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Biomedical subjects

H Yasue

Publications and source records attributed to H Yasue.

At least 217 records · Page 12Linked to original sources
PubMed1996

Development of an animal genome database and its search system.

An animal genome database has been developed on a Unix workstation and maintained by a relational database management system. This database has focused on the comparative gene mapping between species to assist the mapping of the genes related to phenotypic traits in livestock. The linkage maps, cytogenetic maps, polymerase chain reaction primers of pig, cattle, mouse and human, and their references have been included in the database, and the correspondence among species have been stipulated in the database. In order to search the database effectively, the World Wide Web server (http://ws4.niai.affrc.go.jp/) and the electronic mail server system (e-mail: jgbase-mail@ niai.affrc.go.jp) have been developed on different Unix workstations. These servers are connected to the Internet.

Animals↗
PubMed1996

Primary structure of the pig homologue of human IHRP: inter-alpha-trypsin inhibitor family heavy chain-related protein.

The pig counterpart of human IHRP has been isolated from pig serum, and cDNA clones encoding this counterpart were isolated and characterized. The amino acid sequence of pig IHRP predicted from the nucleotide sequence of its cDNA shows reasonable homology to that of human IHRP. The nucleotide sequence of pig IHRP cDNA is identical to that of the mRNA partially determined to be the heavy chain of pig ITI [Buchman et al. (1990) Surgery 108, 560-566]; it is one of the major mRNAs induced in pig liver on cardiogenic shock. Thus we concluded that the reported mRNA should code for IHRP and not for the heavy chain of ITI. The pig IHRP also seems to be identical to pig-MAP, which was recently reported to be a major acute phase serum protein in pig [Gonzalez-Roman et al. (1995) FEBS Lett. 371, 227-230]. The results suggest that IHRP might be involved in acute phase reactions.

Acute-Phase Proteins↗
PubMed1996

Impairment of coronary blood flow regulation by endothelium-derived nitric oxide in dogs with alloxan-induced diabetes.

Diabetes mellitus is a major cause of ischemic coronary artery disease. Endothelial dysfunction is implicated in the pathogenesis of diabetic vascular disease. To examine coronary blood flow (CBF) regulation with endothelium-derived nitric oxide (EDNO) in the diabetic state, we compared the effects of both acetylcholine (ACh) and adenosine (Ado) on left circumflex coronary artery (LCX) blood flow in 12 vehicle-treated and 21 dogs made diabetic with alloxan anesthetized with pentobarbital. All dogs were pretreated with aspirin to inhibit endogenous prostaglandins. None of the hemodynamic parameters were significantly different in the two groups. The percent change in coronary vascular resistance (CVR) after ACh (100 ng/kg) infusion was significantly attenuated in diabetic dogs (-56.5 +/- 1.4%) as compared with vehicle-treated dogs (-64.5 +/- 1.2%) (p < 0.01), whereas the effect of Ado (1 microgram/kg) was not different between the two groups (-71.1 +/- 1.5% in vehicle, -67.0 +/- 1.3% in diabetes). After infusion of incremental doses of NG-nitro-L-arginine methyl ester (L-NAME) 10(-5)-10(-3)M, the effect of ACh was progressively inhibited in both groups and was different no longer between the two groups after the maximal dose. L-Arginine (L-ARG), but not D-ARG, significantly restored the effect of ACh in diabetic dogs but did not affect vehicle-treated dogs. The effect of Ado did not change after L- and D-ARG administration. Cu, Zn-superoxide dismutase (Cu, Zn-SOD) had no effect on any of the effects of ACh and Ado in diabetic dogs. Regulation of CBF with EDNO is impaired in dogs with alloxan-induced diabetes, and this impairment is partially restored by L-ARG.

Acetylcholine↗
PubMed1996

Effect of niceritrol on fibrinolysis and lipoprotein (a) levels in patients with coronary artery disease.

