Biomedical subjects

Y Masuda

Publications and source records attributed to Y Masuda.

At least 91 records · Page 5Linked to original sources

PubMed2000

Dlxin-1, a novel protein that binds Dlx5 and regulates its transcriptional function.

Dlx5, a member of the Dlx family of homeodomain proteins, plays a critical role in bone development and fracture healing. To understand the molecular mechanism underlying the transcriptional regulation by Dlx5, we performed yeast two-hybrid screening and isolated a novel protein, Dlxin-1, that binds Dlx5 and regulates its transcriptional function. Dlxin-1 cDNA encodes a 775-amino acid protein that has a partial homology with necdin at the C terminus and 25 repeats of hexapeptides (WQXPXX) in the middle region. Dlxin-1 mRNA is expressed in various adult tissues, but not the spleen, and also in osteoblastic and chondrogenic cell lines. During embryogenesis, a strong signal for Dlxin-1 mRNA was found in cell layers surrounding cartilaginous elements in bone rudiment during digit formation. Dlxin-1 binds not only Dlx5 but also Dlx7 and Msx2 and forms homomultimers in vivo. Transfection and reporter gene assays indicate that Dlxin-1 activates the transcriptional function of Dlx5. Therefore, Dlxin-1 may act as a regulator of the function of Dlx family members in bone formation.

Amino Acid Sequence↗

PubMed2000

Ghrelin stimulates gastric acid secretion and motility in rats.

Ghrelin, a novel growth-hormone-releasing peptide, was discovered in rat and human stomach tissues. However, its physiological and pharmacological actions in the gastric function remain to be determined. Therefore, we studied the effects of rat ghrelin on gastric functions in urethane-anesthetized rats. Intravenous administrations of rat ghrelin at 0.8 to 20 microgram/kg dose-dependently increased not only gastric acid secretion measured by a lumen-perfused method, but also gastric motility measured by a miniature balloon method. The maximum response in gastric acid secretion was almost equipotent to that of histamine (3 mg/kg, i.v.). Moreover, these actions were abolished by pretreatment with either atropine (1 mg/kg, s.c.) or bilateral cervical vagotomy, but not by a histamine H(2)-receptor antagonist (famotidine, 1 mg/kg, s.c.). These results taken together suggest that ghrelin may play a physiological role in the vagal control of gastric function in rats.

Animals↗

PubMed2000

Peroxisome proliferator-activated receptor activators inhibit lipopolysaccharide-induced tumor necrosis factor-alpha expression in neonatal rat cardiac myocytes.

Peroxisome proliferator-activated receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily. Recently, PPAR activators have been shown to inhibit the production of proinflammatory cytokines in macrophages or vascular smooth muscle cells. It has been reported that tumor necrosis factor-alpha (TNF-alpha) expression is elevated in the failing heart and that TNF-alpha has a negative inotropic effect on cardiac myocytes. Therefore, we examined the effects of PPARalpha and PPARgamma activators on expression of TNF-alpha in neonatal rat cardiac myocytes. Northern blot analysis revealed expression of PPARalpha and PPARgamma mRNA in cardiac myocytes. Immunofluorescent staining demonstrated that both PPARalpha and PPARgamma were expressed in the nuclei of cells. When cardiac myocytes were transfected with PPAR responsive element (PPRE)-luciferase reporter plasmid, both PPARalpha and PPARgamma activators increased the promoter activity. Cardiomyocytes were stimulated with lipopolysaccharide (LPS), and the levels of TNF-alpha in the medium were measured by ELISA. After exposure to LPS, the levels of TNF-alpha significantly increased. However, pretreatment of myocytes with PPARalpha or PPARgamma activators decreased LPS-induced expression of TNF-alpha in the medium. Both PPARalpha and PPARgamma activators also inhibited LPS-induced increase in TNF-alpha mRNA in myocytes. In addition, electrophoretic mobility shift assays demonstrated that PPAR activators reduced LPS-induced nuclear factor-kappaB activation. These results suggest that both PPARalpha and PPARgamma activators inhibit cardiac expression of TNF-alpha in part by antagonizing nuclear factor-kappaB activity and that treatment with PPAR activators may lead to improvement in congestive heart failure.

