Kyushu University Academic Staff Educational and Research Activities Database
List of Presentations
kazunori Nakagawa Last modified date:2019.06.21

Lecturer / Pathobiology / Department of Basic Medicine / Faculty of Medical Sciences


Presentations
1. Yamamoto T, Okada K, Yagi N, Hoshino M, Nakashima Y, Nakagawa K, Tsukube T., Mechanism of Aneurysm Expansion After Endovascular Aortic Repair Analyzed With X-Ray Phase-Contrast Tomography, The American Heart Association's 2018 Scientific Sessions and Resuscitation Science Symposium, 2018.11.
2. K. Yokawa, T. Tsukube, N. Yagi, M. Hoshino, Y. Nakashima, K. Nakagawa, Y. Okita, Quantitative and Dynamic Measurements of Aortic Wall of Acute Type-A Aortic Dissection With X-Ray Phase-Contrast Tomography, The American Heart Association's Arteriosclerosis, Thrombosis and Vascular Biology/Peripheral Vascular Disease 2017 Scientific Sessions, 2017.05.
3. K. Yokawa, T. Tsukube, N. Yagi, M. Hoshino, Y. Nakashima, K. Nakagawa, Y. Okita, Degeneration of Tunica Media in Acute Type-a Aortic Dissection From X-ray Phase-contrast Tomography, American Heart Association Scientific Session 2017, 2017.10.
4. K. Yokawa, T. Tsukube, N. Yagi, M. Hoshino, Y. Nakashima, K. Nakagawa, Y. Okita, Quantitative and Dynamic Measurements of Aortic Wall of Acute Type-A Aortic Dissection with X-ray Phase-contrast Tomography, 31st European Association for Cardio-Thoracic Surgery Annual Meeting, 2017.10.
5. Shuichi Hashimoto, Koichi Takayama, 中川 和憲, Hidenori Shiraha, Yoichi Nakanishi, Stem Cell Marker Lgr6 Expression Analysis in Lung and Oral Cancers, The 23rd General Meeting of the Japanese Association for Dental Science, 2016.10, The signal from R-spondin via Lgr6(leucine-rich repeat containing, G protein-coupled receptor 6), a stem cell marker, augments Wnt/β-catenin signaling pathway. We obtained the results that Lgr6 was specifically expressed in the neoplastic cells in lung and oral carcinomas. Some mutations of Lgr6 were also found in some lung carcinoma cell lines. These results suggest that Lgr6 plays an important role for carcinogenesis or development of lung and oral carcinomas..
6. T. Tsukube, N. Yagi, M. Hoshino, Y. Nakashima, K. Nakagawa, Y. Okada, T. Haraguchi, M. Yoshida, N. Mukohara, S. Kozawa, K. Ogawa, Y. Okita, Impact of synchrotron radiation based phase-contrast X-ray CT findings on understanding onset of acute aortic dissection., American Association for Thoracic Surgery, Aortic Symposium Workshop 2015, 2015.10.
7. Kazunori Nakagawa, Hiroshi Fujii, Yutaka Nakashima, PATHOGENESIS OF EARLY AND INTERMEDIATE LESIONS OF HUMAN CORONARY ATHEROSCLEROSIS: ACCUMULATION OF PLASMA-DERIVED LIPIDS AND DISPERSION
OF SMOOTH MUSCLE CELLS., The 11th International Congress on Coronary Artery Disease, 2015.11.
8. Kazunori Nakagawa, Hiroshi Fujii, Yutaka Nakashima, Pathogenesis of intermediate lesion of human coronary atherosclerosis: Lipid pool formation without necrosis and dispersion of intimal smooth muscle cells., The 82nd Annual Congress of The European Atherosclerosis Society, 2014.06, Aim: Proliferation of smooth muscle cells (SMCs) and deposition of lipids by death of macrophage foam cells are key events in atherosclerosis in animal models. However, different processes occur in human atherosclerosis. The purpose of this study is to clarify the pathogenesis of intermediated lesion (preatheroma) of human atherosclerosis, focusing on intimal SMCs and extracellular lipids.
