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Biomedical subjects

Noriko Inoue

Publications and source records attributed to Noriko Inoue.

At least 19 recordsLinked to original sources
PubMed2007

Reverse perfusion-metabolism mismatch predicts good prognosis in patients undergoing cardiac resynchronization therapy: a pilot study.

BACKGROUND: Cardiac resynchronization therapy (CRT) improves glucose metabolism in the septum of patients with heart failure, so in the present study the predictive value of combined fluorodeoxyglucose (FDG)-positron emission tomography (PET) and metoxy-isobutyl isonitrile (MIBI)-single photon emission computed tomography (SPECT) for the prognosis of patients undergoing CRT was investigated. METHODS AND RESULTS: Fourteen patients (70.3+/-8.2 years) who underwent FDG-PET and MIBI-SPECT before implantation of a biventricular pacemaker were enrolled. The total number of matches, mismatches, reverse mismatches, summed difference score (SDS: sum total of FDG - MIBI scores) and SDS per segment (%SDS) in each of 5 areas of myocardium (septum, anterior, lateral, inferior area, apex) was calculated and compared between the survival groups (all survival: survival group; survival without ischemic heart disease (IHD): non-IHD survival group) and non-survival group. Both the number of reverse mismatch segments and the %SDS in the septum in the non-IHD survival group were significantly greater than in the non-survival group (3.2+/-1.6 vs 0.5+/-0.6, p<0.05; 0.62+/-0.61 vs -0.11+/-0.19, p<0.05). The receiver-operating characteristics curves for prognosis showed that the area under the curve for the number of reverse mismatch segments in the septum (0.93; confidence interval 0.61-0.98) was significantly greater. CONCLUSION: A reverse mismatch pattern in the septum can predict a good prognosis for patients treated with CRT.

Aged↗
PubMed2006

Nerve growth factor, neural stem cells and Alzheimer's disease.

The protein family of the neurotrophins (NTs) comprises structurally and functionally related molecules such as nerve growth factor (NGF) which influences the proliferation, differentiation, survival and death of neuronal cells. In addition to their established functions for cell survival, NTs also mediate higher brain activities such as learning and memory. Changes in NT expression levels have thus been implicated in neurological diseases such as Alzheimer's disease (AD), an age-related neurodegenerative disorder that is characterized by progressive loss of memory and deterioration of higher cognitive functions. The present review provides an overview of the functional role of NGF in neural stem cells and AD while pointing to a potential application of this peptide for the treatment of AD.

Alzheimer Disease↗
PubMed2006

Aquaporin-5 water channel in lipid rafts of rat parotid glands.

Aquaporin-5 (AQP5), an apical plasma membrane (APM) water channel in salivary glands, lacrimal glands, and airway epithelium, has an important role in fluid secretion. The activation of M3 muscarinic acetylcholine receptors (mAChRs) or alpha1-adrenoceptors on the salivary glands induces salivary fluid secretion. AQP5 localizes in lipid rafts and activation of the M3 mAChRs or alpha1-adrenoceptors induced its translocation together with the lipid rafts to the APM in the interlobular ducts of rat parotid glands. This review focuses on the mechanisms of AQP5 translocation together with lipid rafts to the APM in the interlobular duct cells of parotid glands of normal rats and the impairment of AQP5 translocation in diabetes and senescence.

Adrenergic alpha-1 Receptor Agonists↗
PubMed2006

Positive correlations between cerebral choline and renal dysfunction in chronic renal failure.

