Keishiro Kawamura

Osaka Medical College, Takatuki, Ōsaka, Japan

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Publications (109)327.24 Total impact

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    ABSTRACT: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by the progressive replacement of myocardial cells by fat and fibrous tissue. Here we describe the histopathological features of biopsied myocardium from a patient with ARVC. A large amount of adipose tissue was present in the biopsy specimen, and a group of myocardial cells were isolated as an island-like region in the adipose tissue. Electron microscopic examination of cardiomyocytes revealed a large number of intracellular lipid droplets, including some extremely large droplets. Disruptions of the plasma membrane and dissociation of intercellular junctions were associated with discharge of intracellular lipid droplets into the interstitial space. The high accumulation of intracellular lipid droplets may be involved in the pathogenesis of ARVC and may have played an important role in myocardial cell death and progressive replacement of cardiomyocytes by fatty tissue in the current case.
    Heart and Vessels 12/2008; 23(6):440-4. · 2.13 Impact Factor
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    ABSTRACT: The cause of chest pain in patients with normal coronary arteriograms (CAG) remains poorly understood. Left ventricular endomyocardial biopsies from 11 anginal patients with normal CAG and normal left ventriculograms and from seven anginal patients with coronary stenosis were studied by light and electron microscopy. Biopsies from seven non-anginal patients (non-ischemic electrocardiogram abnormalities but no evident heart or systemic diseases) served as controls. In anginal patients with normal CAG, both cardiocytic diameter (17.2 +/- 5.5 microm) and interstitial space percentage area (37.6 +/- 14.9%) were significantly larger than those (13.7 +/- 0.9 microm, 14.9 +/- 2.9%) in control participants. Some cardiocytic nuclei (1.9% of 2000 randomly selected nuclei) exhibited DNA degradation by in-situ nick-end labeling. Electron microscopy revealed cardiocytic nuclei with distinct apoptotic ultrastructures (2.8% of 200 nuclei), phagocytic degradation of cardiocytic cytoplasm, and capillary endothelial swelling (7.1% of 200 capillary transverse sections). No significant infiltration of inflammatory cells was seen. In anginal patients with coronary narrowing (cardiocytic diameter, 16.8 +/- 1.1 microm; interstitial space, 20.1 +/- 5.8%; DNA degraded nuclei, 1.3%), there were however no apoptotic cardiocytic nuclei or cytoplasm and less capillary endothelial swelling (1.6%) in ultrastructure. In biopsies from anginal patients with normal CAG, the presence of cardiocytic hypertrophy and replacement fibrosis are both abnormal. Cardiocytic apoptosis and capillary endothelial swelling, found by others as characteristic of experimental myocardial reperfusion injury, are evident. This supports the possibility of myocardial transient ischemia and reperfusion injury in patients with angina and normal CAG.
    Coronary Artery Disease 03/2002; 13(1):25-35. · 1.30 Impact Factor
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    ABSTRACT: Partial left ventriculectomy (PLV) can be used to treat refractory congestive heart failure caused by dilated cardiomyopathy (DCM). In order to understand the relationship between the underlying myocardial injury and early clinical outcomes after PLV, histopathologic, immunohistochemical and virologic studies of the resected myocardium were performed. The posterolateral left ventricular walls from 27 patients with idiopathic DCM were examined. Cardiomyocyte diameter, degree of myocardial fibrosis, degree of cardiomyocyte degeneration, and degree of inflammatory cell infiltration were compared with mortality rates. Polymerase chain reaction was performed to detect enterovirus genome in the myocardium. Some patients had inflammatory cell infiltrates with focal accumulations of lymphocytes and macrophages, including both cytotoxic/suppressor T-cells and helper/inducer T-cells. The number of inflammatory cells (activated lymphocytes plus macrophages/mm2) was significantly greater in patients who died of cardiac insufficiency after surgery (27.8 +/- 5.7; n = 7) than in the survivors (11.1 +/- 2.5; n = 15). There was no significant difference in the degree of myocardial fibrosis, cardiomyocyte diameter or degree of cardiomyocyte degeneration between the 2 groups. Enterovirus genome was detected in the myocardium of 9 (38%) of 24 patients examined and 5 of these enterovirus-positive hearts had severe inflammatory cell infiltrates (37.9 +/- 2.5/mm2). Early survival in patients undergoing PLV for DCM is significantly affected by the degree of myocardial inflammation, so patients with more severe or ongoing inflammation may have poor clinical outcomes. Chronic myocarditis may play an important role in the etiology and pathophysiology of idiopathic DCM.
