Asami Suzuki

Tokyo Medical and Dental University, Edo, Tōkyō, Japan

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Publications (6)13.24 Total impact

  • Journal of Cardiac Failure 09/2010; 16(9). · 3.07 Impact Factor
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    ABSTRACT: Atherosclerotic plaque that shows echo signal attenuation (EA) without associated bright echoes is sometimes observed by intravascular ultrasound but its clinical significance remains unclear. We investigated the impact of EA on coronary perfusion and evaluated the pathological features of plaque with EA. We studied 687 native coronary lesions in 687 consecutive patients (336 with acute coronary syndrome and 351 with stable angina pectoris) who underwent intravascular ultrasound before percutaneous coronary intervention. By subgroup analysis, 60 lesions (30 lesions with EA) treated with directional coronary atherectomy underwent pathological examination. The Thrombolysis in Myocardial Infarction (TIMI) flow grade and myocardial blush grade after percutaneous coronary intervention were compared between lesions with and without EA in 627 lesions except directional coronary atherectomy subgroup. EA was observed in 245 lesions (35.7%), and coronary flow after percutaneous coronary intervention was worse for lesions with EA than without (final TIMI grade of 0 to 2: 15.4% versus 2.4%, P<0.001; final myocardial blush grade of 0 to 2: 45.6% versus 21.4%, P<0.001). Multivariate analysis revealed a significant association between no reflow (TIMI grade 0 to 2) and EA (odds ratio, 5.59; 95% CI, 2.64 to 11.85; P<0.001), a baseline TIMI grade of 0 to 2 (odds ratio, 5.91; 95% CI, 2.79 to 12.5; P<0.001), and a large reference area (odds ratio, 3.08; 95% CI, 1.40 to 6.76; P=0.005) after controlling for other associated factors. Pathological examination revealed a significantly higher frequency of lipid-rich plaque with microcalcification in lesions with EA. Atherosclerotic plaque with EA showed a significant association with no reflow after percutaneous coronary intervention, suggesting the existence of fragile components susceptible to distal embolization.
    Circulation Cardiovascular Interventions 10/2009; 2(5):444-54. · 6.54 Impact Factor
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    ABSTRACT: It is getting familiar that pathway information greatly contributes to elucidate the molecular basis of human disease with large-scale biological data. We developed a pathway database for molecular pathology in periodontitis named 'Pathogenic Pathway Database for Periodontitis'. Periodontitis is an inflammation disease in periodontal tissue and associated with an increased health risk of angina, myocardial infarction, and fetal cardiovascular events. Despite accumulation of biomedical research on periodontitis pathology at the molecular level, there has been no systematization for biological pathways in periodontitis. We checked 185 reference papers and extracted causal relationships among molecules as well as pathways representing molecular etiology. We also built an ontology that systematizes conceptual terms associated with the pathways. Besides pathways, our ontology provides cellular and tissue specific contextual information that is required to represent pathology at the cellular and tissue specific levels. We implemented in our database an integrated viewer for the association between pathways and ontology. Pathogenic Pathway Database for Periodontitis is freely available at
    In silico biology 01/2009; 9(4):233-43.
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    ABSTRACT: The purpose of the present study was to investigate the genomic markers for periodontitis, using large-scale single-nucleotide polymorphism (SNP) association studies comparing healthy volunteers and patients with periodontitis. Genomic DNA was obtained from 19 healthy volunteers and 22 patients with severe periodontitis, all of whom were Japanese. The subjects were genotyped at 637 SNPs in 244 genes on a large scale, using the TaqMan polymerase chain reaction (PCR) system. Statistically significant differences in allele and genotype frequencies were analyzed with Fisher's exact test. We found statistically significant differences (P < 0.01) between the healthy volunteers and patients with severe periodontitis in the following genes; gonadotropin-releasing hormone 1 (GNRH1), phosphatidylinositol 3-kinase regulatory 1 (PIK3R1), dipeptidylpeptidase 4 (DPP4), fibrinogen-like 2 (FGL2), and calcitonin receptor (CALCR). These results suggest that SNPs in the GNRH1, PIK3R1, DPP4, FGL2, and CALCR genes are genomic markers for severe periodontitis. Our findings indicate the necessity of analyzing SNPs in genes on a large scale (i.e., genome-wide approach), to identify genomic markers for periodontitis.
    Odontology 10/2004; 92(1):43-7. · 1.35 Impact Factor
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    ABSTRACT: Periodontitis is a common inflammatory disease causing destruction of periodontal tissues. It is a multifactor disease involving genetic factors and oral environmental factors. To determine genetic risk factors associated with aggressive periodontitis or severe chronic periodontitis, single nucleotide polymorphisms (SNPs) in multiple candidate genes were investigated in Japanese. We studied 134 patients with aggressive periodontitis, 117 patients with severe chronic periodontitis, and 125 healthy volunteers without periodontitis, under case-control setting, and 310 SNPs in 125 candidate genes were genotyped. Association evaluation by Fisher's exact test (p < 0.01) revealed statistically significant SNPs in multiple genes, not only in inflammatory mediators (IL6ST and PTGDS, associated with aggressive periodontitis; and CTSD, associated with severe chronic periodontitis), but also in structural factors of periodontal tissues (COL4A1, COL1A1, and KRT23, associated with aggressive periodontitis; and HSPG2, COL17A1, and EGF, associated with severe chronic periodontitis). These appear to be good candidates as genetic factors for future study.
    Biochemical and Biophysical Research Communications 05/2004; 317(3):887-92. · 2.28 Impact Factor
  • Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology) 01/2001; 43(4):353-360.