Animals↗

PubMed2000

Central bombesin inhibits food intake and the orexigenic effect of neuropeptide Y in the neonatal chick.

It is well known that central injection of bombesin (BN) suppresses feeding in mammalian and avian species, but the anorexigenic effect of central BN are still open with special reference to the chick. The dose response (0, 0.1 and 0.5 microg) of intracerebroventricular (ICV) injection of BN was examined in Experiment 1. ICV injection of BN inhibited food intake in a dose-dependent manner. Experiment 2 was done to determine whether BN interacts with the orexigenic effect of neuropeptide Y (NPY) in the neonatal chick. Central administration of NPY (2.5 microg) greatly enhanced food intake, but co-injection of BN (0.5 microg) suppressed food intake. The dose response of NPY (2.5 microg) co-injected with three levels of BN (0, 0.1 and 0.5 microg) was examined in Experiment 3. ICV injection of BN attenuated the hyperphagia by NPY in a dose-related fashion. It is suggested that central BN may interact with NPY for the regulation of feeding in the neonatal chick.

Animals↗

PubMed2000

Central administration of alpha-melanocyte stimulating hormone inhibits fasting- and neuropeptide Y-induced feeding in neonatal chicks.

In the present study, the effect of intracerebroventricular (i.c.v.) administration of alpha-melanocyte stimulating hormone (alpha-MSH) on food intake of neonatal chicks was examined. In experiment 1, i.c. v. injection of alpha-MSH (0.04, 0.2 and 1 microg) significantly inhibited food intake of 3-h fasted chicks in a dose-dependent manner. In experiment 2, alpha-MSH strongly inhibited neuropeptide Y-induced feeding when neuropeptide Y (2.5 microg) and several doses of alpha-MSH were given simultaneously i.c.v. These results suggest that alpha-MSH plays an important role in the regulation of food intake of neonatal chicks.

Animals↗

PubMed2000

Synthesis of stable crystals of a self-assembled centered icosahedral samarium cluster formed by bis(L-prolinato)nickel(II) ligands.

A centered icosahedral 12-coordinate samarium cluster formed by six bis(L-prolinato)nickel(II) ([Ni(pro)2]) ligands, [Sm(Ni(pro)2)6]3+, was prepared. The reaction of Sm with [Ni(pro)2] in a small excess (a 2-fold excess) and also in a large excess (even a 10-fold excess) of the latter produced the cluster. Therefore, this system is a self-assembly. In the cluster, each nickel atom is surrounded by six atoms: two amino nitrogens, two carboxylate oxygens which form chelate rings with the nitrogen atoms, and two carboxylate oxygen atoms which link the neighboring nickel atoms. The samarium atom is coordinated by six [Ni(pro)2] ligands, and the metal is in an icosahedral environment formed by 12 oxygen atoms. The icosahedral geometry is almost ideal. Crystals of [Sm(Ni(pro)2)6](ClO4)3.6MeOH, which were prepared from a methanol solution, immediately decompose after filtration because of loosely trapped MeOH molecules in the crystal lattice. Therefore, crystals without MeOH molecules, which must be stable, were prepared by recrystallization from acetonitrile with tetramethylammonium perchlorate (TMAP). According to the X-ray crystal analysis, the cluster is TMA[Sm(Ni(pro)2)6](ClO4)4, cubic of space group F23, with a = 21.273(9) A, V = 9626(1) A3, and Z = 4; R = 0.053 (Rw = 0.049) for 1296 reflections. In addition, several crystals of cluster salts that have different counteranions, i.e., tetrafluoroborate (BF4-), hexafluorophosphate (PF6-), iodide (I-), and nitrate (NO3-), were prepared. The order of increasing ease of crystallization of the cluster salts was I- > PF6- approximately ClO4- > BF4- >> NO3-. The cluster structure is retained in alcohol and acetonitrile solutions; the UV-vis spectra of the solutions are perfectly consistent with the powder diffuse reflection spectrum. Cyclic voltammograms of [Sm(Ni(pro)2)6]3+ in acetonitrile proved that the structure of [Sm(Ni(pro)2)6]3+ is retained in the redox process and that the nickel atoms electrochemically interact with one another. Thermal analysis of the cluster salts with different counteranions was investigated. The results imply that the cluster is very stable until bis(L-prolinato)nickel(II) ligands, which form the cage structure, disintegrate and that the thermal decomposition processes of the cluster salts depend on their counteranions.

