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Biomedical subjects

M Aoki

Publications and source records attributed to M Aoki.

At least 91 records · Page 5Linked to original sources
PubMed2001

Inhibition of neointima by angiotensin-converting enzyme inhibitor in porcine coronary artery balloon-injury model.

Because hepatocyte growth factor (HGF) stimulates growth of endothelial cells exclusively without replication of vascular smooth muscle cells, we hypothesized that HGF may play a role in cardiovascular disease. In human vascular smooth muscle cells, angiotensin II suppressed local vascular HGF production in a dose-dependent manner. Using a rat balloon-injury carotid artery model, we demonstrated that blockade of angiotensin II inhibited neointimal formation, accompanied by a significant increase in local HGF production. However, the relation of vascular HGF to endothelial function was not clarified. Moreover, it is important to test the hypothesis in animal models that are more similar to human restenosis. Thus, in the present study, we used a porcine coronary artery balloon-injury model to study the role of angiotensin II in regulation of the local HGF system in vivo. Expression of HGF mRNA was significantly decreased in balloon-injured coronary arteries versus intact vessels. An angiotensin-converting enzyme (ACE) inhibitor (perindopril) significantly inhibited neointimal formation after balloon injury compared with vehicle (P:<0.05). In addition, vasodilator response of balloon-injured coronary arteries to bradykinin was restored by perindopril treatment, whereas no vasodilator response was observed in balloon-injured vessels treated with vehicle. Vasodilator response of balloon-injured arteries induced by perindopril was completely abolished by N:(w)-nitro-L-arginine methyl ester. Of particular interest, vascular HGF mRNA was significantly increased in balloon-injured vessels treated with perindopril as compared with vehicle. Overall, the present study demonstrated that ACE inhibitor significantly inhibited neointimal formation, accompanied by significant improvement of endothelial dysfunction and a significant increase in local vascular HGF mRNA in vivo in a porcine coronary artery balloon-injury model. Given the strong mitogenic activity of HGF on endothelial cells, improvement of endothelial dysfunction by perindopril might be due to increased local HGF expression through enhancement of reendothelialization after balloon injury, in addition to its direct effect, ACE inhibition. Downregulation of the local vascular HGF system may play an important role in the pathogenesis of cardiovascular disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Mitogenic and antiapoptotic actions of hepatocyte growth factor through ERK, STAT3, and AKT in endothelial cells.

Hepatocyte growth factor (HGF), a member of the angiogenic growth factors, may play a pivotal role in the regulation of endothelial cells, inasmuch as HGF shows mitogenic and antiapoptotic actions in endothelial cells. Because the mechanism of these actions is still unclear, we examined the signal transduction system of HGF in human aortic endothelial cells. Treatment of endothelial cells with recombinant HGF (rHGF) resulted in a significant increase in DNA synthesis as assessed by thymidine incorporation. Importantly, phosphorylation of extracellular signal-related kinase (ERK) and Akt by rHGF was clearly observed. Thus, we further examined the effects of specific inhibitors of ERK or Akt on cell proliferation. Pretreatment with PD98059, a mitogen-activated protein kinase kinase inhibitor, significantly attenuated cell proliferation induced by rHGF, whereas inhibitors of phosphatidylinositol-3-OH kinase, wortmannin, and LY-294002, did not. Interestingly, treatment with rHGF significantly increased the phosphorylation of the signal transducers and activators of transcription (STAT)3 (Ser727), whereas PD98059 attenuated the phosphorylation of Ser727 induced by rHGF. In addition, treatment with rHGF significantly increased the promoter activity of c-fos, which includes the sis-inducible element and serum response element, whereas PD98059 completely attenuated the activation of the c-fos promoter induced by rHGF. In contrast, inhibition of Akt by wortmannin and LY-294002 failed to inhibit the phosphorylation of STAT3 and c-fos activation. On the other hand, treatment with rHGF attenuated the increase in LDH release and caspase-3 activity induced by tumor necrosis factor-alpha stimulation. In contrast to DNA synthesis, wortmannin and LY-294002 markedly attenuated the decrease in caspase-3 activity mediated by rHGF, whereas PD98059 did not. Overall, the present study demonstrated that HGF stimulated cell proliferation through the ERK-STAT3 (Ser727) pathway and had an antiapoptotic action through the phosphatidylinositol-3-OH kinase-Akt pathway in human aortic endothelial cells. These findings provide new perspectives in the role of HGF in cardiovascular disease.

