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Biomedical subjects

S Kamakura

Publications and source records attributed to S Kamakura.

At least 37 records · Page 2Linked to original sources
PubMed2001

Localized right ventricular morphological abnormalities detected by electron-beam computed tomography represent arrhythmogenic substrates in patients with the Brugada syndrome.

AIMS: This study was designed to determine, using electron-beam CT, whether there are morphological abnormalities in patients with the Brugada syndrome and to elucidate the relationship between those abnormalities and arrhythmogenesis. METHODS AND RESULTS: Twenty-six consecutive patients with the Brugada syndrome and 23 age- and gender-matched control subjects (controls) were evaluated for morphological abnormalities using electron beam CT. Electron beam CT demonstrated morphological abnormalities of the right ventricle in 21 (81%) of 26 patients, but in only two (9%) of 23 controls. The sites of morphological abnormalities were the right ventricular outflow tract area in 17 patients and the inferior wall of the right ventricle in four patients. Of the seven patients with monoform premature ventricular contractions recorded only in the acute phase, four of the five patients with premature ventricular contractions from the right ventricular outflow tract area had morphological abnormalities in the right ventricular outflow tract area, and the other two patients with premature ventricular contractions from the inferior wall of the right ventricle had morphological abnormalities in the inferior wall of the right ventricle. CONCLUSION: The sites of morphological abnormalities detected by electron beam CT in patients with the Brugada syndrome were related to the origins of premature ventricular contractions recorded only in the acute phase, which may trigger ventricular fibrillation. These morphological abnormalities may be related to arrhythmogenic substrates in patients with the Brugada syndrome.

Adult↗
PubMed2001

Catecholamines in children with congenital long QT syndrome and Brugada syndrome.

Catecholamines have long been used as a provocative test in some forms of tachyarrhythmias including long QT syndrome (LQTS). In contrast, catecholamines are reported to decrease ST-segment elevation in leads V1-V3 in some patients with Brugada syndrome. Differential effects of catecholamines on QT interval, action potential duration, transmural dispersion of repolarization and Torsade de Pointes between LQT1, LQT2, and LQT3 forms of the LQTS were shown in experimental models of the LQTS by using arterially-perfused wedge preparations as well as in patients with congenital LQTS including children. In our preliminary result of patients with Brugada syndrome including a child, isoproterenol infusion was effective to decrease the ST-segment elevation in leads V1-V2 and to suppress the electrical storm of ventricular fibrillation.

Catecholamines↗
PubMed2001

Comparison of reliability between the modified groin flap and the forearm flap in oral reconstruction.

OBJECTIVE: The groin flap has the advantage of minimum donor-site morbidity, while having the disadvantage of short vascular pedicle of small caliber. Modification of the groin flap has improved the former disadvantage, but the latter one remains. The purpose of this study was to compare the reliability of the modified groin flap with the forearm flap. STUDY DESIGN: Eleven modified groin flaps and 40 forearm flaps consecutively performed by a single surgeon in a hospital for patients with oral cancer were retrospectively reviewed. RESULTS: The rate of total flap loss in the modified groin flap group (8.3%) was higher than that in the forearm flap group (2.5%). The rates of partial flap loss in both flaps were similar to those of total flap loss. The failures of the modified groin flap and the forearm flap were due to arterial and venous complications, respectively. CONCLUSION: The modified groin flap appears to be a little less reliable than is forearm flap; nevertheless, it could be a good option for patients who desire less conspicuous postoperative scars.

Adult↗
PubMed2001

The stereoselective effects of bucolome on the pharmacokinetics and pharmacodynamics of racemic warfarin.

