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Biomedical subjects

Y Ueda

Publications and source records attributed to Y Ueda.

At least 127 records · Page 7Linked to original sources
PubMed2000

Evidence of hepatic endogenous hydrogen peroxide in bile of selenium-deficient rats.

Hepatic endogenous hydrogen peroxide (H(2)O(2)) in bile of selenium-deficient rats (SeD) was for the first time found using the electron spin resonance (ESR) spin-trap technique, and the relationship between glutathione peroxidase (GPX) activity and H(2)O(2) amount is discussed. Normal rats and four groups of rats fed a selenium-deficient diet with different feeding periods were examined. The results showed that the GPX activity decreased depending on the feeding period with the selenium-deficient diet and that the hepatic endogenous H(2)O(2) amount in the bile of the rats fed the selenium-deficient diet for the longest period (a week before birth to 8 weeks old) was drastically higher than those in other groups of rats (P < 0.005). We found that generation of H(2)O(2) due to the decrease in the GPX activity has a threshold value. The results suggest that an exposure to selenium deficiency for long term will cause oxidative stress.

Animals↗
PubMed2000

Increased platelet aggregability in response to shear stress in acute myocardial infarction and its inhibition by combined therapy with aspirin and cilostazol after coronary intervention.

Although antiplatelet therapy with a specific inhibitor of phosphodiesterase-3 cilostazol improves stent patency compared with use of aspirin (ASA) alone, the specific role of cilostazol on platelet aggregation in patients with acute myocardial infarction (AMI) is less well understood. Thirty-six patients with AMI who were successfully treated with primary angioplasty were randomized to 3 antiplatelet regimens: ASA alone (n = 12), ASA + ticlopidine (n = 12), and ASA + cilostazol (n = 12). We measured shear stress-induced platelet aggregation (SIPA) using a modified cone-plate viscometer on admission and on day 7, and evaluated the inhibitory effects of combination therapy with ASA + cilostazol on SIPA. Compared with cases of stable coronary artery disease, significant increases in SIPA and plasma von Willebrand factor activity were observed in patients with AMI before they received antiplatelet therapy. On day 7 after primary angioplasty, ASA did not inhibit SIPA (65 +/- 15% vs 57 +/- 11%, p = 0.086), whereas both combination therapies of ASA + ticlopidine and ASA + cilostazol significantly inhibited SIPA in patients with AMI (ASA + ticlopidine: 61 +/- 15% vs 45 +/- 13%, p <0. 0001; ASA + cilostazol: 64 +/- 14% vs 43 +/- 9%, p <0.005). There was a significant correlation of SIPA with adenosine diphosphate (ADP)-induced platelet aggregation (r = 0.412, p = 0.003) and with plasma von Willebrand factor activity (r = 0.461, p = 0.0008). These data suggest that patients with AMI have increased platelet aggregability in response to high shear stress. Combined antiplatelet therapy with ASA + cilostazol appears to be as effective as therapy with ASA + ticlopidine for reducing SIPA in patients with AMI who are undergoing primary angioplasty.

Aged↗
PubMed2000

Compensatory enlargement of the coronary artery in acute myocardial infarction.

Compensatory enlargement occurred in 71% of lesions in patients with acute myocardial infarction and was more common in these patients than in patients with stable effort angina pectoris. These results suggest that compensatory enlargement may be associated with plaque rupture and subsequent acute myocardial infarction.

Aged↗
PubMed2000

beta-blocker therapy in patients after aortic valve replacement for aortic regurgitation.

BACKGROUND: beta-blocker therapy for dilated or ischemic cardiomyopathy is now an accepted and effective treatment. However, little is known about its efficacy in patients with postoperative impaired left ventricular function. This retrospective study was designed to assess the effects of beta-blocker therapy in patients after aortic valve replacement (AVR) for aortic regurgitation (AR). METHODS: A total of 59 patients who underwent AVR for chronic AR were assigned to four groups. Twelve patients were treated with both ACE inhibitors and beta-blockers, 12 patients with only ACE inhibitors, eight patients with only beta-blockers, and 27 patients without beta-blockers or ACE inhibitors. A postoperative echocardiographic study was performed one year after surgery. RESULTS: The heart rate was significantly reduced in patients with beta-blockers despite the use of ACE inhibitors after surgery. Postoperative left ventricular volume was more significantly decreased in beta patients than in non-beta patients despite the use of ACE inhibitors. There were also significant reductions in left ventricular mass index in ACE+beta patients compared to ACE+non-beta patients. However, there were no significant differences in NYHA functional class and survival rate between beta patients and non-beta patients. CONCLUSIONS: beta-blocker therapy may improve cardiac performance by reducing cardiac volume and mass in patients with impaired LV function after AVR for AR.

