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T Noda

Publications and source records attributed to T Noda.

At least 199 records · Page 11Linked to original sources
PubMed1997

[Transurethral microwave thermotherapy for benign prostatic hyperplasia].

BACKGROUND: We studied the clinical efficacy of transurethral microwave thermotherapy (TUMT) using Endotherm UMW system (OLYMPUS). METHODS: TUMT was performed in 28 patients with benign prostatic hyperplasia (BPH). Three patients of them were catheterized because of urinary retention. The treatment was performed in a single session for an hour. The urethral surface temperature was set at 39 degrees C, and the coolant flow of the urethral applicator (21 Fr balloon catheter) was set at 30 ml/min, to heat up the broad area of the prostate up to 45 degrees C. The clinical efficacy was evaluated by analyzing subjective responses, using the International Prostate Symptom Score (I-PSS) scale (S) and QOL score (L), and objective responses, using peak urinary flow rate (Qmax), average flow rate (Qave), residual urine volume and prostate volume following the treatment. RESULTS: At 24 weeks after the treatment, significant improvement were observed in S score (41%), L score (37%), Qmax (53%) and Qave (62%). Although there was no significant decrease in residual urine and prostate volume. The three patients, with a catheter indwelled because of urinary retention, were all free of the catheter within 4 weeks after the treatment. During and after the treatment, no severe adverse effects, including transient urinary retention needed for indwelling a catheter, was detected. CONCLUSION: A single session of TUMT by Endotherm UMW considered to be safe and useful for symptomatic BPH patients, even who are not indicated for transurethral resection of the prostate (TUR-P) because of underlying disorders.

Aged↗
PubMed1997

Serial histopathologic myocardial findings in a patient with ectopic atrial tachycardia-induced cardiomyopathy.

A 17-year-old woman was found to have ectopic atrial tachycardia by her physician. Echocardiography and cardiac catheterization revealed findings resembling dilated cardiomyopathy at the time of initial presentation. The tachycardia was controlled with atenolol only at a dose of 50 mg/day. However, at the age of 22, the presence of ectopic atrial tachycardia was once again confirmed. We successfully performed catheter ablation for persistent ectopic atrial tachycardia. Serial echocardiographic findings showed the left ventricular dimension and function appeared to return to normal 1 year postablation. However, despite pharmacologic control and catheter ablation therapy, histopathology revealed myocardial fibrosis presumably representing permanent damage of the heart secondary to tachycardia 1 year postablation.

Adolescent↗
PubMed1997

[Modification of gene targeting method for functional analysis of the target gene in vivo].

Gene targeting in ES cells is a powerful tool to generate mice bearing predesigned mutations in the germ line. However, these mice carrying such constitutional mutations are often lethal and, therefore, we cannot study other functional aspects of the gene at later stages or in particular tissues. To inactivate the target gene in particular tissues or at particular stages of development, conditional gene inactivation based on the Cre-loxP recombination system of bacteriophage P1 is considered one of the applicable techniques. To express the Cre gene in a cell-type or developmental stage specific manner, either transgenic or adenoviral technology is most considerable technique in vivo.

Animals↗
PubMed1997

Effects of Albunex infusion on left ventricular inflow velocity in dogs.