The objective of this study was to investigate the stereoselective influence of bucolome on the pharmacokinetics and pharmacodynamics of warfarin in Japanese inpatients with heart disease. Thirty patients were administered a fixed-maintenance dose of warfarin alone once a day for at least 7 days. The other 25 patients were concomitantly administered warfarin and a 300 mg dose of bucolome once a day, and blood samples were collected on days 1, 4, 7, 14, or 21 after administration of bucolome. Serum concentration of warfarin enantiomers was measured by a chiral reversed-phase HPLC-ultraviolet detection method. The PT-INR was used as a measure of the pharmacodynamic effect of warfarin. Coadministration of bucolome and warfarin had no effect on serum (R)-warfarin concentration and significantly increased serum (S)-warfarin concentration compared with warfarin alone. The PT-INR of warfarin alone was significantly lower with bucolome cotreatment. These results indicate that the augmented anticoagulant effect of warfarin by bucolome is due to inhibition of (S)-warfarin metabolism in vivo. When bucolome is added to a stabilized regimen of warfarin therapy, the dose of warfarin should be reduced by about 30% to 60%, and caution should be exercised during the first 7 days after coadministration of bucolome.

Administration, Oral↗
PubMed2001

Initial experience with nifekalant hydrochloride (MS-551), a novel class III antiarrhythmic agent, in patients with acute extensive infarction and severe ventricular dysfunction.

Nifekalant hydrocholoride, a novel class III antiarrhythmic agent, was used as the treatment in 4 patients with extensive anterior infarction and severe ventricular dysfunction. The malignant ventricular tachyarrhythmia was effectively suppressed at a relatively low dose, without compromising the hemodynamics, indicating that this potent K+ channel blocker has therapeutic potential for acute myocardial infarction.

Aged↗
PubMed2001

Implantation of octacalcium phosphate nucleates isolated bone formation in rat skull defects.

OBJECTIVE: Our previous radiographic examinations have indicated that the synthetic octacalcium phosphate (OCP) may provide the core for nucleating multiple osteogenic sites in the experimentally created cranial defect. DESIGN: The present study was designed to confirm the possibility that the implanted OCP causes the osteoinduction as well as the osteoconduction in the rat cranial defect. MATERIALS AND METHODS: Standardized defects were created in male Wistar rat calvaria, and the OCP granules were implanted into the defect. The sham operated rats were processed in the same way except that nothing was implanted. The rats were fixed at 4 weeks after implantation of OCP or the sham operation. We examined bone formed on the implanted OCP, analyzing serial sections histologically combined with immunohistochemistry for the bone specific protein, osteocalcin. RESULTS: In the defects treated with OCP, the radiopacity was scattered throughout the defect besides being observed along the defect margin of the parietal bone. Examination of the serial sections showed that some of new bones on the implanted OCP were formed away from the defect margin of the parietal bone with regard to both histological identification and specific molecular marker. CONCLUSIONS: The present study suggested that the implanted OCP can serve as a core for initiating bone formation and cause the osteoinduction as well as the osteoconduction in the defect.

Animals↗
PubMed2000

Mode of onset of ventricular fibrillation in patients with Brugada syndrome detected by implantable cardioverter defibrillator therapy.

OBJECTIVES: We sought to demonstrate the mode of spontaneous onset of ventricular fibrillation (VF) in patients with Brugada syndrome. BACKGROUND: The electrophysiologic mechanisms of VF in Brugada syndrome have not been fully investigated. METHODS: Nineteen patients (all male, mean age 47 +/- 12 years) with Brugada syndrome were treated with an implantable cardioverter defibrillator (ICD). The implanted devices were capable of storing electrograms during an arrhythmic event. We investigated the mode of spontaneous onset of VF according to the electrocardiographic features during the episode of VF, which were obtained from stored electrograms of ICDs and/or electrocardiographic (ECG) monitoring. RESULTS: During a follow-up of 34.7 +/- 19.4 months (range 14 to 81 months), 46 episodes of spontaneous VF attacks were documented in 7/19 (37%) patients. The event-free period between ICD implantation and the first spontaneous occurrence of VF was 14.6 +/- 12.1 months (range 3.7 to 27.4 months). We investigated 33/46 episodes of VF, for which electrocardiographic features (10 to 20 s before and during VF) were obtained from ICDs and/or ECG monitoring in five patients. A total of 22/33 episodes of VF were preceded by premature ventricular contractions (PVCs), which were almost identical to the initiating PVCs of VF. Furthermore, in three patients who had multiple VF episodes, VF attacks were always initiated by the same respective PVC. The coupling interval of the initiating PVCs of VF was 388 +/- 28 ms. CONCLUSIONS: Spontaneous episodes of VF in patients with Brugada syndrome were triggered by specific PVCs. These findings may provide important insights into the pathophysiological mechanisms causing VF in Brugada syndrome.

