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Biomedical subjects

M Murayama

Publications and source records attributed to M Murayama.

At least 73 records · Page 4Linked to original sources
PubMed1999

Assessment of usefulness of endobronchial ultrasonography in determination of depth of tracheobronchial tumor invasion.

STUDY OBJECTIVE: We assessed the usefulness of endobronchial ultrasonography in the determination of the depth of tumor invasion of the tracheobronchial wall. METHODS: We performed a needle-puncture experiment on normal tissue of 45 specimens to determine the laminar structure of the tracheobronchial wall. In addition, we compared the ultrasonographic determinations of tumor invasion from 24 lung cancer cases with the histopathologic findings. RESULTS: The cartilaginous portions of the extrapulmonary bronchi and the intrapulmonary bronchi exhibited a five-layer structure. Starting on the luminal side, the first layer (hyperechoic) was a marginal echo, the second layer (hypoechoic) was the submucosal tissue, the third layer (hyperechoic) was the marginal echo on the inner side of the bronchial cartilage, the fourth layer (hypoechoic) was bronchial cartilage, and the fifth layer (hyperechoic) was the marginal echo on the outer side of the cartilage. In the membranous portions, the first layer (hyperechoic) was a marginal echo, the second layer (hypoechoic) was smooth muscle, and the third layer (hyperechoic) corresponded to the adventitia. Comparisons between the ultrasonograms and the histopathologic findings in 24 lung cancer cases revealed that depth diagnosis was the same in 23 lesions (95.8%) and was different in 1 lesion (4.2%). In the single case in which the findings were different, lymphocytic infiltration that protruded between the cartilage rings was mistakenly interpreted as tumor infiltration. CONCLUSIONS: This method allows visualization of the laminar structure of the tracheobronchial wall, which is impossible with other diagnostic imaging methods.

Bronchi↗
PubMed1999

Dynamic changes of QT dispersion as a predictor of myocardial ischemia on exercise testing in patients with angina pectoris.

The difference between the maximum and minimum QT intervals on the standard 12-lead ECG (QT dispersion) may be a significant predictor of serious arrhythmias. Dynamic changes in QTd were determined during exercise-induced ischemia in 15 patients with effort angina (> or = 75% coronary stenosis) and 10 normal individuals. Treadmill exercise testing was performed according to Bruce's protocol and the rate-corrected QT dispersion (QTcd) was calculated using Bazett's formula. The resting QTcd before exercise was similar in the angina patients and the controls. After the first stage of exercise, QTcd was significantly increased in the angina patients (p = 0.035), while it remained near baseline in the controls. Five minutes after completing exercise, QTcd was significantly greater in the angina patients than in the controls (p = 0.011). Furthermore, QTcd values after the first stage of exercise were significantly correlated with the maximum ST depression observed on completing exercise in the angina patients (r = 0.714, p = 0.0028). Because QTd may represent the heterogeneity of ventricular repolarization, its significant exercise-induced increase in the angina patients suggests that myocardial ischemia caused repolarization disorders. The significant correlation between QTcd values after the first stage of exercise (before significant ST depression) and the maximum ST depression on completing exercise suggests that an increase in QTcd preceding ischemic ST depression may predict myocardial ischemia. In addition, even daily activities not causing significant ST changes may increase QTcd and the risk of serious arrhythmia in angina patients.

Aged↗
PubMed1999

Specialty-related disparities of readmission in patients with chronic heart failure: the importance of hospital-clinic cooperation.

OBJECT: The purpose of this study was to elucidate differences in readmission rates and late outcome in outpatients with chronic heart failure treated in different clinical settings. PATIENTS AND METHODS: This study included 65 consecutive patients who were admitted to our CCU due to acute heart failure for the first time and discharged from our institution. After their discharge, 31 were cared for by a cardiologist in the outpatient clinic of our institution (group A) and the other 34 were cared for by a general practitioner in a clinic (group B). The various findings during the acute phase and the follow-up period were retrospectively compared between the two groups. In addition, the incidence of unexpected readmission and prolonged outcomes were compared between the two groups. RESULTS: The patients in group B were older than those in group A, but no other differences were noted in patient characteristics. More patients in group A required more than one hospitalization within 6 months from discharge (group A, 35.5%; group B, 8.9%, p<0.01; follow-up period, 17.1+/-5.9 months). There was no difference in the survival rate between the groups. CONCLUSION: We concluded that stabilized outpatients should receive comprehensive care from a general practitioner to avoid the need for readmission after discharge.