    Japanese Circulation Journal 10/2001; 65(9):797-802.
  • Japanese Circulation Journal 01/2001; 65(7):691-694.
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    ABSTRACT: The aim of this study was to evaluate the viral etiology of idiopathic dilated cardiomyopathy (DCM). The demonstration of enteroviral genome in hearts with DCM has reinforced the importance of enteroviruses in the pathogenesis of DCM. However, there is uncertainty about the character and activity of enteroviruses detected in the myocardium. Recently, the association of hepatitis C virus or adenovirus with DCM has been reported. Myocardial specimens from 26 patients with idiopathic DCM, which were obtained at partial left ventriculectomy (PLV), were examined virologically. Strand-specific detection of enteroviral RNA was performed to differentiate active viral replication from latent persistence. Polymerase chain reaction was used to detect genomic sequences of hepatitis C virus, adenovirus, cytomegalovirus, influenza viruses, mumps virus, herpes simplex viruses, varicella-zoster virus and Epstein-Barr virus. Plus-strand enteroviral RNA was detected in 9 (35%) of the 26 patients. Minus-strand enteroviral RNA was determined in seven (78%) of these nine plus-strand RNA-positive patients. Sequence analysis revealed that the enteroviruses detected were coxsackie B viruses, such as coxsackievirus B3 and B4. However, genetic material from other viruses was not detected. Six (86%) of seven minus-strand enteroviral RNA-positive patients died of cardiac insufficiency within the first six months after PLV. Coxsackie B viruses were seen in hearts with idiopathic DCM. Active viral RNA replication appeared to be present in a significant proportion of these cases. Minus-strand coxsackieviral RNA in the myocardium can be a marker for poor clinical outcome after PLV. There was no evidence of persistent infection by other viruses in hearts with DCM.
    Journal of the American College of Cardiology 12/2000; 36(6):1920-6. · 15.34 Impact Factor
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    ABSTRACT: Myocardial integrated backscatter (IB) imaging has been reported to be useful for ultrasonic tissue characterization and delineation of myocardial viability or fibrosis. beta-Blocker therapy has beneficial effects for patients with dilated cardiomyopathy (DCM), but there are no clear findings that indicate which patients with DCM will respond to this therapy. This study was performed to evaluate whether myocardial IB analysis can predict the response to beta-blocker therapy. We prospectively performed echocardiographic examination with IB analysis in 29 patients with DCM (20 men, 9 women) before starting bisoprolol therapy and in 15 normal subjects. Standard echocardiographic examination and IB analysis in the left ventricular wall in the 2-dimensional short-axis view were performed and the magnitude of cyclic variation (CV) of IB and calibrated myocardial IB intensity (subtracted pericardial) were obtained from the interventricular septum and the left ventricular posterior wall. Sixteen patients responded to bisoprolol therapy and 13 did not respond after 12 months of full-dose therapy. Calibrated myocardial IB intensity was lower in responders relative to nonresponders in both the interventricular septum (responders, -20.1 +/- 3.6 dB vs nonresponders, -9.8 +/- 5.1 dB, P <.0001; controls, -20.1 +/- 4.4 dB) and posterior wall (responders, -20.6 +/- 3.6 dB vs nonresponders, -14.6 +/- 4.2 dB, P =.0002; controls, -22.7 +/- 3.3 dB). Also, the lower the myocardial intensity in the interventricular septum or posterior wall, the better left ventricular systolic function improved after beta-blocker therapy. However, CV was lower in both DCM groups than in the controls, and CV in the interventricular septum was lower in nonresponders than in responders (responders, 4.0 +/- 4.1 dB vs nonresponders, -0.8 +/- 6. 1 dB, P <.02; controls, 8.3 +/- 2.4 dB). In addition, CV in the posterior wall showed no difference between the 2 DCM groups (responders, 5.6 +/- 1.3 dB vs nonresponders, 5.1 +/- 3.5 dB, P = not significant; controls, 9.6 +/- 2.5 dB). Also, the percent fibrosis on right ventricular endomyocardial biopsy specimens showed no distinctions between these 2 groups (responders, 25.1% +/- 16.1% vs nonresponders, 24.9% +/- 15.0%, P = not significant). These findings suggest that left ventricular myocardial IB data, especially IB intensity, provide useful information for predicting the response to beta-blocker therapy in patients with DCM. However, right ventricular endomyocardial biopsy findings do not appear to contribute to discriminating between the 2 groups.
