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Dive into the research topics where Hiroki Shioura is active.

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Featured researches published by Hiroki Shioura.


Radiation Research | 2001

Induction of radioresistance by a nitric oxide-mediated bystander effect.

Hideki Matsumoto; Sachiko Hayashi; Masanori Hatashita; Ken Ohnishi; Hiroki Shioura; Toshio Ohtsubo; Ryuhei Kitai; Takeo Ohnishi; Eiichi Kano

Abstract Matsumoto, H., Hayashi, S., Hatashita, M., Ohnishi, K., Shioura, H., Ohtsubo, T., Kitai, R., Ohnishi, T. and Kano, E. Induction of Radioresistance by a Nitric Oxide-Mediated Bystander Effect. To elucidate whether nitric oxide secreted from irradiated cells affects cellular radiosensitivity, we examined the accumulation of inducible nitric oxide synthase, TP53 and HSP72, the concentration of nitrite in the medium of cells after X irradiation, and cellular radiosensitivity using two human glioblastoma cell lines, A-172, which has a wild-type TP53 gene, and a transfectant of A-172 cells, A-172/mp53, bearing a mutated TP53 gene. Accumulation of inducible nitric oxide synthase was caused by X irradiation of the mutant TP53 cells but not of the wild-type TP53 cells. Accumulation of TP53 and HSP72 in the wild-type TP53 cells was observed by cocultivation with irradiated mutant TP53 cells, and the accumulation was abolished by the addition of an inhibitor for inducible nitric oxide synthase, aminoguanidine, to the medium. Likewise, accumulation of these proteins was observed in the wild-type TP53 cells after exposure to conditioned medium from irradiated mutant TP53 cells, and the accumulation was abolished by the addition of a specific nitric oxide scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, to the medium. The radiosensitivity of wild-type TP53 cells was reduced when the cells were cultured in conditioned medium from irradiated mutant TP53 cells compared to conventional fresh growth medium. Collectively, these findings indicate the potential importance of an intercellular signal transduction pathway initiated by nitric oxide in the cellular response to ionizing radiation.


International Journal of Radiation Biology | 2000

Induction of radioresistance to accelerated carbon-ion beams in recipient cells by nitric oxide excreted from irradiated donor cells of human glioblastoma.

Hideki Matsumoto; Sachiko Hayashi; Masanori Hatashita; Hiroki Shioura; T. Ohtsubo; R. Kitai; Takeo Ohnishi; Osami Yukawa; Y. Furusawa; Eiichi Kano

Purpose : To investigate whether nitric oxide excreted from cells irradiated with accelerated carbon-ion beams modulates cellular radiosensitivity against irradiation in human glioblastoma A-172 and T98G cells. Materials and methods : Western-blot analysis of inducible nitric oxide synthase, hsp72 and p53, the concentration assay of nitrite in medium and cell survival assay after irradiation with accelerated carbon-ion beams were performed. Results : The accumulation of inducible nitric oxide synthase was caused by accelerated carbon-ion beam irradiation of T98G cells but not of A-172 cells. The accumulation of hsp72 and p53 was observed in A-172 cells after exposure to the conditioned medium of the T98G cells irradiated with accelerated carbon-ion beams, and the accumulation was abolished by the addition of an inhibitor for inducible nitric oxide synthase to the medium. The radiosensitivity of A-172 cells was reduced in the conditioned medium of the T98G cells irradiated with accelerated carbonion beams compared with conventional fresh growth medium, and the reduction of radiosensitivity was abolished by the addition of an inducible nitric oxide synthase inhibitor to the conditioned medium. Conclusions : Nitric oxide excreted from the irradiated donor cells with accelerated carbon-ion beams could modulate the radiosensitivity of recipient cells. These findings indicate the importance of an intercellular signal transduction pathway initiated by nitric oxide in the cellular response to accelerated heavy ions.PURPOSE To investigate whether nitric oxide excreted from cells irradiated with accelerated carbon-ion beams modulates cellular radiosensitivity against irradiation in human glioblastoma A-172 and T98G cells. MATERIALS AND METHODS Western-blot analysis of inducible nitric oxide synthase, hsp72 and p53, the concentration assay of nitrite in medium and cell survival assay after irradiation with accelerated carbon-ion beams were performed. RESULTS The accumulation of inducible nitric oxide synthase was caused by accelerated carbon-ion beam irradiation of T98G cells but not of A-172 cells. The accumulation of hsp72 and p53 was observed in A-172 cells after exposure to the conditioned medium of the T98G cells irradiated with accelerated carbon-ion beams, and the accumulation was abolished by the addition of an inhibitor for inducible nitric oxide synthase to the medium. The radiosensitivity of A-172 cells was reduced in the conditioned medium of the T98G cells irradiated with accelerated carbon-ion beams compared with conventional fresh growth medium, and the reduction of radiosensitivity was abolished by the addition of an inducible nitric oxide synthase inhibitor to the conditioned medium. CONCLUSIONS Nitric oxide excreted from the irradiated donor cells with accelerated carbon-ion beams could modulate the radiosensitivity of recipient cells. These findings indicate the importance of an intercellular signal transduction pathway initiated by nitric oxide in the cellular response to accelerated heavy ions.