Aged↗
PubMed1999

[Endobronchial ultrasonography for lung cancer].

We assessed the usefulness of endobronchial ultrasonography in the diagnosis of lung cancer. We performed a needle-puncture experiment on 45 normal tissue specimens to determine the luminar structure of the tracheobronchial wall. In addition, we compared the ultrasonographic determination of tumor invasion in 24 lung cancer patients with the histopathological findings. The cartilaginous portions of the extrapulmonary bronchi and the intrapulmonary bronchi exhibited a five-layered structure. Starting on the lumen side, the first layer (hyperechoic) was a marginal echo, the second (hypoechoic) was the submucosal tissue, the third (hyperechoic) was the marginal echo on the inner side of the bronchial cartilage, the fourth (hypoechoic) was bronchial cartilage, and the fifth (hyperechoic) was the marginal echo on the outer side of the cartilage. In the membranous portions, the first layer (hyperechoic) was a marginal echo, the second (hypoechoic) was smooth muscle, and the third (hyperechoic) corresponded to the adventitia. Comparisons between the ultrasonograms and the histopathological findings in 24 lung cancer patients revealed that depth diagnosis was the same in 23 lesions (95.8%) and different in 1 lesion (4.2%). We describe the usefulness of endobronchial ultrasonography in the diagnosis of peribronchial lymph nodes and peripheral pulmonary lesions.

Bronchoscopy↗
PubMed1998

Direct association of presenilin-1 with beta-catenin.

Families bearing mutations in the presenilin-1 (PSI) gene develop Alzheimer's disease (AD). However, the mechanism through which PS1 causes AD is unclear. The co-immunoprecipitation with PS1 in transfected COS-7 cells indicates that PSI directly interacts with endogenous beta-catenin, and the interaction requires residues 322450 of PSI and 445-676 of beta-catenin. Both proteins are co-localized in the endoplasmic reticulum. Over-expression of PS1 reduces the level of cytoplasmic beta-catenin, and inhibits beta-catenin-T cell factor-regulated transcription. These results indicate that PSI plays a role as inhibitor of the beta-catenin signal, which may be connected with the AD dysfunction.

Alzheimer Disease↗
PubMed1998

Presenilin 1 associates with glycogen synthase kinase-3beta and its substrate tau.

Families bearing mutations in the presenilin 1 (PS1) gene develop Alzheimer's disease. Previous studies have shown that the Alzheimer-associated mutations in PS1 increase production of amyloid beta protein (Abeta1-42). We now show that PS1 also regulates phosphorylation of the microtubule-associated protein tau. PS1 directly binds tau and a tau kinase, glycogen synthase kinase 3beta (GSK-3beta). Deletion studies show that both tau and GSK-3beta bind to the same region of PS1, residues 250-298, whereas the binding domain on tau is the microtubule-binding repeat region. The ability of PS1 to bring tau and GSK-3beta into close proximity suggests that PS1 may regulate the interaction of tau with GSK-3beta. Mutations in PS1 that cause Alzheimer's disease increase the ability of PS1 to bind GSK-3beta and, correspondingly, increase its tau-directed kinase activity. We propose that the increased association of GSK-3beta with mutant PS1 leads to increased phosphorylation of tau.

Adult↗
PubMed1998

Characterization of tau phosphorylation in glycogen synthase kinase-3beta and cyclin dependent kinase-5 activator (p23) transfected cells.

