Search PubMed⌕ Search

Biomedical subjects

Y Chiba

Publications and source records attributed to Y Chiba.

At least 37 records · Page 2Linked to original sources

[Thoracic outlet syndrome with arterial complication treated by the subclavicular transsternal approach: report of a case].

A 42-year-old female was referred to our vascular service because of her right arm fatigue and cold sensitivity. On elevation of right arm, her radial pulse was absent with pallor of the hand. Angiography demonstrated a significant stenosis of the right subclavian artery, which was considered to be complication of thoracic outlet syndrome. We performed resection of the first rib using the standard subclavicular approach and the subclavian-subclavian artery bypass using a new transsternal extension approach to the subclavian artery. After follow-up 18 months, she was working and asymptomatic. This transsternal extension is effective to treat the arterial complication after decompression of the thoracic outlet.

Adult↗

Effects of Y-27632 on acetylcholine-induced contraction of intact and permeabilized intrapulmonary bronchial smooth muscles in rats.

In the present study, the effects of a selective Rho-associated coiled-coil forming protein kinase (ROCK) inhibitor, Y-27632 [(+)-(R)-trans-4-(1-aminoethyl)-(4-pyridyl)cyclohexanecarboxamide dihydrochloride] on acetylcholine-induced contraction and Ca(2+) sensitization of rat bronchial smooth muscle were examined. Intact and beta-escin-permeabilized muscles of the third branch of intrapulmonary bronchi were used. In intact muscles, Y-27632 (10(-6)-10(-4) M) concentration-dependently inhibited acetylcholine-induced contractile responses. In acetylcholine (10(-3) M)-precontracted intact muscles, the maximal relaxation (about 50% inhibition of contraction) was obtained by a concentration of 10(-4) M Y-27632, which had no effect on the resting tone. In beta-escin-permeabilized muscles, addition of acetylcholine (10(-5)-10(-3) M) plus GTP (100 microM) induced a further contraction, i.e., Ca(2+) sensitization at a constant Ca(2+) concentration of pCa=6.0. The acetylcholine-induced Ca(2+) sensitization was completely blocked in the presence of 10(-4) M Y-27632, whereas the Ca(2+)-induced contraction itself was not affected by Y-27632. Immunoblot study revealed the expression of ROCK-I and ROCK-II proteins in the intrapulmonary bronchi of rats. These findings suggest that Y-27632 dilates acetylcholine-mediated contraction of rat bronchial smooth muscle by inhibiting RhoA/ROCK-mediated Ca(2+) sensitization.

Acetylcholine↗

PPARgamma ligands inhibit TNF-alpha-induced LOX-1 expression in cultured endothelial cells.

Endothelial dysfunction or activation, elicited by oxidized low-density lipoprotein (OxLDL), has been implicated in the initiation and progression of atherosclerosis. We elucidated whether tumor necrosis factor-alpha (TNF-alpha)-induced endothelial OxLDL receptor, lectin-like OxLDL receptor-1 (LOX-1), mRNA expression is modified by peroxisome proliferator-activated receptor (PPAR) activators in cultured bovine aortic endothelial cells (BAEC). We confirmed that both PPARalpha and PPARgamma were expressed in BAEC by reverse transcription-polymerase chain reaction analysis. Natural PPARgamma ligand 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) and the thiazolidinediones, pioglitazone and troglitazone, decreased TNF-alpha-induced LOX-1 mRNA expression in BAEC. LOX-1 expression induced by phorbol 12-myristrate 13-acetate was also inhibited by 15d-PGJ(2). In contrast, PPARalpha ligands, Wy14643 and fenofibric acid, did not alter TNF-alpha-induced LOX-1 expression. TNF-alpha-induced immunohistochemical staining of LOX-1 was suppressed by 15d-PGJ(2) but not Wy14643. Taken together, PPARgamma activators inhibit TNF-alpha-induced LOX-1 expression in cultured BAEC, which may beneficially influence inflammatory responses in atherosclerosis.

Animals↗

Possible involvement of G(i3) protein in augmented contraction of bronchial smooth muscle from antigen-induced airway hyperresponsive rats.

