Search PubMed⌕ Search

Biomedical subjects

Y Tanabe

Publications and source records attributed to Y Tanabe.

At least 55 records · Page 3Linked to original sources
PubMed2001

Acute encephalopathy associated with nontyphoidal salmonellosis.

The importance of an acute encephalopathy associated with nontyphoidal salmonellosis has recently been recognized, but the disease entity has been poorly established. In this study, we describe two encephalopathic patients associated with nontyphoidal salmonellosis. The patients exhibited a rapid evolution of coma after the onset of lethargy or seizure. Fever and diarrhea due to salmonellosis preceded these events. Secondary factors inducing encephalopathies, such as severe dehydration, sepsis, meningitis, electrolyte or metabolic disturbances, acute renal failure, and multiple organ failure, were excluded in the differential diagnosis at the onset of encephalopathic features. These clinical findings and rapid development of encephalopathic features from localized intestinal infection without any significant abnormalities in a variety of blood tests may suggest a toxic etiology. However, endotoxin was not found in serum from both patients. From these results, we conclude that nontyphoidal salmonellosis can cause a toxic encephalopathy syndrome, like shigellosis or verocytotoxin-producing Escherichia coli infection.

Acute Disease↗
PubMed2001

Th1/Th2 balance alteration in the clinical course of a patient with acute viral myocarditis.

Cytokines have an important role in the pathogenesis and pathophysiology of myocarditis. In this study, subsets of peripheral helper T lymphocytes (Th) in a patient with acute viral myocarditis were analyzed by 3-color flow cytometry. During the clinical course of myocarditis, the Th1/Th2 ratio of peripheral lymphocytes changed. Th1 was dominant in the acute inflammatory phase during which levels of creatine kinase (CK) increased (day 6), then Th2 levels overtook those of Th1 in the recovery phase during which levels of CK decreased (day 13 and 20). At the time of discharge (day 35), Th1 and Th2 had normalized. Thus, it was speculated that the induction of lymphocytic myocarditis was associated with Th1 dominant status, and recovery was related to Th2 polarity. Th subset imbalances may play an important role in the pathogenesis of acute viral myocarditis and these analyses may be useful for understanding the disease activity of myocarditis.

Adult↗
PubMed2001

Significance of end-tidal P(CO(2)) response to exercise and its relation to functional capacity in patients with chronic heart failure.

OBJECTIVES: The value of end-tidal PCO(2) monitoring during exercise in patients with chronic heart failure has not been elucidated. The present study was designed to examine end-tidal PCO(2) response to exercise and its relation to functional capacity in patients with chronic heart failure. METHODS AND RESULTS: Maximal upright ergometer exercise with respiratory gas analysis and arterial blood gas analysis were performed in 105 patients with chronic heart failure (34 patients in New York Heart Association [NYHA] class I, 38 patients in NYHA class II, and 33 patients in NYHA class III) and 14 normal control subjects. Peak O(2) uptake, excessive exercise ventilation as assessed by the slope of the relation between expired minute ventilation and CO(2) output (VE-VCO(2)), and the ratio of physiologic dead space to tidal volume (VD/VT) were determined. Cardiac output was also measured during exercise in 28 patients with chronic heart failure. Arterial PO(2) or PCO(2) values at rest and during exercise were not different among the four groups. However, end-tidal PCO(2) was significantly lower, and arterial to end-tidal PCO(2) difference and VD/VT were significantly higher in NYHA class III patients than other groups during exercise. The maximal end-tidal PCO(2) during exercise was significantly reduced as the severity of chronic heart failure advanced (45.7 +/- 4.0 mm Hg in normal control subjects, 43.5 +/- 4.8 mm Hg in NYHA class I patients, 39.7 +/- 5.1 mm Hg in NYHA class II patients, and 34.9 +/- 5.3 mm Hg in NYHA class III patients). The maximal end-tidal PCO(2) during exercise was significantly correlated with peak O(2) uptake (r = 0.68; p < 0.001) and maximal cardiac index (r = 0.73; p < 0.001), and inversely related to Ve-VCO(2) (r = - 0.84; p < 0.001) and VD/VT at peak exercise (r = -0.65; p < 0.001). CONCLUSIONS: The decreased end-tidal PCO(2) during exercise, which is caused by high ventilation/perfusion ratio mismatching, reflects both reduced cardiac output response to exercise and increased exercise ventilation due to enlarged physiologic dead space in advanced chronic heart failure. The end-tidal PCO(2) during exercise can be used to evaluate the functional capacity of patients with chronic heart failure.

