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T Kurosawa

Publications and source records attributed to T Kurosawa.

At least 37 records · Page 2Linked to original sources
PubMed2001

An experimental study on radiation streaming through a labyrinth in a proton accelerator facility of intermediate energy.

A radiation streaming experiment has been carried out at the Takasaki Ion Accelerator Facility for Advanced Radiation Application at the Japan Atomic Energy Research Institute in a room housing a Cu target irradiated with 68 MeV protons and in a labyrinth of three-legs having a total length of 29 m. In the experiment, neutron and gamma ray energy spectra, neutron reaction rates, and neutron and gamma ray dose equivalent rates were measured using various counters and dosimeters. The experimental data show the applicability of some empirical formulas for estimating the thermal neutron flux in a room and neutrons streaming in a labyrinth designed for a proton accelerator operating in the intermediate energy region. The data suggest that it is mandatory to estimate the gamma ray dose equivalent rate in a labyrinth, which is dominated by the secondary gamma rays due to the neutron capture reaction.

Academies and Institutes↗
PubMed2001

Polymorphisms in the platelet-endothelial cell adhesion molecule-1 (PECAM-1) gene, Asn563Ser and Gly670Arg, associated with myocardial infarction in the Japanese.

We examined three missense polymorphisms of platelet-endothelial cell adhesion molecule-1 (PECAM-1), Val125Leu, Asn563Ser, and Gly670Arg, in 136 Japanese patients with myocardial infarction and 235 healthy Japanese controls. We found that these polymorphisms were in linkage disequilibrium with each other and that frequencies of 125Leu, 563Ser, and 670Arg alleles were significantly increased in patients compared with controls (0.522 vs 0.447, p = 0.048; 0.585 vs 0.502, p = 0.030; and 0.577 vs 0.492, p = 0.032, respectively). The frequencies of homozygotes for 563Ser and 670Arg alleles were also significantly increased in the patients (33.1% vs 23.4%, odds risk [OR] = 1.62, p = 0.040, 95% confidence interval [95%CI] = 1.01-2.58; and 32.4% vs 23.0%, OR = 1.60, p = 0.048, 95%CI = 1.00-2.57, respectively). These observations suggest that the 563Ser/Ser genotype and 670Arg/Arg genotype of PECAM-1 are novel genetic risk factors of myocardial infarction in Japanese. Stratification analysis of the patients showed that the associations of these PECAM-1 genotypes with myocardial infarction were preferentially found in male and younger patients (age of onset of myocardial infarction less than 60 years). In addition, the associations were stronger in patients with three-vessel disease than in the others and appeared independent of conventional risk factors including smoking, hypertension, diabetes mellitus, hyperlipidemia, and obesity.

Amino Acid Substitution↗
PubMed2001

Fetal bile acid metabolism: analysis of urinary 3beta-monohydroxy-delta(5) bile acid in preterm infants.

To elucidate the urinary concentration of total bile acids after birth and the profile of the usual and unusual urinary bile acids, especially 3beta-hydroxy-5-cholen-24-oic acid (Delta(5)-3beta-ol), we measured the concentrations of 13 bile acids in the urine from preterm infants vs. full-term controls by gas chromatography-mass spectrometry. The urinary concentration of total bile acids in early preterm infants below 32 weeks of gestational age significantly exceeded that of the late preterm and full-term infants (p < 0.0005). The major urinary bile acids in early preterm infants were cholic acid, 1beta,3alpha,7alpha,12alpha-tetrahydroxy-5beta-cholan-24-oic acid and Delta(5)-3beta-ol. In conclusion, the high urinary concentrations of total bile acids in preterm infants may be due to an overproduction, or more likely to a low hepatic bile acid clearance. An alternative fetal pathway, the acidic pathway, may be a major route of bile acid biosynthesis in preterm infants.

Bile Acids and Salts↗
PubMed2001

Linkage mapping of the mouse nephrosis (nep) gene to chromosome 15.

ICGN is a partially inbred strain of mice with nephrotic syndrome caused by spontaneous glomerular lesion. It has been reported that the albuminuria in ICGN mouse was controlled by at least a single autosomal recessive gene (nep). In this study, we mapped the nep locus by linkage analysis of backcross progeny between ICGN and MSM mice using DNA pooling method. The linkage analysis revealed that the nep locus was localized on the distal part of chromosome 15.