One of the histopathological markers in Alzheimer's disease is the accumulation of hyperphosphorylated tau in neurons called neurofibrillary tangles (NFT) composing paired helical filaments (PHF). Combined tau protein kinase II (TPK II), which consists of CDK5 and its activator (p23), and glycogen synthase kinase-3beta (GSK-3beta) phosphorylate tau to the PHF-form in vitro. To investigate tau phosphorylation by these kinases in intact cells, the phosphorylation sites were examined in detail using well-characterized phosphorylation-dependent anti-tau antibodies after overexpressing the kinases in COS-7 cells with a human tau isoform. The overexpression of tau in COS-7 cells showed extensive phosphorylation at Ser-202 and Ser-404. The p23 overexpression induced a mobility shift of tau, but most of the phosphorylation sites overlapped the endogenous phosphorylation sites. GSK-3beta transfection showed the phosphorylation at Ser-199, Thr-231, Ser-396, and Ser-413. Triplicated transfection resulted in phosphorylation of tau at 8 observed sites (Ser-199, Ser-202, Thr-205, Thr-231, Ser-235, Ser-396, Ser-404, and Ser-413).

Animals↗
PubMed1998

Accumulation, Metabolism, and Depuration of Organotin Compounds in the Marine Mussels Mytilus graynus and Mytilus edulis under Natural Conditions.

The accumulation, transformation, and depuration of tri-n-butyltin (TBT) were studied over periods of approximately 60-70 days using marine mussels, Mytilus graynus and Mytilus edulis, under natural conditions. M. graynus collected at a lightly polluted site were transplanted to a highly polluted site and M. edulis collected at a highly polluted site were transplanted to a lightly polluted site. TBT taken up in M. graynus showed a bioconcentration factor of 10 500 in the accumulation phase. Di-n-butyl(3-oxobutyl)tin, which is a main metabolite of TBT in M. edulis, showed a longer half-life (8.13 days) than that of the parent compound (4.82 days) in the depuration phase. On the other hand, another metabolite, di-n-butyl(3-hydroxybutyl)tin, showed a shorter half-life (3.98 days) than that of the parent compound. The different half-lives among TBT and its metabolites are responsible for the different metabolic patterns in blue mussels at each sampling time.

Journal Article↗
PubMed1998

Activation of tau protein kinase I/glycogen synthase kinase-3beta by amyloid beta peptide (25-35) enhances phosphorylation of tau in hippocampal neurons.

According to the amyloid hypothesis for the pathogenesis of Alzheimer's disease (AD), amyloid beta peptide (Abeta) directly affects neurons, leading to neurodegeneration and tau phosphorylation, followed by the production of paired helical filaments (PHF) in neurofibrillary tangles (NFT). To analyze the relationship between the phosphorylation sites of tau and the activation of kinases in response to Abeta, we treated cultured rat hippocampal neurons with a peptide fragment of Abeta, Abeta(25-35). Abeta(25-35) treatment activated tau protein kinase I/glycogen synthase kinase-3beta (TPKI/GSK-3beta) but not glycogen synthase kinase-3alpha (GSK-3alpha) or mitogen activated protein kinase (MAP kinase) in primary culture of hippocampal neurons. Using antibodies that recognize phosphorylated sites of tau, we showed that tau phosphorylation was enhanced in at least five sites (Ser199, Ser202, Ser396, Ser404, and Ser413 numbered according to the human tau isoform containing 441 amino acid residues), to an extent that depended on the level of TPK I/GSK-3beta. Treatment with TPK I/GSK-3beta antisense oligonucleotide inhibited the enhancement of tau phosphorylation induced by Abeta(25-35) exposure. Thus, TPK I/GSK-3beta activation by Abeta(25-35) may lead to extensive tau phosphorylation.

Amyloid beta-Peptides↗
PubMed1998

Plasma from patients with cirrhosis increases tissue plasminogen activator release from vascular endothelial cells in vitro.