Bundle-Branch Block↗
PubMed2000

Relation between spatial distribution of late potentials and location of origin of premature ventricular complexes on body surface map in patients with postinfarction ventricular tachycardia.

We studied the relationship between the spatial distribution of late potentials (LPs) and the origin of premature ventricular complexes (PVCs) using body surface maps in 55 patients with postinfarction sustained ventricular tachycardia (VT). Body surface maps were recorded from 87 leads to construct departure maps during sinus rhythm and signal-averaged ECGs were recorded from 32 unipolar leads to construct a LP map. The root-mean-square values during 40 ms intervals behind the QRS end were computed as LPs. The PVC map was recorded simultaneously in 14 patients presenting PVC with similar morphology to VT during LP detection. The origin of PVC was localized at the site of isopotential minimum when the potential exceeded -0.5 mV during the early QRS period. The LP area and the departure area showed a similar distribution. However, the PVC origin was closer to the site of LP maximum than the departure minimum in 11 (79%) patients, and the spatial correlation between the LP maximum and the PVC origin was good in 12 (86%) patients. LP and PVC mapping from the body surface is feasible and of worth to predict noninvasively the site of origin of ventricular arrhythmias in patients with remote myocardial infarction and sustained VT.

Adult↗
PubMed2000

Confocal microscopy of Tomes' granular layer in dog premolar teeth.

Tomes' granular layer is the hypomineralized area of radicular dentin, but knowledge concerning it is limited. The present study was designed to investigate the structural characteristics of Tomes' granular layer in the dog's teeth by confocal microscopy. Permanent premolars of four beagles, two at 7 months and the other two at 14 months of age, were used for observation. During premolar root formation, the 7-month-old dogs were injected with calcein and alizarin red S for vital staining of dentin, and ground sections of the teeth were prepared. Both ground and decalcified-paraffin sections were made from the teeth of the 14-month-old dogs and stained with basic fuchsin or with hematoxylin and eosin. All sections were examined by fluorescence and confocal microscopy. In the ground sections, granules of Tomes' layer and dentinal tubules were stained with basic fuchsin and with calcein. The granules of Tomes' layer stained with calcein were seen only near the labeling lines by calcein. The granules of Tomes' layer appeared as bright spots in cross sections, and as lines in longitudinal sections. When the sections were cut tangentially through the surface of dentin, the granules of Tomes' layer showed a reticular structure. Most of the dentinal tubules were seen to pass between the granules and terminated in the dentin-cementum junction. Looped tubules were not found in this area. In the paraffin sections stained with hematoxylin and eosin, extracellular matrix of dentin showed fluorescence of various intensities and dentinal tubules appeared dark. At the surface of the radicular dentin, the granules of Tomes' layer appeared as fluorescent fibers running parallel to the surface of dentin in the longitudinal sections. The fibers appeared as bright spots in the cross sections and as a mesh in the tangential sections. In the periodontal ligament, collagen fibers showed intense fluorescence, whereas most cells were negative. From these results we conclude that Tomes' granular layer of dog's teeth may be the collagen fiber bundles that remained uncalcified or hypocalcified within the radicular dentin.

Aging↗
PubMed2000

Expression of major bone extracellular matrix proteins during embryonic osteogenesis in rat mandibles.

