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Biomedical subjects

K Yano

Publications and source records attributed to K Yano.

At least 415 records · Page 23Linked to original sources
PubMed1994

Glucose intolerance and 22-year stroke incidence. The Honolulu Heart Program.

BACKGROUND AND PURPOSE: This study was conducted to determine whether glucose intolerance and diabetes increase the risk of thromboembolic, hemorrhagic, and total stroke independent of other risk factors. METHODS: Among 7549 Japanese-American men aged 45 to 68 years and free of coronary heart disease and stroke during 1965 to 1968, history of diabetes, diabetic medication, and nonfasting glucose 1 hour after a 50-g load were used to classify subjects into four glucose tolerance categories. Incidence of stroke over 22 years was ascertained using comprehensive hospital-based surveillance. Age- and risk factor-adjusted relative risks of stroke were determined using a Cox proportional hazards model. RESULTS: A total of 374 thromboembolic, 128 hemorrhagic, and 36 type-unknown strokes occurred. Incidence of thromboembolic but not hemorrhagic stroke increased with worsening glucose tolerance category. Compared with the "low-normal" (glucose < 151 mg/dL) group, subjects in the "high-normal" (151 to 224 mg/dL), "asymptomatic high" (> or = 225 mg/dL), and "known diabetes" groups all had significantly elevated age-adjusted relative risks of thromboembolic stroke. After adjustment for other risk factors, relative risks remained significantly elevated for the asymptomatic high and known diabetes groups (1.43 and 2.45; 95% confidence intervals, 1.00 to 2.04 and 1.73 to 3.47, respectively). Associations were the same in hypertensive and nonhypertensive subjects and similar but slightly stronger in younger (aged 45 to 54 years) than in older (aged 55 to 68 years) men. CONCLUSIONS: Subjects with diabetes and elevated glucose appear to be at increased risk of thromboembolic but not hemorrhagic stroke. These associations were largely independent of other cardiovascular disease risk factors. Excess risk is apparent in older as well as younger diabetic individuals and in hypertensive and nonhypertensive subjects with diabetes.

Aged↗
PubMed1994

Evaluation of aortic distensibility in patients with essential hypertension by using cine magnetic resonance imaging.

In order to evaluate the exact distensibility in various parts of aorta in hypertensive patients, the authors performed cine magnetic resonance (MR) in 30 normal control (NC) subjects and 30 hypertensive (HT) patients whose age and sex were matched. Cine MR was carried out at transverse sections in the ascending, descending, and abdominal aorta. Aortic diameter and area were measured in the frames of the maximum and the minimum aortic area. Aortic distensibility was calculated from the following formula: (Max area-Min area)/(Min area x delta P), where delta P is pulse pressure. Cardiac parameters were measured with echocardiography in all subjects. Aortic distensibility was significantly lower in HT patients than in NC subjects at each transverse section (P < 0.01). Minimum diameter index (Min diameter/body surface area) and cardiac function parameter showed no significant differences between NC and HT groups. From these findings, it is suspected that hypertension is a strongly contributing factor that promotes aortic sclerosis.

Adult↗
PubMed1994

Dexamethasone increases growth hormone receptor messenger ribonucleic acid levels in liver and growth plate.

Glucocorticoid inhibits linear growth and renders target tissues, particularly liver and growth plate, insensitive to GH. We hypothesized that glucocorticoid-induced GH insensitivity is due to decreased gene expression of the GH receptor at the messenger RNA (mRNA) level. To test this hypothesis, we treated 4.5-wk-old male rabbits (n = 6-9 per group) with ip dexamethasone or vehicle and measured GH receptor mRNA levels (by RNase protection assay) and serum GH-binding protein levels (by radioimmunoprecipitation assay). Contrary to our hypothesis, dexamethasone administered in growth-suppressing doses did not decrease GH receptor mRNA levels in liver or growth plate. Instead a tissue-specific stimulation of GH receptor mRNA levels was observed. The dose-response relationship of this effect was biphasic, since the lower growth-suppressing dose of dexamethasone (0.1 mg/kg.day) caused the greater increase in GH receptor mRNA levels, whereas the higher growth-suppressing dose (4 mg/kg.day) had less effect. The dexamethasone-induced increase in GH receptor mRNA was observed in growth plate and liver, target tissues important for linear growth, but not in kidney. Serum GH-binding protein levels also showed a stimulatory response to dexamethasone treatment, with a biphasic dose-response relationship. These data suggest that glucocorticoid-induced GH insensitivity cannot be explained by decreased GH receptor mRNA levels. To the contrary, dexamethasone causes a tissue-specific stimulation in GH receptor mRNA levels with a biphasic dose-response relationship.

