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Biomedical subjects

Issei Komuro

Publications and source records attributed to Issei Komuro.

At least 37 records · Page 2Linked to original sources
PubMed2006

Superiority of synchrony of 256-slice cone beam computed tomography for acquiring pulsating objects. Comparison with conventional multislice computed tomography.

PURPOSE: A prototype 256-slice cone beam computed tomography (CT) provides complete volumetric data within a single gantry rotation (1 s/rotation) with 0.5 mm slice-thickness. MATERIALS AND METHODS: Calcified phantoms (200-400 HU) were attached to the balloon of a pulsating phantom and moved at a rate of 5-90/min. Acquisition was performed during one to-and-fro motion at each pulsation rate without electrocardiogram (ECG)-gating. Each period was divided into 10 phases, and compared to conventional multislice CT scanning without ECG-gating. RESULTS: At 5-20/min, the configuration of calcified phantoms continued to the through-plane without gaps. At 60/min, duplicated calcified phantoms at end-systole and end-diastole were observed without motion. At 90/min, motion could be observed without gaps but was more blurred, and total calcified volume, Agatston scores, mean and max CT values of three phantoms were almost equal compared with those at static state. However, at 60/min, total calcified volume, scores, mean and max CT values of three phantoms were decreased to 64%, 37%, 80% and 56%, respectively, compared with those at static state. In multislice CT, even at lower rates, there were gaps in the through-plane. At 60/min, total calcified volume, scores, mean and max CT values of three phantoms were decreased to only 8%, 3%, 79% and 53%, respectively, compared with static state. CONCLUSION: This new prototype's unique character (synchrony) enables the acquisition of pulsating objects. These can be acquired without gaps in the through-plane even in the absence of ECG-gating. However, its present temporal resolution only permits accurate quantitative evaluation of calcium up to 20/min.

Electrocardiography↗
PubMed2006

Predictive indicators of deep venous thrombosis and pulmonary arterial thromboembolism in 54 subjects after total knee arthroplasty using multislice computed tomography in logistic regression models.

PURPOSE: To determine predictors of deep venous thrombosis (DVT) in the lower extremities and pulmonary arterial thromboembolism (PE) after total knee arthroplasty (TKA), we evaluated the incidence of these events using multislice computed tomography (CT). METHODS: 54 subjects (10 males, 53-81 years old, the first consecutive 25 receiving anticoagulant therapy) underwent enhanced multislice CT (MSCT) before and one week after TKA. RESULTS: DVT, PE, and both were detected in twelve, twelve, and three subjects, respectively, one week after TKA. Hemoglobin and alveolar-arterial oxygen gradient (AaDO2) on the day after TKA, and total amount of operative bleeding (TAOB) were significantly higher in subjects with DVT or PE (P<0.05). In a logistic model for predicting DVT or PE, hemoglobin and AaDO2 levels on the day after TKA and TAOB were associated with an increased incidence of DVT or PE (relative risks 3.51, 1.19 and 1.01 (P<0.05), respectively). From box and whisker plots, we speculated the significant border to predict DVT or PE as 10.5 g/dl for hemoglobin, 34 Torr for AaDO2, and 1280 ml for TAOB. These factors also predicted DVT or PE (relative risks 5.08 (hemoglobin more than 10.5), 6.25 (AaDO2 more than 34 Torr), and 4.95 (TAOB more than 1280 ml) (P<0.05)). CONCLUSIONS: The incidence of DVT or PE one week after TKA was 39% by MSCT. High levels of TAOB, hemoglobin and AaDO2 on the day after TKA may be predictive indicators of DVT or PE one week after TKA.

Aged↗
PubMed2006

Overexpression of Nd1, a novel Kelch family protein, in the heart of transgenic mice protects against doxorubicin-induced cardiomyopathy.