    American Heart Journal 06/2000; 139(5):905-12. · 4.56 Impact Factor
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    ABSTRACT: A cardiac homeobox-containing gene Csx/Nkx2-5, which is essential for cardiac development, is abundantly expressed in the adult heart as well as in the heart primordia. Targeted disruption of this gene results in embryonic lethality due to abnormal heart morphogenesis. To elucidate the role of Csx/Nkx2-5 in the adult heart, we generated transgenic mice which overexpress human Csx/Nkx2-5. The transgene was expressed abundantly in the heart and the skeletal muscle. mRNA levels of several cardiac genes including natriuretic peptides, CARP, MLC2v, and endogenous Csx/Nkx2-5 were increased in the ventricle of the transgenic mice. Electron microscopic analysis revealed that the ventricular myocardium of the transgenic mice had many secretory granules, which disappeared after administration of vasopressin. These results suggest that Csx/Nkx2-5 regulates many cardiac genes and induces formation of secretory granules in the adult ventricle.
    Biochemical and Biophysical Research Communications 05/2000; 270(3):1074-9. · 2.28 Impact Factor
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    ABSTRACT: Heart-type fatty acid-binding protein (H-FABP) is a low molecular weight cytoplasmic protein and present abundantly in the myocardium. When the myocardium is injured, as in the case of myocardial infarction, low molecular weight cytoplasmic proteins including H-FABP are released into the circulation and H-FABP is detectable in a blood sample. We have already developed a direct sandwich-ELISA for quantification of human H-FABP using two distinct types of monoclonal antibodies specific for human H-FABP. In this study we investigated the clinical validity of H-FABP as a biochemical diagnostic marker in the early phase of acute myocardial infarction (AMI). To evaluate the diagnostic usefulness of H-FABP in the early phase of AMI, blood samples were obtained from the following patients within 12 hours after the appearance of symptoms, and serum levels of H-FABP were compared with those of conventional diagnostic markers, such as myoglobin and creatine kinase isoenzyme MB (CK-MB). Blood samples were collected from patients with confirmed AMI (n=140), patients with chest pain who were afterwards not classified as AMI by normal CK-MB levels (non-AMI) (n=49) and normal healthy volunteers (n=75). The serum concentration of H-FABP was quantified with our direct sandwich-ELISA. The concentration of myoglobin mass was measured with a commercial RIA kit. The serum CK-MB activity was determined with an immuno-inhibition assay kit. The overall sensitivity of H-FABP, within 12 hours after the appearance of symptoms, was 92.9%, while it was 88.6% with myoglobin and 18.6% with CK-MB. The overall specificity of H-FABP was 67.3%, while it was 57.1% with myoglobin and 98.0% with CK-MB. The diagnostic efficacy rates with these markers were 86.2% (H-FABP), 80.4% (myoglobin) and 39.2% (CK-MB), respectively. The diagnostic validity of H-FABP was further assessed by receiver operating characteristic (ROC) curve analysis. The area under the curve (AUC) of H-FABP was 0.921, which was significantly greater than with myoglobin (AUC: 0.843) and CK-MB (AUC: 0.654). These parameters, such as sensitivity, specificity, diagnostic efficacy and diagnostic accuracy, obtained for patients with chest pain within 3 hours and/or 6 hours after the onset of symptoms were almost the same as those for patients within 12 hours after symptoms. H-FABP is more sensitive than both myoglobin and CK-MB, more specific than myoglobin for detecting AMI within 12 hours after the onset of symptoms, and shows the highest values for both diagnostic efficacy and ROC curve analysis. Thus, H-FABP has great potential as an excellent biochemical cardiac marker for the diagnosis of AMI in the early phase.