Androstadienes↗
PubMed2001

Endothelial apoptosis induced by oxidative stress through activation of NF-kappaB: antiapoptotic effect of antioxidant agents on endothelial cells.

Injury of endothelial cells has been assumed to be an initial trigger of the development of atherosclerosis. In this study, we investigated the molecular mechanisms of endothelial cell death induced by hypoxia, which leads to oxidative stress. To study the relation between hypoxia-induced cell death and activation of nuclear factor-kappaB (NF-kappaB) in a hypoxic state, we evaluated the effect of 2 antioxidant drugs, probucol and pyrrolidine dithiocarbamate (PDTC), on human endothelial apoptosis. Although hypoxic treatment of human aortic endothelial cells resulted in a significant decrease in cell number and a significant increase in apoptotic cells compared with that of cells under normoxia (P<0.01), treatment with probucol (50 micromol/L) or PDTC (100 micromol/L) significantly attenuated the decrease in cell number (P<0.01) and was accompanied by inhibition of NF-kappaB activation. Furthermore, downregulation of bcl-2 caused by hypoxia was inhibited by these drugs. We further investigated the translocation of bax protein from the cytoplasm to the mitochondrial heavy fraction membrane, as translocation of bax protein is considered to be a determinant of apoptosis. Interestingly, we found that antioxidant treatment inhibited the translocation of bax protein caused by hypoxia. Moreover, upregulation of p53, a proapoptotic molecule, was observed in hypoxia, whereas treatment with probucol attenuated the expression of p53 accompanied by suppression of NF-kappaB activation. These data suggest functional links between p53 and endothelial apoptosis through the activation of NF-kappaB. Overall, the current study demonstrated that oxidative stress induced apoptosis in human aortic endothelial cells through the downregulation of bcl-2, translocation of bax, and upregulation of p53, probably through NF-kappaB activation. Oxidative stress may play an important role in endothelial apoptosis mediated by hypoxia, through the activation of NF-kappaB.

Anticholesteremic Agents↗
PubMed2001

Evaluation of accumulated mucopolysaccharides in the brain of patients with mucopolysaccharidoses by (1)H-magnetic resonance spectroscopy before and after bone marrow transplantation.

In seven patients with mucopolysaccharidoses (1 Hurler, 1 Hurler-Scheie, 4 Hunter, 1 Sly), cranial (1)H-magnetic resonance spectroscopy was performed to evaluate the accumulation of mucopolysaccharides and biochemical changes in the CNS in vivo before and after bone marrow transplantation (BMT). In two of seven patients, (1)H-magnetic resonance spectroscopy was performed before and after BMT. Nuclear magnetic resonance spectra of dermatan sulfate and chondroitin sulfate-C and magnetic resonance spectroscopy of chondroitin sulfate-C and urine from patients with mucopolysaccharidoses showed resonance higher than the chemical shift of myoinositol in the brain (3.7 ppm). The resonance was considered to contain signals from mucopolysaccharide molecules. The resonance was measured as presumptive mucopolysaccharides (pMPS). In white matter lesions detected by magnetic resonance imaging, pMPS/creatine ratios and choline/creatine ratios were consistently higher than control ratios. In white matter without lesions, choline/creatine ratios were higher than control ratios. Patients with higher developmental quotient or intelligence quotient tended to show higher N:-acetylaspartate/creatine ratios and lower pMPS/creatine ratios in basal ganglia. After BMT, the pMPS/creatine ratio in white matter lesions of patient 3, with Hunter syndrome, was slightly decreased, but in none of the patients was the ratio ever below the control ratios, even 7 y after BMT. In white matter without lesions, the pMPS/creatine ratio in patient 3 was decreased to the control ratios after BMT, but although the choline/creatine ratios were gradually decreased, they remained higher than the control ratio, 2 y after BMT. These results suggest that evaluation of pMPS, choline, and N:-acetylaspartate by (1)H-magnetic resonance spectroscopy is an important technique that may provide useful biochemical information in vivo on the neurologic process and the efficacy of BMT in patients with mucopolysaccharidoses.

Adolescent↗
PubMed2001

Medium-mediated bystander effects on HSG cells co-cultivated with cells irradiated by X-rays or a 290 MeV/u carbon beam.

