10 results on '"Imano M"'
Search Results
2. Giant purulent mesenteric cyst
- Author
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Kubota, A., Yonekura, T., Kuroda, D., Yasuda, T., Kato, M., Oyanagi, H., Imano, M., Sato, T., Fukushima, K., and Okada, M.
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- 1996
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3. Efficacy of palliative surgery for gastric cancer patients with peritoneal metastasis who still have residual peritoneal dissemination after chemotherapy.
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Shinkai M, Imano M, Kohda M, Nakanishi T, Hiraki Y, Hagi T, Kato H, Shiraishi O, Yasuda A, Tsubaki M, Nishida S, and Yasuda T
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- Humans, Palliative Care, Peritoneum, Gastrectomy adverse effects, Retrospective Studies, Peritoneal Neoplasms drug therapy, Peritoneal Neoplasms surgery, Peritoneal Neoplasms secondary, Stomach Neoplasms drug therapy, Stomach Neoplasms surgery, Stomach Neoplasms pathology, Laparoscopy
- Abstract
Purpose: Gastric cancer patients with peritoneal metastasis (PM) are generally treated with systemic chemotherapy. When PM has disappeared because of chemotherapy, radical gastrectomy (so-called conversion surgery) is usually performed. We have previously reported the efficacy of conversion surgery, but there are no reports examining the efficacy of palliative gastrectomy for patients with residual PM after chemotherapy. The purpose of this study was to investigate the efficacy of palliative surgery for gastric cancer patients with PM who still have residual peritoneal dissemination after chemotherapy., Methods: Twenty-five gastric cancer patients with PM confirmed by laparoscopy and who had received chemotherapy but who still had residual PM were included in this study. Among the 25 patients, palliative surgery was performed in 20 patients (PS group) and chemotherapy was continued in 5 patients (CTx group), and their therapeutic outcomes were compared., Results: In the PS group, total and distal gastrectomies were performed. Clavien-Dindo grade I postoperative complications occurred in two patients (10%). There were no treatment-related deaths. Postoperative chemotherapy was performed all cases. In the PS group, the median survival time (MST) reached 22.5 months, with 1- and 2-year overall survival (OS) rates of 95% and 45%, respectively, whereas in the CTx group, the MST was 15.8 months, and the 1- and 2-year OS rates were 60% and 0%, respectively. The PS group had significantly longer OS than the CTx group (P=0.044)., Conclusions: Palliative surgery is safe and may prolong survival in gastric cancer patients with residual PM after chemotherapy., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
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- 2023
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4. Efficacy of conversion surgery after a single intraperitoneal administration of paclitaxel and systemic chemotherapy for gastric cancer with peritoneal metastasis.
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Shinkai M, Imano M, Hiraki Y, Momose K, Kato H, Shiraishi O, Yasuda A, Tsubaki M, Nishida S, and Yasuda T
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- Antineoplastic Combined Chemotherapy Protocols therapeutic use, Gastrectomy, Humans, Paclitaxel, Retrospective Studies, Peritoneal Neoplasms drug therapy, Peritoneal Neoplasms secondary, Peritoneal Neoplasms surgery, Stomach Neoplasms drug therapy, Stomach Neoplasms pathology, Stomach Neoplasms surgery
- Abstract
Purpose: The prognosis of gastric cancer patients with peritoneal metastasis (PM) remains dismal with standard systemic chemotherapy. Intraperitoneal (i.p.) chemotherapy with paclitaxel (PTX) has local effects on intra-abdominal cancer cells. According to this phenomenon, we have developed regimens combining single i.p. PTX administration with systemic chemotherapy. This treatment strategy is very promising; however, the effect of "conversion surgery" in patients responding to this chemotherapy is unclear. Therefore, we performed a retrospective study to evaluate the safety and efficacy of conversion surgery for gastric cancer patients with PM., Methods: We enrolled 52 gastric cancer patients with PM who were treated with single i.p. PTX plus systemic chemotherapy between 2005 and 2015. Conversion surgery was performed where PM was eliminated by combination chemotherapy., Results: Among 52 gastric cancer patients, the disappearance of PM was confirmed in 33 patients (63.5%). Gastrectomy with D2 lymph node dissection was performed in all these patients. Histological response of grade ≥ 1b was achieved in 13 patients (39%). Clavien-Dindo grade II postoperative complications occurred in three patients (9%). There were no treatment-related deaths. The median survival time and 1-, 3-, and 5-year overall survival rates of the 33 patients who underwent conversion surgery were 30.7 months and 78.8%, 36.3%, and 24.2%, respectively, and those of the 19 patients who did not undergo surgery were 12.5 months and 52.6%, 5.2%, and 0%, respectively., Conclusion: Conversion surgery is safe and may prolong survival for gastric cancer patients with PM who have responded to single i.p. PTX plus systemic chemotherapy., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
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- 2022
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5. Neuroprotective effect of (-)-epigallocatechin-3-gallate in rats when administered pre- or post-traumatic brain injury.