    Clinical Chemistry and Laboratory Medicine 04/2000; 38(3):231-8. · 2.96 Impact Factor
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    ABSTRACT: Scanning electron microscopy (SEM) with secondary electron emissions is useful for the study of cardiomyocyte architecture, however, the information is limited from the cell surface. Whereas backscattered electron (BSE) emission can give a high-resolution image of the specimen's intracellular structure after heavy metal staining. In this study, we applied BSE imaging analysis to the study of the arrangement of cardiomyocytes in the myocardium. The tissue specimens from a normal fresh monkey heart, normal human heart obtained at autopsy, and surgically resected tissue from a patient with old myocardial infarction in the left ventricular aneurysmectomy were used. The tissue specimens were fixed in neutral formalin, treated with NaOH and then stained with Gomori's silver methenamine reagent followed by tannic acid and osmium tetroxide. After dehydration and drying, the specimens were coated with carbon and examined by SEM with a BSE detector. In the tissue preparations, the A bands of sarcomeres were selectively stained with silver so that the arrangements of subsarcolemmal myofibrils and the intercalated discs were clearly seen in the BSE images. In the left ventricular aneurysmal walls of old myocardial infarction, atrophied cardiomyocytes with disarray of subsarcolemmal myofibrils were observed. The results strongly suggest that BSE images are further applicable to the study of the architecture of cardiac myocytes and their branches, and the arrangement of intracellular myofibrils in various diseased myocardium.
    Cardiovascular Pathology 03/2000; 9(2):103-109. · 2.34 Impact Factor
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    ABSTRACT: Cardiocyte loss during myocardial hypertrophy leads to progressive dysfunction in human hearts with chronic hemodynamic overload. The mechanism for such cell elimination is unknown. We examined lysosomal participation in cardiocytic degradation present in human cardiac biopsies, utilizing electron microscopic cytochemistry (acid phosphatase). Lysosomes were significantly increased in number (t-test, P<0.001) in 50 hemodynamically overloaded hearts (375+/-69, mean+/-s.e.m., per 5,000 microm(2) cardiocytic area; eight controls, 38+/-11). Secondary lysosomes were prominent near degenerative intracellular organelles in both hypertrophic and atrophic cardiocytes. Increased lysosomal and phagocytic activity in the cytoplasm without typical nuclear apoptosis resembled cytoplasmic degradation in developmental programmed cell death described in different tissues. We also demonstrated cardiocytic DNA degradation (in situ nick-end labeling) in autopsy hearts, including 299 nuclei normalized per 10(6) observed nuclei from five concentrically hypertrophied hearts, 1961 nuclei from five eccentrically hypertrophied hearts, and no positive nuclei in five controls. We postulate a chronic self-controlled cytoplasmic proteolysis in cardiocytes, not initially associated with either nuclear degradation or intercellular dehiscence but later possibly accompanied by apoptotic nuclear elimination, and leading to apoptotic cell death.
    Journal of Molecular and Cellular Cardiology 02/2000; 32(1):161-75. · 5.22 Impact Factor
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    ABSTRACT: To examine whether warfarin therapy had any influence on left atrial spontaneous echo contrast, we performed serial transesophageal echocardiography with integrated backscatter analysis in 12 patients with non-valvular atrial fibrillation. We found that the integrated backscatter intensity of the left atrial cavity did not change after 1 to 2 months of warfarin therapy, and concluded that this therapy does not influence spontaneous echo contrast.
    The American Journal of Cardiology 11/1999; 84(7):857-9, A8. · 3.43 Impact Factor
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    ABSTRACT: Many of the myocardial wall motion abnormalities in heart donors are reversible after transplantation, indicating that the presence of wall motion abnormalities should not automatically lead to the exclusion of donor hearts. The present study observes the natural course of brain death-induced myocardial dysfunction, and investigates whether low-dose dobutamine stress echocardiography could identify reversible myocardial dysfunction in brain-dead patients. We prospectively measured the serial changes of left ventricular fractional shortening (FS) using echocardiography and cardiac troponin T from admission to the time of cardiac standstill in 30 brain-dead patients. Patients were divided into 2 groups according to FS at the time of brain death; group I (FS > or =30%) and group II (FS <30%). Dobutamine stress echocardiography was performed in group II. Twenty-three patients were in group I and 7 patients were in group II. Four patients among 7 patients in group II showed dobutamine-nonresponsive wall motion (group IIa) and the remaining 3 patients showed dobutamine-responsive wall motion (group IIb). Troponin T at the time of brain death was markedly higher in group IIa than in groups I and IIb (5.13+/-3.79 vs 0.23+/-0.20, 0.22+/-0.16 ng/ml, p <0.0001, respectively). FS remained normal and troponin T was not increased until cardiac standstill in group I. FS remained decreased and troponin T remained elevated until cardiac standstill in group IIa, whereas FS became normal at 7 days after brain death with no change in troponin T in group IIb. Thus, some brain death-induced myocardial dysfunction is reversible and low-dose dobutamine stress echocardiography may identify reversible myocardial dysfunction.