Journal Article↗

PubMed2000

Aminoguanidine prevents concanavalin A-induced hepatitis in mice.

Aminoguanidine is an inhibitor of the inducible form of nitric oxide synthase (iNOS). In the present study, the effect of aminoguanidine on concanavalin A-induced hepatitis was examined. Treatment of mice with concanavalin A (10 mg/kg, i.v.) induced interferon-gamma and iNOS mRNA expression in the liver before the elevation of plasma alanine aminotransferase activity. Immunohistochemical study showed the induction of iNOS protein expression in the area of necrosis. Aminoguanidine (1, 3 and 10 mg/kg, i.p.) inhibited the concanavalin A-induced elevation of alanine aminotransferase activity. Aminoguanidine (10 mg/kg, i.p.) did not inhibit concanavalin A-induced interleukin-2, interferon-gamma, tumor necrosis factor-alpha or iNOS mRNA expression in the liver. The plasma nitrite/nitrate level was elevated at 6 and 24 h after concanavalin A treatment. The elevation of nitrite/nitrate was inhibited by aminoguanidine (10 mg/kg, i.p.). From these results, we conclude that nitric oxide formed by iNOS may be involved in the development of concanavalin A-induced hepatitis.

Alanine Transaminase↗

PubMed2000

The induction of hepatic microsomal UDP-glucuronosyltransferase by the methylsulfonyl metabolites of polychlorinated biphenyl congeners in rats.

The effects of nine methylsulfonyl (MeSO(2)) metabolites of tetra-, penta- and hexachlorinated biphenyls (tetra-, penta- and hexaCBs; 20 micromol/kg once daily for 4 days) on the hepatic microsomal UDP-glucuronosyltransferase (UDP-GT) were investigated in male Sprague-Dawley rats. Each of the seven 3-MeSO(2)-PCBs, 3-MeSO(2)-2, 2',4',5-tetraCB (3-MeSO(2)-CB49), 3-MeSO(2)-2,3',4',5-tetraCB (3-MeSO(2)-CB70), 3-MeSO(2)-2,2',3',4',5-pentaCB (3-MeSO(2)-CB87), 3-MeSO(2)-2,2',4',5,5'-pentaCB (3-MeSO(2)-CB101), 3-MeSO(2)-2,2',3', 4',5,6-hexaCB (3-MeSO(2)-CB132), 3-MeSO(2)-2,2',3',4',5,5'-hexaCB (3-MeSO(2)-CB141), 3-MeSO(2)-2,2',4',5,5',6-hexaCB (3-MeSO(2)-CB149) and 4-MeSO(2)-2,2',4',5,5'-pentaCB (4-MeSO(2)-CB101) increased the activities of UDP-GT toward chloramphenicol, 4-nitrophenol and 4-methylumbelliferone. 4-MeSO(2)-2,2',4',5,5',6-hexaCB (4-MeSO(2)-CB149) increased the activity of UDP-GT toward chloramphenicol (UGT2B1) but not toward 4-nitrophenol (UGT1A6) and 4-methylumbelliferone (UGT1A6). The activity of UDP-GT toward thyroxine (T(4)) significantly increased after the administration of each of the seven 3-MeSO(2)-PCBs and 4-MeSO(2)-CB101. Significant correlation was found between the activity of UDP-GT toward T(4) and serum total T(4) concentration after the administration of each of the MeSO(2) derivatives except 4-MeSO(2)-CB149. In conclusion, seven 3-MeSO(2)-PCBs and 4-MeSO(2)-CB101 induce both UGT2B1 and UGT1A6, and 4-MeSO(2)-CB149 induces UGT 2B1. The results from the present study indicate that increase in the hepatic T(4) glucuronidation after the administration of the seven 3-MeSO(2)-PCBs and 4-MeSO(2)-CB101 possibly because of the induction of both UGT1A1 and UGT1A6 caused the reduction of serum T(4) levels.