To investigate a possible involvement of pertussis toxin (PTX)-sensitive heterotrimeric G proteins in the pathogenesis of airway hyperresponsiveness, the effect of PTX treatment on the augmented contractile response to acetylcholine (ACh) in bronchial smooth muscle of antigen-induced airway hyperresponsive rats was determined. In bronchial smooth muscle of airway hyperresponsive rats that were actively sensitized and repeatedly challenged with 2,4-dinitrophenylated Ascaris suum antigen, ACh-induced contractions were markedly augmented. The augmented contractile responses in the airway hyperresponsive group were significantly inhibited after treatment with PTX (1 microg/mL for 6 hr, 37 degrees ), whereas only a slight attenuation was observed in the normal control group. The level of G(alpha)i3 (measured by immunoblotting), but not other alpha-subunits of G(i/o) family proteins, in bronchial smooth muscle of the airway hyperresponsive rats was significantly increased as compared with that of control animals. It is concluded that PTX-sensitive muscarinic contractile responses of bronchial smooth muscle might be augmented upon antigen-induced airway hyperresponsiveness in rats, probably due to an up-regulation of G(alpha)i3 protein of bronchial smooth muscle.

Acetylcholine↗

Pluronic F-127 gels incorporating highly purified unsaturated fatty acids for buccal delivery of insulin.

The present study investigated the release profiles of insulin from Pluronic F-127 (PF-127) gel containing unsaturated fatty acids such as oleic acid (18:1), eicosapentaenoic acid (20:5) or docosahexaenoic acid (22:6) and the hypoglycemic effect of insulin following the buccal administration of the gel formulations in normal rats. Insulin release from the gels decreased in the presence of unsaturated fatty acids. Remarkable and continuous hypoglycemia was induced by all PF-127 gels (insulin dose, 25 IU/kg) containing unsaturated fatty acids. PF-127 gels containing oleic acid showed the highest pharmacological availability (15.9+/-7.9%). Our finding demonstrate that 20% PF-127 gels containing unsaturated fatty acids are potential formulations for the buccal delivery of insulin.

Animals↗

Overexpression of HUT1 gene stimulates in vivo galactosylation by enhancing UDP-galactose transport activity in Saccharomyces cerevisiae.

Transfer of activated sugar-nucleotides from the cytoplasm to the lumen of the Golgi is an essential requirement for glycosylation of glycoproteins, proteoglycans and glycosphingolipids. Although mannosylation is the major modification in the yeast Saccharomyces cerevisiae, several reports suggest the presence of galactose residues on yeast proteins and sphingolipids. We have detected alpha-galactosylated O-linked chitinase by lectin blotting from cells that functionally express the gma12(+) gene, encoding alpha 1,2-galactosyltransferase from Schizosaccharomyces pombe. This result implies the presence of a UDP-galactose transporter in S. cerevisiae. A conserved gene, HUT1, which encodes a putative multi-transmembrane protein, was cloned and characterized for its possible involvement in galactosylation. The HUT1 gene is not essential and is expressed at a relatively low level under the physiological conditions we examined. The disruption of this gene did not show any apparent impairments in glycosylation. However, a temperature- and concentration-dependent increase in UDP--galactose transport activity was detected from cells overexpressing HUT1 in the presence of gma12(+). The surface of these cells was confirmed to carry galactose residues by staining with FITC-conjugated alpha-galactose-specific lectin. These results suggest a role for Hut1p in the transport of UDP--galactose from the cytosol into the Golgi lumen in S. cerevisiae.

Amino Acid Sequence↗

Activation of rho is involved in the mechanism of hydrogen-peroxide-induced lung edema in isolated perfused rabbit lung.

Acute lung injury is attributed primarily to increased vascular permeability caused by reactive oxygen species derived from neutrophils, such as hydrogen peroxide (H2O2). Increased permeability is accompanied by the contraction and cytoskeleton reorganization of endothelial cells, resulting in intercellular gap formation. The Rho family of Ras-like GTPases is implicated in the regulation of the cytoskeleton and cell contraction. We examined the role of Rho in H2O2-induced pulmonary edema with the use of isolated perfused rabbit lungs. To our knowledge, this is the first study to examine the role of Rho in increased vascular permeability induced by H2O2 in perfused lungs. Vascular permeability was evaluated on the basis of the capillary filtration coefficient (Kfc, ml/min/cm H2O/100 g). We found that H2O2 (300 microM) increased lung weight, Kfc, and pulmonary capillary pressure. These effects of H2O2 were abolished by treatment with Y-27632 (50 microM), an inhibitor of the Rho effector p160 ROCK. In contrast, the muscular relaxant papaverine inhibited the H2O2-induced rise in pulmonary capillary pressure, but did not suppress the increases in lung weight and Kfc. These findings indicate that H2O2 causes pulmonary edema by elevating hydrostatic pressure and increasing vascular permeability. Y-27632 inhibited the formation of pulmonary edema by blocking both of these H2O2-induced effects. Our results suggest that Rho-related pathways have a part in the mechanism of H2O2-induced pulmonary edema.