Animals↗
PubMed1994

A sporadic case of male-limited precocious puberty has the same constitutively activating point mutation in luteinizing hormone/choriogonadotropin receptor gene as familial cases.

Familial male-limited precocious puberty (FMPP) is an autosomal dominant disorder characterized by marked elevation of serum testosterone despite low levels of gonadotropin. Recently, a single point mutation in the LH/hCG receptor (LH/CGR) gene was found in FMPP families that constitutively activates the LH/CGR, causing Leydig cell activation and precocious puberty. Among the Japanese population, only four sporadic cases of male-limited precocious puberty have been reported. In the current study, we examined one of the four reported Japanese patients with sporadic male-limited precocious puberty and found the same mutation as that in the FMPP families. Genomic DNA was isolated, and the polymerase chain reaction (PCR) was performed to amplify a fragment of LH/CGR DNA encoding amino acid residues that include transmembrane helixes 5 and 6. Sequencing of the PCR products revealed a heterozygous adenosine-guanine transition at nucleotide 1733 in codon 578. The mutation encodes an aspartic acid578-glycine substitution in transmembrane helix 6. The mutant LH/CGR, created by site-directed mutagenesis in vitro, exhibited constitutively higher cAMP levels in transfected COS-7 cells than the wild-type LH/CGR, as described previously; however, basal inositol phosphate levels were not increased by transfection with complementary DNA for the mutant receptor. The concentration and affinity of [125I]hCG-binding sites were similar in cells transfected with the mutant and wild-type LH/CGR complementary DNAs, indicating that the mutant did not alter the production of receptor or its ability to bind human LH/CG. The sporadic occurrence of this case was confirmed by further studies. The mutation creates a recognition site for the restriction endonuclease MspI. Restriction digestion was positive for the mutant not digested by MspI, indicating that the patient's mutant allele was not inherited from his parents. DNA analysis of the patient and the parents, using microsatellite repeat markers, was compatible with biological paternity and maternity. We conclude that the aspartic acid578-->glycine mutation in the LH/CGR has arisen in the Japanese population and is the cause of a sporadic case of male-limited precocious puberty.

Aspartic Acid↗
PubMed1994

Somatostatin-related peptides isolated from the eel gut: effects on ion and water absorption across the intestine of the seawater eel.

Four somatostatin-related peptides were isolated from eel guts. Two of them were the same as eel SS-25II (eSS-25II) and eel SS-25I (eSS-25I) isolated from European eel pancreas. The remaining two peptides were C-terminal tetradecapeptides (eSS-14II and eSS-14I) of eSS-25II and eSS-25I, respectively. These four peptides all enhanced the serosa-negative transepithelial potential difference and short-circuit current across the seawater eel intestine after pretreatment with isobutylmethylxanthine, serotonin (5-HT) and methacholine, an agonist of acetylcholine (ACh). Among these peptides, eSS-25II was the most potent enhancer, followed by eSS-25I and eSS-14II. Since the large peptide (eSS-25II) acts at a lower concentration than the small somatostatin (eSS-14II), the 11 N-terminal amino acid residues seem to potentiate somatostatin action in the eel intestine. In contrast, eSS-14II was more potent than mammalian SS-14, indicating that the three amino acid residues (Tyr18, Gly21, Pro22) in the C-terminal portion also contribute to the potency of somatostatin. Endogenous somatostatin (eSS-25II) activated net Na+, Cl- and water fluxes across the seawater eel intestine. This stimulatory action was not inhibited by tetrodotoxin or yohimbine, an adrenergic antagonist, indicating that eSS-25II does not act through neuronal firing or through catecholamine release. Thus, eel somatostatins may act directly on the enterocytes, but on a distinct receptor from that for adrenaline, to antagonize the inhibition of NaCl and water absorption by 5-HT and ACh in the seawater eel intestine.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Specific binding of 12-O-tetradecanoylphorbol-13-acetate to histone H1.