BACKGROUND: Lipoprotein (a) [Lp(a)] is an independent risk factor for coronary artery disease and niceritrol (a prodrug of nicotinic acid) is known to reduce Lp(a) levels. Patients with coronary artery disease often have impairment of the fibrinolytic system. METHODS: To elucidate the effect of niceritrol on fibrinolysis and Lp(a) levels, we examined plasminogen activator inhibitor (PAI) activity, tissue-type plasminogen activator (t-PA) antigen, and serum Lp(a) levels before and after administration of niceritrol to coronary artery disease patients with high baseline Lp(a) levels (> or = 20 mg/dl). Niceritrol was administered to 26 patients for 12 weeks at 750 mg/day. Fasting blood samples were obtained at 0800 h from each patient before treatment, after administration of niceritrol for 12 weeks and 4 weeks after the discontinuation of therapy. RESULTS: There were significant reductions in PAI activity (9.9 +/- 1.8 compared with 5.4 +/- 1.6 IU/ml, P < 0.01), t-PA antigen levels (10.0 +/- 0.5 compared with 8.8 +/- 0.6 ng/ml, P < 0.05), and Lp(a) levels (49.3 +/- 5.9 compared with 42.5 +/- 5.4 mg/dl, P < 0.01) after 12 weeks of niceritrol administration. Four weeks after the discontinuation of niceritrol treatment, all these parameters returned to baseline. CONCLUSIONS: This study demonstrated that niceritrol administration decreases PAI activity and t-PA antigen levels together with Lp(a) levels in patients with coronary artery disease. These observations suggest that niceritrol administration may tend to normalize fibrinolysis in such patients.

Adult↗
PubMed1996

Effect of purified eicosapentaenoate ethyl ester on fibrinolytic capacity in patients with stable coronary artery disease and lower extremity ischaemia.

BACKGROUND: Lower extremity ischaemia is often complicated by coronary artery disease (CAD). Patients with CAD often have impaired fibrinolytic capacity. Plasma plasminogen activator inhibitors (PAI) levels are known to be associated with levels of atherogenic lipids. Purified eicosapentaenoic acid reduces atherogenic lipid levels. OBJECTIVE: To examine the effect of purified eicosapentaenoic acid ethyl ester (EPA) on the fibrinolytic capacity in patients with stable CAD and arteriosclerosis obliterans (ASO). METHODS: Plasma levels of PAl activity and tissue-type plasminogen activator (t-PA) antigen were measured. We administered 1800 mg/day EPA for 8 weeks to 25 patients. RESULTS: Mean baseline plasma PAI activity (P < 0.01) and t-PA antigen (P < 0.01) levels were higher in the patient group than they were in the control group. At the conclusion of EPA administration, significant reductions in PAI activity (P < 0.01), t-PA antigen (P < 0.01) and serum levels of triglyceride (P < 0.01), total (P < 0.05) and low-density lipoprotein (P < 0.05) cholesterols were observed. Changes in PAI activity levels caused by EPA administration showed positive linear correlations with those in low-density lipoprotein cholesterol (r = 0.411, P < 0.05) and triglyceride (r = 0.652, P < 0.01). CONCLUSION: These findings indicate that the fibrinolytic capacity in patients with CAD and ASO is decreased by increased PAI activity, but that EPA may correct this fibrinolytic impairment by decreasing PAI activity via its inhibitory effect on atherogenic lipids.

Administration, Oral↗
PubMed1996

A swine SINE (PRE-1 sequence) distribution in swine-related animal species and its phylogenetic analysis in swine genome.

The distribution of PRE-1 sequence (a swine SINE) among the animal species related to Sus scrofa, i.e. Phacochoerus aethiopicus and Tayassu tajacu, was examined by dot-blot analysis using PRE-1 sequences as a probe. This revealed that Phacochoerus aethiopicus and Tayassu tajacu contained PRE-1 sequences, amounts of which in their genomes are almost the same as that in the swine genome, indicating that these species separated after PRE-1 sequences proliferated to diversify in the genome. In order to estimate the time when the PRE-1 started to diversify in the swine genome, PRE-1 sequences were extracted from GenBank DNA database by homology analysis using the PRE-1 consensus sequence as a probe. The 22 PRE-1 sequences obtained were aligned and their phylogenetic relation was calculated by the neighbour-joining method. The result of the calculation combined with the mutation rate of the pseudogenes (r = 4.6 x 10(-9)) indicated that the PRE-1 sequence diversified at least 43.2 million years ago. Taken together, the period of time since the separation of the three species, Sus scrofa, Phacochoerus aethiopicus and Tayassu tajacu, is currently estimated to be less than 43.2 million years.

Animals↗
PubMed1996

Double atrial responses to a single ventricular impulse in long RP' tachycardia.