International Journal of Radiation Oncology Biology Physics | 1998

Suppression of heat-induced HSF activation by CDDP in human glioblastoma cells

Hideki Matsumoto; Sachiko Hayashi; Hiroki Shioura; Toshio Ohtsubo; Ryuhei Kitai; Ken Ohnishi; Nobushige Hayashi; Takeo Ohnishi; Eiichi Kano

PURPOSE The kinetics of the accumulation of inducible 72-kD heat shock protein (hsp72) and the activation of heat shock transcriptional factor (HSF) after hyperthermia and/or CDDP treatment in two human glioblastoma cell lines, A-172 having the wild-type p53 gene and T98G having the mutated p53 gene were evaluated. METHODS AND MATERIALS Western blot analysis of hsp72, gel-mobility shift assay of HSF, cell survival, and development of thermotolerance were examined. RESULTS The prominent suppression of heat-induced hsp72 accumulation by CDDP was seen in A-172 cells, but not in T98G cells. This was due to the p53-dependent inhibition of heat-induced HSF activation by CDDP. The interactive hyperthermic enhancement of CDDP cytotoxicity was observed in A-172 cells, but not in T98G cells. In addition, the heat-induced thermotolerance was suppressed by the presence of CDDP in the pretreatment. CONCLUSION Suppression of heat-induced hsp72 accumulation by CDDP contributes to an interactive hyperthermic enhancement of CDDP cytotoxicity in the cells bearing the wild-type p53 gene.


International Journal of Molecular Medicine | 2011

Thermosensitization and induction of apoptosis or cell-cycle arrest via the MAPK cascade by parthenolide, an NF-κB inhibitor, in human prostate cancer androgen-independent cell lines

Sachiko Hayashi; Ken Koshiba; Masanori Hatashita; Takefumi Sato; Yutaka Jujo; Ryuta Suzuki; Yukie Tanaka; Hiroki Shioura

Parthenolide (PTL), a nuclear factor-κB (NF-κB) inhibitor, has a significant thermo-enhancement effect. Modification of thermosensitivity by treatment with PTL prior to hyperthermia was investigated in the human prostate cancer androgen-independent cell lines PC3 and DU145. In addition, we analyzed the mechanisms related to induction of apoptosis or G₂/M cell-cycle arrest via the effects of ERK1/2, p38 and SAPK/JNK signaling on mitogen-activated protein kinase (MAPK). Lethal damage caused by mild hyperthermia at 41.0˚C or 42.0˚C in both cell lines resulted in a low level of thermosensitivity, while sequential combination with PTL showed significant thermosensitization. Step-up hyperthermia (SUH) (42˚C for 30 min, 43.0˚C or 43.5˚C for various periods) reduced the thermosensitivity of the cells to second heating. However, PTL given as pre-treatment prior to SUH prevented SUH-induced thermal tolerance and resulted in significant thermosensitization. Induction of apoptosis by the combination of PTL and hyperthermia at 44.0˚C was determined by the ratio of sub-G1 division cells using flow cytometry, which was increased significantly in comparison with single treatment, and was more effective in PC3 than DU145 cells. The behavior of ERK1/2, p38, and SAPK/JNK signaling in the MAPK cascade by treatment with PTL and hyperthermia were examined by Western blotting. As for PC3 cells, ras-downstream p-ERK1/2 was activated and p-p38 slightly activated by combined treatment with PTL and hyperthermia in comparison with each alone. As for DU145 cells, ERK1/2 was not changed, while p38 and SAPK/JNK were slightly activated by combination treatment. These results were related to increases in the induction of apoptosis, G₂/M cell cycle arrest, and lethal damage of cells via the MAPK cascade. Together, our findings demonstrate that PTL is an effective thermosensitizing agent for multidisciplinary therapy for human prostate cancer.