INTRODUCTION: Cerebral metabolism in chronic renal failure (CRF) patients has not been fully evaluated. This study examined cerebral metabolites in CRF, using proton magnetic resonance spectroscopy (MRS). METHODS: Subjects comprised 19 CRF patients and 21 healthy volunteers. Spectra were acquired from voxels of interest positioned in the parietal gray and white matter, and concentrations of the following cerebral metabolites were measured: N-acetyl group (NA), creatine + phosphocreatine (Cr), choline-containing compounds (Cho), myo-inositol and glutamate + glutamine. Among the 19 CRF patients, 9 who were started on hemodialysis (HD) underwent careful follow-up. Proton MRS was performed before and about 2 weeks after starting HD. In six patients in whom follow-up was possible, a third MRS was performed after about 18 months. RESULTS: The NA/Cr ratio was not significantly changed in CRF. However, elevations in the Cho/Cr ratio were found in both gray and white matter compared with controls. To the best of our knowledge, this is the first report of positive correlations between the Cho/Cr ratio in both regions and serum osmotic pressure. Compared with baseline data, no significant changes in cerebral metabolite ratios were found about 2 weeks after starting HD. About 18 months after starting HD, however, the elevated Cho/Cr ratio was significantly reduced in the gray matter and tended to be reduced in the white matter. CONCLUSIONS: Cho appear to play an important role in the regulation of cerebral metabolism to compensate for alterations in serum osmotic pressure in CRF, and HD may correct this abnormal cerebral metabolism.

Adult↗
PubMed2006

Correlation between plasma brain natriuretic peptide concentration and lung thallium-201 uptake on exercise thallium perfusion images.

The plasma brain natriuretic peptide (BNP) concentration at rest correlates with left ventricular end-diastolic pressure (LVEDP), left ventricular ejection fraction (LVEF), and pulmonary capillary wedge pressure (PCWP). High lung thallium-201 uptake has been reported to be associated with hemodynamic variables such as LVEDP, LVEF, and PCWP. However, there is no study that has investigated the correlation of plasma BNP concentration with lung thallium-201 uptake. We examined whether the plasma BNP concentration was related to lung thallium-201 uptake. Before exercise, venous blood samples were obtained from 39 patients with old myocardial infarction. We investigated the correlations between plasma BNP concentration and lung thallium-201 uptake, and whether they were related to LVEF, extent of nonviable myocardium, and ischemic myocardium, respectively, with thallium-201 exercise stress testing. The plasma BNP concentration significantly correlated with lung thallium-201 uptake (P < 0.05), nonviable segments (P < 0.01), and LVEF (P < 0.01). Lung thallium-201 uptake correlated with nonviable segments (P < 0.01). Our results suggest that increased secretion of BNP is related to increased lung thallium-201 uptake, and they are related to the extent of nonviable myocardium and decreased left ventricular function. Plasma BNP concentration and lung thalium-201 uptake may reflect the extent of myocardial fibrosis causing myocyte stretch.

Aged↗
PubMed2006

Interactive segmentation of the cerebral lobes with fuzzy inference in 3T MR images.

Measurement of volume and surface area of the frontal, parietal, temporal and occipital lobes from magnetic resonance (MR) images shows promise as a method for use in diagnosis of dementia. This article presents a novel computer-aided system for automatically segmenting the cerebral lobes from 3T human brain MR images. Until now, the anatomical definition of cerebral lobes on the cerebral cortex is somewhat vague for use in automatic delineation of boundary lines, and there is no definition of cerebral lobes in the interior of the cerebrum. Therefore, we have developed a new method for defining cerebral lobes on the cerebral cortex and in the interior of the cerebrum. The proposed method determines the boundaries between the lobes by deforming initial surfaces. The initial surfaces are automatically determined based on user-given landmarks. They are smoothed and deformed so that the deforming boundaries run along the hourglass portion of the three-dimensional shape of the cerebrum with fuzzy rule-based active contour and surface models. The cerebrum is divided into the cerebral lobes according to the boundaries determined using this method. The reproducibility of our system with a given subject was assessed by examining the variability of volume and surface area in three healthy subjects, with measurements performed by three beginners and one expert user. The experimental results show that our system segments the cerebral lobes with high reproducibility.

Algorithms↗
PubMed2006

Evaluation of myocardial glucose metabolism before and after recovery of myocardial function in patients with tachycardia-induced cardiomyopathy.