Double atrial responses (DARs) to a single ventricular impulse have been described in patients with long RP' tachycardia. To define the determinants for the occurrence of DARs, 8 cases with long RP' tachycardia were examined. The mechanism of long RP' tachycardia was the orthodromic atrioventricular reciprocating tachycardia (AVRT) involving a slow conducting concealed accessory pathway in 4 cases and uncommon (fast-slow) type of atrioventricular nodal reentrant tachycardia (AVNRT) in the other 4 cases. Programmed and rapid ventricular pacing was performed during sinus rhythm and also rapid ventricular pacing during tachycardia (i.e., entrainment). The retrograde effective refractory period (ERP) and the retrograde maximal 1:1 conduction rate of the fast and slow conducting pathways were examined. In 1 of the 4 cases with AVRT, DARs were observed during programmed and rapid ventricular pacing, performed during sinus rhythm and also during entrainment. In 1 of the 4 cases with AVNRT, DARs were observed only during entrainment. The determinants of DARs in cases with long RP' tachycardia were: (1) presence of two different retrogradely conducting pathways; (2) short ERP of the retrograde fast and slow conducting pathways and a short minimal pacing cycle length at which 1:1 ventriculoatrial conduction occurs via these pathways; (3) crucial conduction delay in the slow conducting pathway; and (4) preexisting antegrade unidirectional block in the slow conducting pathway or the antegrade block in the slow conducting pathway produced by collision with a previous retrograde impulse during entrainment.

Adult↗
PubMed1996

Role of adenosine in regulation of coronary flow in dogs with inhibited synthesis of endothelium-derived nitric oxide.

Endothelium-derived nitric oxide (NO) regulates coronary blood flow, but it is unclear how NO synthesis inhibition affects myocardial metabolism. In pentobarbital sodium-anesthetized dogs, myocardial oxygen metabolism, adenosine release, lactate extraction rate (LER), and systolic ventricular wall thickening (SWT) at baseline and during atrial pacing were estimated before and after intracoronary NG-nitro-L-arginine methyl ester (L-NAME) infusion. Coronary blood flow and PO2 in the anterior interventricular vein at baseline were both significantly decreased by L-NAME (3 x 10(-4) M in the coronary blood). Coronary flow was increased during pacing, which was not affected by L-NAME. Myocardial adenosine release remained unchanged during pacing before L-NAME, but it was significantly increased after L-NAME infusion. Neither LER nor SWT changed during pacing performed before and after L-NAME. The experiment was also performed in dogs pretreated with 8-phenyltheophyl-line. After L-NAME, pacing-induced increase in coronary flow was suppressed, and both LER and SWT were significantly decreased during pacing. In conclusion, when NO synthesis is inhibited, adenosine release is increased in response to the increase in myocardial oxygen demand. With this compensatory adenosine release, coronary flow is increased and ventricular function is unaffected.

Adenosine↗
PubMed1996

Suppression of atherosclerotic changes in cholesterol-fed rabbits treated with an oral inhibitor of neutral endopeptidase 24.11 (EC 3.4.24.11).

Neutral endopeptidase 24.11 (NEP), widely distributed in the body, hydrolyzes and inactivates a number of endogenous vasoactive peptides, some of which could alter various functions of cells present in the arterial wall. Recently NEP has been found to exist in the vascular endothelium. The aim of this study was to assess the influence of chronic NEP inhibition by daily administration of UK79300 (candoxatril), an orally active NEP inhibitor (NEPI), on the development of atherosclerotic changes in high-cholesterol-fed rabbits. Male New Zealand White rabbits were fed for 8 weeks as follows: normal rabbit diet (Normal, n = 15), 1.5% cholesterol diet (Cholesterol, n = 15), or 1.5% cholesterol diet containing NEPI (20 mg.kg-1.d-1) (Cholesterol+NEPI, n = 15). At the end of the dietary period, NEPI treatment was found to suppress the surface area of the aorta covered by plaques (% surface area: Cholesterol, 59 +/- 6 versus Cholesterol+NEPI, 36 +/- 7, P < .01) and decreased contents of cholesterol and cholesterol esters in the aortas. NEPI also reduced plasma total cholesterol by 27% of Cholesterol rabbits (1781 +/- 130 mg/dL). The endothelial function, estimated by the endothelium-dependent relaxation of the isolated aortas in response to acetylcholine, was preserved in Cholesterol+NEPI rabbits compared with that in Cholesterol rabbits. NEP enzymatic activities in plasma and the particulate fraction of the homogenates from the aortas in Cholesterol rabbits were both increased, 3.1- and 3.9-fold, respectively, above those in Normal rabbits, but the activities in Cholesterol+NEPI rabbits were significantly lower than those in Cholesterol rabbits. UK73967, an active form of UK79300, or phosphoramidon partly reversed the atherosclerotic impairment of relaxation of the isolated thoracic aortic rings from Cholesterol rabbits in response to exogenous additions of C-type natriuretic peptide (CNP) and substance P, which are NEP substrates known to exist endogenously in the vascular endothelium. The results suggest that the increased NEP activity plays a significant role in atherogenesis, and NEPIs might be therapeutically useful in the prevention of atherosclerosis. Reduction of plasma cholesterol and suppression of degradations in the arteries of endogenously released CNP, substance P, or possibly other kinins known to have anti-atherosclerotic actions may at least partially contribute to the inhibitory effects of NEPIs on atherosclerotic changes.