Doxorubicin is one of the most effective drugs available for cancer chemotherapy. However, the clinical use of doxorubicin has been greatly limited because of severe side effects on cardiomyocytes. Since Nd1-L, a novel actin-binding protein, is expressed most abundantly in the heart of adult mice, we examined a role of Nd1-L in doxorubicin-induced cardiomyopathy. When doxorubicin (5 mg/kg x 4 times) was injected into adult mice at a 3-day-interval, approximately 50% of injected mice died within 4 weeks of the first injection. Nd1-L mRNA expression in the heart decreased within 3 weeks after the first injection and many cardiomyocytes of injected mice died by apoptosis. Overexpression of Nd1-L in the heart of transgenic mice protected the cardiomyocytes from apoptosis and improved survival rate after doxorubicin injection. Furthermore, activation of Erk1/2 was observed in cultured cells overexpressing Nd1-L. Thus, Nd1-L plays a critical role in protecting the heart from doxorubicin-induced cardiomyopathy.

Animals↗
PubMed2006

Effect of plaque volume on subsequent vessel remodeling at edges of sirolimus-eluting stents.

Serial (baseline and 9-month follow-up) intravascular ultrasound analysis was performed at 5-mm reference segments immediately proximal and distal to the sirolimus-eluting stent (SES) in 33 lesions. Proximal and distal reference segments were divided into 1-mm subsegments. Between postintervention and follow-up intravascular ultrasound studies, there were significant decreases in the lumen and increases in plaque & media areas in the subsegment closest to the distal edge, with no change in external elastic membrane area. There was no significant change in external elastic membrane, lumen, and plaque & media areas within the other subsegments. At the nearest 1-mm subsegment from the proximal and distal edges, baseline plaque & media area was associated with subsequent vessel remodeling. In conclusion, a large amount of plaque at the SES edge may be a risk of negative remodeling at follow-up (stent edge restenosis). It supports the importance of "normal-to-normal" SES deployment.

Aged↗
PubMed2006

Angiotensin II induces premature senescence of vascular smooth muscle cells and accelerates the development of atherosclerosis via a p21-dependent pathway.

BACKGROUND: Angiotensin II (Ang II) has been reported to contribute to the pathogenesis of various human diseases including atherosclerosis, and inhibition of Ang II activity has been shown to reduce the morbidity and mortality of cardiovascular diseases. We have previously demonstrated that vascular cell senescence contributes to the pathogenesis of atherosclerosis; however, the effects of Ang II on vascular cell senescence have not been examined. METHODS AND RESULTS: Ang II significantly induced premature senescence of human vascular smooth muscle cells (VSMCs) via the p53/p21-dependent pathway in vitro. Inhibition of this pathway effectively suppressed induction of proinflammatory cytokines and premature senescence of VSMCs by Ang II. Ang II also significantly increased the number of senescent VSMCs and induced the expression of proinflammatory molecules and of p21 in a mouse model of atherosclerosis. Loss of p21 markedly ameliorated the induction of proinflammatory molecules by Ang II, thereby preventing the development of atherosclerosis. Replacement of p21-deficient bone marrow cells with wild-type cells had little influence on the protective effect of p21 deficiency against the progression of atherogenesis induced by Ang II. CONCLUSIONS: We demonstrated that Ang II promotes vascular inflammation by inducing premature senescence of VSMCs both in vitro and in vivo. Our results suggest a critical role of p21-dependent premature senescence of VSMCs in the pathogenesis of atherosclerosis.

Aging, Premature↗
PubMed2006

Predictors of non-calcified plaques in the coronary arteries of 242 subjects using multislice computed tomography and logistic regression models.

