg/ml) than in healthy subjects (10.4 +/- 5.5 pg/ml, p < 0.001). In particular, in one patient with SAH and one of two nonsurvivors, plasma endotoxin levels were markedly high relative to the other cases. In most survivors, plasma endotoxin levels decreased in the recovery phase, whereas they further increased at the terminal stage in one of two nonsurvivors. Serum interleukin (IL)-6 and IL-8 levels in the acute phase were significantly higher in patients with AH and LC+AH as compared with healthy subjects. These levels were especially high in nonsurvivors and in one patient with SAH. IL-10 increased in two nonsurvivors, one patient with SAH, and one with LC+AH. In the recovery phase, these cytokine levels in survivors tended to decrease, but in nonsurvivors, IL-6 remained high, and IL-8 and IL-10 further increased. Tumor necrosis factor-alpha levels were below the detection limit throughout the course in all patients. Serum lipopolysaccharide binding protein (LBP) generally was elevated in the acute phase and decreased in the recovery phase in all survivors, but in one of the nonsurvivors, LBP was elevated markedly at the terminal stage. In the acute phase, plasma endotoxin levels were correlated positively with white blood cell counts, neutrophil counts, and serum IL-8. IL-8 was correlated positively with neutrophil counts and negatively with serum cholinesterase, hepaplastin test, and serum albumin levels. IL-6 was correlated positively with white blood cell and neutrophil counts, C-reactive protein, and serum total bilirubin and negatively with hepaplastin test and serum total protein levels. Serum LBP was correlated positively with white blood cell and neutrophil counts. CONCLUSIONS: Endotoxemia and related elevation of IL-8 may play an important role in the activation and migration of neutrophils in patients with alcoholic hepatitis. Marked elevation of inflammatory cytokines, IL-6 and IL-8, are related to severity and poor prognosis of alcoholic hepatitis. Serum LBP may serve as an index of inflammatory reaction in alcoholics.

Acute-Phase Proteins↗
PubMed1999

Central nervous system-mediated hyperglycemic effects of NIK-247, a cholinesterase inhibitor, and MKC-231, a choline uptake enhancer, in rats.

We investigated the effects of intracerebroventricular administration of NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclo-penta(b)-quinoline monohydrate hydrochloride; a cholinesterase inhibitor) or MKC-231 (2-(2-oxypyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofur o[2,3-b]quinolin-4-yl) acetoamide; a choline uptake enhancer) on plasma glucose level in comparison with that of neostigmine administration in rats. The extents of NIK-247- and MKC-231-induced hyperglycemia were considerably less than that by neostigmine, suggesting that the potencies of the drugs to produce the peripheral hyperglycemia may be pharmacologically negligible.

Aminoquinolines↗
PubMed1999

A thymidine to cytosine substitution for codon 26 of exon 3 of apolipoprotein C-II gene in a patient with apolipoprotein C-II deficiency.

A 52-year-old Japanese woman was evaluated for severe hypertriglyceridemia and recurrent acute pancreatitis. This hypertriglyceridemia was found to be due to the absence of serum apolipoprotein C-II (apo C-II) which was identified by Western blotting using polyclonal anti-apo C-II antiserum. DNA sequence analysis of the apo C-II gene from the patient revealed a homozygous nucleotide change: a thymidine (T) to cytosine (C) substitution in codon 26 (TGG->CGG) at the third exon of the apo C-II gene, that resulted in a Trp26 to Arg substitution. The mutation was also confirmed by restriction fragment length polymorphism (RFLP) analysis with the restriction enzyme Hpa II. The same mutation has been found in a case previously reported in Japan, and was named apo C-II Wakayama. However, the case in Wakayama prefecture showed two concomitant point mutations at the 5'-flanking region upstream from the first exon, which were not identified in our case by RFLP analysis with the restriction enzyme BstXI. Considering that the prefectures of these two cases, Nara and Wakayama, are next to each other, the mutation in our case may be a genetic forebear of apo C-II Wakayama. However, no familial relationship between the two cases has been documented.

Apolipoprotein C-II↗
PubMed1998

Centrally administered TRH-induced insulin secretion is impaired in the Otsuka-Long-Evans-Tokushima Fatty rats, a model of spontaneous non-insulin-dependent diabetes mellitus.

To investigate whether insulin secretion induced by stimulation of the vagus nerve is preserved or impaired in Otsuka-Long-Evans-Tokushima Fatty (OLETF) rats, we injected 10(-8) mol of thyrotropin-releasing hormone (TRH) into the third cerebral ventricle and determined the serum level of insulin in the unanesthetized, unrestrained rats. Intracerebroventricular (i.c.v.) injection increased the serum levels of glucose and insulin in both OLETF and Long-Evans-Tokushima-Otsuka (LETO) rats, a nondiabetic control strain, at 8-12 weeks of age. At 24-28 weeks of age, the increased level of glucose in OLETF rats was comparable to LETO rats but that of insulin was lower than control after the i.c.v. injection of TRH. Pretreatment with i.v. atropine had no significant effect on such hyperglycemia. However, the increases in the serum levels of insulin were suppressed in both OLETF and LETO rats. The plasma levels of epinephrine, norepinephrine, and glucagon rose significantly after TRH. There was no significant difference in the levels of any hormones between the two groups. In OLETF rats at 24-28 weeks of age, i.v. glucose load induced significantly higher serum levels of glucose and insulin than LETO rats. The results suggest that the vagus nerve-mediated insulin secretion is impaired in OLETF rats, similar to an autonomic diabetic neuropathy in the early stage of diabetes. This impairment may play some role in deteriorating glucose tolerance in this spontaneously developed diabetes model.