Animals↗

PubMed2000

Brain-derived mast cells could mediate histamine-induced inhibition of food intake in neonatal chicks.

In the present study, the effect of intracerebroventricular (i.c.v.) administration of histamine on food intake of neonatal chicks was examined over 2 h. Histamine (100, 200 or 400 nmol, respectively) was injected in the lateral ventricle of 2-day-old chicks, and cumulative food intakes were measured. i.c.v. injection of histamine significantly inhibited food intake in a dose-dependent manner. In addition, compound 48/80, which causes degranulation of mast cells and release of histamine, or thioperamide, which is an antagonist of the histamine H3 autoreceptor and increases histamine release from histaminergic nerve terminals, was injected i.c.v. to clarify whether mast cell- or neuron-derived histamine in the central nervous system of chicks is essential to the feeding inhibition. Central administration of compound 48/80 inhibited food intake with a dose-dependent manner, but thioperamide had no effect on feeding. An inhibitor of mast cell degranulation, sodium cromoglycate, somewhat attenuated food intake inhibited by compound 48/80. These results suggest that brain-derived mast cells could be a major source of histamine in the inhibition of food intake of neonatal chicks.

Animals↗

PubMed2000

Hemodynamic, renal, and hormonal effects of adrenomedullin infusion in patients with congestive heart failure.

BACKGROUND: Experimental studies have shown that adrenomedullin (AM) causes vasodilatation, diuresis, and a positive inotropic effect. In humans, however, whether infusion of AM has beneficial effects in congestive heart failure (CHF) remains unknown. METHODS AND RESULTS: Hemodynamic, renal, and hormonal responses to intravenous infusion of human AM (0.05 microg. kg(-1). min(-1)) were examined in 7 patients with CHF and 7 normal healthy subjects (NL). In NL group, AM significantly decreased mean arterial pressure (-16 mm Hg, P<0. 05) and increased heart rate (+12 bpm, P<0.05). In CHF group, AM also decreased mean arterial pressure (-8 mm Hg, P<0.05) and increased heart rate (+5 bpm, P<0.05), but to a much lesser degree (P<0.05 versus NL). AM markedly increased cardiac index (CHF, +49%; NL, +39%, P<0.05) while decreasing pulmonary capillary wedge pressure (CHF, -4 mm Hg; NL, -2 mm Hg, P<0.05). AM significantly decreased mean pulmonary arterial pressure only in CHF (-4 mm Hg, P<0.05). AM increased urine volume (CHF, +48%; NL, +62%, P<0.05) and urinary sodium excretion (CHF, +42%; NL, +75%, P<0.05). Only in CHF, plasma aldosterone significantly decreased during (-28%, P<0.05) and after (-36%, P<0.05) AM infusion. These parameters remained unchanged in 7 patients with CHF and 6 healthy subjects who received placebo. CONCLUSIONS: Intravenous infusion of AM has beneficial hemodynamic and renal effects in patients with CHF.

Adrenomedullin↗

PubMed2000

Palladium-catalyzed borylation of aryl halides or triflates with dialkoxyborane: A novel and facile synthetic route to arylboronates

A direct borylation of aryl halides or triflates with dialkoxyborane was investigated. The coupling reaction of pinacolborane with aryl halides or triflates in the presence of a catalytic amount of PdCl(2)(dppf) together with a base provided arylboronates in high yields. The product distributions were strongly dependent on the base employed, and the tertiary amine, especially Et(3)N, was effective for the selective formation of the boron-carbon bond. The reaction conditions were so mild that arylboronates having a variety of functional groups such as carbonyl, cyano, and nitro groups were readily prepared.

Journal Article↗

PubMed2000

A case report of intravenous leiomyomatosis extending into the heart.

The patient was a 47-year-old woman who underwent total hysterectomy for uterine leiomyoma in 1994. Two years later, intracaval and intravenous tumors were found by ultrasonic cardiography, magnetic resonance imaging, enhanced chest computed tomography, and venography. The patient underwent total removal of these tumors. Pathological findings indicated that these tumors were leiomyomas. After comparing the present findings with those of similar cases in the literature, we concluded that our patient had intravenous leiomyomatosis extending into the heart.