This study examined the effects of Albunex (sonicated 5% human serum albumin) infusion on left ventricular inflow velocity by Doppler echocardiography. Left ventricular pressure and left ventricular inflow velocity were recorded simultaneously under eight different conditions in dogs: 1) baseline 1 (control), 2) Albunex 0.2 ml/kg, 3) baseline 2, 4) Albunex 0.5 ml/kg, infusion of dextran 100 ml, 5) baseline 3, 6) Albunex 0.2 ml/kg, 7) baseline 4, and 8) Albunex 0.5 ml/kg. In the normal state (no dextran), Albunex (0.2 ml/kg) caused no hemodynamic changes or inflow velocity changes. In contrast, infusion of Albunex (0.5 ml/kg) caused time velocity integrals of early filling to increase from the baseline (5.51 +/- 1.13 vs 7.19 +/- 1.14 cm, p < 0.05). After dextran infusion (100 ml), Albunex (0.2 ml/kg) caused peak early filling velocity to increase (62.4 +/- 6.9 vs 67.3 +/- 9.4 cm/sec, p < 0.05), and infusion of Albunex (0.5 ml/kg) also caused peak early filling velocity to increase from baseline (64.6 +/- 8.5 vs 73.7 +/- 14.5 cm/sec, p < 0.05). Infusion of Albunex (0.5 ml/kg) after dextran infusion caused increases in left ventricular pressure at the mitral valve opening (12.7 +/- 3.1 vs 15.2 +/- 3.3 mmHg, p < 0.05) and in left atrial driving force (13.5 +/- 3.6 vs 16.7 +/- 5.9 mmHg, p < 0.05). Clinicians should be cautious about using Albunex at doses of greater than 0.2 ml/kg when evaluating the pressure gradient of the left ventricle in patients with elevated left ventricular diastolic pressure. In patients with normal hemodynamics, Albunex infusion at doses of less than 0.2 ml/kg apparently did not affect the velocity measurement.

Albumins↗
PubMed1997

Assessment of left atrial operative mean stiffness using simultaneous recordings of left ventricular pressure and M-mode echocardiography of the left atrium and mitral valve.

Left atrial (LA) operative mean stiffness was measured using simultaneous recordings of the left ventricular (LV) pressure and M-mode echocardiography of the LA and mitral valve. The LA operative passive mean stiffness value was obtained during LV systole using LV pressure at the mitral valve opening and the pre-atrial contraction where the LV and LA pressure curves cross each other. Before the LA stiffness measurement, the LA volume calculated by biplane left atriography was compared with the dimension of the LA M-mode echocardiogram at three points (maximum volume, pre-atrial contraction and minimum volume) in another 23 patients (5 normal subjects, 4 patients with angina pectoris, 14 patients with myocardial infarction), and the regression equation was obtained by power fitting (y = ax3+ b). Using this equation, the LA volumes were calculated and used for the measurement of LA operative mean stiffness. Eleven normal subjects (C group), 14 patients with myocardial infarction (ejection fraction: EF > or = 55%; NF group), and 12 patients with myocardial infarction (EF < 55%; F group) were studied. The measured operative mean stiffness values based on the LA dimension and LV pressure [K(D)] were 0.69 +/- 0.40, 1.0 +/- 0.37, and 2.0 +/- 0.61 mmHg/mm, respectively (p < 0.01 in C vs F). The mean stiffness values calculated with LA volume [K(V)] were 0.48 +/- 0.23, 0.42 +/- 0.19, and 0.66 +/- 0.25 mmHg/ml, respectively (p < 0.05 in NF vs F). In F group, both the K(D) and K(V) values were high. The K(D) value can thus be used clinically as an easily obtained index of the LA operative mean stiffness. The high LA operative mean stiffness in F group appeared to be related to the increased LA pressure at the mitral valve opening. This method of measurement of the LA operative mean stiffness can be easily applied and used as a routine measurement providing additional information regarding left ventricular function.

Aged↗
PubMed1996

Marked expression of plasma brain natriuretic peptide is a special feature of hypertrophic obstructive cardiomyopathy.