Animals↗
PubMed2001

Immunohistochemical analysis of molecular events in tubulo-interstitial fibrosis in a mouse model of diffuse mesangial sclerosis (ICGN strain).

Diffuse mesangial sclerosis (DMS) is one of the hereditary glomerular diseases and histologically characterized by severe glomerulosclerosis and subsequent tubulo-interstitial fibrosis (TIF). In DMS patients, renal dysfunction correlates well with TIF, rather than with glomerular lesions. Thus, molecular mechanisms whereby TIF in DMS progresses should be addressed. Previously, we found that nephrotic ICGN mice manifest DMS-like lesions and develop renal dysfunction in accordance with onset of TIF. In the present study, we investigated fibrogenic events involved in the progression of TIF after DMS manifestation, using the DMS mouse model. Immunohistochemistry revealed that expression of transforming growth factor-beta (TGF-beta) was rare in the interstitial cells of the nephrotic mice at the early-stage of DMS, while the TGF-beta expression became evident in the late-stage DMS mice. Platelet-derived growth factor (PDGF) was mildly expressed in the distal tubules of the early-stage DMS mice, whereas the PDGF expression markedly increased at the late-stage of DMS. As a result, alpha-actin-positive myofibroblastic cells were found dominant in the interstitial spaces of the late-stage DMS mice. Finally, TIF became severe in accordance with the overexpressions of these molecules. Our results suggest that in our murine model: 1) persistent proteinuria leads to over-expression of TGF-beta and PDGF in non-glomerular areas; 2) these cytokines provoke interstitial myofibroblast accumulation; and 3) the myofibroblasts produce fibrotic matrix proteins in the interstitial spaces. This process may possibly contribute to the development of TIF in DMS patients.

Albuminuria↗
PubMed2001

Immunohistochemical evaluation of a malignant phecochromocytoma in a wolfdog.

A malignant pheochromocytoma with multiple metastases was diagnosed in a 7-year-old male wolfdog that resulted from a cross between an eastern timber wolf (Canis lupus lycaon) and an Alaskan malamute. A yellowish white neoplastic mass approximately 10 cm diameter was found in the right adrenal gland. The neoplasm penetrated through the wall of the caudal vena cava. A diagnosis of pheochromocytoma was established by histopathologic and immunohistochemical procedures. Immunohistochemically, the neoplastic cells expressed chromogranin A, substance P, synaptophysin, Leu-7, protein gene product 9.5, methionine-enkephalin, S100 protein, and galanin. Multiple metastatic tumors were found in the kidneys, spleen, lungs, heart, and liver.

Adrenal Gland Neoplasms↗
PubMed2001

Usefulness of BMIPP SPECT to evaluate myocardial viability, contractile reserve and coronary stenotic progression after reperfusion in acute myocardial infarction.

Using combined 123I-BMIPP (BMIPP), 201Tl (Tl) and 99mTc-PYP (PYP) myocardial SPECT imaging, risk areas of acute myocardial infarction were documented in the acute stage, and then these images were evaluated for how well they reflected muscle viability, contractile reserve and coronary stenotic progression subsequent to reperfusion therapy. Patients who only experienced a first attack of myocardial infarction were enrolled. In total, 36 cases who had had the occluded artery successfully reperfused were examined during the past year. They had no significant vessel disease except for the culprit single artery. The patients were comprised of 32 men and 4 women. The mean age was 59.5 years. All patients underwent coronary angiography and left ventricular (LV) angiography in the emergency room. BMIPP/Tl and PYP myocardial SPECT were conducted in the acute stage and chronic stage. In the chronic stage LV angiography was repeated to assess the improvement of LV wall motion. The response to postextrasystolic potentiation (PESP) testing was performed to estimate myocardial contractile reserve. The risk area of acute myocardial infarction (AMI) was documented by reduced BMIPP accumulation. The size of reduced BMIPP accumulation was larger than that of PYP accumulation. A BMIPP/Tl discrepancy and PYP accumulation were documented to assess myocardial viability. Both improvement in LV wall motion and augmentation of PESP response were more closely related to a BMIPP/Tl discrepancy in the presence or absence of PYP accumulation. Therefore, it would be possible to evaluate myocardial viability and contractile reserve by the BMIPP/Tl discrepancy. In patients with good viability, it is important to predict whether there is coronary stenotic progression or not. In this study, we demonstrated that most patients with improved BMIPP images had no significant progression at the site of intervention. Serial observation of BMIPP images from the acute stage to the chronic stage might enable us to predict the progression of coronary stenosis.