The mechanisms of medium-mediated bystander effects on cell survival and micronucleus (MN) induction were investigated by co-cultivating unirradiated HSG cells with cells irradiated by X-rays or 290 MeV/u carbon beams. It was found that the survival of the irradiated cells exponentially decreased along with the dose, and that the plating efficiency (PE) of the unirradiated recipient cells was obviously more enhanced than that of the control cells. Moreover, MN was induced in the unirradiated recipient cells and its yield had a maximum distribution corresponding to the donor dose, which was different from the linear-quadratic dose response of the yield of MN in the irradiated cells. The treatment of PTIO, a scavenger of nitric oxide (NO), decreased both PE and MN of the unirradiated recipient cells to control levels. Moreover, nitrite was detected in the co-culture medium, and its concentration was related to the donor dose. These results indicated that NO was involved in the above mentioned medium-mediated bystander effects. In addition, an equation was deduced to well fit the induction of MN of the unirradiated recipient cells.

Bystander Effect↗
PubMed2001

Relative biological effectiveness of the 235 MeV proton beams at the National Cancer Center Hospital East.

A therapy-dedicated cyclotron was installed in the National Cancer Center Hospital East (NCCHE) at Kashiwa in 1997. Prior to the start of clinical use, we investigated the biological effectiveness of therapeutic proton beams for cell lethality. The proton beams accelerated up to 235 MeV were horizontally extracted from the cyclotron, and scattered by a bar-ridge filter to produce a Spread-Out-Bragg-Peak (SOBP) of 10-cm width. The biological systems used here were mouse intestinal crypt cells and three in vitro cell lines, including SCC61 human squamous cell carcinoma, NB1RGB human fibroblasts and V79 Chinese hamster cells. The dose responses after irradiation at either the entrance plateau or the middle portion of SOBP were compared with those after linac 6 MV X-ray irradiation. The fit of a linear quadratic model to survival curves showed that proton irradiation increased the alpha value of SCC61 and the beta value of V79 cells with a least change for alpha/beta ratio of NB1RGB cells. The isoeffect dose that reduces either cell survivals to 10% or mouse jejunum crypts to 10 per circumference was termed D10. The relative biological effectiveness (RBE) of protons obtained by comparing the D10 values between protons and X-rays ranged from 0.9 to 1.2. The depth distribution of cell lethality was measured by replating V79 cells after irradiation from a "cell stack chamber" that received a single dose of 7 Gy at the middle position of SOBP. The thus-obtained cell survivals at various depths coincided well with the estimated survivals, but tended to decrease at the distal end of SOBP. We conclude that an RBE of 1.1 would be appropriate for 235 MeV proton beams at the NCCHE.

Animals↗
PubMed2001

Acute cholestatic hepatitis caused by a probable allergic reaction to paracetamol in an adolescent.

We reported on an adolescent who suffered from cholestatic hepatitis after taking a low dose of paracetamol. It was suspected that the condition was brought about by an allergic reaction to paracetamol. Paracetamol is one of the representative intrinsic hepatotoxic drugs. There have been only a few reports on liver damage due to an allergic reaction to paracetamol. There is a need to call attention to this particular reaction.

Acetaminophen↗
PubMed2001

Effects of dobutamine on coronary flow velocity response and their relations to age.

The purpose of this study was to assess the effects of low-dose dobutamine on left ventricular (LV) functional and coronary flow reserves using transthracic echocardiography. The study group consisted of 30 children aged from 5 months to 16 years (mean 4.8 +/- 4.4 years). Echocardiographic studies were repeated before and during dobutamine infusion (5 microg/kg per minute). The peak diastolic velocity in the left descending coronary artery (LAD) was recorded by pulsed-Doppler under the guidance of color Doppler flow mapping. The coronary flow velocity (CFV) response was calculated as the ratio of LAD peak flow velocity at dobutamine infusion to basal LAD peak flow velocity. Left ventricular contractility was calculated by two-dimensionally directed M-mode echocardiography. The rate-corrected mean velocity of circumferential fiber shortening (mVcfc) and LV end-systolic wall stress (ESS) were used as indices of contractility. Adequate spectral Doppler recordings of the LAD peak flow velocity for the assessment of CFV response were obtained in 26 of 30 patients (87%). The LAD peak flow velocity at dobutamine infusion increased significantly compared with the basal values. The CFV response in the younger children was low and increased significantly with age. The CFV response did not show significant correlations with the changes in heart rate, systolic blood pressure, rate-pressure product, nor ESS during dobutamine infusion. However, a significant relationship between the CFV response and the percent change of mVcfc was observed. In the present study using high frequency transthoracic echocardiography, we demonstrated the age-related changes in CFV response and LV functional reserve by dobutamine infusion. Responses of LV contractility and coronary flow to dobutamine are less sensitive in youngerchildren and increased with increasing age.