Adrenergic beta-Antagonists↗
PubMed2000

In vivo electron spin resonance spectroscopy on signal decay of intrastriatal nitroxide radical after acute administration of haloperidol in rats.

Sequential changes in the electron spin resonance (ESR) signal intensity of nitroxide radical perfused in the striatum of rats treated with haloperidol (HPD) were evaluated using a 700-MHz ESR spectrometer. Nitroxide radical was perfused in the striatum by in vivo microdialysis. Nitroxide used was 3-carbamoyl-2,2,5, 5-tetramethylpyrrolidine-1-oxyl. Following 6-h perfusion of the nitroxide radical by dialysis at the rate of 2 microl/min through the radical introducer that had been stereotaxically implanted in the rat's striatum, HPD or saline was injected intraperitoneally into the rats in the resonator. The sequential changes in the ESR spectrum of the nitroxide radical were then evaluated. Spectra were successively observed in all animals. The half-life, which was estimated on the basis of the exponential decay in signal intensity, was used as a parameter of decay rate of the ESR signal intensity of nitroxide radical. The half-life in the rats injected with HPD was significantly longer than that in controls. This finding suggests that the reducing ability of the striatal extracellular space of a rat acutely treated with HPD was decreased in comparison with that of the control.

Animals↗
PubMed2000

[Healing in the intestinal anastomosis--comparison of the Albert-Lembert and Gambee methods].

An experimental comparative histomorphological study was made on intestinal healing processes following an Albert-Lembert suture with approximation of the serosal surface and Gambee's layer to layer anastomosis of a dog. There was no obvious complications such as postoperative hemorrhage, anastomotic stenosis or anastomotic leakage. Although both anastomoses resulted in a good healing process, Gambee's layer to layer suture, which caused the submucosal layers to face each other, showed better wound healing at the anastomosis in terms of layer to layer attachment. As a conclusion, Gambee's layer to layer anastomosis seemed to be a better anastomotic technique in terms of wound healing for the intestinal anastomosis.

Anastomosis, Surgical↗
PubMed2000

Clinical and radiographic evaluation of disc excision for lumbar disc herniation with and without posterolateral fusion.

STUDY DESIGN: A prospective study evaluating the clinical and radiographic results in 95 patients with lumbar disc herniation. OBJECTIVES: To evaluate the results of disc excision, with and without posterolateral fusion. SUMMARY OF BACKGROUND DATA: The effect of posterolateral fusion on the outcomes and radiologic changes in patients with lumbar disc herniation has rarely been reported. METHODS: Forty-four patients underwent disc excision, and 51 patients underwent disc excision and fusion. Clinical symptoms were evaluated using the Japanese Orthopaedic Association Back scores. All medical and surgical records were examined with regard to intraoperative blood loss, operation time, and other data. Preoperative and follow-up radiographs were analyzed to determine the spinal motion and disc height. RESULTS: Clinical outcome was excellent or good in 73% of the nonfusion group and in 82% of the fusion group (P = 0.31). The reduction in lower back pain after surgery was greater in the fusion group. The rate of recurrent disc herniation at the surgical level in the nonfusion group increased, but intraoperative blood loss, operation time, length of hospital stay, and total cost of procedure were all significantly less in the patients undergoing disc excision alone than in the fusion group. The radiologic analysis provided evidence that the disc height at the level of disc excision and posterolateral fusion in the fusion group decreased with time, as in the nonfusion group. The changes in disc height and spinal motion were not related to the clinical results. CONCLUSIONS: Although there is still controversy regarding the pros and cons of fusion in association with disc excision, there is seldom an indication for primary fusion for lumbar disc herniation.

Adolescent↗
PubMed2000

Functional impairment of p73 and p51, the p53-related proteins, by the human T-cell leukemia virus type 1 Tax oncoprotein.