OBJECTIVES: We detected non-calcified plaques (NCPs) in the coronary arteries using multislice computed tomography (MSCT) in order to determine the predictors of NCPs using logistic regression models. METHODS: Two hundred and forty-two consecutive subjects (141 males; overall age range, 17-91 years old) underwent enhanced electrocardiogram-gated MSCT to detect NCPs. Logistic models for predicting NCPs were developed which incorporated age, sex, coronary calcified-plaque (CP), and the following coronary risk factors (RFs): hypertension (HT), diabetes mellitus (DM), hyperlipidemia (HL), a smoking habit, and obesity. RESULTS: NCPs were detected in 76 subjects (59 males, 35-82 years old [median=67]) whose average number of coronary RFs was 2.6, 75% of whom presented with HT, 30% with DM, 51% with HL, 64% were present or past cigarette smokers, and 32% were obese. In the 76 subjects with NCPs, the incidence of male sex, presence of HT, a smoking habit, CP and the number of coronary RFs were significantly higher than in the 166 subjects without NCP. Of the 101 female subjects, 17 showed NCPs and in every case the subject was more than 50 years old. In a logistic regression model, male sex, HT and smoking habit (relative risks 2.7, 2.0, and 2.7 [95% confidence interval=1.3-5.6, 1.0-4.0, and 1.5-4.9, respectively]) were associated with increased incidence of NCPs. CONCLUSIONS: The incidence of NCPs was significantly increased in the presence of HT and a smoking habit, suggesting that lesions may be caused by HT or smoking-induced vessel injury even in the young male.

Abstracting and Indexing↗
PubMed2006

Characterization and morphology of atherosclerotic plaque of coronary arteries: utility of electron-beam tomography to detect non-calcified plaque: a comparison with conventional coronary angiography and intravascular ultrasound.

BACKGROUND: Electron-beam tomography (EBT) may provide useful information about characterization and morphology of atherosclerotic plaque of coronary arteries. MATERIALS AND METHODS: Twenty-six subjects (20 male, 6 female) with suspected coronary heart disease had two routine (r) and one enhanced (e) EBT scans to detect non-calcified plaque (NCP) in the coronary arterial lumen, and were compared with conventional coronary angiograms (CAG) and intravascular ultrasound (IVUS). RESULTS: Three had the sites, which did not have high CT values suggesting calcification in rEBT, nor which was not enhanced by contrast material in eEBT. One had the site with positive CT values that were supposed to be the proliferation intima or organized thrombus and at the corresponding site mixed plaque was observed in the IVUS image. The other two had the site with negative CT values that were supposed to be fat tissue with significant stenosis in CAG. We also made the cross-sectional images of the vessel and the morphology of the NCP, which projected into the lumen, could be evaluated. CONCLUSIONS: We could detect the NCP, differentiate fat tissue from soft tissue and evaluate the morphology of the plaque in EBT.

Aged↗
PubMed2006

Feeding artery of a recurrent pheochromocytoma from the left internal thoracic artery demonstrated by multislice computed tomography.

A 53-year-old female presented to our hospital because of an abnormal shadow on chest X-ray. She had previously undergone surgical removal of a pheochromocytoma. Enhanced multislice CT was performed and three-dimensional volume rendered images revealed two tumors in the thorax and neck, suggesting pheochromocytoma. There was an aberrant artery originating from the left internal thoracic artery (ITA) leading to the tumor, which we identified as the feeding artery of the pheochromocytoma. We planned to eliminate the tumors surgically, and based on the multislice CT findings, we also planned to simultaneously eliminate the feeding artery from the left ITA.

Female↗
PubMed2006

Molecular mechanism underlying inverse agonist of angiotensin II type 1 receptor.

