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N Takeda

Publications and source records attributed to N Takeda.

At least 181 records · Page 10Linked to original sources
PubMed1998

Pressure-induced structural rearrangements of bovine pancreatic trypsin inhibitor studied by FTIR spectroscopy.

Fourier transform infrared (FTIR) spectroscopy combined with resolution enhancement techniques, second-derivative and difference spectroscopies, have been used to characterize pressure-induced changes in the structural rearrangements of bovine pancreatic trypsin inhibitor (BPTI) in D2O solution at 25.0 degrees C. According to the observed changes in the amide I' band up to 550 MPa, the secondary structure elements of BPTI, such as the alpha-helix, 3(10)-helix, beta-sheet, and beta-turn, are scarcely rearranged except for the loop structure of residues of 9-17 and 36-43. The polypeptide backbone is not extensively unfolded up to 550 MPa. The minor pressure-induced structural rearrangements are completely reversible. A further increase in pressure above 1000 MPa associated with the precipitation of BPTI in D2O buffer solution induces the partial structural rearrangements of the alpha-helix, beta-turn and/or 3(10)-helix, and beta-sheet. The polypeptide backbone of BPTI is not fully unfolded even above 1000 MPa. Most of the protected backbone amide protons involved in the beta-sheet remain intact in the pressure range where BPTI is not precipitated, while those involved in the alpha-helix and beta-turn and/or 3(10)-helix are exchanged with solvent deuterons. The protected backbone amide protons located near the surface regions are more easily exchanged with solvent deuterons by application of high pressure than those involved in the core.

Animals↗
PubMed1998

Haemodynamic evaluation of cerebral gliomas using XeCT.

The purpose of this study was to characterize regional blood flow (BF) in untreated cerebral gliomas (CG) using stable Xe-enhanced computed tomography (XeCT). XeCT of 38 patients with untreated CG were analyzed and compared with CT and magnetic resonance images (MRI) and histopathological findings. Individual averaged BF values for tumour in 29 high grade gliomas (HGGs) and 9 low grade gliomas (LGGs) were intermediate between averaged BF values for cortex and white matter in the non-tumour bearing hemisphere. All averaged BF values for cyst and central necrosis were very low. In 27 HGGs, BF in tumour was relatively high in ring-enhancement lesions on CT and MRI, but was low even in viable tumour centers showing no contrast enhancement. In the other 2 HGGs, BF was low in tumour center and relatively high in tumour periphery regardless of homogeneous enhancement. In 5 HGGs, averaged BF value of the cortex outside surrounding oedema was higher than that of cortex in the non-tumour bearing hemisphere. In LGGs, BF distribution in tumour was homogeneously low in 3 small-sized and heterogeneous in 6 large-sized lesions including moderately high and low BF regions. These differences in BF pattern between HGGs and LGGs on XeCT might be helpful in considering to some extent the histopathology of untreated cerebral glioma pre-operatively.

Adolescent↗
PubMed1998

Prospective echocardiographic analysis of progressive obstruction of the proximal pulmonary artery in congenital heart disease and obstructed pulmonary flow.

BACKGROUND: It is uncertain whether proximal pulmonary artery (PA) obstruction exists soon after birth and whether its progress relates directly to postnatal ductal constriction in congenital heart disease and obstructed pulmonary flow. METHODS: Serial morphometric analyses of the PA branches by echocardiogram were performed in 28 patients (mean age at initial study 2.5 days) until severe constriction of the ductus occurred (mean age 47 days). These patients were divided into 2 groups by subsequent angiographic or postmortem confirmation; 10 with proximal PA obstruction (group 1) and 18 without obstruction (group 2). RESULTS: At the time of initial examination, the mean indexed diameter of the proximal PA on the side of the ductus arteriosus in group 1 was significantly smaller than that on the contralateral side (5.2+/-0.7 versus 9.0+/-0.7 mm/BSA0.5, P < .001) or that in group 2 (8.0+/-0.4 mm/BSA0.5, P < .001). In group 1, 8 patients had a proximal PA index on the ductal side < or = 5.5 mm/BSA0.5, which was less than those of any group 2 patients. After severe constriction of the ductus, the proximal PA index on the ductal side further decreased only in group 1 (P < .01). CONCLUSIONS: These data indicate that unilateral obstructive lesion of branch PA is present shortly after birth and its progression relates directly to ductal constriction. Neonates with branch PA obstruction can be identified on their initial echocardiogram as having a proximal PA index on the ductal side < or = 5.5 mm/BSA0.5.