AIMS/BACKGROUND: In patients with severe liver disease, blood levels of many coagulation and fibrinolytic factors are lowered due to a diminished synthetic capability in the liver. Tissue plasminogen activator (t-PA) is synthesized by the vascular endothelial cells, however, and is increased in such patients. METHODS: Amounts of t-PA secreted were determined by immunosorbent assay after plasma from patients with cirrhosis was added to cultured human umbilical vein endothelial cells to determine whether a plasma factor directly enhanced t-PA secretion from vascular endothelial cells. RESULTS: Release of t-PA was significantly higher with exposure to plasma from patients with decompensated cirrhosis than when plasma from patients with compensated cirrhosis or normal subjects was used (p < 0.01 and p < 0.05, respectively). Plasminogen activator inhibitor 1 (PAI-1) concentrations were measured similarly but did not differ among the three groups. CONCLUSIONS: Our results indicate that factors in plasma from patients with decompensated cirrhosis directly stimulate t-PA release from the vascular endothelial cells, while any increased PAI-1 release observed in comparable in vivo situations is probably an indirect response to an increase of t-PA or a result of impaired hepatic clearance.

Cells, Cultured↗
PubMed1998

Neuronal mechanisms underlying the facilitatory control of uropod steering behaviour during treadmill walking in crayfish. I. Antagonistically regulated background excitability of uropod motoneurones

One of the postural reflexes of crayfish, the uropod steering response, is elicited by specific sensory inputs while the animal is walking. It is not elicited, however, by the same inputs when the animal is at rest. To clarify the neuronal mechanisms underlying this facilitatory control of body posture in the active animals, we used intracellular recordings to analyse the synaptic activities of uropod motor system neurones in an unanaesthetized whole-animal preparation. Several uropod motoneurones were found to receive sustained depolarizing inputs during walking, whereas the walking leg motoneurones sampled always showed rhythmic activity. The membrane conductance of the uropod motoneurones increased during the sustained synaptic activity. Premotor nonspiking interneurones showed depolarizing or hyperpolarizing membrane potential changes during walking that were also accompanied by increases in membrane conductance. Some of these interneurones enhanced uropod motoneurone activity, whereas others suppressed it during walking. These results suggest that the background excitability of uropod motoneurones is kept at an intermediate level during walking by the antagonistic inputs from premotor nonspiking interneurones so that the uropod motor system can be responsive to both further excitatory and inhibitory inputs resulting from postural changes.

Journal Article↗
PubMed1998

Neuronal mechanisms underlying the facilitatory control of uropod steering behaviour during treadmill walking in crayfish. II. Modulation Of uropod motoneurone excitation by leg proprioception

The synaptic activities underlying the uropod steering behaviour of crayfish evoked by tilting the substratum beneath the legs have been studied intracellularly in unanaesthetized animals standing or walking on a treadmill. The uropod motoneurones showed little or no synaptic response when the treadmill was tilted while the animal was in a quiescent state and the membrane potential was at its resting value. When the same stimulus was given while the animal was walking or in an active stance on the treadmill, the motoneurones showed transient much-enhanced excitatory or inhibitory responses to tilt, depending on the tilt direction. These responses were superimposed on a sustained level of background excitation so that the spike activity of the motoneurones either increased or decreased. Premotor nonspiking interneurones also showed little or no synaptic response to the tilt stimulus while the animal was resting, but greatly enhanced responses, in either a depolarizing or a hyperpolarizing direction, while the animal was walking or in the active-standing state. The results indicate that the proprioceptor inputs converging onto the uropod motoneurones, either directly or through premotor nonspiking interneurones, are gated not only in the uropod motor system in the terminal abdominal ganglion but also at as yet unidentified sites upstream in anterior ganglia, thus suggesting multiple gate control of the descending proprioceptor pathway.

Journal Article↗
PubMed1998

Efficacy of oral magnesium administration on decreased exercise tolerance in a state of chronic sleep deprivation.

We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% less than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p<0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration.

Administration, Oral↗
PubMed1998

Influence of aerobic exercise training on brain natriuretic peptide secretion in patients in the chronic phase of myocardial infarction.