Adolescent↗
PubMed2001

Phosphorylation of p38 mitogen-activated protein kinase downstream of bax-caspase-3 pathway leads to cell death induced by high D-glucose in human endothelial cells.

Because high D-glucose significantly stimulates endothelial cell death, we examined the molecular mechanisms of high D-glucose-induced endothelial apoptosis. Treatment of human aortic endothelial cells with high D-glucose (25 mmol/l), but not mannitol and L-glucose, resulted in a significant decrease in cell number and a significant increase in apoptotic cells as compared with a physiological concentration (5 mmol/l). Interestingly, high D-glucose treatment significantly increased bax protein, accompanied by translocation of bax protein from cytosol to mitochondria-enriched heavy membrane fraction. In contrast, the expression and distribution of bcl-2 protein were not altered by high D-glucose. In addition, the activity of caspase-3 proteases was increased after exposure to high glucose, whereas caspase inhibitors prevented endothelial cell death induced by high D-glucose. On the other hand, p38 mitogen-activated protein kinase (MAPK) was markedly phosphorylated and showed sustained phosphorylation after stimulation. A specific inhibitor of p38 MAPK, SB 203580, and the overexpression of kinase-inactive p38 MAPK significantly attenuated cell death induced by high D-glucose in human aortic endothelial cells, whereas at 6 h after high D-glucose treatment, SB 203580 and overexpression of kinase-inactive p38 MAPK did not attenuate caspase-3 activation induced by high D-glucose. Importantly, caspase inhibitors significantly attenuated the sustained phosphorylation of p38 MAPK induced by high D-glucose. Thus, we finally focused the MAPK kinase (MEK) kinase 1 (MEKK1) to further examine the cross-talk between p38 MAPK and the bax-caspase proteases pathway. High D-glucose treatment induced MEKK1 cleavage, whereas caspase inhibitors significantly attenuated the cleavage. Importantly, kinase-inactive MEKK1 also blocked the phosphorylation of p38 MAPK induced by high D-glucose. Here, we demonstrated that high D-glucose induced apoptosis in human endothelial cells through activation of the bax-caspase proteases pathway and through phosphorylation of p38 MAPK mediated by MEKK1. Phosphorylation of p38 MAPK downstream of the bax-caspase pathway may play a pivotal role in endothelial apoptosis mediated by high D-glucose.

Animals↗
PubMed2001

[Gene therapy for arteriosclerotic diseases].

Recent progress in molecular biology gives us gene therapy, as a new strategy for treatment of cardiovascular diseases. Targeted diseases have been wide-spread from single gene-deficient diseases to more complexed adult diseases such as restenosis after angioplasty and ischemic diseases. Clinical gene therapy for restenosis and angina using VEGF gene have already performed in USA and they can show beneficial effects of such strategies. On the other hand, we have just started a clinical trial using E2F decoy for restenosis after PTA or PTCA, since April 2000. E2F decoy is expected to become a new treatment for restenosis as a gene therapy. Also, the feasibility of a novel therapeutic strategy using angiogenic growth factors such as VEGF to augment collateral artery development has recently entered the realm of treatment of ischemic diseases. We focus on HGF, which is a novel endothelial growth factor. HGF-based therapeutic angiogenesis would possibly result a new treatment for severe ischemic diseases.

Angioplasty, Balloon, Coronary↗
PubMed2001

Antiasthmatic effect of YM976, a novel PDE4 inhibitor, in guinea pigs.