BACKGROUND: We assessed left ventricular (LV) function and myocardial glucose metabolism by fluoro-18-deoxyglucose (18F-FDG) positron emission tomography (PET) in patients with tachycardia-induced cardiomyopathy (TC). METHODS: The subjects were 42 patients with heart disease, consisting of 7 patients with TC (61.4 +/- 19.0 years, LVEF 34.1%+/- 10.6%) and 35 with ischemic heart disease (IHD) (63.1 +/- 10.8 years, LVEF 49.9%+/- 13.5%). Five volunteers with normal ECG were the control group. All of the patients underwent 18F-FDG PET and echocardiography, and all of the patients with TC underwent 18F-FDG PET and echocardiography before and 6 months after antitachycardia therapy. Six patients underwent radiofrequency catheter ablation (RFCA) and 1 patient was medically treated with antitachycardia therapy. Myocardial glucose metabolism was assessed semiquantitatively by using the % dose uptake of 60 kg of BW (% dose uptake). RESULTS: Mean % dose uptake of the control group was 5.52 +/- 0.54%. After antitachycardia therapy, LVEF significantly improved (34.1 +/- 10.6% vs 54.3 +/- 13.6%, P < 0.01), and % dose uptake also significantly improved (1.26 +/- 0.55% vs 1.49 +/- 0.62%, P < 0.05). Patients with IHD showed higher % dose uptake than those with TC before antitachycardia therapy (3.18 +/- 1.36 vs 1.26 +/- 0.55%, P < 0.01), controls showed higher value of % dose uptake than TC before antitachycardia therapy (5.52 +/- 0.54% vs 1.26 +/- 0.55%, P < 0.01). CONCLUSION: Semiquantitative analysis of 18F-FDG PET showed that antitachycardia therapy improved myocardial glucose metabolism in patients with TC.

Cardiomyopathies↗
PubMed2006

Assessment of atrial regional wall motion using strain Doppler imaging during biatrial pacing in the bradycardia-tachycardia syndrome.

INTRODUCTION: Biatrial pacing is expected to have preventive effects on atrial fibrillation. METHODS: We evaluated atrial regional wall motion by strain Doppler imaging (SDI) in 6 patients (62.5 +/- 11.3 [SD] years), who suffered from atrial fibrillation, with an implanted biatrial pacemaker. SDI was performed and atrial regional wall motion was estimated during biatrial (BiA) and right atrial appendage (RAA) pacing. RESULTS: There was no significant difference in the interval from the pacing spike to the peak strain of the atrium in the lateral right atrium (LRA) between BiA and RAA pacing. However, there was a significant difference in the septal atrium (SA) between BiA and RAA pacing (225.0 +/- 19.9 vs 267.2 +/- 15.7 ms, P < 0.0001) and in the lateral left atrium (LLA) between BiA and RAA pacing (216.7 +/- 21.6 vs 275.0 +/- 16.2 ms, P < 0.0001). There were significant differences in the time difference of peak strain between BiA and RAA pacing in each atrial segment (LRA-AS: 2.2 +/- 5.9 vs 45.0 +/- 11.9 ms, P = 0.0016, SA-LLA: -8.3 +/- 5.5 vs 7.8 +/- 2.7 ms, P < 0.0011, LRA-LLA: -6.1 +/- 3.9 vs 52.8 +/- 13.2 ms, P = 0.0002). There was no significant difference in the interval from the pacing spike to the inflection point of atrial strain (S-I) of LRA. However, there were significant differences in S-I of SA (83.9 +/- 24.1 vs 129.9 +/- 30.6 ms, P = 0.0086) and LLA (102.2 +/- 37.9 vs 166.1 +/- 13.4 ms, P = 0.0028). CONCLUSION: BiA pacing improved the synchronicity of regional wall motion of both atrium.

Adult↗
PubMed2006

Suppression of atrial fibrillation by atrial pacing.