Arterial Occlusive Diseases↗
PubMed1998

Subcellular remodeling and heart dysfunction in chronic diabetes.

Heart dysfunction in chronic diabetes has been observed to be associated with depressed myofibrillar adenosine triphosphatase activities as well as abnormalities in the sarcoplasmic reticular and sarcolemmal calcium transport processes. The evidence has been presented to show that alterations in the expression of myosin isozymes and regulatory proteins as well as myosin phosphorylation contribute to the development of myofibrillar remodeling in the diabetic heart. Defects in sarcoplasmic reticular and sarcolemmal calcium transport appear to be due to the accumulation of lipid metabolites in the membrane. Different agents, such as calcium-antagonists, beta-adrenoceptor blockers, angiotensin converting enzyme inhibitors, metabolic interventions and antioxidants, have been reported to exert beneficial effects in preventing subcellular remodeling and cardiac dysfunction in chronic diabetes. Clinical and experimental investigations have suggested that increased sympathetic activity, activated cardiac renin-angiotensin system, myocardial ischemia/functional hypoxia and elevated levels of glucose for a prolonged period, due to insulin deficiency, result in oxidative stress. It is proposed that oxidative stress associated with a deficit in the status of the antioxidant defense system may play a critical role in subcellular remodeling, calcium-handling abnormalities and subsequent diabetic cardiomyopathy.

Calcium↗
PubMed1998

Effects of troglitazone on hepatic and peripheral insulin resistance induced by growth hormone excess in rats.

It is well known that short-term growth hormone (GH) administration in humans and animals induces insulin resistance and glucose intolerance. The purpose of the present study was to clarify whether troglitazone, a new insulin-sensitizing drug of the thiazolidinedione class, counteracts the insulin antagonistic effects of recombinant human (rh) GH on glucose metabolism in rats. Male Wistar rats weighing 184 to 226 g were treated either with rhGH (n = 8) or rhGH plus troglitazone (n = 8). rhGH (20 IU/kg body weight/d) was given by subcutaneous injection twice daily for 2 days. Troglitazone was given at 100 mg/kg/d orally for 5 days before and 2 days during rhGH. Saline was injected to the control rats (n = 7). Euglycemic clamp studies with an insulin infusion rate of 8 mU/kg/min were performed in these rats after an overnight fast. Hepatic glucose output (HGO), glucose infusion rate (GIR), and glucose disappearance rate (GDR) were measured. Fasting levels of plasma glucose (6.6 +/- 0.1, 6.1 +/- 0.3, 6.5 +/- 0.2 mmol/L), insulin (187.5 +/- 24.1, 206.4 +/- 24.1, 182.3 +/- 31.0 pmol/L), and serum free fatty acid (FFA) (1.58 +/- 0.18, 1.43 +/- 0.16, 1.61 +/- 0.25 mEq/L) were comparable among rats treated with rhGH, rhGH plus troglitazone, and controls, respectively. Basal HGO was also comparable among the three treatment groups. HGO was suppressed significantly during the hyperinsulinemic glucose clamp in control rats, but not in rhGH rats. When troglitazone was coadministered with rhGH, suppressibility of HGO during the glucose clamp was comparable to that of controls. GIR (13.5 +/- 4.5 v 24.1 +/- 4.1 mg/kg/min) and GDR (18.1 +/- 5.8 v 30.3 +/- 5.2 mg/kg/min) were decreased by rhGH treatment compared with control values. They returned to normal levels in rats treated with both rhGH and troglitazone (GIR, 22.4 +/- 5.9; GDR, 24.7 +/- 7.1). From these results, it is evident that rhGH treatment impaired insulin's ability to suppress HGO and stimulate peripheral glucose utilization. Troglitazone could block the insulin antagonistic effects of GH on hepatic glucose output and peripheral glucose utilization.

Administration, Oral↗
PubMed1998

Effects of troglitazone on dexamethasone-induced insulin resistance in rats.