YM976 is a novel and specific phosphodiesterase 4 inhibitor. In our previous report, we indicated that YM976 has less emetogenicity, a major adverse effect of PDE4 inhibitors, than rolipram. In the present study, we examined the antiasthmatic effects of YM976 in guinea pigs. YM976 orally administered exhibited inhibition of antigen-induced bronchoconstriction, airway plasma leakage, airway eosinophil infiltration, and airway hyperreactivity (AHR), with ED(50) values of 7.3, 5.7, 1.0, and 0.52 mg/kg, respectively. Rolipram also dose dependently suppressed these responses. Prednisolone suppressed eosinophil infiltration and AHR, whereas it failed to inhibit bronchoconstriction and plasma leakage. Theophylline moderately suppressed bronchoconstriction and edema, but neither eosinophil infiltration nor AHR. YM976 suppressed the peroxidase activity in the bronchoalveolar lavage fluid, and elevated the intracellular peroxidase activity and cAMP contents of infiltrated cells, suggesting that YM976 inhibited not only the infiltration but also the activation of leukocytes. In vitro studies revealed that YM976 potently suppressed eosinophil activation (EC(30) = 83 nM), and exerted a little relaxation on LTD(4)-precontracted tracheal smooth muscle (EC(50) = 370 nM). Rolipram exhibited a potent tracheal relaxation activity (EC(50) = 50 nM). In vivo studies indicated that the inhibitory effect of YM976 on LTD(4)-induced bronchospasm was marginal even at 30 mg/kg p.o., although rolipram significantly inhibited the bronchospasm at the same dose. These results suggested that YM976, unlike rolipram, showed the inhibition of antigen-induced airway responses due to anti-inflammatory effects, but not to direct tracheal relaxation. In conclusion, YM976 may have potential therapeutic value in the treatment of asthma through its anti-inflammatory activities.

Animals↗
PubMed2001

[A family of early childhood-onset Charcot-Marie-Tooth disease type 2].

We reported a man and his son with Charcot-Marie-Tooth disease (CMT) type 2. Their age at onset was about 5 years. Their clinical examinations revealed muscle atrophy and weakness of both distal lower limbs, foot-drop, a reduction of the reflex in both Achilles tendons and sensory impairment of the glove and stocking type. Nerve conduction studies revealed remarkably low amplitude of compound muscle action potential compared to conduction velocity. The nerve biopsy of their sural nerves revealed loss of large myelinated fiber. We presumed that the clinical features of their disease were compatible with CMT2A or 2B. DNA analysis of our family members performed with microsatellite markers linked to the candidate regions of CMT2A and 2B, did not show apparent positive results. We speculate that this family was a novel gene locus of CMT type 2.

Adult↗
PubMed2001

Double-Switch operation for congenitally corrected transposition.

Double-switch operation was performed in 76 patients with congenitally corrected transposition of the great arteries at the Heart Institute of Japan, Tokyo Women's Medical University. Detailed surgical techniques of Mustard and Senning procedures for inlet switch, as well as arterial switch operation, pulmonary reconstruction by direct right ventricular-pulmonary arterial anastomosis, and external conduit repair for outlet switch are described in detail.

Adolescent↗
PubMed2001

Studies on mechanisms of low emetogenicity of YM976, a novel phosphodiesterase type 4 inhibitor.

YM976 is a novel and selective inhibitor of phosphodiesterase type 4 (PDE4) with a different chemical structure from rolipram. Orally administered YM976 showed anti-inflammatory activity (ED(50) = 2.8 mg/kg) similar to rolipram (3.5 mg/kg). On the other hand, the emetogenicity of YM976, one of the main adverse effects of PDE4 inhibitors, was lower (maximal non-emetic dose = 10 mg/kg) than that of rolipram (1 mg/kg). The reasons for this low emetogenicity of YM976 remain unclear, and the present study endeavored to elucidate the mechanisms. Candidates for the possible mechanisms included 1) PDE4 subtype selectivity, 2) binding affinity for HAR-conformation, and 3) brain penetration. YM976 exhibited affinity for high affinity for rolipram-conformation (HAR-conformation) (IC(50) = 2.6 nM) identical to that of rolipram (1.2 nM), and failed to show significant selectivity for the individual PDE4 subtype. These results suggested that neither subtype selectivity nor the affinity for HAR-conformation may be related to the low emetogenicity of YM976. YM976 showed a minor effect on reserpine-induced hypothermia, in contrast to rolipram. To estimate brain penetration, we then measured cAMP contents in peripheral tissues (peritoneal macrophages) and in the brain. YM976 increased the cAMP content of peritoneal macrophages, but caused no significant increase in brain cAMP levels, while rolipram elevated the cAMP content of both tissues at the same dose. In conclusion, YM976 shows an apparent dissociation between its anti-inflammatory effects and emetogenicity, perhaps because of the poor brain penetration.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2001

[Tuberculosis control strategy in the 21st century in Japan--for elimination of tuberculosis in Japan].