We have previously demonstrated that the human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein represses the trans-activation function of p53 tumor suppressor protein. Recently, several proteins with sequence homology to p53 have been identified. In this study, we demonstrated that Tax represses the trans-activation functions of p73alpha, p73beta, and p51A, the p53-related proteins, as well as p53. Moreover, a mutant Tax of coactivator CBP-binding site (K88A), which activated NF-kappaB but not CREB pathway, could not repress the p73 nor p51 trans-activation functions, indicating that CBP-binding domain of Tax is essential for the suppression of their functions. Using proteins of Gal4-fused N-terminal region of p73 and p51, we showed that Tax-mediated inactivation of p73 or p51 requires for their N-terminal trans-activation domains. Furthermore, only the putative N-terminal trans-activation domains of them did not have enough transcriptional activities and their adjacent regions are essential for their full trans-activation, suggesting the existence of their second trans-activation subdomains. Thus, HTLV-1 Tax inactivated the p53-related proteins through their N-terminal trans-activation domains.

DNA-Binding Proteins↗
PubMed2000

Nifedipine-induced coronary vasodilation in ischemic hearts is attributable to bradykinin- and NO-dependent mechanisms in dogs.

BACKGROUND: Dihydropyridine calcium channel blockers protect endothelial cells against ischemia and reperfusion injury, suggesting that nifedipine may increase the in vivo cardiac NO level and thus coronary blood flow (CBF) in ischemic hearts. We tested this hypothesis. METHODS AND RESULTS: In open-chest dogs, coronary perfusion pressure (CPP) was reduced in the left anterior descending coronary artery so that CBF decreased to one third of the control level, and thereafter CPP was maintained constant (103+/-8 to 43+/-3 mm Hg, n=9). We obtained fractional shortening (FS) and lactate extraction ratio (LER) as indices of regional myocardial contraction and metabolism. Both FS (26.4+/-2.1% to 6.7+/-2.0%, n=9, P<0.001) and LER (32+/-6% to -37+/-5%, n=9, P<0.001) showed a decrease when CPP was reduced. After intracoronary infusion of nifedipine (4 microgram. kg(-1). min(-1)), CBF increased from 30+/-1 to 48+/-4 mL. 100 g(-1). min(-1) (P<0.01) without a change of CPP (n=9). Both FS (14.0+/-1.9%, n=9) and LER (-9+/-7%, n=9) also increased (P<0.01). Nifedipine increased the difference in the level of metabolites of NO (nitrate+nitrite; 9+/-3 to 25+/-5 nmol/mL, n=9, P<0.01) and bradykinin (22+/-5 to 58+/-4 pmol/mL, n=9, P<0.01) between coronary venous and arterial blood. L-NAME (an NO synthase inhibitor) or HOE-140 (a bradykinin receptor antagonist) attenuated (P<0.05) the increase in CBF (29+/-3 and 35+/-2 mL. 100 g(-1). min(-1), n=5 each), FS (4.8+/-0.6% and 6.9+/-1.7%, n=5 each), LER (-47+/-8% and -35+/-9%, n=5 each), and nitrate+nitrite (3+/-2 and 8+/-4 nmol/mL, n=5 each) due to nifedipine infusion. CONCLUSIONS: These results indicate that the calcium channel blocker nifedipine mediates coronary vasodilation and improves myocardial ischemia through both bradykinin/NO-dependent and -independent mechanisms.

Animals↗
PubMed2000

Sequential changes in glutamate transporter mRNA levels during Fe(3+)-induced epileptogenesis.

Severe head injury in humans can cause recurrent seizures; this form of epilepsy appears to correlate with the occurrence of parenchymal hemorrhage. The injection of ferric cations, one component of hemoglobin, into rat amygdala, causes lipid peroxidation, and recurrent spontaneous seizures. We wondered whether the regulation of glutamate might be perturbed as a result of severe head injury, which might then act as a mechanism of chronic epileptogenesis. Levels of glutamate transporter glutamate-aspartate transporter (GLAST), glutamate transporter-1 (GLT-1), and excitatory amino-acid carrier (EAAC-1) mRNA were measured in ipsilateral and contralateral hippocampi and cerebral cortex removed from rats at 60 min, 24 h, and 5, 15 and 30 days after FeCl(3) injection into the amygdaloid body. While the neuronal transporter EAAC-1 mRNA was elevated bilaterally for up to 30 days following the microinjection that initiated seizures, GLT-1 mRNA, derived from glial cells, returned to basal levels. At 15 and 30 days after injection, however, when the experimental animals were experiencing spontaneous limbic behavioral seizures, GLAST mRNA was down-regulated. Epileptogenesis may correlate with the impairment of glial glutamate transport, leading to an excitation and imbalance of transmitter influences within the hippocampi and cerebral cortex.