Methods and Results: Step and serial frozen sections of the right coronary artery were obtained from 43 Japanese autopsied subjects (from 15 to 49 years of age) with no or earlier atherosclerotic lesions. The lesions were classified into 4 categories according to the grade of atherosclerosis; diffuse intimal thickening (DIT), initial lesion, foam cell lesion and intermediate lesion. DIT is a physiological intimal thickening with plenty of SMCs and no lipid deposition. Initial lesions and foam cell lesions exhibited mild deposition of extracellular lipids and accumulation of macrophage foam cells in the SMC-rich intima, respectively. Intermediate lesions consisted of lipid pools with abundant extracellular lipids in the thickened intima, in addition to many SMCs and macrophage foam cells. No necrosis or lytic changes were observed in the lipid pools, and the extracellular lipids colocalized with ApoB and fibrinogen, suggesting that the penetration of plasma lipoproteins play an important role in lipid pool formation. The density of intimal SMCs was significantly decreased in the foam cell lesion and the intermediate lesion, but the number of the cells showed no significant change. No MIB-1-positive cells or TUNEL-positive cells were observed, and only a few SMCs showed positive immunostain for BAX, LC3B and NLRP3, suggesting that SMCs were spread out in the intima as the lesion progressed without undergoing excessive proliferation or death.
Conclusion: Intermediate lesion of human atherosclerosis develops primarily by infiltration of plasma lipoproteins and lipid pool formation, and dispersion of pre-existing intimal SMCs..
9. Takuro Tsukube, Naoto Yagi, Masato Hoshino, Kentaro Uesugi, Yutaka Nakashima, Kazunori Nakagawa, Katsuhiko Nakamae, Tomonori Haraguchi, Ritsu Matsukawa, Shuichi Kozawa, Yutaka Okita, Acute Aortic Dissection is Associated with Alteration of Elastic Architecture of Aortic Media Assessed by Synchrotron Phase-Contrast X-ray Computed Tomography., 第78回日本循環器学会学術集会, 2014.03, Objectives: To investigate alteration of the elastic architecture of the media of aortic dissection, we have applied synchrotron phase-contrast X-ray computed tomography imaging (PCXI) to provide detailed two and three-dimensional visualization of aortic wall structures in excised human aorta. Methods: Human aortic walls of the ascending aorta were obtained during aortic replacement, including aortic dissection (group-A: n=17) and Marfan syndrome (group-M: n=3). Normal aorta was obtained from autopsy (group-N: n=3). Ex vivo PCXI was performed using a synchrotron radiation source (SPring-8), and samples were also histologically analyzed. Results: In all samples, unprecedented structural contrast and resolution were obtained. In group-N, PCXI revealed minimal changes in density of media. In group-M, PCXI demonstrated bimodal peaks in density and intra-medial low density zone was connected to cystic medial necrosis and aortic dissection. In group-A, PCXI revealed low density area in the outer layer of the media of the non-dissecting part of the aortic wall, which were well correlated with irregularity of the elastic layers. The mass density of media in group-A and M were significantly lower than normal aorta.Conclusions: PCXI revealed details about the spatial relationships of the elastic architecture in the aortic wall. These findings may indicate that changes in elastic architecture of the media are initial presentations, prior to onset of acute aortic dissection..
10. Regulation of mitochondrial release of apoptosis-inducing factor is a mechanism for neuroprotective activity of pigment epithelium-derived factor in retinal degeneration. .
11. Paracrine loop between VEGF-C/Flt-4 and PDGF-BB/PDGFR-beta systems contribute therapeutic angiogenesis using FGF-2 gene transfer in ischemic hind limbs..
12. Flk-1 identifies pluripotent precursor in fetal mous liver..
13. Fibroblast growth factor-2(FGF-2) gene transfer can stimulate endogenous PDGF-B mRNA via VEGF-C/Flt-4 system in murine ischemic hind limbs..
14. Involvement of VEGF-C/flt-4 system in therapeutic angiogenesis of FGF-2 gene transfer in murine ischemic hind limb..
15. Inhibition of Tissue Factor Synthesis by Antisense Transfection Suppresses Tissue Factor / Factor VIIa - induced uPAR Upregulation.
16. Highly efficient intramuscular gene transfer using Sendai virus vector: VEGF is necessary, but seriously toxic without FGF-2 to treat critical limb ischemia..
17. Slight increase of serum ceruloplasmin via somatic hepatocyte transplantation is sufficient to improve the prognosis of rat model of Wilson's disease..
18. Serious adverse effect of intramuscular gene transfer of VEGF165 for limb salvage in mice with critical limb ischemia..