Troglitazone, a thiazolidinedione derivative, has been shown to counteract insulin resistance in obesity and non-insulin-dependent diabetes mellitus (NIDDM). To test its effects on dexamethasone-induced insulin resistance, we measured hepatic glucose production (HGP) and the insulin-stimulated glucose disposal rate (Rd) by a euglycemic-hyperinsulinemic glucose clamp technique coupled with 3-3H-glucose infusion in male Wistar rats treated with low-dose dexamethasone ([LoDex] 0.05 mg/kg/d, n = 7), high-dose dexamethasone ([HiDex] 0.1 mg/kg/d, n = 7), or dexamethasone plus troglitazone (LoDex + T, n = 8; HiDex + T, n = 6). Dexamethasone was injected subcutaneously for 4 days. Troglitazone was administered orally at 20 mg/d for 3 days before and for 4 days along with the dexamethasone treatment. The glucose clamp study was performed after an overnight fast in chronically catheterized conscious rats with a continuous insulin infusion of 57.4 pmol/kg/min. Basal HGP was comparable among the control (45.8 +/- 2.1 micromol/kg/min, n = 7), LoDex (47.9 +/- 4.7 micromol/kg/min), LoDex + T (46.0 +/- 2.6 micromol/kg/min), and HiDex + T (54.7 +/- 3.4 micromol/kg/min) groups. It increased about twofold in the HiDex group (80.1 +/- 5.2 micromol/kg/min, P < .05 v control). Under hyperinsulinemia, HGP was suppressed to a similar level in the control (11.3 +/- 8.8 micromol/kg/min), LoDex (10.2 +/- 8.4 micromol/kg/min), and LoDex + T (7.8 +/- 7.9 micromol/kg/min) groups. The suppressive effect of insulin on steady-state HGP during the clamp was impaired in HiDex (63.7 +/- 9.7 micromol/kg/min, P < .05) and HiDex + T (64.0 +/- 6.5 micromol/kg/min, P < .05). Rd decreased 27% in LoDex (81.5 +/- 5.8 micromol/kg/min, P < .05) and 36% in HiDex (71.3 +/- 9.4 micromol/kg/min, P < .05) compared with the controls (111.4 +/- 7.4 micromol/kg/min). Troglitazone prevented the decrease in Rd in LoDex + T (102.6 +/- 5.7 micromol/kg/min), but not in HiDex + T (67.0 +/- 6.4 micromol/kg/min). These results indicate that the development of peripheral insulin resistance was prevented by troglitazone in LoDex rats. Troglitazone may be a useful drug to treat steroid-induced diabetes.

Animals↗
PubMed1998

Phimosis as a manifestation of chronic graft-versus-host disease after allogeneic bone marrow transplantation.

Chronic GVHD is one of the major complications of BMT, involving a variety of organs, but rarely involving the genitourinary system. We report a patient who simultaneously developed extensive chronic GVHD and phimosis after BMT. From the clinical course and pathological findings, chronic GVHD was considered to be responsible for the phimosis. Despite intensive immunosuppressive therapy, the phimosis persisted. Phimosis is a rare complication after BMT, which may often remain neglected. Possibility of this complication should be considered in patients with chronic GVHD.

Adult↗
PubMed1998

Depressive disorders as psychiatric complications after obesity surgery.

Three case reports of morbidly obese patients (two women and a man) who underwent vertical banded gastroplasty and who subsequently fell into depression, are presented here. The psychiatric diagnosis according to DSM-III-R (Diagnostic and Statistical Manual of Mental Disorders, 3rd edition, revised), the eating pattern before obesity surgery, the past history of mental disorder, social adaptation before surgery, psychological gain from their obese state, and the presence of unrealistic expectations of obesity surgery were investigated. Case 1 was diagnosed postoperatively as having a major depressive episode without a personality disorder. Case 2 was diagnosed post-operatively as having a major depressive episode. Case 3 had a depressive disorder not otherwise specified. Cases 2 and 3 had a social phobia with comorbidity of personality disorders. Binge eating disorder was confirmed in all patients before obesity surgery. There were differences between case 1 and cases 2 and 3 based on the presence of personality disorder and the time of onset of depression. When some psychiatric characteristics are confirmed in obese patients, obesity surgery should be undertaken more prudently because the patients may manifest depression postoperatively. The pre-operative psychiatric assessment is essential for a decision on indication of obesity surgery.