Carbon Dioxide↗
PubMed2001

A case of effusive-constrictive pericarditis after cardiac surgery.

A 60-year-old woman who had undergone repair of an atrial septal defect was readmitted to the hospital with dyspnea, abdominal distention, and leg edema 31 months after surgery. An echocardiogram demonstrated massive pericardial effusion. Cardiac catheterization revealed elevation and equilibrium of the 4-chamber diastolic pressure and a dip-and-plateau pattern in the right and the left ventricular pressures. Despite removal of pericardial fluid by pericardiocentesis, the findings and symptoms did not improve. The patient underwent both parietal and visceral pericardiectomy after which striking hemodynamic and symptomatic improvement occurred. Effusive-constrictive pericarditis is uncommon but should be considered in patients with refractory heart failure and massive pericardial effusion showing no improvement after removal of pericardial fluid.

Aged↗
PubMed2001

[A case of systemic fat embolism in mixed connective tissue disease associated with interstitial pneumonia during steroid treatment].

A 67-year-old man with a four-year history of mixed connective tissue disease (MCTD) associated with interstitial pneumonia was admitted to our hospital with a complaint of dyspnea and moist cough. Because the interstitial pneumonia was exacerbated, he was given high-dose steroid treatment (pulse therapy and sequential oral treatment of PSL 50 mg/day). After treatment his general condition showed some improvement, but then he suddenly died of acute respiratory failure. Autopsy disclosed fat emboli in the lungs, kidneys, liver and myocardium. The fat embolism may have been a consequence of the steroid treatment. Fat embolism should be taken into account as one of the causes of the acute respiratory failure in collagen vascular disease patients receiving steroid treatment.

Acute Disease↗
PubMed2000

Tau pathology in diffuse neurofibrillary tangles with calcification (DNTC): biochemical and immunohistochemical investigation.

Diffuse neurofibrillary tangles with calcification (DNTC) represents a primary and sporadic presenile dementia that is characterized by temporal or fronto-temporal atrophy with diffuse neurofibrillary tangles (NFTs), neuropil threads and Fahr-type calcification without senile plaques. We examined the tau pathology in five autopsy cases of DNTC by immunoblotting and immunohistochemistry using phosphorylation-dependent and -independent anti-tau antibodies. The pattern of staining for different epitopes of beta-amyloid (A beta) was also investigated. NFTs were immunopositive with all the anti-tau antibodies used in this study. On the immunoblots, sarkosyl-insoluble tau appeared as three major bands of 60, 64 and 68 kDa, and as a minor band at 72 kDa. The majority of extracellular NFTs were weakly immunopositive only with the antibody recognizing the 40 carboxyl-terminal of A beta in DNTC. These results suggest that Alzheimer's disease-like tau pathology could exist independently of A beta deposits in DNTC.

Aged↗
PubMed2000

Methamphetamine decreases calcium-calmodulin dependent protein kinase II activity in discrete rat brain regions.

A Ca(2+)/calmodulin-dependent signaling cascade has been implicated in the regulation of dopaminergic neurotransmission after chronic administration of amphetamine and methamphetamine (METH). We found a decrease in Ca(2+)/calmodulin-dependent protein kinase II (CaM-kinase II) activity in five regions of the rat brain (parietal cortex; frontal cortex; hippocampus; striatum; and nucleus accumbens) after a single injection of METH. Pretreatment with the selective dopamine D1 receptor antagonist SCH 23390 prevented the acute METH-induced decrease in CaM-kinase II activity in the parietal cortex, striatum, nucleus accumbens, and substantia nigra/ventral tegmental area (SN/VTA). Pretreatment with the N-methyl-D-aspartate receptor antagonist MK-801 significantly restored the acute METH-induced decrease in CaM-kinase II activity in the parietal cortex, nucleus accumbens, and SN/VTA. Striatal CaM-kinase II activity was still significantly lower than that of the chronic saline-treated controls after a 1-week, but not a 4-week, abstinence from chronic administration of METH. A METH challenge after a 4-week abstinence period induced a more pronounced decrease in CaM-kinase II activity in rats chronically injected with METH than in rats chronically injected with saline. Western blot analysis revealed that the amount of CaM-kinase II protein was not altered after a single METH injection or after chronic METH injections, compared with saline-treated controls. However, amounts of phosphorylated (Thr(286)) CaM-kinase II in the parietal cortex, striatum and SN/VTA were significantly decreased at 3 h after an acute METH injection compared with saline-treated controls. These results suggest that dephosphorylation of CaM-kinase II may contribute to the decreased enzyme activities induced by acute METH administration, and that chronic treatment with METH leads to an enhanced capacity of METH to decrease CaM-kinase II activity after an extended withdrawal period.