It is not known how bone proteins appear in the matrix before and after calcification during embryonic osteogenesis. The present study was designed to investigate expressions of the five major bone extracellular matrix proteins--i.e. type I collagen, osteonectin, osteopontin, bone sialoprotein and osteocalcin--during osteogenesis in rat embryonic mandibles immunohistochemically, and their involvement in calcification demonstrated by von Kossa staining. Wistar rat embryos 14 to 18 days post coitum were used. Osteogenesis was not seen in 14-day rat embryonic mandibles. Type I collagen was localized in the uncalcifed bone matrix in 15-day mandibles, where no other bone proteins showed immunoreactivity. Osteonectin, osteopontin, bone sialoprotein and osteocalcin appeared almost simultaneously in the calcified bone matrix of 16-day mandibles and accumulated continuously in 18-day mandibles. The present study suggested that type I collagen constitutes the basic framework of the bone matrix upon which the noncollagenous proteins are oriented to lead to calcification, whereas the noncollagenous proteins are deposited simultaneously by osteoblasts and are involved in calcification cooperatively.

Animals↗
PubMed2000

Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome.

INTRODUCTION: Brugada syndrome is characterized by an ST segment elevation in leads V1-V3 and a high incidence of ventricular fibrillation (VF). A mutation in a cardiac Na+ channel gene, SCN5A, has been linked to Brugada syndrome, and sodium channel blockers have been shown to be effective in unmasking the syndrome when concealed. The aim of this study was to examine the effects of Na+ channel blockers on ST segment elevation, QRS, corrected QT (QTc) interval, and ventricular arrhythmias in patients with Brugada syndrome. METHODS AND RESULTS: We examined the effects of three different Na+ channel blockers (flecainide, disopyramide, and mexiletine) on the amplitude of the ST segment 20 msec after the end of QRS (ST20), QRS duration, QTc interval measured from 12-lead ECG, and ventricular arrhythmias in 12 Brugada and 10 control patients. Maximum ST20 observed in the V2 or V3 leads under baseline conditions was greater in the Brugada patients than in control patients, whereas QRS duration and maximum QTc interval were no different between the two groups. Flecainide and disopyramide, but not mexiletine, significantly increased maximum ST20 and QRS duration in both groups, although these effects were much more pronounced in the Brugada patients. The increases in ST20 and QRS duration with flecainide were significantly larger than those with disopyramide. An increase of 0.15 mV in ST20 with flecainide separated the two groups without overlap. Ventricular premature complexes developed only with flecainide in Brugada patients (3/12) displaying a marked ST elevation but not widening of QRS. CONCLUSION: Our findings suggest that Na+ channel blockers amplify existing I(Na) and possibly other ion channel defects, with a potency inversely proportional to the rate of dissociation of the drug from the Na+ channel, thus causing a prominent elevation of the ST segment and, in some cases, prolongation of QRS duration in patients with Brugada syndrome.

Adult↗
PubMed2000

Clinical characteristics of patients with spontaneous or inducible ventricular fibrillation without apparent heart disease presenting with J wave and ST segment elevation in inferior leads.

INTRODUCTION: The clinical characteristics of three patients with spontaneous or inducible ventricular fibrillation (VF) without apparent heart disease, who presented with J wave and ST segment elevation in inferior leads, are described. METHODS AND RESULTS: All patients were male and experienced syncope. Their symptoms occurred at night or early in the morning. Holter ECG revealed infrequent premature ventricular complexes. Injection with disopyramide 2 mg/kg augmented ST segment elevation. CONCLUSION: These characteristics were very similar to those of patients with Brugada syndrome. These three patients with these specific features might have a variant of Brugada syndrome.

Adult↗
PubMed2000

Recovery time dispersion measured from 87-lead body surface potential mapping as a predictor of sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy.