OBJECTIVES: We examined whether plasma brain natriuretic peptide levels are abnormally elevated in hypertrophic obstructive cardiomyopathy compared with other cardiac diseases. BACKGROUND: We previously reported that plasma brain and atrial natriuretic peptide levels were elevated in hypertrophic cardiomyopathy. METHODS: We compared plasma concentrations of brain and atrial natriuretic peptide and hemodynamic and echocardiographic data in 50 patients with hypertrophic obstructive cardiomyopathy (n = 15, mean [+/-SD] intraventricular pressure gradient 37 +/- 16 mm Hg), hypertrophic nonobstructive cardiomyopathy (n = 15), aortic stenosis (n = 10, mean pressure gradient 41 +/- 18 mm Hg) and hypertensive heart disease (n = 10, mean systolic/diastolic blood pressure 203 +/- 16/108 +/- 11 mm Hg, respectively) and 10 normal subjects. RESULTS: Plasma brain natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group (397.1 +/- 167.8 pg/ml*) than in the hypertrophic nonobstructive cardiomyopathy (60.0 +/- 48.1 pg/ml*), hypertensive heart disease (53.9 +/- 31.4 pg/ml*), aortic stenosis (75.4 +/- 54.3 pg/ml*) and normal groups (9.8 +/- 6.4 pg/ml [*p < 0.05 vs. normal group, p < 0.05 vs. hypertrophic obstructive cardiomyopathy group]). Although plasma atrial natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group than the other patient groups, the brain/atrial natriuretic peptide ratio in the hypertrophic obstructive cardiomyopathy group was higher (4.5 +/- 2.3) than those in the other three patient groups (1.1 to 1.4) and the normal group (0.7 +/- 0.5). Left ventricular end-diastolic pressure and left ventricular end-diastolic volume index were similar among the four patient groups. The interventricular septal thickness and the ratio of interventricular septal thickness to left ventricular posterior wall thickness were similar between the hypertrophic obstructive and nonobstructive cardiomyopathy groups. CONCLUSIONS: Abnormal elevations of plasma brain natriuretic peptide levels are difficult to explain on the basis of hemodynamic and echocardiographic data and are a special feature of hypertrophic obstructive cardiomyopathy.

Adult↗
PubMed1996

Cytoplasm-to-vacuole targeting and autophagy employ the same machinery to deliver proteins to the yeast vacuole.

The vacuolar protein aminopeptidase I (API) uses a novel cytoplasm-to-vacuole targeting (Cvt) pathway. Complementation analysis of yeast mutants defective for cytoplasm-to-vacuole protein targeting (cvt) and autophagy (apg) revealed seven overlapping complementation groups between these two sets of mutants. In addition, all 14 apg complementation groups are defective in the delivery of API to the vacuole. Similarly, the majority of nonoverlapping cvt complementation groups appear to be at least partially defective in autophagy. Kinetic analyses of protein delivery rates indicate that autophagic protein uptake is induced by nitrogen starvation, whereas Cvt is a constitutive biosynthetic pathway. However, the machinery governing Cvt is affected by nitrogen starvation as targeting defects resulting from API overexpression can be rescued by induction of autophagy.

Aminopeptidases↗
PubMed1996

G protein-coupled cholecystokinin-B/gastrin receptors are responsible for physiological cell growth of the stomach mucosa in vivo.

Many peptide hormone and neurotransmitter receptors belonging to the seven membrane-spanning G protein-coupled receptor family have been shown to transmit ligand-dependent mitogenic signals in vitro. However, the physiological roles of the mitogenic activity through G protein-coupled receptors in vivo remain to be elucidated. Here we have generated G protein-coupled cholecystokinin (CCK)-B/gastrin receptor deficient-mice by gene targeting. The homozygous mice showed a remarkable atrophy of the gastric mucosa macroscopically, even in the presence of severe hypergastrinemia. The atrophy was due to a decrease in parietal cells and chromogranin A-positive enterochromaffin-like cells expressing the H+,K(+)-ATPase and histidine decarboxylase genes, respectively. Oral administration of a proton pump inhibitor, omeprazole, which induced hypertrophy of the gastric mucosa with hypergastrinemia in wild-type littermates, did not eliminate the gastric atrophy of the homozygotes. These results clearly demonstrated that the G protein-coupled CCK-B/gastrin receptor is essential for the physiological as well as pathological proliferation of gastric mucosal cells in vivo.

Animals↗
PubMed1996

Disorganization of microtubular network in postischemic liver dysfunction: its functional and morphological changes.