Modern tuberculosis control programme has been launched in 1951 by the major revision of the previous Tb. Control Law in Japan. Main control measures were BCG vaccination programme for tuberculin negatives, annual screening of Tb. by miniature radiophotography (MMR), charge free diagnosis and treatment of Tb. patients, registration and case-holding at Health Centres throughout the country and so on. Thanks to the efforts of the Government and people concerned, Tb. incidence has decreased with the annual reduction rate of 11% during 1961 and 1977. However, Tb. decrease has stagnated after that, and it is increasing slowly in these 3 years since 1998. Moreover, regional variations of Tb. incidence are considerable, and Tb. is concentrated in specific risk groups such as elderly persons, homeless, foreign born individuals and so on. However, the present Tb. Control measures were introduced prior to the discovery of most major anti-Tb. drugs and all modern internationally accepted Tb. Control strategies, so that it is strongly desired to improve the present control programme from rather classical present Tb. control measures to global standard one to overcome the resurgence of Tb. in Japan. At first, the author stressed that the priority of Tb. Control Programme should be changed according to the development of science and the change of epidemiological situations. BCG vaccination and Tb. screening by MMR might be very important when the annual risk of Tb. infection was very high--about 4% in 1950. Now it is around 0.05% and the incidence of Tb. among 0-14 years of age is 1.1 per 100,000 so that the priority should be given on treatment of the detected cases instead of BCG vaccination or MMR. The doctors in the public health field should give more strong concern on clinical aspects of Tb. Control Programme at present. It was considered that the main urgent problems to be improved in the present Tb. control measures are as follows. 1. It is strongly recommended to spread the global standard regimen with 2HRZE/4HR (E) more widely and rapidly. Because the standard regimen is used in only 50% of new smear positive cases at present although 15.3% of Tb. patients are 80 years or more, or 56.3% of them are 60 years or more, and the side effects by PZA are higher among elderly patients. 2. Shortening of the hospitalization duration is required because 76.7% of newly detected bacilli positive cases are hospitalized at first, and the median of the period of hospitalization is 4 months, and 18.4% of them are hospitalized 6 months or more at present. 3. DOT treatment has been introduced for special groups in the big cities in 2000 for the first time in Japan, but it is needed to spread DOT treatment more widely, for example, by increasing health insurance payment for the institutions where DOT treatment is being implemented. 4. It is recommended to build special rooms to accept Tb. patient at general hospitals and/or university hospitals to avoid the neglect of Tb. by general medical doctors. 5. Follow-up of Tb. patients after treatment completion at Health Centres is not needed now, because the relapse rate is so low. 6. Indiscriminative screening programme for all the people aged 19 years old or more should be stopped, at least up to 39 years of age, because Tb. detection rate has become so low as 0.0069% at present. As Tb. decrease is so slow, or is increasing in some areas, that the contact surveys among the young aged 20 to 39 should be strengthened in the future. 7. As Japan Anti-Tb. Association is being carrying out mass screening programme extensively at present, so that the Association has started to discuss the future health check system. Because of the rapid and constant increase of the lung cancer, the Association is discussing the method to detect the lung cancer, too. In any way, it is needed to focus the screening programme for special high risk groups instead of indiscriminative screening. 8. BCG vaccination for infants should be continued a little more, because BCG vaccination can protect the development of 7 miliary Tb. and/or meningitis cases during 15 years if BCG is given 70% of the infants in 2000. However, it was strongly recommended to stop re-vaccination of BCG, because it is not so effective, and disturb the diagnosis of Tb. infection by tuberculin testing. 9. Treatment of latent Tb. infection will become more and more important, so that it's indication should be expanded to the adults in the future instead of the present indication up to 29 years of age. It is needed to revise Tuberculosis Control Low to improve control programme in Japan. The author hoped that the members of Japan Tuberculosis Society will promote the improvement and to support the Government to improve the Law.

Age Factors↗
PubMed2001

[Case report of CABG for progressive coronary artery stenosis after 22-year history of Kawasaki disease].

More than 30 years has passed since Kawasaki disease was recognized as an independent disease entity, but the cardiovascular complications of Kawasaki disease are still not well known. We report an 22-year-old woman who underwent triple coronary artery bypass grafting because of a coronary artery aneurysm and multiple coronary artery stenoses, 22 years after the diagnosis of Kawasaki disease. A 2 cm coronary artery aneurysm due to Kawasaki disease was diagnosed when she was 10 years old, when she first presented with the symptom of dyspnea on effort. Since then, she was followed at the outpatient clinic. When she was 19 years old, the first coronary catheterization was performed. Two years later, the second coronary catheterization revealed progression of coronary artery disease. Therefore, coronary artery bypass grafting was performed. This case is rare from the point of view of long-term progression of coronary artery disease.

Adult↗