Animals↗
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

Molecular phylogeny of parasitic zygomycota (Dimargaritales, zoopagales) based on nuclear small subunit ribosomal DNA sequences.

We analyzed sequence data of the 18S rDNA gene from representatives of nine mycoparasitic or zooparasitic genera to infer the phylogenetic relationships of these fungi within the Zygomycota. Phylogenetic analyses identified a novel monophyletic clade consisting of the Zoopagales, Kickxellales, Spiromyces, and Harpellales. Analyses also identified a monophyletic mycoparasitic-zooparasitic Zoopagales clade in which Syncephalis, Thamnocephalis, and Rhopalomyces form a sister group to a Piptocephalis-Kuzuhaea clade. Although monophyly of the mycoparasitic Dimargaritales received strong bootstrap and decay index support, phylogenetic relationships of this order could not be resolved because of the unusually high rate of base substitutions within the 18S rDNA gene. Overall, the 18S gene tree topology is weak, as reflected by low bootstrap and decay index support for virtually all internal nodes uniting ordinal and superordinal taxa. Nevertheless, the 18S rDNA phylogeny is mostly consistent with traditional phenotypic-based classification schemes of the Fungi.

Classification↗
PubMed2000

Tau-negative astrocytic star-like inclusions and coiled bodies in dementia with Lewy bodies.

To evaluate glial lesions in cases of dementia with Lewy bodies (DLB), we studied the brains of four patients with DLB. Astrocytic star-like inclusions, which resembled tufted astrocytic fibrillary tangles in shape, were found in the cortex of two of these cases. In addition, coiled bodies were found in the white matter of the cerebrum in two cases. The astrocytic star-like inclusions were immunohistochemically negative for tau protein, ubiquitin and alpha-synuclein. The coiled bodies were immunohistochemically negative for tau protein but immunopositive for ubiquitin and alpha-synuclein. These results suggest that in DLB a primary degenerative process takes place in both glial cells and neurons.

Aged↗
PubMed2000

Determinants of delayed improvement in exercise capacity after percutaneous transvenous mitral commissurotomy.

BACKGROUND: Percutaneous transvenous mitral commissurotomy (PTMC) results in short-term hemodynamic and symptomatic improvements. We have previously shown that the immediate symptomatic relief is related to the improvement in excessive exercise ventilation. The exercise capacity, however, does not improve in the short term but does improve gradually over several months. The pathophysiologic basis for the delayed improvement in exercise capacity has not been fully evaluated. METHODS: To elucidate the determinants of improvement in exercise capacity late after PTMC, maximal ergometer exercise with respiratory gas analysis and exercise hemodynamic measurements were performed in 22 patients with symptomatic mitral stenosis before, immediately after, and 7 months after PTMC. RESULTS: Mitral valve area increased from 0.9 +/- 0.2 cm(2) to 1.7 +/- 0.4 cm(2) after PTMC (P <.01). Significant improvements were observed in symptoms, cardiac output at peak exercise (6.6 +/- 1.5 L/min vs 8.6 +/- 1.9 L/min, P <.01), and mean pulmonary artery pressure at peak exercise (54.1 +/- 15.6 mm Hg vs 42.3 +/- 9.5 mm Hg, P <.01) immediately after PTMC. Excessive exercise ventilation, as assessed by the slope of the regression line between expired minute ventilation and carbon dioxide output (VE-VCo(2)), decreased significantly from 38.2 +/- 8.2 to 33.3 +/- 4.9 (P <.01). There were no significant changes in peak oxygen uptake (from 17.5 +/- 3.2 mL/kg per minute to 17.9 +/- 3.6 mL/kg per minute) immediately after PTMC. At 7 months, improved mitral valve area, symptoms, cardiac output at peak exercise, mean pulmonary artery pressure at peak exercise, and VE-VCo(2) were unchanged compared with values immediate after PTMC. Significant improvement was observed in peak oxygen uptake (19.7 +/- 3.0 mL/kg per minute [P <.01 compared with pre-PTMC or immediate post-PTMC values]). The increase in exercise cardiac output or the decrease in pulmonary artery pressure was not correlated with the late improvement in peak oxygen uptake. The short- or long-term improvements in VE-VCo(2), however, were significantly correlated with the late improvement in peak oxygen uptake. CONCLUSIONS: Our results suggest that ventilatory improvement, not increased exercise cardiac output, contributed at least in part to the late improvement in exercise capacity after PTMC.