Administration, Oral↗
PubMed1996

The cDNA sequence of porcine vitronectin and its expression in liver and skeletal muscle of GH-supplemented pigs.

A cDNA (1555 bp) (DNA database accession number, D61396) having a homology with human vitronectin (Vn) was isolated from a porcine liver cDNA library, and its sequence was determined. The open reading frame in the cDNA was found to code a protein with 388 amino acids, then the amino acid sequence of the protein (porcine putative Vn) was aligned to the other mammalian (mouse, rabbit, and human) Vns previously reported. The alignment revealed that the functional amino acid sequences reported as the cell attachment site, the heparin binding site, the region involved in glycosylation, and plasminogen activator inhibitor I-binding domain were conserved in the porcine putative Vn. These findings together with the fact that the calculated molecular weight and the N-terminal amino acid sequence of the putative Vn agreed with those reported by biochemical analysis on porcine Vn, led us to conclude that the cDNA isolated in the present study coded for the porcine Vn. Then, a time course study was performed to examine whether the administration of growth hormone (GH) affects Vn mRNA expression in liver and skeletal muscle, since the level of Vn mRNA was reported to be affected by inflammation, and since GH was reported to be involved in inflammation. This revealed that GH has no effect on the level of liver Vn mRNA, and that Vn mRNA level in skeletal muscle seemed to be affected following GH-injection.

Amino Acid Sequence↗
PubMed1996

Enhancement of myocardial reactive hyperemia with manganese-superoxide dismutase: role of endothelium-derived nitric oxide.

OBJECTIVE: To test the hypothesis that superoxide radicals generated during myocardial ischemia and reperfusion influence reactive hyperemia (RH) by reacting with endothelium-derived nitric oxide (EDNO), we examined the effect of manganese (Mn)-superoxide dismutase (SOD) on RH in anesthetized dogs. METHODS: Twelve dogs were pretreated with 8-phenyltheophylline (8PT) to block adenosine's effect. Five dogs were pretreated with 8PT and NG-nitro-L-arginine methyl ester (L-NAME) to block adenosine's and EDNO's effects. Following occlusion of the left circumflex artery (LCX) for 10 and 60 s, RH was observed before and after Mn-SOD. In another group of 6 dogs pretreated with 8PT, RH following 60-s LCX occlusion was observed before and after Mn-SOD and catalase. For comparison with the effect of Mn-SOD, that of copper, zinc (Cu,Zn)-SOD was also examined in another group of 5 dogs. RESULTS: In the dogs pretreated with 8PT, Mn-SOD significantly increased excess flow and repayment of flow debt during RH after 60-s LCX occlusion but did not affect RH after 10-s LCX occlusion. Mn-SOD-induced augmentation of RH following 60-s LCX occlusion was not affected by catalase, while it was completely abolished by L-NAME. In contrast to Mn-SOD, Cu,Zn-SOD showed no effect on RH following 60-s LCX occlusion in the dogs pretreated with 8PT. CONCLUSIONS: Superoxide radicals generated during ischemia for 60 s and reperfusion attenuates myocardial RH through inactivation of EDNO. Mn-SOD shows more beneficial effects on myocardial RH than Cu,Zn-SOD.

Adenosine↗
PubMed1996

Effects of sphingomyelinase and sphingosine on arterial vasomotor regulation.

The sphingomyelin pathway is an important signal transduction system regulating various cellular functions. However, little is known about the effect of sphingomyelin metabolites on vasomotor function. We examined the vascular effects of sphingomyelin, sphingosine, and sphingomyelinase (SPMase) in vitro. In pig coronary rings precontracted with prostaglandin F2 alpha, sphingosine and SPMase evoked initial contraction and subsequent gradual relaxation; however, sphingomyelin did not influence the tone. The initial contractions in response to either SPMase (40 microU/ml to 0.4 U/ml) or sphingosine (0.5-10 microM) treatment were abolished in rings denuded of endothelium. This initial contraction in response to sphingosine treatment was significantly attenuated by a cyclo-oxygenase inhibitor indomethacin, but not altered by either a nitric oxide synthase inhibitor, N omega-monomethyl-L-arginine (L-NMMA), a protein kinase C (PKC) inhibitor staurosporine, or superoxide dismutase (SOD, 100 U/ml). Incubation of coronary rings with sphingosine (10 microM) or SPMase (0.4 U/ml) for 120 min significantly attenuated subsequent endothelium-dependent relaxation in response to thrombin and A23187, but did not affect endothelium-independent relaxation in response to sodium nitroprusside. In contrast, sphingomyelin (10 microM) did not alter the endothelium-dependent relaxation. In conclusion, in the sphingomyelin pathway, sphingosine induces vasoconstriction in coronary arteries that seems to be mediated by the release of cyclooxygenase-sensitive vasoconstrictor prostanoids from the endothelium. Sphingosine also induced endothelial dysfunction characterized by impaired endothelium-dependent relaxation. Thus, the sphingomyelin pathway may be an important regulator of vascular function.