Cancer Letters | 1996

Suppression of heat-induced hsp72 accumulation by cisplatin in human glioblastoma cells

Hideki Matsumoto; Sachiko Hayashi; Hiroki Shioura; Toshio Ohtsubo; Takeo Ohnishi; Eiichi Kano

The accumulation of the inducible hsp72 (72-kDa heat shock protein) after hyperthermia and/or cisplatin treatment in human glioblastoma cell line (A-172) was studied by Western blot analysis. The level of hsp72 increased to eight-fold 10 h after hyperthermia alone (44 degrees C for 20 min, D50) and to three-fold 10 h after cisplatin treatment (5 microg/ml) at 37 degrees C for 15 min (D50). In contrast, when the cells were simultaneously heated with cisplatin, the accumulation of hsp72 was suppressed. The level of hsp72 increased to about six-fold and two-fold 10 h after hyperthermia (44 degrees C, 15 min) in the presence of 1 and 10 microg/ml (D50 or D10) of cisplatin, respectively. In addition, we found both the enhancement of thermosensitivity and the suppression of thermotolerance by the simultaneously combined treatment of hyperthermia and cisplatin. It has been reported that the enhancement of cisplatin cytotoxicity by hyperthermia is due to increase of both cisplatin uptake and DNA damage by hyperthermia. Our results suggest that the interactive cytotoxic enhancement by the combination of hyperthermia and cisplatin may be also due to the suppression of heat-induced hsp72 accumulation by cisplatin.


Journal of Experimental & Clinical Cancer Research | 1999

Thermosensitivity, incidence of apoptosis and accumulations of hsp72 and p53 proteins of murine L cells in wild type status of p53 gene.

Sachiko Hayashi; Eiichi Kano; Hideki Matsumoto; Masanori Hatashita; Toshio Ohtsubo; T Nishida; Hiroki Shioura; Ryuhei Kitai

Murine L cells showed markedly high lethal thermosensitivity. Survivals from fractionated heating at 44 degrees C with variety of interval time at 37 degrees C (44 degrees C for 10 min--variety of interval time at 37 degrees C-44 degrees C for 10 min) increased markedly in accordance with elongation of the internal time; i.e. survival fraction of 0.9% from 44 degrees C for 20 min alone without the interval time to those of 25% from the fractionated heating with interval time at 37 degrees C for 3-10 hrs. Incidence of apoptosis of the L cells from heating at 44 degrees C for 6.5 min (LD50) increased from 7% immediately after the heating to 30% 6-12 hrs after the post-incubation time at 37 degrees C. Accumulation of both hsp72 and p53 proteins markedly increased after a heating at 44 degrees C for 10 min alone in accordance with elongation of post-incubation time at 37 degrees C, representing a peak 6 hrs after the post incubation. Status of p53 gene in L cells were determined with Reverse Transcription-Polymerase Chain Reaction-Single Strand Conformational Polymorphism (RT-PCR-SSCP), i.e. wild type.


Journal of Neuro-oncology | 1998

Sensitization to hyperthermia by intracellular acidification

Ryuhei Kitai; Masanori Kabuto; T. Kubota; Hidenori Kobayashi; Hideki Matsumoto; Sachiko Hayashi; Hiroki Shioura; Toshio Ohtsubo; Kanji Katayama; Eiichi Kano

Hyperthermia has been introduced as a new modality of treatment for glioma. In these experiments, the cytotoxicity of hyperthermia in C6 glioma cells was enhanced by increasing the intracellular acidity with amiloride and/or 4,4′-diisothiocyanatostilbene-2,2′disulfonic acid (DIDS). Intracellular pH (pHi) is regulated mainly by Na’u/H’u and HCOplus’3minus/Clminus antiports through the cell membrane, and amiloride acts on the former, DIDS on the latter to lower pHi. The cellular thermosensitivity to clinically achievable brain hyperthermia at 42° C was enhanced by 0.5 mM amiloride (Na’u/H’u antiport inhibitor). T0 values (T0 = the heating period required to reduce experimental survival rate by 1/e) at 42° C without and with amiloride was 192 and 81 min, respectively. The addition of DIDS (HCO3minus/Clminus antiport inhibitor) further enhanced. T0 value was 25 min. Fluorophotometric measurement of pHi was employed using the pH sensitive dye, bis(carboxyethyl)carboxyfluorescein, which is trapped in viable cells. The average pHi in control C6 glioma cells in pH 7.2 media was 7.21. In the untreated cells heated at 42° C for 1 hour, the pHi was 7.12. The pHi of the cells heated in the presence of amiloride was decreased to 6.83. The pHi was further lowered to 6.67 by the treatment with amiloride in combination with DIDS for 2 hours. Hyperthermia with amiloride and DIDS may be a more effective treatment for malignant gliomas.