Amides↗

Site difference in RhoA expression between rat bronchial and tracheal smooth muscles after antigen challenge--relation to development of hyperresponsiveness.

OBJECTIVE: The present study compared the effects of repeated antigen exposure on the development of hyperresponsiveness and the expression of RhoA in the main bronchial and lower tracheal smooth muscles of sensitized METHODS: Actively sensitized rats were repeatedly challenged by antigen inhalation. Twenty-four hours after the final antigen challenge the isometrical contractions of the bronchial and tracheal smooth muscles were measured. Immunoblottings were also performed using bronchial and tracheal homogenates and the density ratios of RhoA/beta-actin were calculated to quantify the levels of RhoA. RESULTS: Acetylcholine-induced contraction of bronchial, but not tracheal, smooth muscle of antigen-treated rats was significantly augmented as compared with that of control rats, indicating that airway hyperresponsiveness appeared by antigen challenge in bronchial smooth muscle. RhoA expression in bronchial, but not tracheal, smooth muscle was significantly increased in the antigen-treated animals. CONCLUSION: The increased expression of RhoA is suggested to have an important role in developing hyperresponsiveness of bronchial smooth muscle.

Acetylcholine↗

Increased expression of G12 and G13 proteins in bronchial smooth muscle of airway hyperresponsive rats.

OBJECTIVE: To obtain information on the activation pathway of the monomeric G protein, RhoA, in bronchial smooth muscle, the expression of G alpha12 and G alpha13 in bronchial smooth muscle of the rat was determined. The levels of these G proteins were also compared between antigen-induced airway hyperresponsive and normal control groups. METHODS: Actively sensitized rats were repeatedly challenged by antigen inhalation. Twenty-four hours after the final antigen challenge, membrane preparations of bronchial smooth muscles were prepared. Immunoblottings were performed, and the density ratios of G alpha12/beta-actin and G alpha13/beta-actin were calculated to quantify the levels of these G-protein alpha subunits. RESULTS: Both G alpha12 and G alpha13 proteins were expressed in rat bronchial smooth muscle. The levels of bronchial G alpha12 and G alpha13 proteins in the repeatedly antigen challenged rats were significantly increased as compared with those in control animals; the magnitude of upregulation in the airway-hyperresponsive group was 89% and 68% in the control group, respectively. CONCLUSION: G alpha12 and G alpha13 proteins were expressed in rat bronchial smooth muscle. Considering the probable involvement of G12 and G13 proteins in Ca2+ sensitization through Rho protein, the augmented expression of such G proteins after repeated antigen challenge may be responsible for the hyperresponsiveness of bronchial smooth muscle contraction in rats.

Animals↗

Hyperamylasemia and subclinical pancreatitis after cardiac surgery.

Hyperamylasemia after cardiac surgery is common but typically causes no clinical concern because it consists mainly of the salivary isoenzyme. In this study we evaluated the incidence, source, and time course of postoperative hyperamylasemia with special attention to the possibility of subclinical pancreatitis. In 88 patients prospectively tested for serum amylase and lipase concentrations, elastase 1 activity, and amylase isoenzyme characteristics, 57 (64%) showed hyperamylasemia during the early postoperative period. In most cases early hyperamylasemia was not of pancreatic origin, but two patients were diagnosed with subclinical pancreatitis. Among the last 23 patients, 5 of 10 patients with early hyperamylasemia exceeding 1000 IU/L showed late hyperamylasemia on the seventh postoperative day, when it represented mainly the pancreatic isoenzyme. Lipase concentrations and elastase 1 activities were elevated in these cases. Late hyperamylasemia following cardiac surgery may be of pancreatic origin and indicative of subclinical pancreatitis, even if early hyperamylasemia was of salivary origin.

Adult↗

Surgical outcome of infectious aneurysm of the abdominal aorta with or without SIRS.