Microtubules in the hepatocytes have been implicated to serve as lines of cytoplasmic transport of secretory materials, but are highly labile structures sensitive to pathological conditions in the cytosol. We examined the role of ischemia/reperfusion-induced cytoskeletal alterations in postischemic liver dysfunction. Rabbit livers were subjected to 60-min warm ischemia followed by 1 h or 24 h of reperfusion. Liver function was assessed by directly measuring hepatic clearance of indocyanine green (ICG), an organic anion whose cytoplasmic transport is assumed to depend on intact microtubules, using near-infrared spectroscopy. Structural alterations of microtubules were observed immunohistochemically using tissue sections stained with monoclonal anti-beta-tubulin antibody. ICG removal from hepatocytes into bile canaliculi deteriorated 1 h but reversed 24 h after reperfusion. Immunohistochemistry showed fragmentation of microtubules at the end of liver ischemia. This cytoskeletal alteration was evident 1 h but was not observed 24 h after reperfusion. Treatment with prostaglandin E1 exerted its beneficial effect by preserving ICG clearance and microtubular network. These results demonstrate that liver ischemia and subsequent reperfusion both affect the organization of microtubular network and suggest that structural disruption of microtubules may be a cause of postischemic liver dysfunction.

Actin Cytoskeleton↗
PubMed1996

Generation and characterization of mutant mice lacking ryanodine receptor type 3.

The ryanodine receptor type 3 (RyR-3) functions as a Ca2+-induced Ca2+ release (CICR) channel and is distributed in a wide variety of cell types including skeletal muscle and smooth muscle cells, neurons, and certain non-excitable cells. However, the physiological roles of RyR-3 are totally unclear. To gain an insight into the function of RyR-3 in vivo, we have generated mice lacking RyR-3 by means of the gene targeting technique. The mutant mice thus obtained showed apparently normal growth and reproduction. Although Ca2+-induced Ca2+ release from intracellular Ca2+ stores of the mutant skeletal muscle differed in Ca2+ sensitivity from that of wild-type muscle, excitation-contraction coupling of the mutant muscle seemed to be normal. Moreover, we could not find any significant disturbance in the smooth muscle and lymphocytes from the mutant mice. On the other hand, the mutant mice showed increased locomotor activity, which was about 2-fold greater than that of the control mice. These results indicate that the loss of RyR-3 causes no gross abnormalities and suggest that the lack of RyR-3-mediated Ca2+ signaling results in abnormalities of certain neurons in the central nervous system.

Animals↗
PubMed1996

Ornithine decarboxylase activity in rat intestinal mucosa and liver is stimulated by central administration of 2-deoxy-D-glucose but not of 2,5-anhydro-D-mannitol.

It has been shown that 2-deoxy-D-glucose (2-DG) inhibits glucose utilization and elicits feeding through the lateral hypothalamus. In contrast, 2,5-anhydro-D-mannitol (2,5-AM), blocking glycogenolysis and/or gluconeogenesis, elicits feeding through the ventromedial hypothalamus. The aim of the present study was to determine whether ornithine decarboxylase (ODC) activity in the rat small intestine is stimulated by infusion into the third ventricle of 2-DG or of 2,5-AM. Under anesthesia, a cannula was implanted into the third ventricle one week before the experiment. Each rat was infused with 6, 12, and 24 mumol 2-DG or 2,5-AM into the third ventricle without disturbing the behavior. Ingestive behavior was observed for one h after the infusion. ODC activity in the intestinal mucosa and the liver was measured 2 h after the infusion. Additionally, ODC activity was measured in vagotomized rats. Both test solutions elicit feeding at 24 mumol/rat. Infusion of 2-DG into the cerebroventricle significantly increased ODC activity in the duodenal and jejunal mucosa and the liver. In contrast to 2-DG, infusion of 2,5-AM did not increase ODC activity in the intestinal mucosa or liver. Truncal vagotomy attenuated the increase of ODC activity in the intestinal mucosa and liver induced by 2-DG. The present study showed that 2-DG, but not 2,5-AM, increased ODC activity in the peripheral organs, indicating that glucose-metabolism at specific sites of the central nervous system, including the lateral hypothalamus, is important for stimulatory signals to ODC activity. It is also indicated that the stimulatory signals from the central nervous system are mediated, at least in part, via the efferent vagal nerve.

Animals↗
PubMed1996

Loss of cerebellar Purkinje cells in aged mice homozygous for a disrupted PrP gene.