Adult↗
PubMed1998

RNA metabolism in uremic patients: accumulation of modified ribonucleosides in uremic serum. Technical note.

To determine the metabolism of ribonucleic acid (RNA) in uremia, serum and urine levels of ribonucleosides in uremic patients were analyzed using reversed-phase high-performance liquid chromatography. The serum levels of xanthosine and all modified ribonucleosides were increased in undialyzed patients with chronic renal failure (CRF), and patients undergoing hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD). The serum level of pseudouridine was markedly increased in all the uremic patients especially CAPD patients (32 times higher than normal). By contrast, the serum level of adenosine did not show any significant change in the uremic patients. Interestingly, the serum and urine levels of inosine were significantly decreased in all the uremic patients, suggesting that the production of inosine is decreased in uremic patients. The serum level of uridine was significantly elevated only in the HD patients. The serum levels of all ribonucleosides except inosine and uridine decreased significantly after HD. The urinary excretion of inosine, 1-methyladenosine, 1-methylguanosine, N2,N2-dimethylguanosine and N4-acetylcytidine was significantly decreased in the CRF patients, leading to the accumulation of these modified ribonucleosides in the uremic serum. CAPD patients showed markedly increased serum levels of modified ribonucleosides such as pseudouridine, 1-methylinosine, and N2,N2-dimethylguanosine and N4-acetylcytidine as compared with the HD patients. These results demonstrate that there was an altered metabolism of RNA in uremic patients with marked accumulation of modified ribonucleosides.

Chromatography, High Pressure Liquid↗
PubMed1998

Histaminergic influence on vestibular stimulation-induced locus coeruleus inhibition in rats.

In previous reports we have shown that caloric stimulation (CS) of the vestibular apparatus inhibits locus coeruleus (LC)-noradrenergic neuronal activity in urethane-anaesthetized rats. The present study examined the effect of neural histamine depletion by alpha-fluoromethylhistidine (alpha-FMH) on CS-induced LC inhibition. In alpha-FMH treated rats, LC neuronal inhibition caused by CS was still observed. This finding indicates that the central histaminergic neuron system does not participate in the CS-induced LC-noradrenergic inhibition. It is suggested that the noradrenergic neuron system is involved in the development of vestibulo-autonomic response, independent of the histaminergic neuron system.

Animals↗
PubMed1998

An implication of protein phosphatase 2A-beta in the rat flocculus for lesion-induced vestibular plasticity.

The differential display method was applied to identify genes, the expression of which is up-regulated in the cerebellar flocculus after unilateral labyrinthectomy (UL). Total RNA from sham-operated and labyrinthectomized rat flocculi was isolated, amplified by polymerase chain reaction (PCR) using a single arbitrary primer and separated by electrophoresis on a polyacrylamide gel. PCR products in amounts significantly higher in samples from labyrinthectomized animals than in those from controls were cut out of the gel and sequenced. One of the cDNA fragments showed 100% nucleotide sequence identity to the rat protein phosphatase 2A (PP2A)-beta catalytic subunit mRNA. In situ hybridization histochemistry and Northern blot analysis showed that PP2A-beta mRNA expression was intensely localized to the floccular Purkinje cell layer and up-regulated with a maximum increase within 2 days after UL. In labyrinthectomized rats, UL-induced nystagmus gradually disappeared within 3 days after UL. However, in animals with continuous floccular infusion of okadaic acid, a potent inhibitor of PP2A, UL-induced nystagmus lasted significantly longer. All these findings suggest that up-regulation of PP2A-beta mRNA in floccular Purkinje cells after UL is involved in lesion-induced vestibular plasticity. So far, various kinds of neural plasticity-associated molecules have been investigated mainly by slice in vitro studies. This paper indicates that differential display is the feasible molecular biological in vivo method for an investigation about the mechanism of neural plasticity.

Animals↗
PubMed1998

Accelerated aging of dermal fibroblast-like cells from the senescence-accelerated mouse (SAM): acceleration of changes in DNA ploidy associated with in vitro cellular aging.