Brain natriuretic peptide (BNP) secretion increases after myocardial infarction (MI); its plasma level may reflect the degree of left ventricular dysfunction. This study examines how aerobic exercise therapy for MI influences BNP secretion. Subjects included 70 patients (mean age, 62.0+/-11.3 years) who were divided into four groups: (1) 20 patients with an anterior MI and exercise training; (2) 20 patients with an anterior MI and no exercise training; (3) 15 patients with an inferior MI and exercise training; and (4) 15 patients with an inferior MI and no exercise training. The training groups performed aerobic exercise 3 times a week for 2 months. Exercise intensity was defined as a heart rate of anaerobic threshold (AT), derived from the treadmill cardiopulmonary exercise testing at 1 month after the onset of MI. The subjects underwent cardiopulmonary exercise testing again at 3 months after the onset of MI. To measure BNP, blood samples were obtained in the resting state and immediately after the peak exercise. AT and peak oxygen uptake increased in the training group with anterior MI and in both the training and nontraining groups with inferior MI. Significant serial change in plasma BNP level was not observed in the inferior MI groups. Plasma BNP level decreased longitudinally only in the nontraining anterior MI group. It was concluded that exercise training in patients with an anterior MI could delay the recovery of left ventricular function, but will increase exercise tolerance.

Aged↗
PubMed1998

Beneficial effects of mechanical reperfusion therapy on left ventricular remodeling and late outcome following myocardial infarction.

The long-term relative benefits of thrombolysis and mechanical reperfusion therapy following acute myocardial infarction (AMI) have not been established. The purpose of this study was to compare left ventricular function, left ventricular remodeling and late outcome after AMI for different reperfusion therapies. Thirty consecutive patients suffering their first anterior wall myocardial infarction with coronary stenoses limited to the left anterior descending coronary artery were studied. They included 10 patients who underwent intracoronary thrombolysis (ICT), 10 who underwent PTCA and 10 who underwent noninterventional medical treatment. All patients underwent coronary angiography (CAG) during the acute phase of AMI and also during the follow-up period, and left ventriculography during the follow-up period and clinical follow-up was performed (mean clinical follow-up period: 53 +/- 31 months). No significant difference in global ejection fraction was noted among the groups, although the end-diastolic volume index (EDVI) in the PTCA group (79.4 +/- 17.5 ml/m2) was significantly smaller than in the noninterventional (106.1 +/- 25.1 ml/m2) and ICT (107.9 +/- 28.3 ml/m2) group (p < 0.05). The regional wall motion index (RWMI) for the anterior region in the PTCA group (-2.7 +/- 0.8) was greater (p < 0.05) than in the noninterventional (-3.4 +/- 0.6) and ICT (-3.3 +/- 0.6) groups. A significant linear correlation was found between EDVI and % diameter stenosis and also between RWMI and % diameter stenosis following reperfusion (p = 0.01). There was no difference in the incidence of cardiac death, nonfatal reinfarction, bypass surgery or congestive heart failure among the groups. Disturbed left ventricular regional wall motion and remodeling benefit most from angioplasty because of prompt restoration of adequate blood flow. However, there was no difference in late outcomes following AMI among the three groups.

Adult↗
PubMed1998

Heart failure in 3 patients with acromegaly: echocardiographic assessment.

We evaluated 3 patients with acromegaly who developed heart failure. Heart failure appeared to be due to acromegalic cardiomyopathy in 2 patients who did not have hypertension or evidence of coronary artery disease, and it was possibly due to acromegalic cardiomyopathy combined with familiar hypertrophic cardiomyopathy in 1 patient. The common echocardiographic findings in the present three cases were: 1) enlargement of the left atrium, 2) markedly dilated left ventricular cavity with diffuse hypokinesis, 3) decrease of indices of the left ventricular systolic function, and 4) no evidence of left ventricular hypertrophy. Echocardiographic findings in acromegaly with congestive heart failure resemble those of idiopathic dilated cardiomyopathy.

Acromegaly↗