Adult↗
PubMed2000

Prolonged recovery of cardiac output after maximal exercise in patients with chronic heart failure.

OBJECTIVES: The aim of this study was to characterize the kinetics of cardiac output during recovery from maximal exercise in patients with chronic heart failure (CHF). BACKGROUND: Recent studies have shown that oxygen uptake kinetics during recovery from exercise are delayed in patients with CHF. However, the kinetics of cardiac output during recovery from maximal exercise in CHF has not been examined. METHODS: Thirty patients with CHF performed maximal upright ergometer exercise with respiratory gas analysis. Kinetics of oxygen uptake (VO2) and carbon dioxide output (VCO2) during recovery were characterized by T1/2, the time to reach 50% of the peak values. Cardiac output was measured at 1-min intervals during exercise and recovery. Kinetics of cardiac output during recovery were characterized by the ratios of cardiac output during the first 4 min of recovery to cardiac output at peak exercise. Overshoot of cardiac output was defined as a further increase in cardiac output at 1 min of recovery above the cardiac output at peak exercise. RESULTS: Both T1/2 VO2 and T1/2 VCO2 increased as CHF worsened. The ratios of cardiac output during recovery to cardiac output at peak exercise were significantly correlated with T1/2 VO2 (r = 0.47 to 0.62, p < 0.05) and T1/2 VCO2 (r = 0.40 to 0.70, p < 0.05). There was a negative correlation between cardiac index at peak exercise and both T1/2 VO2 (r = -0.65, p < 0.001) and T1/2 VCO2 (r = -0.60, p < 0.001). Overshoot of cardiac output was recognized in 11 of 30 patients. Cardiac index at peak exercise was significantly lower in patients with overshoot (4.5 +/- 0.9 L/min/m2) than in those without overshoot (6.1 +/- 2.1 L/min/m2, p < 0.05). However, because of a continued increase in cardiac output at 1 min of recovery in patients with overshoot, there were no differences in cardiac index after the first minute of recovery. Heart rate at peak exercise and recovery of heart rate did not differ between these groups. Overshoot of cardiac output was caused by a rebound increase in stroke volume which was due to a reduction in systemic vascular resistance. CONCLUSIONS: Prolonged kinetics of VO2 or VCO2 during recovery from maximal exercise represent impairment of circulatory response to exercise and delayed recovery of cardiac output after exercise. Overshoot of cardiac output at 1 min of recovery was characteristic of severe CHF with poor cardiac output response to exercise.

Analysis of Variance↗
PubMed2000

Stress transmission through Ti-Ni alloy, titanium and stainless steel in impact compression test.

Impact stress transmission of Ti-Ni alloy was evaluated for biomedical stress shielding. Transformation temperatures of the alloy were investigated by means of DSC. An impact compression test was carried out with use of split-Hopkinson pressure-bar technique with cylindrical specimens of Ti-Ni alloy, titanium and stainless steel. As a result, the transmitted pulse through Ti-Ni alloy was considerably depressed as compared with those through titanium and stainless steel. The initial stress reduction was large through Ti-Ni alloy and titanium, but the stress reduction through Ti-Ni alloy was more continuous than titanium. The maximum value in the stress difference between incident and transmitted pulses through Ti-Ni alloy or titanium was higher than that through stainless steel, while the stress reduction in the maximum stress through Ti-Ni alloy was statistically larger than that through titanium or stainless steel. Ti-Ni alloy transmitted less impact stress than titanium or stainless steel, which suggested that the loading stress to adjacent tissues could be decreased with use of Ti-Ni alloy as a component material in an implant system.

Journal Article↗
PubMed2000

Mechanical stretch augments PDGF receptor beta expression and protein tyrosine phosphorylation in pulmonary artery tissue and smooth muscle cells.