BACKGROUND: Atrial fibrillation (AF) is a common arrhythmia in patients with an implanted pacemaker, but the role of atrial pacing in preventing AF is still unclear. METHODS AND RESULTS: Sixty-six patients (67.8+/-12.1 years) were enrolled: 54 with sick sinus syndrome (SSS), 11 with atrioventricular blocks (AVB), and 1 with SSS and AVB. The prevalence of AF was investigated. In 22 patients with AF, the AF burden was estimated under "back-up pacing" (40-50 beats/min), then under "atrial pacing" (60-85 beats/min). The prevalence of AF in the SSS group tended to be higher than that in the AVB group (48.1% vs 18.2%, p=0.06). The AF burden in patients with a percentage of atrial pacing (% atrial pacing) <50% was significantly greater than that in patients with % atrial pacing >or=50% (12.5+/-21.1% vs 4.2+/-10.3%, p<0.05). AF disappeared immediately after "atrial pacing" in 4 patients (18.2%). In 9 patients (40.9%), the AF burden decreased gradually, and AF disappeared in 6 patients (27.3%) after 207.9+/-130.2 days. CONCLUSION: The prevalence of AF may be higher in patients with SSS than in those with AVB. Atrial pacing has a preventive effect on AF, and the effect of atrial pacing is not always immediate but is progressive in some patients.

Aged↗
PubMed2006

Daily shock impedance measured by implantable cardioverter defibrillator is useful in the management of congestive heart failure.

BACKGROUND: Clinical data suggest that changes in intrathoracic impedance and fluid accumulation in the lung are inversely related. METHODS AND RESULTS: Daily shock impedance (S-IMP) was evaluated in 29 patients in whom a Ventak Prizm 2 was implanted (61+/-14 years old). The mean follow-up period was 45+/-18 weeks, during which 6 patients had episodes of decompensated heart failure (DHF group) and the others did not (NHF group). There was no significant difference between the DHF group and NHF group in the mean value of the S-IMP (46.4 +/-3.3 vs 45.4+/-5.4 Omega). The range of S-IMP in individual patients in the DHF group was significantly greater than that in the NHF group (13.8+/-0.38 vs 7.0+/-3.1 Omega, p<0.0001). Mean weekly change of S-IMP in individual patients in the DHF group was significantly greater than that in the NHF group (1.583+/-0.630 vs 1.092+/-0.361 Omega, p<0.0176). When the cut-off value was set at >1.242 Omega, sensitivity was 100% and specificity was 69.6% for a diagnosis of DHF. There was a significant negative correlation between the percent increases in brain natriuretic peptide (BNP) and S-IMP (correlation coefficient: -0.775 p<0.0001) in the DHF group. There was an inverse relation between BNP and S-IMP. CONCLUSIONS: Measurement of shock impedance may be useful in the management of congestive heart failure.

Aged↗
PubMed2006

[Improvement of central sleep disordered breathing with severe congestive heart failure by biventricular pacing therapy: a case report].

A 74-year-old man with ischemic cardiomyopathy was repeatedly admitted for congestive heart failure. His left ventricular ejection fraction was 21% and diastolic left ventricular dimension was 73.5mm by echocardiography. He was treated with biventricular pacing and heart failure improved from New York Heart Association class III to II. Before the treatment, brain natriuretic peptide was 600.5 pg/ml. Apnea hypopnea index was 23.8 and all events were central type. After biventricular pacing, apnea hypopnea index was improved to 21.9 after 11 days, 14.0 after 33 days, and 4.8 after 48 days. His left ventricular ejection fraction was 36%, diastolic left ventricular dimension was 71.4mm, and brain natriuretic peptide was 383.8 pg/ml. In this patient, central sleep disordered breathing was improved by biventricular pacing therapy after only 48 days.

Aged↗
PubMed2006

NF-kappaB regulates B-cell-derived nerve growth factor expression.

In the mammalian brain, four neurotrophins have been identified: nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4/5 (NT-4/5). NGF exerts an important role in the development and functions of the central and peripheral nervous system. However, it has recently been documented that several types of immune cells, such as mast cells, lymphocytes, basophils and eosinophils, produce, store and release NGF. Accumulating preclinical and clinical data indicate that dysfunctions of NGF and the other neurotrophins may contribute to impaired immune responses and concentration of NGF frequently correlates with disease severity. Thus, the aim of this study was to elucidate the potential signaling mechanisms of cytokine- neurotrophins interactions contributing to increased NGF levels. Our data show that the transcription factor NF-kappaB plays a pivotal role in regulating B-cell-derived NGF expression.