12-O-Tetradecanoylphorbol-13-acetate (TPA) binds specifically to histone H1 prepared from HeLa cells and to calf histone H1 with dissociation constants of 4.3 x 10(-7) and 9.3 x 10(-7) M, respectively. The TPA-binding to histone H1 was confirmed immunologically using a monoclonal antibody directed against an evolutionally conserved epitope of histone H1. This binding would influence DNA structure and the basal level of transcription, and may, in turn, account for the cell growth-regulatory activity of TPA.

Amino Acid Sequence↗
PubMed1994

Effects of intravenous verapamil on atrial vulnerability.

To investigate the effects of verapamil on indicators of atrial vulnerability, we examined 30 patients with paroxysmal supraventricular tachycardia who received intravenous verapamil during an electrophysiologic study. Single atrial extrastimuli were given before and after intravenous administration of verapamil to induce repetitive atrial firing (RAF) or atrial fibrillation, and to examine the maximum A2/A1, which was defined as the maximum ratio of the duration of the atrial electrogram resulting from premature stimulation (A2) to that resulting from the basic drive beat (A1). The maximum A2/A1 increased from 145 +/- 20% to 154 +/- 25% (p < 0.02) after verapamil administration. The maximum A2/A1 in patients in whom neither RAF nor atrial fibrillation were induced both before and after verapamil were smaller than those in patients in whom RAF was induced only after verapamil (before; 138 +/- 20% vs 165 +/- 15%, p < 0.02. after; 144 +/- 22% vs 172 +/- 17%, p < 0.05). RAF or atrial fibrillation was induced only after verapamil in 6 patients, who showed a maximum A2/A1 before verapamil of 150% or more. These data suggest that verapamil may induce repetitive atrial firing and possibly atrial fibrillation in some predisposed patients, especially in those that have a greater maximum A2/A1, which may be an indicator of local intraatrial conduction delay before drug infusion.

Adolescent↗
PubMed1994

Effects of hydrocortisone on transmembrane currents in guinea pig ventricular myocytes--possible evidence for positive inotropism.

Steroid hormones are thought to have a positive inotropic action, but the precise electrophysiological effects which underlie this positive inotropism remain unknown. The effects of hydrocortisone on the L-type calcium current (ICa) of the isolated guinea pig ventricular cells were investigated under the whole-cell voltage-clamp recording. Hydrocortisone (10(-6) to 10(-5) M) increased the amplitude of ICa without any changes in the voltage-dependency in ICa. This agent retarded the fast inactivation component of ICa, but not the slow component. On the other hand, hydrocortisone slightly reduced the slope conductance of inward rectifying potassium current (IK1) at potentials less than -50mV. This effect on IK1 is favorable for the activation of ICa. Thus, these results indicate that the positive inotropism of hydrocortisone is mediated, at least in part, by a direct potentiating effect on ICa.

Animals↗
PubMed1994

A survey of Campylobacter jejuni in broilers from assignment to slaughter using DNA-DNA hybridization.

A survey of Campylobacter jejuni in the cecal contents of broilers raised on a farm was carried out by the DNA-DNA hybridization method from the day of assignment to slaughter at about 1-week intervals. C. jejuni was detected in chickens as early as 1 week of age, and was widely detected at each week of age throughout the growing period. In addition, of 20 chickens tested just after assignment, 7 (35%) were C. jejuni positive. It is suggested that newly introduced chickens may have already been contaminated with C. jejuni. The hybridization method was able to detect C. jejuni in the chickens from the day of assignment to 3 weeks of age, but C. jejuni was never detected in the same chickens by the enriched culture method. Therefore, it is suggested that the hybridization method is more sensitive than the enriched culture method.