The surgical outcome of infectious abdominal aortic aneurysms was evaluated based on the preoperative presence or absence of systemic inflammatory response syndrome (SIRS). Nine patients were divided into two groups according to the criteria for SIRS such as body temperature, heart rate, respiratory rate, and white blood cell count. In the group with SIRS, rupture and impending rupture of aneurysms occurred in three of the four patients (75%). All aneurysms were resected with a small part as a remnant; two in situ and two extraanatomic reconstructions were performed. Three patients died after surgery: one after in situ (cerebral infarction) and two after extraanatomic reconstruction (sepsis and multiple organ failure). In the group without SIRS, closed en bloc resection in two patients and resection of the aneurysm with a small part as a remnant in three patients were performed. In situ reconstruction in all patients and omentum wrapping in two patients were performed. One of the five patients died of massive hematemesis 70 days after surgery. The overall mortality rate was 75% in the group with SIRS versus 20% in the group without SIRS. The surgical outcome of infectious abdominal aortic aneurysm depends upon the severity of underlying infection. A possibility exists that SIRS is a useful indicator for predicting the surgical outcome of patients.

Aged↗

Transmyocardial laser revascularization induced angiogenesis correlated with the expression of matrix metalloproteinases and platelet-derived endothelial cell growth factor.

OBJECTIVE: Transmyocardial laser revascularization (TMLR) has been widely evaluated as a treatment for ischemic myocardium. However, its mechanism remains unclear. One mechanism is angiogenesis. This study examines the relationship between TMLR and angiogenesis from the viewpoint of matrix metalloproteinases and platelet-derived endothelial cell growth factor. METHODS: The left anterior descending coronary artery (LAD) was ligated permanently in 12 beagle dogs. TMLR was accomplished in six of the 12 dogs using a carbon dioxide laser. No laser treatment was done in the six control dogs. Two weeks after the initial operation, dogs were euthanized and transmural samples (each of approximately 0.5 g) were cut from the center of the infarcted LAD territory, right ventricular wall, left circumflex artery perfuse area and interventricular septum except the LAD perfuse area. They were snap-frozen in liquid nitrogen for matrix metalloproteinases and platelet-derived endothelial cell growth factor activity analysis. Hematoxylin and eosin staining, double immunohistologic staining with anti-proliferating cell nuclear antigen and von Willebrand factor antibody, and immunohistologic staining with antibody against platelet-derived endothelial cell growth factor were performed for histologic studies. The activities of matrix metalloproteinases were examined by gelatin zymography. The activity of platelet-derived endothelial cell growth factor was examined by a spectrophotometric method. RESULTS: The channels were found to be infiltrated with granulation tissue and fibrosis. In the laser group, the active matrix metalloproteinase-2 and platelet-derived endothelial cell growth factor activity in the area of the left anterior descending coronary artery was significantly higher than in the control group (P<0.0001 and P=0.037, respectively). Within the channel remnants or close to these areas, the number of von Willebrand factor positive microvessels and proliferating cell nuclear antigen with correlating von Willebrand factor positive microvessels were significantly higher than in the control group (P=0.001 and P=0.0006, respectively). These increases in microvessels significantly correlated with the expression of matrix metalloproteinases and platelet-derived endothelial cell growth factor. CONCLUSION: Based on these findings it was concluded that transmyocardial laser revascularization induced angiogenesis correlated with the expression of active matrix metalloproteinases-2 and platelet-derived endothelial cell growth factor.

Animals↗

Augmented acetylcholine-induced translocation of RhoA in bronchial smooth muscle from antigen-induced airway hyperresponsive rats.

Acetylcholine (ACh)-induced translocation of RhoA in bronchial smooth muscle of repeatedly antigen-challenged rats that have a marked airway hyperresponsiveness (AHR) was examined. ACh induced time- and concentration-dependent translocation of RhoA to the plasma membrane, indicating an activation of RhoA in bronchial smooth muscle. The level of ACh-induced RhoA translocation was further increased markedly in the AHR group as compared to that in the control group. It is suggested that the augmented activation of RhoA observed in the hyperresponsive bronchial smooth muscle might be responsible for the enhanced ACh-induced Ca(2+) sensitization of bronchial smooth muscle contraction associated with AHR.

Acetylcholine↗

Contraindication of magnesium sulfate in a pregnancy complicated with late-onset diabetes mellitus and sensory deafness due to mitochondrial myopathy.