INTRODUCTION: The clinical usefulness of QT dispersion in 12-lead ECG has been controversial in identifying subjects at risk for sustained ventricular tachycardia (VT) in patients with idiopathic dilated cardiomyopathy (DCM). We hypothesized that increasing the spatial resolution of the ECG improves the accuracy of risk stratification. The purpose of this study was to test the ability of recovery time dispersion measured from 87-lead body surface potential mapping (BSPM) to identify patients at risk for sustained VT in idiopathic DCM. METHODS AND RESULTS: We obtained 87-lead BSPM and 12-lead ECG in 33 patients with idiopathic DCM (15 patients with a history of sustained VT [VT(+) group] and 18 patients without a history of sustained VT [VT(-) group]) and in 20 normal control subjects. We measured the corrected QT dispersion and corrected recovery time dispersion from 12-lead ECG (QTc-12 dispersion and RTc-12 dispersion, respectively) and 87-lead BSPM (QTc-87 dispersion and RTc-87 dispersion, respectively). Signal-averaged ECG also was recorded in 25 patients. Neither the QTc-12 nor QTc-87 dispersion discriminated between the VT(+) and VT(-) groups patients. The VT(+) group patients had a larger but insignificant RTc-12 dispersion than the VT(-) group patients. In contrast, the RTc-87 dispersion was significantly larger in the VT(+) group patients than in the VT(-) group patients (236 +/- 39 msec vs 184 +/- 28 msec, P < 0.001). Receiver operating curve analysis indicated that the RTc-87 dispersion was as good as late potentials in predicting susceptibility to sustained VT; its sensitivity, specificity, and negative predictive value were 73%, 76%, and 76%, respectively (cutoff value 200 msec). RTc-87 dispersion >200 msec combined with positive late potentials provide high sensitivity (92%) and high negative predictive value (88%) for sustained VT. CONCLUSION: The RTc-87 dispersion is a useful tool to identify subjects at risk for sustained VT in patients with idiopathic DCM.

Body Surface Potential Mapping↗
PubMed2000

Hypokalemia-induced long QT syndrome with an underlying novel missense mutation in S4-S5 linker of KCNQ1.

Congenital long QT syndrome (LQTS) is caused by mutations in at least five genes coding for cardiac potassium or sodium channels that regulate the duration of ventricular action potentials. Acquired LQTS often is associated with drugs or metabolic abnormalities. A 47-year-old woman who presented with marked QT prolongation (QTc = 620 msec(1/2)) and repeated episodes of torsades de pointes associated with hypokalemia (2.6 mEq/L) was screened for mutations in LQTS genes using polymerase chain reaction/single-strand conformation polymorphism (PCR/SSCP). We identified a novel missense mutation in the intracellular linker of S4-S5 domains of KCNQ1, resulting in an amino acid substitution of cysteine for arginine at position 259 (R259C). Whole cell, patch clamp experiments were conducted on COS7 cells transfected with wild-type and/or R259C KCNQ1 with or without KCNE1. Functional analyses of the mutant KCNQ1 subunit on COS7 cells revealed its functional channels in the homozygous state, producing a significantly smaller current than the KCNQ1 channels and a less severe dominant-negative effect on I(Ks). The novel KCNQ1 mutation R259C is the molecular basis for I(Ks) dysfunction underlying an apparently sporadic case of hypokalemia-induced LQTS, consistent with a mild mutation likely to disclose the clinical manifestation of LQTS in a context of severe hypokalemia. Our findings suggest that gene carriers with such mild mutations might not be so rare as commonly expected in patients with acquired LQTS, and stress the importance of mutational analysis for detecting either "silent" forms of congenital LQTS or de novo mutations.

Female↗
PubMed2000

Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms.

INTRODUCTION: Body surface distribution and magnitude of ST segment elevation and their reflection in 12-lead ECGs have not been clarified in Brugada syndrome. METHODS AND RESULTS: Eighty-seven-lead body surface potential mapping and 12-lead ECGs were recorded simultaneously in 25 patients with Brugada syndrome and 40 control patients. The amplitude of the ST segment 20 msec after the end of QRS (ST20) was measured from all 87 leads, and an ST isopotential map was constructed. The maximum ST elevation (maxST20) was distributed in an area of the right ventricular outflow tract in all Brugada patients, and it was larger than that in control patients (0.37 +/- 0.13 vs 0.12 +/- 0.04 mV; P < 0.0005). The maximum was observed on the level of the parasternal fourth intercostal space, on which the V1 and V2 leads of the standard 12-lead ECG were located, in 18 of the 25 Brugada patients in whom typical coved- or saddleback-type ST elevation was seen in leads V1 and V2. The maximum was located on the second intercostal space in the remaining seven Brugada patients in whom only a mild saddleback-type ST elevation was seen in leads V1 and V2 of the 12-lead ECG. Typical ST segment elevation was recognized in leads V1 and V2, which were recorded on the second or third intercostal space. ST elevation in Brugada patients was dramatically normalized by isoproterenol, a beta-adrenergic agonist (maxST20 = 0.17 +/- 0.08 mV; P < 0.0005 vs control conditions), and accentuated by disopyramide, an Na+ channel blocker (maxST20 = 0.50 +/- 0.15 mV; P < 0.0005 vs control conditions), without any change in the location of the maxST20. CONCLUSION: Our data indicate that recordings of leads V1-V3 of the 12-lead ECG on the parasternal second or third intercostal space would be helpful in diagnosing suspected patients with Brugada syndrome. The data suggest that Na+ channel blockers are capable of accentuating ST elevation in leads V1-V3.