Female↗

PubMed2000

Effect of mental stress on left ventricular ejection fraction and its relationship to the severity of coronary artery disease.

To evaluate the relationship between the mental stress-induced decrease in left ventricular ejection fraction (LVEF) and the severity of exercise-induced ischaemia, 20 patients with stable coronary artery disease (CAD) underwent radionuclide ventriculography during mental stress testing and stress myocardial perfusion single-photon emission tomography (SPET). We also examined whether changes in haemodynamic and neurohormonal parameters are related to changes in LVEF during mental stress. The LVEF decreased from 54.8% +/- 17.7% to 49.8% +/- 16.2% with mental stress (P < 0.0005). Ten of the 20 patients (50.0%) had a > or = 5% decrease in LVEF The remaining ten patients had no or a <5% decrease in LVEF There was a significant correlation between the change in LVEF during mental stress and the size of the reversible defect on stress myocardial perfusion SPET (r = -0.80, P < 0.0005), with close regional correspondence (75% identical). This correlation was less strong in the 12 patients with a total defect score at rest of <10 (r = -0.69, P = 0.014) than in the eight patients with a total defect score at rest of > or = 10 (r = -0.94, P = 0.001). The changes in blood pressure and heart rate were not significantly correlated with the change in LVEF, but the percent change in adrenaline concentration correlated with the change in LVEE It is suggested that mental stress impairs systolic function by inducing transient myocardial ischaemia. The effect of neurohormonal responses during mental stress on LV systolic function may also be important in patients with CAD.

Aged↗

PubMed2000

Viability of cryopreserved semilunar valves: an evaluation of cytosolic and mitochondrial activities.

BACKGROUND: Despite long-standing, widespread use of cryopreserved allografts, the basic cellular biology of these tissues is still yet unknown. The present investigation was undertaken to study cryopreserved heart valves from the standpoint of cytosolic esterase and mitochondrial dehydrogenase activities. METHODS: Cryopreserved porcine aortic cusps were observed in an unfixed fresh condition with a confocal laser scanning microscope using fluorescent dye. Porcine cusps and cultured human umbilical vein endothelial cells were divided into three groups, including fresh, cold-preserved, and cryopreserved specimens, and cytosolic esterase activity and mitochondrial dehydrogenase activity were analyzed in each. RESULTS: Confocal laser scanning microscope findings disclosed a widely distributed fluorescence in the cusp. Cytosolic esterase activity within human umbilical vein endothelial cells (28%+/-9.0%) after cryopreservation was significantly less than that it was in the cusps (72%+/-21%). Mitochondrial dehydrogenase activity of cryopreserved human umbilical vein endothelial cells and that of cusps fell to 44%+/-6.1% and 64%+/-17% respectively; the difference between the two values was not significant. CONCLUSIONS: Cryopreservation appeared to produce serious damage to cytosolic and mitochondrial functions of endothelial cells. The cytosolic function of cusps, mainly consisting of fibroblasts, was comparatively preserved after cryopreservation, but mitochondrial function of the cusps was more diminished.

Animals↗

PubMed2000

The mechanism of geranylgeraniol-induced apoptosis involves activation, by a caspase-3-like protease, of a c-jun N-terminal kinase signaling cascade and differs from mechanisms of apoptosis induced by conventional chemotherapeutic drugs.