Animals↗
PubMed1997

NG-methyl-L-arginine, an inhibitor of nitric oxide synthase, affects the central nervous system to produce peripheral hyperglycemia in conscious rats.

To determine whether the nitric oxide (NO) system in the central nervous system (CNS) is involved in the peripheral metabolism of carbohydrate we injected NG-methyl-L-arginine (L-NMA), an inhibitor of NO synthase, into the third cerebral ventricle of unanesthetized, unrestrained rats and determined the plasma level of glucose. This intracerebroventricular (i.c.v.) injection of the drug increased the plasma level of glucose dose-dependently, whereas an intravenous (i.v.) injection had no effect. The hyperglycemia thus induced was suppressed by concomitant i.c.v. or prior i.v. administration of L-arginine. Concomitant administration of D-arginine did not affect hyperglycemia by L-NMA. The i.c.v. injection of 5 x 10(-6) mol L-NMA increased plasma levels of glucose, epinephrine and norepinephrine, and serum levels of glucagon. However, plasma levels of insulin were unchanged, despite the presence of hyperglycemia. The hyperglycemia produced by L-NMA was completely inhibited by bilateral adrenalectomy. It was also inhibited by prior intraperitoneal injection of phentolamine, but not of propranolol or naloxone. Results suggest that L-NMA acts on the CNS to stimulate adrenal secretion of epinephrine and, subsequently, to elevate glucose levels in the peripheral blood. The NO system thus seems to be involved in the neural regulation of the adrenal by the GNS, which in turn regulates peripheral blood glucose levels.

Adrenalectomy↗
PubMed1997

The pressor response induced by repeated injections of neostigmine into the central nervous system is desensitized in adrenalectomized, but not in intact rats.

To investigate whether or not pressor responses to repeated stimulation of central cholinoceptive neurons are desensitized, mean arterial blood pressure (MAP) and heart rate (HR) were measured following repeated injections of neostigmine, an acetylcholinesterase inhibitor, into the third cerebral ventricle in conscious, unrestrained intact or adrenalectomized (ADX) rats. Neostigmine (5 x 10(-9) or 5 x 10(-8) mol) in 1 milliliter saline increased MAP dose-dependently and increased HR in intact rats. The peak values in MAP and HR after three repeated injections at 4 hour intervals did not wane. Neostigmine (5 x 10(-8) mol) also increased MAP in ADX rats, and the peak values after the first injection were higher in the ADX rats than in the intact rats. The pressor responses to the second and third injection, however, were less than to the first injection in the ADX rats. HR responses to the repeated injections in the ADX rats were identical to those in the intact rats. These findings suggest that the adrenal gland plays a role in antagonizing the development of desensitization in the neostigmine-induced pressor response.

Adrenalectomy↗
PubMed1996

Increase in insulin release from rat pancreatic islets by quinolone antibiotics.

1. The present study was undertaken to elucidate the mechanism(s) of hypoglycaemia caused by quinolone antibiotics. We investigated the effects of various quinolone antibiotics on insulin release in rat pancreatic islets. 2. At a non-stimulatory concentration of 3 mM glucose, lomefloxacin (LFLX) or sparfloxacin at 1 mM and pipemidic acid (0.1-1 mM) induced slight insulin release but tosufloxacin or enoxacin up to 100 microM did not. 3. At the stimulatory concentration of 10 mM glucose, all quinolones augmented insulin release in a dose-dependent manner. LFLX (100 microM) shifted the dose-response curve of glucose-induced insulin release to the left without altering the maximal response. 4. At 10 mM glucose, LFLX (100 microM) increased insulin release augmented by forskolin (5 microM) or 12-O-tetradecanoyl phorbol-13-acetate (100 nM) but not by raising the K+ concentration from 6 to 25 mM. 5. Verapamil (50 microM) or diazoxide (50-400 microM) antagonized the insulinotropic effect of LFLX. 6. These data suggest that quinolone antibiotics may cause hypoglycaemia by increasing insulin release via blockade of ATP-sensitive K+ channels.

4-Quinolones↗
PubMed1995

Effects of imidazoline antagonists of alpha 2-adrenoceptors on endogenous adrenaline-induced inhibition of insulin release.

We studied the effects of adrenoceptor antagonists and imidazoline derivatives on endogenous adrenaline-induced inhibition of insulin release in anesthetized rats. The intracerebroventricular injection of neostigmine increased plasma levels of catecholamines and glucose but not insulin. Pretreatment with an i.p. injection with phentolamine caused a dose-dependent increase in insulin secretion. When atropine was coadministered with phentolamine, the phentolamine-induced increase in insulin secretion was inhibited. Neither phentolamine nor atropine affected plasma levels of catecholamine. Yohimbine and idazoxan, which are alpha 2-adrenoceptor antagonists, and tolazoline, a non-selective alpha-adrenoceptor antagonist, also reversed adrenaline-induced inhibition of insulin secretion. Phenoxybenzamine, prazosin, propranolol, and antazoline, an imidazoline without alpha 2-adrenoceptor activity, did not affect insulin levels. When agents were preinjected i.p. in rats that were given saline into the third cerebral ventricle, phentolamine and antazoline, but not yohimbine and idazoxan, increased plasma levels of insulin. The results suggest that the inhibition of insulin release induced by adrenaline was reversed by antagonism of alpha 2-adrenoceptors. Phentolamine and antazoline, both of which are imidazoline derivatives, induced insulin secretion independently of the adrenoceptors only under the resting conditions.

Adrenergic alpha-2 Receptor Agonists↗