Magnetic Resonance Imaging | 2013

Monitoring of extra-axial brain tumor response to radiotherapy using pseudo-continuous arterial spin labeling images: Preliminary results

Tatsuya Yamamoto; Kazuyuki Kinoshita; Nobuyuki Kosaka; Yoshitaka Sato; Hiroki Shioura; Hiroaki Takeuchi; Hirohiko Kimura

INTRODUCTION Technological developments have increased the ease of performing perfusion MRI by arterial spin labeling (ASL) in clinical settings. The objective of this study was to evaluate the effects of radiotherapy on extra-axial brain tumors by using MR perfusion images obtained using the pseudo-continuous arterial spin labeling (pcASL) method. MATERIALS AND METHODS Six consecutive patients (nine lesions) with extra-axial brain tumors treated only with radiotherapy were enrolled in this study. MR examinations, including pcASL imaging, were performed before and after radiotherapy. Cerebral blood flow, maximum tumor blood flow (mTBF), tumor volume and the ratio of signal enhancement by contrast material (enhancement ratio) were evaluated in serial examinations during the course of radiotherapy. Both the percentage change in mTBF (mTBF ratio) and the percentage change in volume (volume ratio) were calculated using values obtained before and after radiotherapy. The correlation between the volume ratio and the mTBF ratio was assessed using linear regression analysis and Spearmans rank correlation coefficient (rs). RESULTS A strong correlation was demonstrated between the tumor volume ratio and the mTBF ratio before and after radiotherapy (rs=0.93, P<.01). However, no significant correlation was identified between changes in enhancement and volume ratio (rs=0.20) or between changes in enhancement and mTBF ratio (rs=0.30) before and after radiotherapy. CONCLUSION The mTBF measured using pcASL may serve as an additive index for tumor volume when determining tumor response to radiotherapy even in the absence of contrast material.


International Scholarly Research Notices | 2014

Alpha 1-Adrenoceptor Blocker May Improve Not Only Voiding But Also Storage Lower Urinary Tract Symptoms Caused by 125I Brachytherapy for Prostate Cancer

Nobuyuki Oyama; Yoshitaka Aoki; Hideaki Ito; Yoshiji Miwa; Hironobu Akino; Yoshitaka Sato; Hiroki Shioura; Hirohiko Kimura; Osamu Yokoyama

Purpose. To assess changes in lower urinary tract symptoms (LUTS) within 1 year after brachytherapy in patients receiving alpha 1-adrenoceptor antagonists. Methods. We retrospectively evaluated 116 patients who underwent 125I prostate brachytherapy in our institute. Seventy-one patients were treated with a combination of external beam radiation therapy and brachytherapy. Alpha 1-adrenoceptor antagonists were prescribed to all patients after brachytherapy. International Prostate Symptom Score (IPSS) forms and postvoid residual urine volume were recorded at all follow-up visits. Results. Forty-nine patients were given tamsulosin hydrochloride, 32 were given silodosin hydrochloride, and 35 were given naftopidil for up to 6 months after seed implantation. Patients given tamsulosin or naftopidil tended to show a higher peak IPSS and slower recovery to baseline values than those given silodosin. The patients given naftopidil showed an insufficient recovery in storage symptoms in naftopidil group in comparison with tamsulosin group at 3 months and with silodosin group at 6 and 9 months. Conclusions. In the management of LUT after brachytherapy, silodosin may provide a more favorable improvement. Silodosin and tamsulosin may have an advantage in improving not only voiding but also storage lower urinary tract symptoms after brachytherapy.


Acta radiologica short reports | 2014

Arterial spin labeling perfusion-weighted MRI for long-term follow-up of a cerebral arteriovenous malformation after stereotactic radiosurgery

Kazuhiro Shimizu; Nobuyuki Kosaka; Tatsuya Yamamoto; Hiroki Shioura; Toshiaki Kodera; Ken-ichiro Kikuta; Hirohiko Kimura

We present a longitudinal series of arterial spin-labeling magnetic resonance imaging (ASL-MRI) in a patient with cerebral arteriovenous malformations (AVMs) treated by stereotactic radiosurgery (SRS). Pretreatment ASL-MRI showed high signal intensity in both the nidus and draining veins, and the latter signal abnormality gradually moved proximally by 14 months after SRS. At 24 months, the signal abnormalities finally disappeared, indicating complete obliteration of the nidus. The hemodynamic changes in the AVM were clearly visualized in the longitudinal ASL-MRI series, thus this non-invasive MR method may be useful not only for detecting AVMs but also for assessment of their response after SRS.

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Ken Ohnishi

Nara Medical University

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