Adult↗
PubMed2001

Microbiological contamination in genetically modified animals and proposals for a microbiological test standard for national universities in Japan.

The Biosafety Committee of the Japanese Association of Laboratory Animal Facilities of National Universities (JALAN) investigated recent episodes of microbiological contamination in genetically modified mice (GMM), and the countermeasures taken when the contaminated GMM were introduced into animal facilities, by questionnaires addressed to 53 animal facilities belonging to JALAN and serological tests. Although almost all of the contaminated GMM were accepted with conditions such as rederivation after or before reception and housing in designated rooms, contamination with a spectrum of microorganisms was demonstrated in GMM transferred domestically and from abroad. In serological tests, Mycoplasma pulmonis, mouse parvovirus, and mouse encephalomylitis virus were detected in GMM transferred from domestic facilities and from abroad. The present results of the questionnaires and serological tests suggest that GMM are highly and widely contaminated with microorganisms compared with mice from commercial breeders. Thus, we propose a microbiological requirement, including microbiological status--excellent, common, and minimum--as a guide for the transfer and procurement of mice and rats in Japan.

Animals↗
PubMed2001

Metabolic changes in human CD36 deficiency displayed by glucose loading.

Previous in vitro studies have shown that CD36 participates in cellular fatty acid (FA) uptake. In vivo evidence for a physiologic role of CD36 in this process is poor and mostly obtained in animals. To examine the metabolic role of human CD36, we performed a glucose loading test for normals (n = 16) and subjects with CD36 deficiency, both Type I (n = 5) and Type II (n = 16). After 30 min, FA levels had fallen by 60.1% in normals but by only 31.7% in Type II deficiency (P <0.01 vs. normals) and 16.5% in Type I deficiency which remained significantly higher than the other two groups out to 2 h. Further, changes in triglyceride and glucose metabolism were observed in the both types of CD36 deficiency. Impaired fast FA clearance by muscle and consequently increased hepatic FA uptake seem to underlie these changes. We conclude that human CD36 deficiency causes systemic metabolic changes.

Adult↗
PubMed2000

Reciprocal balance of hepatocyte growth factor and transforming growth factor-beta 1 in renal fibrosis in mice.

BACKGROUND: Transforming growth factor-beta 1 (TGF-beta 1) plays a central role in the pathogenesis of renal fibrosis. In contrast, hepatocyte growth factor (HGF) may be an important molecule for tissue repair. As TGF-beta 1 is a suppressor molecule for HGF expression, we asked whether a decrease in HGF expression would be accompanied by an increase in TGF-beta 1 and whether the progression of renal fibrosis would be modulated. METHODS: We used the ICR strain-derived glomerulonephritis (ICGN) mice as a model of chronic renal disease and examined changes in local HGF expression during the natural course of renal fibrosis. To determine the significance of intrinsic HGF noted during progression of renal fibrosis, we administered an anti-HGF antibody to mice at the early stage of renal fibrosis. RESULTS: At an early stage of renal fibrosis, the mice showed strong peritubular HGF expression, coinciding with tubular proliferation. In the late stages, the renal HGF level was markedly decreased, coinciding with a reduction in proliferative tubular areas. Renal TGF-beta 1 levels were increased in accordance with expansion of fibrotic areas. Notably, the anti-HGF antibody treatment of early-stage mice decreased the HGF level and reduced tubular areas, whereas collagen-deposited areas were expanded in parallel with increased TGF-beta 1 levels. Consequently, in HGF-neutralized mice, there was a rapid progression of renal dysfunction. CONCLUSIONS: Not only an increase in TGF-beta 1 level, but also a decrease in local HGF expression may be responsible for the manifestation of renal fibrosis, particularly tubular destruction.