Action Potentials↗
PubMed1999

Distinct domains of mouse dishevelled are responsible for the c-Jun N-terminal kinase/stress-activated protein kinase activation and the axis formation in vertebrates.

Recent studies have shown that Drosophila Dishevelled (Dsh), an essential component of the wingless signal transduction, is also involved in planar polarity signaling through the c-Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) pathway in Drosophila. Here, we show that expression of a mouse homolog of Dsh (mDvl-1) in NIH3T3 cells activates JNK/SAPK, and its activator MKK7. A C-terminal half of mDvl-1 which contains the DEP domain was sufficient for the activation of JNK/SAPK, whereas an N-terminal half of mDvl-1 as well as the DEP domain is required for stimulation of the TCF/LEF-1-dependent transcriptional activation, a beta-catenin-dependent process. A single amino acid substitution (Met for Lys) within the DEP domain (mDvl-1 (KM)) abolished the JNK/SAPK-activating activity of mDvl-1, but did not affect the activity to activate the LEF-1-dependent transcription. Ectopic expression of mDvl-1 (KM) or an N-terminal half of mDvl-1, but not the C-terminal, was able to induce secondary axis in Xenopus embryos. Because the secondary axis formation is dependent on the Wnt/beta-catenin signaling pathway, these results suggest that distinct domains of mDvl-1 are responsible for the two downstream signaling pathways, the beta-catenin pathway and the JNK/SAPK pathway in vertebrates.

3T3 Cells↗
PubMed1999

Activation of the protein kinase ERK5/BMK1 by receptor tyrosine kinases. Identification and characterization of a signaling pathway to the nucleus.

ERK5 (also known as BMK1), a member of the mitogen-activated protein kinase (MAPK) superfamily, was known to be activated strongly by oxidant and osmotic stresses. Here we have found that ERK5 is strongly activated by epidermal growth factor and nerve growth factor, whose receptors are tyrosine kinases. The activation of ERK5 was inhibited by expression of dominant-negative Ras and induced by expression of active Ras in PC12 cells, indicating a requirement for Ras in ERK5 activation. The epidermal growth factor-induced activation of ERK5 was found to be inhibited by PD98059 and U0126 inhibitors, which were previously thought to act specifically on classical MAPK kinase (also known as MEK1) and readily reversed by CL100 and MKP-3 dual-specificity phosphatases for which classical MAPKs were previously shown to serve as preferred substrates. The reporter assays demonstrated that the serum-induced enhancement of transcription from serum response element was significantly inhibited by expression of a dominant-negative form of MEK5, which was a direct and specific activator for ERK5 and that transcription from serum response element mediated by the Ets-domain transcription factor Sap1a, but not by Elk1, was stimulated by coexpression of ERK5 and active MEK5. In addition, Sap1a was shown to be phosphorylated by ERK5 in vitro and by the activation of the ERK5 pathway in cells. Moreover, the serum-induced c-Fos expression was markedly inhibited by expression of dominant-negative MEK5. These results reveal a novel signaling pathway to the nucleus mediated by ERK5 that functions downstream of receptor tyrosine kinases to induce immediate early genes, in parallel with the classical MAPK cascade.

Amino Acid Sequence↗