In the present study, we investigated the effects of geranylgeraniol (GGO), a potent inducer of apoptosis in various lines of human tumor cells, on signal transduction cascades involved in apoptosis in human leukemia cells. GGO strongly induced the activation of c-Jun N-terminal kinase (JNK/SAPK) within 2 h in U937 and K562 cells, while neither ERK nor p38 was activated to any considerable extent during GGO-induced apoptosis. Transient expression of a constitutively active mutant form of mitogen-activated protein kinase kinase 1 (MEKK1), deltaMEKK1, or of deltaMEKK1-green fluorescent protein (GFP) in K562 cells activated JNK, but not a caspase-3-like protease, and was insufficient to induce cell death but rendered cells susceptible to GGO-induced cell death. Stable expressions of deltaMEKK1-GFP in U937 cells gave similar results. In contrast to VP-16-induced apoptosis, GGO-induced activation of JNK was almost completely inhibited by benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (Z-DEVD) and by benzyloxycarbonyl-Asp-CH2OC[O]-2,6,-dichlorobenzene (Z-Asp), indicating that the JNK-activation step is located downstream of the caspase signaling pathway in GGO-induced apoptosis. Moreover, apoptosis induced by GGO was significantly inhibited in two lines of cells with a dominant-negative deletion mutation in c-Jun, indicating a requirement for JNK signaling. In addition, unlike the effects on other inducers of apoptosis, the activation of JNK and of the caspase-3-like protease by GGO was significantly delayed by 12-O-tetradecanoylphorbol-13-acetate (TPA), suggesting that the site of inhibition by TPA might be located upstream of the protease and JNK in the GGO-induced apoptotic signaling pathway.

Antineoplastic Agents↗

PubMed2000

Behavioral effect of mouse fibrinopeptide A on mouse forced swimming.

A specific dopamine 2 receptor antagonist, (-)sulpiride, induced an anti-depressive behavior, climbing, in mice forced to swim for 6 h after the injection. The effective fraction was divided from the mouse serum using an ion exchanger and an ultra filtration method. This fraction contained fibrinopeptide A. A peptide synthesized according to the primary 6-amino acid sequence (TDTEDK) of fibrinopeptide A also remarkably increased the behavior. The present findings clearly indicate that a peptide with TDTEDK showed anti-depressive activity.

Amino Acid Sequence↗

PubMed2000

Ibotenic acid-induced lesions of the medial septum increase hippocampal membrane associated protein kinase c activity and reduce acetylcholine synthesis: prevention by a phosphatidylcholine/vitamin B12 diet.

Ibotenic acid infusion into the medial septum (MS) results in biochemical alterations in the hippocampus. The biochemical events involved in this neuronal lesion are poorly understood. We investigated the effect of a purified diet supplemented with egg phosphatidylcholine (PC) and vitamin B(12) on ibotenic acid-medicated biochemical changes in the rat hippocampus and crude synaptosomal membranes. Male Wistar rats with this MS lesion were fed a purified diet (control diet) or a purified diet supplemented with 5.7 g PC and 125 microg vitamin B(12) per 100 g (experimental diet) for 18 days. Sham-operated rats were fed the control diet. Compared with the sham-operated rats, MS-lesioned rats fed the control diet showed increased activity of membrane-bound protein kinase C (PKC), decreased activity of choline acetyltransferase, and decreased concentrations of acetylcholine in the hippocampus. The ratio of cholesterol to phospholipid in the crude synaptic membrane was lower in the lesioned rats than in the sham-operated rats, but this was not accompanied by any alteration in membrane lipid fluidity. MS-lesioned rats fed the experimental diet showed lowered PKC activity and elevated acetylcholine concentrations than did rats fed the control diet, but there were no significant effects on choline acetyltransferase activity and the lipid ratio. The ibotenic acid-mediated elevation of PKC activity was observed as early as 2 days postinjury in the control diet-fed rats but not in the experimental diet-fed rats. We propose that ibotenic acid mediates pathophysiologic actions through the activation of PKC and that PC combined with vitamin B(12) ameliorates the second messenger-mediated injury.

Journal Article↗

PubMed2000

Intracerebroventricular injection of mammalian motilin, melanin-concentrating hormone or galanin does not stimulate food intake in neonatal chicks.

1. Several neural peptides are known to stimulate feeding behaviour in mammalian species. The aim of this study was to elucidate whether central injection of mammalian motilin, melanin-concentrating hormone (MCH) or galanin stimulates feeding in the neonatal chick. 2. None of the peptides applied here enhanced the food intake of the chick. 3. It is suggested that motilin, MCH and galanin, at least those of mammalian origin, may not regulate feeding in neonatal chicks, when administered to the central nervous system.

Animals↗