Animals↗
PubMed2005

Identification of AQP5 in lipid rafts and its translocation to apical membranes by activation of M3 mAChRs in interlobular ducts of rat parotid gland.

Aquaporin-5 (AQP5), an apical plasma membrane (APM) water channel in salivary glands, lacrimal glands, and airway epithelium, has an important role in fluid secretion. M(3) muscarinic acetylcholine receptor (mAChR)-induced changes in AQP5 localization in rat parotid glands were investigated with immunofluorescence or immunoelectron microscopy, detergent solubility, and gradient density floatation assays. Confocal microscopy revealed AQP5 localization in intracellular vesicles of interlobular duct cells in rat parotid glands and AQP5 trafficking to the APM 10 min after injection of the mAChR agonist cevimeline. Conversely, 60 min after injection, there was a diffuse pattern of AQP5 staining in the cell cytoplasm. The calcium ionophore A-23187 mimicked the effects of cevimeline. Immunoelectron microscopic studies confirmed that cevimeline induced AQP5 trafficking from intracellular structures to APMs in the interlobular duct cells of rat parotid glands. Lipid raft markers flotillin-2 and GM1 colocalized with AQP5 and moved with AQP5 in response to cevimeline. Under control conditions, the majority of AQP5 localized in the Triton X-100-insoluble fraction and floated to the light-density fraction on discontinuous density gradients. After 10-min incubation of parotid tissue slices with cevimeline or A-23187, AQP5 levels decreased in the Triton X-100-insoluble fraction and increased in the Triton X-100-soluble fraction. Thus AQP5 localizes in the intracellular lipid rafts, and M(3) mAChR activation induces AQP5 trafficking to the APM with lipid rafts via intracellular Ca(2+) signaling and induces AQP5 dissociation from lipid rafts to nonrafts on the APM in the interlobular duct cells of rat parotid glands.

Animals↗
PubMed2005

Sorcin interacts with sarcoplasmic reticulum Ca(2+)-ATPase and modulates excitation-contraction coupling in the heart.

Sorcin is a 21.6-kDa Ca(2+) binding protein of the penta-EF hand family. Several studies have shown that sorcin modulates multiple proteins involved in excitation-contraction (E-C) coupling in the heart, such as the cardiac ryanodine receptor (RyR2), L-type Ca(2+) channel, and Na(+)-Ca(2+) exchanger, while it has also been shown to be phosphorylated by cAMP-dependent protein kinase (PKA). To elucidate the effects of sorcin and its PKA-dependent regulation on E-C coupling in the heart, we identified the PKA-phosphorylation site of sorcin, and found that serine178 was preferentially phosphorylated by PKA and dephosphorylated by protein phosphatase-1. Isoproterenol allowed sorcin to translocate to the sarcoplasmic reticulum (SR). In addition, adenovirus-mediated overexpression of sorcin in adult rat cardiomyocytes significantly increased both the rate of decay of the Ca(2+) transient and the SR Ca(2+) load. An assay of oxalate-facilitated Ca(2+) uptake showed that recombinant sorcin increased Ca(2+) uptake in a dose-dependent manner. These data suggest that sorcin activates the Ca(2+)-uptake function in the SR. In UM-X7. 1 cardiomyopathic hamster hearts, the relative amount of sorcin was significantly increased in the SR fraction, whereas it was significantly decreased in whole-heart homogenates. In failing hearts, PKA-phosphorylated sorcin was markedly increased, as assessed using a back-phosphorylation assay with immunoprecipitated sorcin. Our results suggest that sorcin activates Ca(2+)-ATPase-mediated Ca(2+) uptake and restores SR Ca(2+) content, and may play critical roles in compensatory mechanisms in both Ca(2+) homeostasis and cardiac dysfunction in failing hearts.