Age Factors↗
PubMed1994

Possible role of supernormal atrial conduction in the genesis of atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation.

OBJECTIVE: The occurrence of supernormal excitability and conduction in the atrium has been attributed to the internodal pathways in several animal experiments. However, little is known about the role of supernormal atrial conduction (SNC) in the genesis of arrhythmias. The specific aim of this study was to evaluate prospectively the relationship between SNC, atrial conduction defects and atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation. METHODS: Programmed atrial stimulation was performed in 38 control patients (group 1), and 21 patients with idiopathic paroxysmal atrial fibrillation (group 2) to assess some determinants of atrial conduction defects, SNC, and atrial fibrillation inducibility. RESULTS: The mean P-wave duration was 99 +/- 8 ms in group 1, and 110 +/- 12 ms in group 2; p < 0.001. The maximum interatrial conduction delay was 36 +/- 40 ms in group 1, and 56 +/- 21 ms in group 2; p < 0.005. Supernormal atrial conduction was observed in 27 (71 percent) patients of group 1, and in 5 (24 percent) of group 2; p < 0.0003. The SNC zone was 70 +/- 29 ms in group 1, and 16 +/- 31 ms in group 2; p < 0.0001. The maximum decrease in conduction time during the period of SNC was 12 +/- 4 ms in group 1 and 3 +/- 6 ms in group 2; p < 0.0005. The SNC zone showed a significant inverse correlation with the P-wave duration (r = -0.53; p < 0.0005), and with the maximum conduction delay (r = -0.38; p < 0.005). CONCLUSIONS: Patients with idiopathic paroxysmal atrial fibrillation have a significantly decreased incidence of SNC than controls. There is an inverse relation between the atrial conduction defects and the SNC. The association of the absence of SNC with defects in atrial conduction may play some role in the development of atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation.

Adult↗
PubMed1994

Delayed cerebral ischemia manifesting as peduncular hallucinosis after aneurysmal subarachnoid hemorrhage--three case reports.

Three cases of peduncular hallucinosis occurred in patients with aneurysmal subarachnoid hemorrhage. All patients underwent early clipping of the ruptured aneurysms of the anterior circulation. Several days after onset of subarachnoid hemorrhage, the patients complained of vivid visual hallucinations associated with abnormal sleep-waking rhythms, suggesting a diagnosis of peduncular hallucinosis. The hallucinations disappeared with administration of an increased dose of dobutamine. These findings indicated that peduncular hallucinosis might be a manifestation of delayed cerebral ischemia after subarachnoid hemorrhage. No other possible cause of neurological deficits such as hydrocephalus, cerebral infarcts, or metabolic encephalopathies was identified. Damage to the ascending reticular activating system has been implicated in the pathogenesis of peduncular hallucinosis. Cerebral vasospasm in the perforating arteries of the ascending reticular activating system was probably the cause of the hallucinosis in our patients.

Adult↗
PubMed1994

RES-701-1, a novel and selective endothelin type B receptor antagonist produced by Streptomyces sp. RE-701. II. Determination of the primary sequence.

The structure of RES-701-1, a novel microbial endothelin type B receptor antagonist, was determined. Protein chemical data and FAB-MS have identified RES-701-1 to be a cyclic polypeptide consisting of 16 common L-amino acids. This compound is so stable against proteolysis that its enzymatic digestion under standard conditions proved to be very difficult. Therefore, the primary sequence of RES-701-1 was determined by the application of advanced protein chemical methods to be Gly1-Asn2-Trp3-His4-Gly5-Thr6-Ala7-Pro8-++ +Asp9-Trp10-Phe11-Phe12-Asn13- Tyr14-Tyr15-Trp16. The compound is cyclized between the beta-carboxyl group of Asp9 and the alpha-amino group of Gly1.

Amino Acid Sequence↗
PubMed1994

Modulation of adrenergic receptors during regression of cardiac hypertrophy.