Animals↗
PubMed2000

Resuscitation from fulminant myocarditis associated with refractory ventricular fibrillation.

Resuscitation was possible in a case of fulminant myocarditis with refractory ventricular fibrillation (Vf) using a percutaneous cardiopulmonary support system (PCPS). A 46-year old Japanese man suddenly experienced cardiopulmonary dysfunction shortly after the onset of flu symptoms, was promptly diagnosed as having fulminant myocarditis and PCPS was immediately initiated. On the second day in the hospital, refractory Vf occurred, which lasted for approximately 2h despite repeated efforts to terminate it. Finally, a large dose of steroids was administered. From the third day of hospitalization and onwards, the Vf disappeared totally. The patient completely recovered from such a serious state in 6 months. During the following 3 years, he has had no clinical symptoms of worsening. As in this case demonstrates, most myocarditis is curable and invasive measures are very helpful in rescuing patients from the fulminant type with refractory Vf.

Anticoagulants↗
PubMed2000

Metabolic significance and expression of Caenorhabditis elegans type II 3-oxoacyl-CoA thiolase.

The authors cloned the cDNA of the nematode Caenorhabditis elegans encoding a 44-kDa protein (P-44), which is similar to sterol carrier protein x (SCPx). Genomic DNA data and Northern blot analysis excluded the possibility of P-44 forming SCPx-like fusion protein. P-44 is required in the formation of bile acid in vitro from CoA esters of their enoyl-form intermediate in the presence of D-3-hydroxyacyl-CoA dehydratase/D-3-dehydrogenase bifunctional protein. Also, rat SCPx converts 24-hydroxy-form intermediate to bile acid under similar conditions. From this and other evidence, P-44 and SCPx were categorized as type II thiolase. The mRNA encoding P-44 was detected in every developmental stage of C. elegans: egg, larval stages, and adult. P-44, therefore, seems essential for the normal functioning of this organism.

Acetyl-CoA C-Acyltransferase↗
PubMed2000

Factors predicting mortality in patients after myocardial infarction caused by left main coronary artery occlusion: significance of ST segment elevation in both aVR and aVL leads.

Acute left main coronary artery obstruction is rare and most patients in this clinical setting die of sudden death or cardiogenic shock. During the past 8 years, we encountered 13 patients with acute myocardial infarction caused by total occlusion of the left main coronary artery (LMCA-AMI). Thus, we surveyed these patients, and attempted to elucidate helpful predictors related to the prognosis. Six of 13 patients with LMCA-AMI survived. Successful left coronary artery dilatation was achieved in all survivors (group S), and in 5 (71%) non-survivors (group non-S). The age was not different between the two groups. A past history of angina was confirmed in 83% of group S. while only in 29% of group non-S. Clinical findings such as time of onset of AMI, interval from the AMI onset to admission, elapsed period from the AMI onset to recanalization of LMCA and the value of CK on admission were not different between the two groups. However, cardiogenic shock occurred in only 1 patient (17%) in group S compared with 5 patients (71%) in group non-S. As emphasized in the literature, good collateral circulation to the left anterior descending artery was observed in 5 patients (83%) in group S, while not observed in group non-S. Electro cardiographically, ST elevation in the aVR lead was very characteristic. This finding was confirmed in 69% of the total patients. Noticeably, 5 out of 6 non-survivors (83%) showed ST elevation not only in leads aVR but also in the aVL lead. In addition to the absence of collateral circulation, this electrocardiographic finding, which obviously indicates the presence of extensive myocardial ischemia in the diseased heart, is a simple and important predictor suggesting a poor prognosis in LMCA-AMI patients.

Angioplasty, Balloon, Coronary↗
PubMed2000

Expression of alpha-smooth muscle actin and fibronectin in tubulointerstitial lesions of cats with chronic renal failure.