Animals↗
PubMed1996

[Evaluation of simultaneous acquisition of transmission and emission data on thallium-201 myocardial SPECT].

This study evaluates the usefulness of attenuation correction on regional myocardial tracer distributions defined by Thallium-201 myocardial SPECT images obtained from cardiac phantoms and patients with or without coronary heart disease. A three-detector SPECT system equipped with a Technetium-99m line source and a fan-beam collimator was used for simultaneous transmission and emission data acquisition. All three detectors were equipped with fan-beam collimators. Thallium-201 myocardial scintigraphy was performed on phantom study and 19 patients. Transmission images, uncorrected and corrected emission images were iteratively reconstructed with a EM-ML algorithm. Attenuation map computed from the transmission data was utilized for the attenuation correction. For the phantom study, circumferential profile analysis was applied to both datasets of horizontal long-axis slices through the center of the phantom. The maximum profile value in the circumferential profile set to 100% in the normalized uncorrected and corrected profiles. The uncorrected circumferential profiles from cardiac insert model 7070 and RH-2 cardiophantom showed decrease in activity in basal regions which appeared improvement in the attenuation corrected profiles. In clinical study, the inferior-to-anterior activity ratio, changed from 0.78 +/- 0.10 to 0.97 +/- 0.11 on stress images in patients with inferior ischemia and from 0.96 +/- 0.12 to 1.15 +/- 0.13 on 4 hour delayed or rest images in normal cases. The anteroapical wall of the attenuation corrected images, however, showed a decrease in activity relative to the inferior wall in normal cases. The increase in activity in inferior wall on attenuation corrected images was observed frequently in clinical study but not in phantom study. A presence of scatter from the liver or bowels may cause the increase in activity in the inferior wall in clinical study. In conclusion, transmission scan is one of the useful methods for the attenuation correction. Scatter correction, however, is also necessary to make an accurate attenuation corrected images.

Heart↗
PubMed1996

Menstrual cyclic variation of endothelium-dependent vasodilation of the brachial artery: possible role of estrogen and nitric oxide.

Estrogens have been reported to influence endothelial functions. This article's aim is to examine whether endothelium-dependent vasodilation of brachial arteries is changed in parallel with the physiological variation of the ovarian hormones during the menstrual cycle in young healthy female subjects. With high-resolution ultrasonography, we measured the diameter and blood flow of brachial arteries at rest, during reactive hyperemia, and after sublingual nitroglycerin administration in 15 young healthy female subjects (mean 29.6 +/- 2.6 years). All female subjects were studied in each of three different phases of one menstrual cycle (M, menstrual phase; F, follicular phase; L, luteal phase). The increase in arterial diameter during reactive hyperemia was lowest in the menstrual phase and highest in the follicular phase (4.9 +/- 0.8% in M; 14.1 +/- 0.9% in F; 9.2 +/- 1.1% in L; p < 0.005 between any two means among the groups). No significant difference was apparent in the percentage of increase in blood flow during reactive hyperemia among the three phases. The percentage of increase in arterial diameter after nitroglycerin administration also was not significantly different among the three phases of the cycle. The serum estradiol level was lowest in the menstrual phase and was highest in the follicular phase (17.5 +/- 1.6 pg/ml in M, p < 0.0005, M versus F and L; 107.8 +/- 18.0 pg/ml in F, p < 0.05, F versus L; 74.4 +/- 7.3 pg/ml in L). The serum level of nitrite-nitrate, measured by the Griess reaction, was highest in the follicular phase and was lowest in the menstrual phase of the three different phases (40.4 +/- 7.9 mumol/l in M, p < 0.01, M versus F, and p < 0.05, M versus L; 106.7 +/- 17.6 mumol/l in F, p < 0.05, F versus L; 62.2 +/- 6.2 mumol/l in L). In conclusion, a significant variation of the endothelium-dependent vasodilation parallels the levels of serum estradiol and nitrite-nitrate during the menstrual cycle in female subjects.

Adult↗