ATP-Binding Cassette Transporters↗
PubMed2000

Latent hepatitis B virus infection in healthy individuals with antibodies to hepatitis B core antigen.

Several recent reports have shown that hepatitis B virus (HBV) could be frequently transmitted to the recipients from donors who have antibodies to hepatitis B core antigen (anti-HBc) through liver transplantation. We provide here the molecular evidence of latent HBV infection accompanied with ongoing viral replication in the liver tissue of anti-HBc-positive healthy individuals. HBV DNA was detectable in 13 of 14 healthy donors who were positive for both anti-HBc and antibodies to hepatitis B surface antigen (anti-HBs), but in none of 3 who were positive for anti-HBs alone. The detected HBV genomes from these subjects included covalently closed circular DNA and pregenomic RNA, the replication intermediate of HBV. Notably, 5 of 7 cases tested were predominantly infected with wild type HBV strains without any mutations in the precore and core promoter regions under the presence of circulating antibody to hepatitis B e antigen. Interestingly, a predominant clone detected in one donor showed a 63-nucleotide deletion in the precore region including an encapsidation signal sequence. Our findings indicate that the majority of healthy individuals positive for anti-HBc, which had been assumed to denote a past history of transient HBV infection, were latently infected with the episomal form of HBV accompanied by ongoing viral replication and few nucleotide mutations in the precore and core regions.

Adult↗
PubMed2000

Immunohistochemical localization of cathepsin D in colorectal tumors.

PURPOSE: Although it has been suggested that cathepsin D, a lysosomal protease, is involved in tumor invasion and metastasis in human colorectal cancers, conflicting studies have also been reported recently. In addition, this issue has been only rarely studied in human colorectal tumors by use of immunohistochemical methods. The aim of the study presented here was to clarify not only the correlation between cathepsin D expression and tumor invasion or metastasis but also the correlation between the intracellular immunostaining pattern of cathepsin D and tumor invasion and metastasis in human colorectal tumors. METHODS: Thirty-four primary colorectal adenocarcinomas and 24 adenomas were immunostained by use of an anticathepsin D antibody. Both the incidence and the immunostaining patterns of cathepsin D were investigated in all tissue samples. RESULTS: Three different immunostaining patterns, i.e., supranuclear, basal, and diffuse, were observed in samples containing cathepsin D. Although the incidence of cathepsin D-positive carcinomas was not correlated with tumor progression, invasion, or metastasis, the immunostaining pattern was significantly correlated with lymphatic invasion. CONCLUSIONS: The results of this study suggest that abnormal cathepsin D immunostaining patterns (basal or diffuse) can be used to predict a potential for lymphatic invasion in colorectal carcinoma.

Adenocarcinoma↗
PubMed2000

Sarpogrelate reduces mechanical hemolysis in patients with heart valve prostheses.

OBJECTIVE: We evaluate the clinical efficacy of sarpogrelate, an antiplatelet drug that improves red blood cell deformability, to reduce the intravascular hemolysis problems suffered frequently by patients implanted with heart valve prostheses. SUBJECTS: Subjects were 34 patients undergoing mechanical heart valve replacement and having serum lactate dehydrogenase concentrations 20% above the maximum normal range. METHOD: Sarpogrelate was given daily, 100 mg orally for the first 6 months and 200 mg thereafter. RESULTS: Average serum lactate dehydrogenase decreased significantly from 423 +/- 108 IU/l, to 391 +/- 83 IU/l with the 100 mg dose, and to 361 +/- 86 IU/l with the 200 mg dose. The percentage of reticulocytes decreased from 15.5 +/- 5.3/1000 to 15.3 +/- 5.7/1000 at the 100 mg dose and 13.1 +/- 4.0/1000 at the 200 mg dose. Serum iron concentrations increased significantly from 63.2 +/- 24.8 micrograms/dl to 76.2 +/- 16.2 micrograms/dl at the 100 mg dose, and to 70.9 +/- 26.2 micrograms/dl with the 200 mg dose. CONCLUSION: Sarpogrelate is a useful drug for patients with implanted heart valve prostheses and subsequent high serum lactate dehydrogenase because it works as an antiplatelet drug and reduces mechanical hemolysis.

Adult↗
PubMed2000

Coronary surgery through partial sternotomy in a patient with tracheostoma.

We report successful coronary artery bypass grafting through a lower partial sternotomy for a patient with a tracheostoma. He required a tracheotomy for serious laryngeal edema which developed during anesthetic induction prior to elective conventional coronary surgery. A safe alternative approach, comprising a lower midline skin incision with a lower partial sternotomy distant from the stoma, facilitated coronary artery bypass grafting to the left and right coronary arteries after four weeks.

