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Featured researches published by Hiroyuki Kurosawa.
Circulation Research | 2007
Kensuke Kimura; Masaki Ieda; Hideaki Kanazawa; Takashi Yagi; Makoto Tsunoda; Shin Ichi Ninomiya; Hiroyuki Kurosawa; Kenji Yoshimi; Hideki Mochizuki; Kazuto Yamazaki; Satoshi Ogawa; Keiichi Fukuda
Neuronal function and innervation density is regulated by target organ-derived neurotrophic factors. Although cardiac hypertrophy drastically alternates the expression of various growth factors such as endothelin-1, angiotensin II, and leukemia inhibitory factor, little is known about nerve growth factor expression and its effect on the cardiac sympathetic nerves. This study investigated the impact of pressure overload-induced cardiac hypertrophy on the innervation density and cellular function of cardiac sympathetic nerves, including kinetics of norepinephrine synthesis and reuptake, and neuronal gene expression. Right ventricular hypertrophy was induced by monocrotaline treatment in Wistar rats. Newly developed cardiac sympathetic nerves expressing β3-tubulin (axonal marker), GAP43 (growth-associated cone marker), and tyrosine hydroxylase were markedly increased only in the right ventricle, in parallel with nerve growth factor upregulation. However, norepinephrine and dopamine content was paradoxically attenuated, and the protein and kinase activity of tyrosine hydroxylase were markedly downregulated in the right ventricle. The reuptake of [125I]-metaiodobenzylguanidine and [3H]-norepinephrine were also significantly diminished in the right ventricle, indicating functional downregulation in cardiac sympathetic nerves. Interestingly, we found cardiac sympathetic nerves in hypertrophic right ventricles strongly expressed highly polysialylated neural cell adhesion molecule (PSA-NCAM) (an immature neuron marker) as well as neonatal heart. Taken together, pressure overload induced anatomical sympathetic hyperinnervation but simultaneously caused deterioration of neuronal cellular function. This phenomenon was explained by the rejuvenation of cardiac sympathetic nerves as well as the hypertrophic cardiomyocytes, which also showed the fetal form gene expression.
Investigative Radiology | 2015
Michiko Nagai; Masayuki Yamaguchi; Kensaku Mori; Toshihiro Furuta; Hiroki Ashino; Hiroyuki Kurosawa; Hiroyuki Kasahara; Manabu Minami; Hirofumi Fujii
Objective The objective of this study was to demonstrate experimentally that radiofrequency ablation (RFA) of ferucarbotran-accumulated healthy liver tissues causes excess iron deposition in the ablated liver tissues on postablation days and produces sustained T2*-weighted low signals indicative of ablative margins surrounding hepatic tumors. Materials and Methods We conducted 3 experiments using 30 rats. In experiment 1, we administered either ferucarbotran (n = 6) or saline (n = 4), acquired T2*-weighted images (T2*-WIs) of the liver by using a 3-T magnetic resonance scanner, and subsequently performed RFA of healthy liver lobes. We acquired follow-up T2*-WIs up to day 7 and histologically analyzed the liver specimens. In another 4 rats, we performed sham operation, instead of RFA, in ferucarbotran-accumulated liver lobes, followed by the same image acquisition and histological analysis. In experiment 2, we administered 59Fe-labeled ferucarbotran, subsequently performed either RFA (n = 4) or sham operation (n = 4) in the liver, and acquired autoradiograms of the liver specimens on day 7. In experiment 3, we conducted RFA treatment for 8 rats bearing orthotopic hepatic tumors after ferucarbotran administration and monitored tumor growth by using serial T2*-WIs. Results On days 4 and 7 of the experiment 1, T2*-WIs of 6 rats with systemic ferucarbotran administration and subsequent hepatic RFA showed low-signal regions indicative of ablated liver tissues, whereas high-signal areas were seen in 4 saline-administered rats. Neither high nor low signal areas were detected in 4 sham-operated rats. Histologically, larger amounts of iron were observed in the RFA-induced necrotic liver tissues in the ferucarbotran-administered rats than in the saline-administered-rats. The 59Fe autoradiography of the rats in experiment 2 revealed accumulation of ferucarbotran-derived iron in necrotic liver tissues. Among 6 hepatic tumors grown in 6 rats of the experiment 3, a total of 4 tumors were stable in size, but the other 2 increased markedly on day 7. Retrospectively, T2*-WIs showed the former tumor sites surrounded completely by low-signal areas on day 4. Conclusions The RFA of ferucarbotran-accumulated healthy liver tissues in the rats caused excess iron deposition in the ablated liver tissues and produced sustained T2*-weighted hypointense regions. Similar hypointense regions surrounding hepatic tumors were indicative of ablative margins.
Pacing and Clinical Electrophysiology | 2017
Mari Amino; Koichiro Yoshioka; Sachie Tanaka; Noboru Kawabe; Hiroyuki Kurosawa; Keisuke Uchida; Shinobu Oshikiri; Tadashi Hashida; Shigetaka Kanda; Sadaki Inokuchi; Yuji Ikari
Iodine‐123 metaiodobenzylguanidine (123I‐MIBG) is useful for detecting sympathetic innervation in the heart, and has been closely associated with fatal arrhythmias. However, such imaging is typically calibrated to the area of highest uptake and thus is unable to identify areas of hyperinnervation. We hypothesized that normal 123I‐MIBG uptake regions in the denervated heart would demonstrate nerve sprouting and correlate with the potential for arrhythmogenesis.
The Journal of Nuclear Medicine | 2002
Chio Okuyama; Naoki Sakane; Toshihide Yoshida; Keiji Shima; Hiroyuki Kurosawa; Kenzo Kumamoto; Yo Ushijima; Tsunehiko Nishimura
Annals of Nuclear Medicine | 2009
Shigeki Ito; Hiroyuki Kurosawa; Hiroyuki Kasahara; Satomi Teraoka; Eiji Ariga; Shizuhiko Deji; Masahiro Hirota; Takuya Saze; Kunihide Nishizawa
Society of Nuclear Medicine Annual Meeting Abstracts | 2007
Katsutoshi Tsuchiya; Tsuneaki Kawaguchi; Isao Takahashi; Masatoshi Tanaka; Hiroyuki Kasahara; Hiroyuki Kurosawa; Keisuke Uchida; Kensuke Amemiya
Annals of Nuclear Medicine | 2014
Hiroyuki Kurosawa; Kazuhisa Sakurai; Hideaki Hasegawa; Keisuke Uchida; Hiroyuki Kasahara; Masatoyo Nakajo; Masayuki Nakajo
Journal of Nuclear Cardiology | 2002
Shinji Hasegawa; Hideo Kusuoka; Kaoru Maruyama; Hiroyuki Kurosawa; Syusaku Tazawa; Satoshi Ishida; Minoru Inoue; Masatsugu Hori; Tsunehiko Nishimura
Circulation Research | 2012
Michiaki Hiroe; Naohide Ageyama; Yasuhiro Yasutomi; Hiroyuki Kurosawa; Ousuke Fujimoto; Yasushi Arano; Kyoko Imanaka-Yoshida
The Journal of Nuclear Medicine | 2008
Keisuke Uchida; Hiroyuki Kurosawa; Hiroyuki Kasahara; Keita Utsunomiya; Atsuro Suzuki; Katsutoshi Tsuchiya; Isao Takahashi; Tsuneaki Kawaguchi; Kensuke Amemiya