A primipara affected by late-onset diabetes and sensory deafness because of mitochondrial myopathy was hospitalized for threatened preterm delivery. Magnesium sulfate was started for tocolysis, resulting in general muscle damage, although the mitochondrial myopathy did not deteriorate during pregnancy. Magnesium sulfate may be contraindicated in pregnancy with mitochondrial myopathy.

Adult↗

Prenatal diagnosis of QT prolongation by fetal magnetocardiogram--use of QRS and T-wave current-arrow maps.

To determine the T wave of a fetal magnetocardiogram (FMCG), we have evaluated the T/QRS ratio and obtained current-arrow maps that indicate weak currents. We measured FMCG signals for 52 normal fetuses and two abnormal fetuses with prolonged QT waves by using three superconducting quantum interference device (SQUID) systems: a nine-channel system, a 12-channel vector system and a 64-channel system. The T/QRS ratio was calculated for all the normal fetuses from the maximum magnitudes of the QRS complex and the T wave. Current-arrow maps of the QRS complex (R wave) and T wave were obtained by using the 64-channel system, and the phase differences of the total-current vectors were calculated by using the current-arrow maps. The results showed that the T/QRS ratio had a wide variability of 0.35 for the normal fetuses. However, the magnitude of the prolonged T wave was as weak as the detection limit of the SQUID magnetometer. Although the T/QRS ratios for the fetuses with QT prolongation were within the normal range (< 0.35), the weak magnitude of the prolonged T wave could be evaluated. On the other hand, by comparing the current-arrow maps of the R and T waves for the normal fetuses, we found that the maximum-current arrows were indicated as either in the same direction or in opposite directions. These patterns could be identified clearly by the phase differences. Very weak prolonged T waves for the two abnormal fetuses could be determined by using these current-arrow maps and phase differences. Consequently, although the T/QRS ratios of FMCG signals have a wide distribution, we have concluded that the current-arrow map and phase difference can be used to determine the T wave of an FMCG signal.

Adult↗

A new beta-1,2-N-acetylglucosaminyltransferase that may play a role in the biosynthesis of mammalian O-mannosyl glycans.

Recent studies have shown that O-mannosyl glycans are present in several mammalian glycoproteins. Although knowledge on the functional roles of these glycans is accumulating, their biosynthetic pathways are poorly understood. Here we report the identification and initial characterization of a novel enzyme capable of forming GlcNAc beta 1-2Man linkage, namely UDP-N-acetylglucosamine: O-linked mannose beta-1,2-N-acetylglucosaminyltransferase in the microsome fraction of newborn rat brains. The enzyme transfers GlcNAc to beta-linked mannose residues, and the formed linkage was confirmed to be beta 1-2 on the basis of diplococcal beta-N-acetylhexosaminidase susceptibility and by high-pH anion-exchange chromatography. Its activity is linearly dependent on time, protein concentration, and substrate concentration and is enhanced in the presence of manganese ion. Its activity is not due to UDP-N-acetylglucosamine: alpha-3-D-mannoside beta-1,2-N-acetylglucosaminyltransferase I (GnT-I) or UDP-N-acetylglucosamine: alpha-6-D-mannoside beta-1,2-D-acetylglucosaminyltransferase II (GnT-II), which acts on the early steps of N-glycan biosynthesis, because GnT-I or GnT-II expressed in yeast cells did not show any GlcNAc transfer activity against a synthetic mannosyl peptide. Taken together, the results suggest that the GlcNAc transferase activity described here is relevant to the O-mannosyl glycan pathway in mammals.

Animals↗

The first exon coding region of cystathionine gamma-synthase gene is necessary and sufficient for downregulation of its own mRNA accumulation in transgenic Arabidopsis thaliana.

Expression of the gene for cystathionine gamma-synthase (CGS), which catalyzes the key step of methionine biosynthesis, is feedback regulated at the level of mRNA stability. The first exon polypeptide of CGS is suggested to be involved in this regulation and amino acid sequence alterations caused by mto1 mutations in that region lead to an overaccumulation of CGS mRNA [Chiba et al. (1999) Science 286: 1371-1374]. Transgenic Arabidopsis thaliana harboring chimeric constructs in which wild-type or mto1 mutant CGS exon 1 are fused in-frame to reporter genes and driven by the cauliflower mosaic virus 35S RNA promoter were constructed. Studies with these transgenic lines demonstrated that the coding region of CGS exon 1 is necessary and sufficient for downregulation of its own mRNA accumulation in response to methionine application and that this region acts in cis in this process.

Arabidopsis↗