Adenoviridae↗
PubMed2005

Long-term follow-up of atrioventricular delay optimization in patients with biventricular pacing.

BACKGROUND: Atrioventricular (AV) delay optimization may be important in patients with biventricular pacing and the optimal AV delay can be predicted using Doppler echocardiography and the formula: optimal AV delay = AV delay-the interval between the end of A wave and complete closure of the mitral valve when the AV delay is set at slightly prolonged AV delay. METHODS AND RESULTS: In the present study the efficacy of this method was evaluated in 5 patients (67.4+/-8.0 (SD) years old) with biventricular pacing. Cardiac output (CO) and diastolic filling time were measured by Doppler echocardiography. When the AV delay was set at the predicted optimal AV delay -25 ms, the predicted optimal AV delay (133+/-66 ms) and predicted optimal AV delay + 25 ms, the respective CO were 4.5+/-0.9, 5.3+/-1.0, 4.8+/-1.0 L/min (p<0.05, ANOVA) and the diastolic filling times were 364 +/-100, 373+/-105, 335+/-84 ms (p<0.05, ANOVA). Congestive heart failure improved from New York Heart Association class 3.6+/-0.5 to 1.4+/-0.5 (p<0.001). CONCLUSIONS: AV delay optimization is important in patients with biventricular pacing and can be easily achieved by the new method.

Aged↗
PubMed2004

Molecular mechanisms and drug development in aquaporin water channel diseases: the translocation of aquaporin-5 from lipid rafts to the apical plasma membranes of parotid glands of normal rats and the impairment of it in diabetic or aged rats.

Salivary secretion from rat salivary glands occurs in response to stimulation by acetylcholine and norepinephrine released from nerve endings. Aquaporin-5 (AQP5) localizes in lipid rafts under control conditions and is induced to traffic to the apical plasma membrane in interlobular ducts of rat parotid glands by the activation of M3 muscarinic acetylcholine receptors or alpha1-adrenoceptors. This review will focus on the mechanisms of the translocation of AQP5 from lipid rafts to the apical plasma membrane in the interlobular duct cells of parotid glands of normal rats and the impairment of its translocation in diabetic or senescent rats.

Aging↗
PubMed2004

Rapid electrical stimulation of contraction modulates gap junction protein in neonatal rat cultured cardiomyocytes: involvement of mitogen-activated protein kinases and effects of angiotensin II-receptor antagonist.

OBJECTIVES: The aim of this study was to investigate the effects of rapid electrical stimulation (RES) of contraction on the expression of connexin (Cx)43 gap junction in neonatal rat cultured ventricular myocytes and the consequent changes of conduction properties. BACKGROUND: The expression and distribution of gap junctions in cardiac muscle can be changed readily under a variety of pathological conditions because of dynamic turnover of Cxs. The effects of RES of contraction on gap junction remodeling are not well understood. METHODS: Neonatal rat ventricular myocytes cultured for five days were subjected to RES (field stimulation) at 3.0 Hz for up to 120 min. RESULTS: Rapid electrical stimulation resulted in a significant upregulation of Cx43 (by approximately 1.5-fold in protein and by approximately 1.9-fold in messenger ribonucleic acid at 60 min). Immunoreactive signal of Cx43 was also increased. Angiotensin II (AngII) content was increased significantly by RES >15 min. Phosphorylated forms of extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinases, and p38 mitogen-activated protein kinases (MAPKs) were all increased dramatically by RES with peaks at 5 - 60 min. Propagation of excitation was visualized by extracellular potential mapping by using a multiple electrode array system. Conduction velocity was increased significantly by RES for 60 to 90 min (25% - 27% increase). Treatment of myocytes with losartan (100 nmol/l) prevented most of these effects of RES; RES-induced upregulation of Cx43 was also prevented by specific inhibitors for ERK and p38 MAPKs. CONCLUSIONS: A short-term RES causes upregulation of Cx43 in cardiomyocytes and a concomitant increase of conduction velocity, mainly through an autocrine action of AngII to activate ERK and p38 MAPKs.

Angiotensin Receptor Antagonists↗