Coronary Artery Bypass↗
PubMed2000

Nephrotoxicity of D-proparglyglycine in mice.

When D-propargylglycine was injected intraperitoneally into mice, polyuria, glycosuria, and aminoaciduria were observed as has been previously reported in rats. The urine of the mice treated with D-propargylglycine contained twice as much protein as that of the control mice. Polyacrylamide gel electrophoresis showed a new protein of approximately 62 kDa in the urine of the D-propargylglycine-treated mice. Protein sequencing revealed that this protein was serum albumin. Since the above-mentioned symptoms suggested dysfunction of the renal proximal tubules, the activity of urinary N-acetyl-beta-D-glucosaminidase, a marker enzyme of injury to the proximal tubules, was measured. The urinary enzyme activity was 2.6 times higher in the D-propargylglycine-treated mice than in the control mice. Light- and electron-microscopy showed degenerative and necrotic cells in the straight part of the proximal tubules of the treated mice. However, none of these symptoms was observed in D-propargylglycine-treated mutant mice, lacking D-amino-acid oxidase. These results indicate that D-propargylglycine itself is not nephrotoxic but its metabolite produced by the D-amino-acid oxidase reaction is nephrotoxic and injures proximal tubular cells, resulting in an impairment of the reabsorption of water, glucose, amino acids, and proteins.

Alkynes↗
PubMed2000

Molecular regulation of glutamate and GABA transporter proteins by valproic acid in rat hippocampus during epileptogenesis.

Epileptiform discharges and behavioral seizures may be the consequences of the presence of either excessive excitation associated with the neurotransmitter glutamate or from inadequate inhibitory effects associated with gamma-aminobutyric acid (GABA). Synaptic effects of these neurotransmitters are terminated by the action of transporter proteins that remove these amino acids from the synaptic cleft. The glial transporters glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1), and the neuronal transporter excitatory amino acids carrier-1 (EAAC-1) limit excitation initiated by synaptic release of glutamate. Transporter proteins GABA transporter-1 (GAT-1) and GABA transporter-3 (GAT-3) remove GABA from synaptic regions. To assess the molecular effects of the antiepileptic drug valproate, albino rats with chronic, spontaneous, recurrent seizures induced by amygdalar injection of FeCl3 were treated for 14 days with either valproic acid or with saline as an injection control. Regions of the hippocampus were assayed for glutamate and GABA transporters by western blot. While epileptogenesis is thought to correlate with the downregulation of GLAST and upregulation of EAAC-1, valproate caused an increase in the quantity of GLAST protein measured in the hippocampus. Valproate treatment decreased GLT-1 in both control and experimental animals in both hippocampi. EAAC-1 was unchanged by valproate treatment. GABA transporters GAT-1 and GAT-3 in the hippocampus were upregulated by FeCl3 injection into the amygdala. However, valproate caused the downregulation of these GABA transporters in both control and experimental animals. Altered molecular regulation of glutamate appears to be critical in the development of sustained, spontaneous limbic seizures. Our data suggest that valproate may have unique mechanisms of action; specifically, it may affect the removal of glutamate by upregulating GLAST and decreasing GABA transport, which could result in increased tissue concentrations of GABA.

ATP-Binding Cassette Transporters↗
PubMed2000

Kindling phenomena induced by the repeated short-term high potassium stimuli in the ventral hippocampus of rats: on-line monitoring of extracellular glutamate overflow.

We observed in this study that transient periodic stimuli in response to high potassium (40 mM, 5 min at 40-min intervals, 13-15 stimuli) perfusion in the ventral hippocampus of rats led to the appearance of a kindling-like phenomenon. In this kindling-like phenomenon, we confirmed the augmentation of glutamate release and the prolongation of spike discharge. Changes in the extracellular glutamate levels before and after the stimuli were monitored by the application of in vivo microdialysis combined with on-line enzyme fluorometric detection of glutamate. This kindling-like phenomenon was not observed when microdialysis was carried out using a Ca++-free medium. The augmentation of glutamate release and the prolongation of spike discharge with epileptic convulsions are completely Ca++ dependent. These data show that repeated short-term increases in extracellular glutamate levels results in the enhancement of excitatory neuronal systems, causing an excessive propagation of seizure activity and culminating in secondary generalized seizures.

Action Potentials↗