Accelerated changes in the DNA ploidy associated with in vitro aging were examined in fibroblast-like cells isolated from the dorsal dermis of newborn SAMP11 (accelerated senescence-prone, short-lived) mice, and were compared to changes observed in cell lines from SAMR1 (accelerated senescence-resistant, long-lived) mice. Flow cytometric analysis of the DNA content in confluent cells and chromosome analysis in mitoses revealed that the diploid cells were being replaced with tetraploid cells until a growth crisis; thereafter, hypotetraploid cells became predominant, accompanied by immortalization. The number of mitoses decreased as the crisis ensued, then increased. Although these changes were observed in the cell lines from both strains of mice, the changes occurred more rapidly and at earlier population doublings in the cell lines from the SAMP11 mice. These results suggest that the cell lines from SAMP11 mice might have higher susceptibility to factors that cause polyploidization, including oxidative stress.

Aging↗
PubMed1998

Complete nucleotide sequence and genetic organization of Aichi virus, a distinct member of the Picornaviridae associated with acute gastroenteritis in humans.

The complete nucleotide sequence of a novel enteric virus, Aichi virus, associated with nonbacterial acute gastroenteritis in humans was determined. The Aichi virus genome proved to be a single-stranded positive-sense RNA molecule with 8,251 bases excluding a poly(A) tail; it contains a large open reading frame with 7,302 nucleotides that encodes a potential polyprotein precursor of 2,433 amino acids. The genome contains a 5' nontranslated region (NTR) with 712 bases and a 3' NTR with 240 bases followed by a poly(A) tail. The structure of the genome, VPg-5' NTR-leader protein-structural proteins-nonstructural proteins-3' NTR-poly(A), was found to be typical of a picornavirus. The VP0-VP3 and VP3-VP1 cleavage sites were determined to be Q-H and Q-T, respectively, by N-terminal amino acid sequence analyses using purified virion proteins. Possible cleavage sites, Q-G, Q-A, and Q-S, which cleave P2 and P3 polyproteins were found to be similar to those of picornaviruses. A dendrogram based on 3Dpol proteins indicated that Aichi virus is genetically distinct from the known six genera of picornaviruses including entero-, rhino-, cardio-, aphtho-, and hepatovirus and echovirus 22. Considering this together with other properties of the virus (T. Yamashita, S. Kobayashi, K. Sakae, S. Nakata, S. Chiba, Y. Ishihara, and S. Isomura, J. Infect. Dis. 164:954-957, 1991), we propose that Aichi virus be regarded as a new genus of the family Picornaviridae.

Acute Disease↗
PubMed1998

Electrocardiographic Changes and Mortality Due to Myocardial Infarction in Rats With or Without Imidapril Treatment.

BACKGROUND: Various angiotensin-converting enzyme inhibitors are known to improve heart function and prolong survival in patients and animals after myocardial infarction. Because myocardial infarction is known to induce arrhythmias, this study tested the hypothesis that early treatment with the angiotensin converting enzyme inhibitor imidapril reduces mortality during acute myocardial infarction because of protective effects against arrhythmogenesis. METHODS AND RESULTS: Rats were randomly divided into four groups: sham control, myocardial infarction, sham plus imidapril, and myocardial infarction plus imidapril. Myocardial infarction was produced by ligation of the left anterior descending coronary artery. Treated rats received imidapril (1 mg/kg/day) through a gastric tube beginning 1 hour after coronary occlusion; control rats received tap water. Electrocardiogram (ECGs) were recorded 1, 3, 7, and 21 days postocclusion. Infarct size and scar weight were determined at 21 days in the myocardial infarction groups with and without imidapril treatment. ECGs of untreated rats showed ST-segment changes, abnormal Q waves, premature ventricular complexes, and QT(c) prolongation 1-21 days after coronary occlusion. Total mortality in 21 days averaged 35% in untreated rats; mortality within 48 hours was 30%. On the other hand, imidapril-treated rats showed fewer ST-segment changes, fewer abnormal Q waves, and a decreased incidence of premature ventricular complexes after coronary occlusion; the ST-segment and QT(c) interval returned to basal values within 1 week after occlusion. Imidapril treatment did not affect the ECG pattern in sham-treated control animals. Total mortality in the imidapril-treated group in 21 days after infarction was 22.5%; mortality within 48 hours was 20% (P <.05 compared with the untreated infarction group). Infarct size and scar weight caused by coronary occlusion did not differ in the untreated and imidapril-treated groups. CONCLUSIONS: Early treatment with imidapril markedly decreases mortality in rats after acute myocardial infarction. The lower mortality is not associated with a decrease in infarct size but is consistent with a protective effect of the drug against arrhythmogenesis.