    The American Journal of Cardiology 09/1999; 84(5):578-82. · 3.43 Impact Factor
  • Journal of Cardiac Failure 09/1999; 5(3):62-62. · 3.07 Impact Factor
  • Journal of Cardiac Failure 09/1999; 5(3):77-77. · 3.07 Impact Factor
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    ABSTRACT: Leukocyte tyrosine kinase (LTK) is a receptor-type protein tyrosine kinase belonging to the insulin receptor superfamily. To elucidate its biological role, we generated transgenic mice expressing LTK under the control of cytomegarovirus enhancer and beta-actin promoter. The transgenic mice exhibited growth retardation and most of the transgenic mice died within several months after birth. Interestingly, although LTK was expressed in several major organs, the activation (tyrosine-phosphorylation, kinase activity, and multimerization) of LTK was observed selectively in the heart, where LTK was localized on intracellular membrane, presumably on endoplasmic reticulum. Echocardiography showed that the transgenic heart underwent severe concentric hypertrophy, which resulted in reduced cardiac output, low blood pressure, and increased heart rate. Histological examination of the heart exhibited focal degeneration of cardiomyocytes. These histological changes were considered to be due to apoptosis, based on the finding that the sarcolemmas of the degenerative cardiomyocytes were well preserved. In addition, expression of fetal genes, such as atrial natriuretic peptide and skeletal alpha-actin, was markedly induced in the transgenic heart. These results indicate that a certain tissue-specific mechanism of activating LTK exists in the heart and that the activated LTK resulted in cardiac hypertrophy, cardiomyocyte degeneration and gene reprogramming. These findings will provide novel insights into the activating mechanism and biological role of LTK in vivo.
    Oncogene 08/1999; 18(26):3821-30. · 8.56 Impact Factor
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    ABSTRACT: Multivessel spasm in variant angina is believed to be a major prognostic factor. Three patterns of multivessel spasm have been detected: (1) spasm at different sites on different occasions (migratory spasm); (2) spasm sequentially affecting 2 different sites (sequential spasm); and (3) simultaneous spasm at more than 1 site (simultaneous spasm). The present study investigated the prognosis based on this factor for variant angina without fixed coronary stenosis and examined the influence of multivessel spasm on cardiac events. Twenty-six patients were diagnosed as having variant angina without fixed coronary stenosis using 12-lead 24-h ECG recording system and coronary cineangiography. These patients were followed up prospectively for 57.1+/-7.6 months. Of the 26 patients 13 had single-vessel spasm, 6 had migratory multivessel spasm angina, and 7 showed sequential and/or simultaneous multivessel spasm angina. The survival free of serious cardiac events and of all cardiac events was significantly lower for patients with sequential and/or simultaneous multivessel spasm than for those with migratory multivessel spasm (p<0.05, p<0.05), whereas for patients with migratory multivessel spasm the difference comparison with single-vessel spasm did not attain statistical significance (p = ns, p = ns). The results of this study suggest that there seems to be a high-risk subgroup (i.e., sequential and/or simultaneous multivessel spasm) among patients with variant angina.
    Japanese Circulation Journal 07/1999; 63(7):509-13.
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    ABSTRACT: The mechanism of cardiac uptake of long-chain free fatty acids has not been fully determined. We encountered a hypertrophic cardiomyopathy patient who showed a lack of cardiac uptake of 2 different types of long-chain fatty acid analogues on the scintigraphic images. Flow cytometric analysis revealed no platelet or monocyte CD36 molecule expression (type I CD36 deficiency) and his CD36 gene showed homozygous mutation for 478C to T substitution, leading to an abnormal CD36 amino acid sequence. These findings strongly suggest that a specific transporting system rather than a simple diffusion is commonly involved in the cardiac uptake of long-chain free fatty acids in humans, and that the CD36 protein is the most likely candidate for the specific transporter and to explain scintigraphic defects on fatty acid imaging.
    Japanese Circulation Journal 05/1999; 63(4):319-22.