To delineate the molecular mechanism underlying the inverse agonist activity of olmesartan, a potent angiotensin II type 1 (AT1) receptor antagonist, we performed binding affinity studies and an inositol phosphate production assay. Binding affinity of olmesartan and its related compounds to wild-type and mutant AT1 receptors demonstrated that interactions between olmesartan and Tyr113, Lys199, His256, and Gln257 in the AT1 receptor were important. The inositol phosphate production assay of olmesartan and related compounds using mutant receptors indicated that the inverse agonist activity required two interactions, that between the hydroxyl group of olmesartan and Tyr113 in the receptor and that between the carboxyl group of olmesartan and Lys199 and His256 in the receptor. Gln257 was found to be important for the interaction with olmesartan but not for the inverse agonist activity. Based on these results, we constructed a model for the interaction between olmesartan and the AT1 receptor. Although the activation of G protein-coupled receptors is initiated by anti-clockwise rotation of transmembrane (TM) III and TM VI followed by changes in the conformation of the receptor, in this model, cooperative interactions between the hydroxyl group and Tyr113 in TM III and between the carboxyl group and His256 in TM VI were essential for the potent inverse agonist activity of olmesartan. We speculate that the specific interaction of olmesartan with these two TMs is essential for stabilizing the AT1 receptor in an inactive conformation. A better understanding of the molecular mechanisms of the inverse agonism could be useful for the development of new G protein-coupled receptor antagonists with inverse agonist activity.

Amino Acid Sequence↗
PubMed2006

Granulocyte colony stimulating factor directly inhibits myocardial ischemia-reperfusion injury through Akt-endothelial NO synthase pathway.

OBJECTIVE: Granulocyte colony stimulating factor (G-CSF) has been reported recently to prevent cardiac remodeling and dysfunction after acute myocardial infarction through signal transducer and activator of transcription 3 (STAT3). In this study, we examined acute effects of G-CSF on the heart against ischemia-reperfusion injury. METHODS AND RESULTS: Rat hearts were subjected to global 35-minute ischemia and 120-minute reperfusion in Langendorff system with or without G-CSF (300 ng/mL). G-CSF administration was started at the onset of reperfusion. Triphenyltetrazolium chloride staining revealed that G-CSF markedly reduced the infarct size. G-CSF strongly activated Janus kinase 2 (Jak2), STAT3, extracellular signal-regulated kinase (ERK), Akt, and endothelial NO synthase (NOS) in the hearts subjected to ischemia followed by 15-minute reperfusion. The G-CSF-induced reduction in infarct size was abolished by inhibitors of phosphatidylinositol 3-kinase, Jak2, and NOS but not of mitogen-activated protein kinase kinase (MEK). CONCLUSIONS: These results suggest that G-CSF acts directly on the myocardium during ischemia-reperfusion injury and has acute nongenomic cardioprotective effects through the Akt-endothelial NOS pathway.

Animals↗
PubMed2006

Critical roles of muscle-secreted angiogenic factors in therapeutic neovascularization.

The discovery of bone marrow-derived endothelial progenitors in the peripheral blood has promoted intensive studies on the potential of cell therapy for various human diseases. Accumulating evidence has suggested that implantation of bone marrow mononuclear cells effectively promotes neovascularization in ischemic tissues. It has also been reported that the implanted cells are incorporated not only into the newly formed vessels but also secrete angiogenic factors. However, the mechanism by which cell therapy improves tissue ischemia remains obscure. We enrolled 29 "no-option" patients with critical limb ischemia and treated ischemic limbs by implantation of peripheral mononuclear cells. Cell therapy using peripheral mononuclear cells was very effective for the treatment of limb ischemia, and its efficacy was associated with increases in the plasma levels of angiogenic factors, in particular interleukin-1beta (IL-1beta). We then examined an experimental model of limb ischemia using IL-1beta-deficient mice. Implantation of IL-1beta-deficient mononuclear cells improved tissue ischemia as efficiently as that of wild-type cells. Both wild-type and IL-1beta-deficient mononuclear cells increased expression of IL-1beta and thus induced angiogenic factors in muscle cells of ischemic limbs to a similar extent. In contrast, inability of muscle cells to secrete IL-1beta markedly reduces induction of angiogenic factors and impairs neovascularization by cell implantation. Implanted cells do not secret angiogenic factors sufficient for neovascularization but, instead, stimulate muscle cells to produce angiogenic factors, thereby promoting neovascularization in ischemic tissues. Further studies will allow us to develop more effective treatments for ischemic vascular disease.

Aged↗