With regard to the mechanotransduction mechanisms of vasculature involved in hypertensive diseases, we aimed to identify tyrosine-phosphorylated proteins in pulmonary artery that responded to mechanical stress. Mechanical stretch simultaneously augmented protein-tyrosine phosphorylation in p55, p95, p105, p115, p130, p165, p180 in pulmonary artery tissue and pulmonary artery-derived smooth muscle cells (PASMC), whereas p115 and p55 were preferentially phosphorylated by the stretch in endothelial cells (PAEC). A series of experiments designed to characterize these proteins indicated that p115 and p180 were focal adhesion kinase (FAK) and platelet-derived growth factor receptor beta (PDGF-Rbeta), respectively, and that stretch augmented the surface-expression of PDGF-Rbeta in PASMC but not in PAEC. Moreover, a significant increase in the steady-state mRNA level for PDGF-Rbeta was observed in the pulmonary artery of rats with monocrotaline-induced pulmonary hypertension, where the artery should be overstretched due to increasing pulmonary arterial blood pressure. These results suggest that stretch-induced overexpression of cell-surface PDGF-Rbeta as well as augmentation of yrosine phosphorylation of proteins including FAK in PASMC might be involved in the mechanotransduction of pulmonary artery.

Animals↗
PubMed2000

Attenuation of pressure-induced myogenic contraction and tyrosine phosphorylation by fasudil, a cerebral vasodilator, in rat cerebral artery.

The mechanism by which fasudil inhibits pressure-induced myogenic contraction was studied with regard to tyrosine phosphorylation in rat cerebral artery. Intracellular Ca(2+) concentration ([Ca(2+)](i)) and vessel diameter were simultaneously measured. Total tyrosine phosphorylation level and phosphorylation of tyrosine 419 on pp60(src) required for its full catalytic activity were immunocytochemically detected in situ. Fasudil (1 - 100 microM) partially suppressed the increase in [Ca(2+)](i), and totally attenuated contraction elicited by pressurization from 10 to 60 mmHg. Furthermore, fasudil (100 microM) significantly attenuated tyrosine phosphorylation and the activity of pp60(src) augmented in situ by pressure. Herbimycin A (1 - 100 nM) and genistein (3 - 30 microM), tyrosine kinase inhibitors, effectively attenuated the pressure-induced increase in [Ca(2+)](i), contraction, tyrosine phosphorylation, and activation of pp60(src). Both fasudil and herbimycin A directly inhibited the pp60(src) activity in a cell free system. Orthovanadate (100 microM), a tyrosine phosphatase inhibitor, significantly potentiated the pressure-induced increase in [Ca(2+)](i) and contraction. Nicardipine (100 nM), a Ca(2+) antagonist, completely inhibited pressure-induced increase in [Ca(2+)](i) and contraction, but affected neither tyrosine phosphorylation nor activity of pp60(src) in the pressurized arteries. Arginine-glycine-aspartic acid-serine peptide (1 - 100 microM) concentration-dependently reduced the pressure-induced contraction. In addition to the hitherto reported vasodilatory actions of fasudil, the present results suggest the inhibition by fasudil of pressure-induced tyrosine phosphorylation and pp60(src) activation. The wide spectrum of inhibitory actions of fasudil may contribute to the effective attenuation of the pressure-induced contraction in the cerebral artery.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2000

Specific inhibition of stretch-induced increase in L-type calcium channel currents by herbimycin A in canine basilar arterial myocytes.

The effects of protein-tyrosine kinase (PTK) and protein-tyrosine phosphatase (PTP) inhibitors on voltage-activated barium currents (I(Ba)) through L-type calcium channels increased by hypotonic solution were investigated in canine basilar arterial myocytes by the whole-cell patch-clamp technique. I(Ba) was elicited by depolarizing step from a holding potential of -80 to +10 mV and identified by using an L-type calcium channel agonist, Bay K 8644 (100 nM), and an L-type calcium channel blocker, nicardipine (1 microM). Hypotonic superfusate induced cell swelling and acted as a stretch stimulus, which reversibly increased peak I(Ba) amplitude at +10 mV. I(Ba) was also decreased by nicardipine (1 microM) under the hypotonic condition. PTK inhibitors such as herbimycin A (30 nM), genistein (10 microM), and lavendustin A (10 microM) decreased I(Ba) enhanced by hypotonic solution. Genistein also decreased I(Ba) in a concentration-dependent manner under the isotonic condition. The inactive genistein analogue daidzein (10 microM) had no effect on I(Ba) under either the isotonic or hypotonic condition. By contrast, herbimycin A did not decrease I(Ba) under the isotonic condition. Sodium orthovanadate (10 microM), a PTP inhibitor, increased I(Ba) under both conditions. The present results suggest that cell swelling by hypotonic solution increases the L-type calcium channel currents in canine basilar artery and that herbimycin-sensitive PTK activity is primarily involved in the enhancement of calcium channel currents.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