Journal Article↗
PubMed1998

Hepatitis C virus infection and heart diseases: a multicenter study in Japan.

As a collaborative research project of the Committees for the Study of Idiopathic Cardiomyopathy, a questionnaire was sent out to 19 medical institutions in Japan in order to examine the possible association between hepatitis C virus (HCV) infection and cardiomyopathies. Hepatitis C virus antibody was found in 74 of 697 patients (10.6%) with hypertrophic cardiomyopathy (mean age, 57.7 years) and in 42 of 663 patients (6.3%) with dilated cardiomyopathy (mean age, 56.5 years); these prevalences were significantly higher than that found in volunteer blood donors in Japan (2.4%, 50-59 years of age, each p<0.0001). The prevalence was significantly higher in patients suffering from hypertrophic cardiomyopathy as opposed to those with dilated cardiomyopathy (p<0.01). The presence of HCV antibody was detected in 650 of 11,967 patients (5.4%) patients seeking care in 5 academic hospitals. Various cardiac abnormalities were found among these patients, arrhythmias being the most frequent. These observations suggest that HCV infection is an important cause of a variety of otherwise unexplained heart diseases.

Cardiomyopathies↗
PubMed1998

Cell cycle of myocytes of cardiac and skeletal muscle in mitochondrial myopathy.

Patients who have mitochondrial myopathy can present with specific pathological conditions (eg, diabetes mellitus and deafness). A 36-year-old woman presented with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). An investigation was conducted into whether the abnormalitiy of mitochondrial DNA (a T to C transition at position 3271 in the mitochondrial tRNA [Leu(UUR)] gene) influences nuclear DNA synthesis by cells in the heart, skeletal muscles, and brain. Myocardium, skeletal muscle, and brain tissues were stained with hematoxylin-eosin, and Masson trichrome for histopathology. Target nuclei taken from the myocardial and skeletal muscles and brain tissue were purified after removing debris by the modified Hedley method. These nuclei were stained with propidium iodide (PI) for analysis by flow cytometry. The number of nuclei in the G2M phase was bigger in myocytes of MELAS than in normal myocytes (Control) (MELAS myocyte: Control myocyte=24.9+/-7.3: 6.1+/-1.6%, p<0.005), but there was no significant increase in the G2M phase in brain tissue. The G1 phase was far more reduced in MELAS myocytes and skeletal muscle than in Controls (MELAS myocyte: Control myocyte=65.8+/-9.1: 88.0+/-3.2%, p<0.005; MELAS skeletal muscle: Control skeletal muscle=85.1+/-2.2: 90.1+/-3.2%, p<0.05), while there was no significant decrease of nuclei in the G1 phase in brain tissue. Increased amount of nuclei in the G2M phase in cardiac myocytes and skeletal muscle cells compared with that in neurons might depend on the capacity for proliferation and differentiation of these cells as compared with brain tissue. It was concluded that the mitochondrial DNA mutation (3271T-to-C) of MELAS may influence the nuclear DNA synthesis of cells in various tissues depending on their level of mitotic activity.

Adult↗
PubMed1998

Subependymoma in the lateral ventricle incidentally detected by routine brain examination--case report.

A 42-year-old male visited our hospital for a routine brain examination, which incidentally identified an intraventricular mass lesion (2.7 x 1.6 x 1.2 cm3). Magnetic resonance imaging showed the tumor was isointense on the T1-weighted image and hyperintense on the T2-weighted and proton images. The intraventricular tumor was totally extirpated through the interhemispheric ipsilateral transcallosal approach. The histological diagnosis was subependymoma. Neuroimaging cannot differentiate this benign neoplasm from other more aggressive tumors. Widespread use of the medical checkup system is expected to find a higher incidence of otherwise non-identified asymptomatic lesions. Surgical extirpation is one of the treatment options to establish the correct diagnosis and to prevent symptoms.

Adult↗