OBJECTIVE: To examine renal expression of alpha-smooth muscle actin (alpha-SMA) and fibronectin in cats with tubulointerstitial nephritis (TIN) for use in predicting progression to renal fibrosis. ANIMALS: 19 cats with TIN and 9 cats without nephritis. PROCEDURE: Serum creatinine and BUN concentrations were measured. Indices for glomerular extra-cellular matrix (ECM), tubular injury (TI), and fibronectin were determined in renal specimens to quantify the extent of injury and fibrotic lesions. Expression of alpha-SMA in renal tissue was immunohistochemically detected, and correlations were evaluated between the alpha-SMA index and other histologic and clinical variables. RESULTS: The alpha-SMA index in tubulointerstitial areas (1.63 +/- 0.78) was significantly higher in cats with TIN, especially in the periglomerular and peritubular areas, than in cats without nephritis (0.20 +/- 0.14). The alpha-SMA index was significantly associated with the TI index (r2 = 0.70), fibronectin index (r2 = 0.95), BUN concentration (r = 0.64), and serum creatinine concentration () = 0.66). Of special interest was that interstitial alpha-SMA expression appeared evident in the kidneys at an early stage of TIN, prior to the onset of ECM deposition. CONCLUSION AND CLINICAL RELEVANCE: Analysis of results of histologic and clinical examinations revealed that interstitial alpha-SMA expression may have clinical importance and may be a useful early histologic marker for development of chronic renal failure in cats. An immunohistochemical examination for fibrogenic molecules (such as alpha-SMA expression) may provide fundamental information on the pathogenesis of early-stage renal disease and aid clinical management of cats with chronic renal failure, including TIN.

Actins↗
PubMed1999

Apoptotic DNA fragmentation and upregulation of Bax induced by transient ischemia of the rat retina.

This study was performed to examine the involvement of apoptosis and the expression of bcl-2 family genes in ischemia-induced retinal injury. Retinal ischemia was induced in adult rats by raising the intraocular pressure to 130 mmHg for 45 min. Selective damage to the inner retina was observed 7 days after ischemia. No terminal deoxynucleotidyl-transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) positive cells were observed in the normal retina, but there was a significant number of TUNEL positive cells 6-48 h after transient ischemia followed by a decrease at 96 and 168 h. The number of TUNEL positive cells reached a maximum at 24 h after ischemia. DNA laddering was observed on agarose gel electrophoresis with the retinas 24 and 48 h after ischemia but not in the normal retina. Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) revealed that bax gene expression did not change immediately after cessation of ischemia, but gradually increased as early as 6 h, reached a peak at 24 h, then decreased to near baseline levels at 168 h. On the other hand, bcl-2 gene expression showed no obvious changes at any time after transient ischemia. Moreover, intense Bax protein immunoreactivity was detected in the retinal sections at 24 h after ischemia although little immunoreactivity was present in the normal sections. These results suggest that apoptosis associated with the expression of Bax is involved in retinal cell loss after ischemic insult.

Animals↗
PubMed1999

Immunohistochemical demonstration of bovine viral diarrhoea virus antigen in the pancreatic islet cells of cattle with insulin-dependent diabetes mellitus.

The pancreatic islets were studied in seven cattle with insulin-dependent diabetes mellitus (IDDM) associated with persistent bovine viral diarrhoea virus (BVDV) infection. BVDV antigen was detected immunohistochemically in the pancreatic islet cells. There was a decrease in the size and number of islets, vacuolar degeneration of residual islet cells, and lymphocytic insulitis. The atrophied islets were composed of small uniform cells with limited amounts of cytoplasm, containing a small number of insulin- and chromogranin-positive granules. Enlarged islets consisting of islet cells with vacuolated cytoplasm were also frequently observed. Many of the vacuolated islet cells differed from the cells of normal islets in containing fewer cytoplasmic insulin- and chromogranin-positive granules. Mild lymphocytic insulitis was observed frequently in enlarged islets but rarely in atrophied islets. Immunoreactivity with BVDV antibody was found in the acinar cells of the pars exocrina in all seven cattle and in the residual cells of the islets of Langerhans of four cattle. BVDV antigen-positive cells were seen more frequently in the enlarged islets than in the atrophied islets. Some islets with lymphocytic infiltrates showed a small number of antigen-positive cells. These findings suggest that autoimmune IDDM was induced by persistent BVDV infection, resulting in gradual destruction of the islet beta cells.

Animals↗