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    ABSTRACT: Scanning electron microscopy was used to compare the shape, size, and connection of left ventricular (LV) myocytes between spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) at 3, 8, 15, 35, and 63 weeks of age. For either strain at each age, five rats were studied, in which LV myocytes consisted of a cylindrical trunk with series (SB) and/ or lateral branch(es) (LB) and step formations; cell junctions had 12 common basic patterns. The length (L), width (W), and L/W ratio of the myocytes, and various indices for SB, LB, and three selected types of cell junctions were measured in 100 cells from each heart and averaged for comparison studies. In the growing period (3-8 weeks of age), the LV myocytes were similar in shape and width in the two age-matched strains and grew similarly with the same L/W ratio. In adolescent (15-week-old) WKY, LV cells grew with the same L/W ratio as in the younger rats, whereas in adolescent SHR, the cells showed a much greater increase in width than in length (disproportionate hypertrophy), the LB proliferated significantly, and the numbers of step-to-step and side-to-side junctions were diminished. In adult (15-35-week-old) WKY, LV cells continued to grow without much change in SB, LB, and the cell junctions, whereas in adult SHR, LV hypertrophy progressed with enhanced cardiomyocyte hypertrophy, increased number of SB, LB, and step-to-end junctions, and reduction in the number of step-to-step and side-to-side junctions per cell. In aged (63-week-old) WKY and SHR, the indices of LV myocytes, SB, LB, and cell junctions did not differ from those in adult WKY and SHR, except for LB thinning in the WKY and significant LB loss in the SHR. Age-related reductions in side-to-side- and step-to-step junctions, and LB loss with myocardial fibrosis in adult and aged SHR may indicate increased loss of gap junctions which couple the cells for transverse conduction, and contribute to anisotropic discontinuous propagation and potential reentrant LV arrhythmias.
    Heart and Vessels 02/1999; 14(1):15-28. · 2.11 Impact Factor
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    ABSTRACT: Patients can present with hypertrophied papillary muscles in the left ventricle, even without hypertrophy in other segments, and they have electrocardiographic (ECG) abnormalities suggestive of hypertrophic cardiomyopathy (HCM). This study was performed to evaluate whether the solitary papillary muscle hypertrophy was related to HCM. By analyzing 6731 echocardiographic studies between 1990 and 1994, the incidence of patients with papillary muscle hypertrophy was retrospectively examined, as well as the ECG features and family history related to HCM in these patients. After the normal size of the anterolateral and posteromedial papillary muscles was obtained from echocardiographic studies in 40 healthy subjects (0.7 +/- 0.2 cm for each of the vertical and horizontal axis), papillary muscle hypertrophy was defined as follows: either the vertical or horizontal diameter of at least one of the 2 papillary muscles was more than 1.1 cm (mean+2SD in the normal subjects). Using this definition, 29 patients with papillary muscle hypertrophy were identified, of whom 14 (48%) showed high voltage QRS complexes, 10 (34%) showed T wave inversion, and 6 (21%) showed abnormal Q waves. Ten patients (34%) had a family history of HCM. In 2 patients that were followed for 18 and 11 years, respectively, the voltages of the QRS complexes and inverted T waves progressed with the hypertrophy of the papillary muscle. These findings suggest that solitary papillary muscle hypertrophy is related to HCM and that papillary muscle hypertrophy is a newly identified subtype of or an early form of HCM.
    Japanese Circulation Journal 12/1998; 62(11):811-6.
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    ABSTRACT: In patients with malignant lymphoma, the first signs and symptoms are frequently noncardiac and clinical manifestations of cardiac involvement are often nonspecific. This case report presents a patient with malignant lymphoma whose first manifestation was characteristic of heart failure, mainly due to diastolic dysfunction, and whose postmortem examination revealed massive myocardial invasion.
    Japanese Circulation Journal 12/1998; 62(11):863-7.

Publication Stats

2k Citations
327.24 Total Impact Points

Institutions

  • 1983–2008
    • Osaka Medical College
      • • First Department of Internal Medicine
      • • Third Department of Internal Medicine
      Takatuki, Ōsaka, Japan
  • 1992–2000
    • University of Texas Medical Branch at Galveston
      • Department of Pathology
      Galveston, Texas, United States
  • 1997
    • Fujita Health University
      • Department of Internal Medicine
      Nagoya, Aichi, Japan
  • 1996
    • Kyushu University
      Hukuoka, Fukuoka, Japan
  • 1991
    • Nagoya University
      • Division of Biological Chemistry
      Nagoya-shi, Aichi-ken, Japan