Prion protein (PrP) is a glycoprotein constitutively expressed on the neuronal cell surface. A protease-resistant isoform of prion protein is implicated in the pathogenesis of a series of transmissible spongiform encephalopathies. We have developed a line of mice homozygous for a disrupted PrP gene in which the whole PrP-coding sequence is replaced by a drug-resistant gene. In keeping with previous results, we find that homozygous loss of the PrP gene has no deleterious effect on the development of these mice and renders them resistant to prion. The PrP-null mice grew normally after birth, but at about 70 weeks of age all began to show progressive symptoms of ataxia. Impaired motor coordination in these ataxic mice was evident in a rotorod test. Pathological examination revealed an extensive loss of Purkinje cells in the vast majority of cerebellar folia, suggesting that PrP plays a role in the long-term survival of Purkinje neurons.

Animals↗
PubMed1996

Ataxia and epileptic seizures in mice lacking type 1 inositol 1,4,5-trisphosphate receptor.

The inositol 1,4,5-trisphosphate (InsP3) receptor acts as an InsP3-gated Ca2+ release channel in a variety of cell types. Type 1 InsP3 receptor (IP3R1) is the major neuronal member of the IP3R family in the central nervous system, predominantly enriched in cerebellar Purkinje cells but also concentrated in neurons in the hippocampal CA1 region, caudate-putamen, and cerebral cortex. Here we report that most IP3R1-deficient mice generated by gene targeting die in utero, and born animals have severe ataxia and tonic or tonic-clonic seizures and die by the weaning period. An electroencephalogram showed that they suffer from epilepsy, indicating that IP3R1 is essential for proper brain function. However, observation by light microscope of the haematoxylin-eosin staining of the brain and peripheral tissues of IP3R1-deficient mice showed no abnormality, and the unique electrophysiological properties of the cerebellar Purkinje cells of IP3R1-deficient mice were not severely impaired.

Animals↗
PubMed1996

Effects of heart rate on flow velocity of the left atrial appendage in patients with nonvalvular atrial fibrillation.

BACKGROUND AND HYPOTHESIS: Flow velocity of the left atrial appendage (LAA) is thought to be important in thrombus formation in association with blood stasis and the development of spontaneous echo contrast. The effects of heart rate on peak flow velocity of LAA have not been studied in patients with nonvalvular atrial fibrillation. METHODS: Using transesophageal Doppler echocardiography, peak flow velocity of the LAA was measured at the junction between the left atrium and the LAA during left ventricular (LV) systole and diastole in 21 patients with nonvalvular atrial fibrillation. In six cases, the average peak flow velocity of the LAA for 10 consecutive beats with moderately long R-R intervals (LI beats) was compared with those of 3-5 consecutive beats with extremely short R-R intervals (SI beats). RESULTS: Average peak flow velocity of the LAA during LV diastole was significantly higher than that during LV systole (26.5 +/- 15.7 vs. 19.3 +/- 10.4 cm/s, p < 0.01). In SI beats, average peak flow velocity of the LAA was significantly lower than that in LI beats (17.1 +/- 12.1 vs. 21.2 +/- 12.9 cm/s, p < 0.01). CONCLUSION: An increased heart rate reduced the peak flow velocity of the LAA in patients with nonvalvular atrial fibrillation, which would promote blood stasis in the LAA.

Adult↗
PubMed1996

Atrial reservoir and active transport function after cardioversion of chronic atrial fibrillation.