OBJECTIVE: To determine whether alpha 1- or beta-adrenergic receptors are altered during regression of cardiac hypertrophy produced by antihypertensive agents. DESIGN AND METHODS: Cardiac hypertrophy was induced in rats by aortic banding. After 6 weeks banding the rats were treated with an angiotensin converting enzyme (ACE) inhibitor (enalapril), an alpha 1-adrenergic antagonist (bunazosin) or a beta-adrenergic antagonist (propranolol) for 6 weeks to induce regression. The numbers of alpha 1- and beta-adrenergic receptors, haemodynamics, tissue noradrenaline content and tissue ACE activity were measured. RESULTS: Regression of cardiac hypertrophy occurred after treatment of aortic banded rats with a high dose of enalapril, bunazosin or propranolol, and was accompanied by a reduction in systolic blood pressure. The number of alpha 1- or beta-adrenergic receptors was unchanged by propranolol treatment, but the number of alpha 1-adrenergic receptors was increased in the hearts of rats treated with bunazosin. A low dose of enalapril (3 mg/kg body weight) caused regression of hypertrophy without a concomitant reduction in blood pressure, and decreased the number of alpha 1-adrenergic receptors. The dissociation constants for alpha 1- and beta-adrenergic receptors were not different among the experimental groups, and the positive derivatives of left ventricular pressure was unaltered in rats treated with a low dose of enalapril but was reduced by the other drugs. CONCLUSION: Of the three drugs tested, only the low dose of enalapril affected adrenergic receptors during regression of cardiac hypertrophy, causing a decrease in alpha 1-adrenergic receptor number without a reduction in blood pressure. This effect may be explained by non-haemodynamic actions of the ACE inhibitor enalapril, probably by modulation of peripheral sympathetic activity.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Glutamate substitution for glutamine at position 5 or 6 reduces somatostatin action in the eel intestine.

Isolating a new somatostatin-like peptide from eel gut, the active residues to potentiate somatostatin action in the eel intestine were determined. In the newly-isolated peptide, the 5th or 6th Gln of the eel somatostatin (eSS-25II) was replaced with Glu. Although this peptide also enhanced the short-circuit current (Isc) across the intestine of the seawater eel, higher concentrations (approximately 30 fold) were required to obtain the same effects as eSS-25II. Since the Isc is due to active Cl- transport, this indicates that a structure formed by Gln-Gln residues at position 5 and 6 potentiates the somatostatin action to enhance ion and water transport across the intestine of the eel.

Amino Acid Sequence↗
PubMed1994

Epidemiology of stroke among Japanese men in Hawaii during 24 years of follow-up: the Honolulu Heart Program.

This report present epidemiologic data on stroke incidence and mortality as well as on risk factors for total stroke and subtypes of stroke among Japanese men in Hawaii, who were known to have much lower stroke morbidity and mortality than indigenous Japanese men. Of 7,893 men aged 45 to 68 and free of stroke at baseline examination (1965-68), 587 developed first episodes of stroke during 24 years of follow-up through 1989. Comparing the distribution of stroke subtypes before and after the advent of CT scanning in 1976, there was an increase in thromboembolic stroke (67% to 74%), a decrease in subarachnoid hemorrhage (9% to 6%) and unknown type (7% to 2%), and little change in intracerebral hemorrhage (18% to 19%). Total stroke incidence declined from 5.1 to 2.4 per 1,000 person years between 1969 and 1988, with a mean annual rate of decline of 5%. Total stroke mortality in the target population (examined and nonexamined men combined) also declined markedly, at a rate similar to that reported for U.S. white men of comparable ages. The one-month case fatality ratio fell dramatically in hemorrhagic stroke (75% to 29%) and only slightly (13% to 11%) in thromboembolic stroke during the same period. Relationships between a variety of biological, sociocultural and lifestyle factors and the risk of stroke subtypes were evaluated by means of bivariate and multivariate Cox regression models. Hypertension was the strongest and most consistent risk factor for all subtypes of stroke. Other risk factors showed inconsistent patterns of association with stroke subtypes in multivariate analysis.

Age Factors↗