Atrial reservoir function has not been studied after successful cardioversion of chronic atrial fibrillation. Using transthoracic and transesophageal Doppler echocardiography, we measured flow velocity-time integrals of the systolic forward (Sa), diastolic forward (Da), and diastolic reversed (rAa) waves of flow velocity waveforms in the pulmonary vein and the superior vena cava, and those of the early diastolic (Ea) and late diastolic (Aa) waves of the transmitral and transtricuspid flow velocity waveforms. The left and right atrial storage fractions (LASF, RASF), indexes of atrial reservoir function, were determined as the ratios of the atrial storage volume to the ventricular stroke volume; (Sa - rAa)/(Sa - rAa + Da). The left and right atrial active contraction fractions (LAACF, RAACF), indexes of atrial active transport function, were also determined as the ratios of the atrial active contraction volume to the left ventricular stroke volume; Aa/(Ea + Aa). These indices were evaluated periodically in 12 patients with non-valvular chronic atrial fibrillation before and 1-4 days after direct current cardioversion of atrial fibrillation; in 8 of the patients, the indices were also evaluated 1-3 months after the cardioversion. An additional 10 patients in sinus rhythm served as controls. Both the LASF and RASF were low during atrial fibrillation; the values increased significantly 14 days after successful cardioversion (P < 0.01 P < 0.01), and continued to increase at 1-3 months. The LASF and RASF values 1-3 months after cardioversion were comparable to those in control subjects. Both the LAACF and RAACF also increased significantly from 1-4 days to 1-3 months after cardioversion (P < 0.05, P < 0.01), becoming comparable to those in control subjects. During the 3 months after successful cardioversion of non-valvular chronic atrial fibrillation, left and right atrial reservoir function and left and right atrial active transport function increased progressively, becoming comparable to values in the control subjects.

Aged↗
PubMed1996

The role of Ca2+ release from sarcoplasmic reticulum in the regulation of sinoatrial node automaticity.

The role of Ca2+ release channels in the sarcoplasmic reticulum in modulating physiological automaticity of the sinoatrial (SA) node was studied by recording transmembrane action potentials and membrane ionic currents in small preparations of the rabbit SA node. Ryanodine, which modifies the conductance and gating behavior of the Ca2+ release channels, was used to block Ca2+ release from the sarcoplasmic reticulum. Superfusion of 1-mM ryanodine decreased the spontaneous firing frequency as well as the maximal rate of depolarization of the SA, and these reductions reached a steady state within approximately 5 min. The action potential recordings revealed that the latter part of diastolic depolarization was depressed and that the take-off potential became less negative. This suggested that the negative chronotropic effect of ryanodine resulted from the blockade of physiological Ca2+ release from the sarcoplasmic reticulum. In voltage clamp experiments, using double-microelectrode techniques, ryanodine did not markedly reduce the Ca2+ current (ICa) but decreased the delayed rectifying K+ current (IK), the steady-state inward current (Iss), and the hyperpolarization-activated inward current (Ih). These observations suggest that, even when the function of C2+ channels in the cell membrane is normally maintained, depression of Ca2+ release channels in the sarcoplasmic reticulum would prevent sufficient elevation of the Ca2+ concentration in SA node cells for the activation of various ionic currents, and, thus adversely affect the physiological automaticity of this primary cardiac pacemaker.

Action Potentials↗
PubMed1996

Changes in splenic volume after partial splenic embolization in children.

AIM: The authors studied changes in splenic volume after partial splenic embolization (PSE) in children who had thrombocytopenia caused by splenomegaly. MATERIALS AND METHODS: Five children with hypersplenism (ages of 1, 6, 7, 10, and 14 years) underwent PSE. The follow-up period ranged from 1 month to 8 years 9 months. Whole and infarcted splenic volumes were measured from computed tomography images obtained before and after PSE. RESULTS: Within 2 weeks after PSE, the whole splenic volume increased to 110% to 140% of the pre-PSE volume. The infarcted area disappeared 3 to 4 months after PSE, and the whole splenic volume decreased markedly. The decreased volume tended to be stable during the follow-up period. The splenic enlargement before PSE ranged from 7.2 to 14.2 times the standard splenic volume for a corresponding body weight. The splenic volume did not become normal after PSE; it remained between 2 and 7 times larger than standard. Platelet counts stayed above 10 x 10(4) /mm3 when the splenic volume reduced to 2 times the standard volume. CONCLUSION: The first 4 weeks after PSE is the most dangerous period for the development of splenic capsule. The infarcted parenchyma is absorbed 3 to 4 months after PSE, and the whole splenic volume is reduced. Thereafter, the splenic volume is stable for several years. Reembolization is not likely to be necessary in the majority of patients who have had splenic embolization with an infarction rate of > or = 80%.

Adolescent↗