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Itoh T, Tabuchi M, Mizuguchi N, Imano M, Tsubaki M, Nishida S, Hashimoto S, Matsuo K, Nakayama T, Ito A, Munakata H, and Satou T
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- 8-Hydroxy-2'-Deoxyguanosine, Aldehydes metabolism, Animals, Brain Edema etiology, Brain Edema prevention & control, Brain Injuries complications, Brain Injuries pathology, Catechin therapeutic use, DNA, Single-Stranded metabolism, Deoxyguanosine analogs & derivatives, Deoxyguanosine metabolism, Disease Models, Animal, Drug Administration Schedule, Glial Fibrillary Acidic Protein metabolism, Lipid Peroxidation drug effects, Male, Maze Learning drug effects, Neurons drug effects, Neurons metabolism, Phosphopyruvate Hydratase metabolism, Proto-Oncogene Proteins c-bcl-2 metabolism, Rats, Rats, Wistar, Time Factors, Brain Injuries prevention & control, Catechin analogs & derivatives, Neuroprotective Agents therapeutic use
- Abstract
Our previous study indicated that consuming (-)-epigallocatechin gallate (EGCG) before or after traumatic brain injury (TBI) eliminated free radical generation in rats, resulting in inhibition of neuronal degeneration and apoptotic death, and improvement of cognitive impairment. Here we investigated the effects of administering EGCG at various times pre- and post-TBI on cerebral function and morphology. Wistar rats were divided into five groups and were allowed access to (1) normal drinking water, (2) EGCG pre-TBI, (3) EGCG pre- and post-TBI, (4) EGCG post-TBI, and (5) sham-operated group with access to normal drinking water. TBI was induced with a pneumatic controlled injury device at 10 weeks of age. Immunohistochemistry and lipid peroxidation studies revealed that at 1, 3, and 7 days post-TBI, the number of 8-Hydroxy-2'-deoxyguanosine-, 4-Hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells, and levels of malondialdehyde around the damaged area were significantly decreased in all EGCG treatment groups compared with the water group (P < 0.05). Although there was a significant increase in the number of surviving neurons after TBI in each EGCG treatment group compared with the water group (P < 0.05), significant improvement of cognitive impairment after TBI was only observed in the groups with continuous and post-TBI access to EGCG (P < 0.05). These results indicate that EGCG inhibits free radical-induced neuronal degeneration and apoptotic death around the area damaged by TBI. Importantly, continuous and post-TBI access to EGCG improved cerebral function following TBI. In summary, consumption of green tea may be an effective therapy for TBI patients.
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- 2013
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6. Appearance of neural stem cells around the damaged area following traumatic brain injury in aged rats.
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Itoh T, Imano M, Nishida S, Tsubaki M, Nakayama T, Mizuguchi N, Yamanaka S, Tabuchi M, Munakata H, Hashimoto S, Ito A, and Satou T
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- 8-Hydroxy-2'-Deoxyguanosine, Aging, Aldehydes analysis, Animals, Cell Differentiation physiology, DNA, Single-Stranded analysis, Deoxyguanosine analogs & derivatives, Deoxyguanosine analysis, Deoxyguanosine biosynthesis, Disease Models, Animal, Fluorescent Antibody Technique, Immunohistochemistry, Intermediate Filament Proteins analysis, Intermediate Filament Proteins biosynthesis, Male, Nerve Tissue Proteins analysis, Nerve Tissue Proteins biosynthesis, Nestin, Neural Stem Cells metabolism, Rats, Rats, Wistar, Brain Injuries metabolism, Brain Injuries pathology, Lipid Peroxidation physiology, Neural Stem Cells cytology
- Abstract
We have previously reported free radical production after traumatic brain injury (TBI), which induces neural stem cell (NSC) degeneration and death. However, the effects of aging on NSC proliferation around the damaged area following TBI have not been investigated. Therefore, in this study, we used 10-week (young group) and 24-month-old (aged group) rat TBI models to investigate the effects of aging on NSC proliferation around damaged tissue using immunohistochemical and ex vivo techniques. Young and aged rats received TBI. At 1, 3 and 7 days after TBI, immunohistochemical and lipid peroxidation studies were performed. Immunohistochemistry revealed that the number of nestin-positive cells around the damaged area after TBI in the aged group decreased significantly when compared with those in the young group (P < 0.01). However, the number of 8-hydroxy-2'-deoxyguanosine-, 4-hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells and the level of peroxidation around the damaged area after TBI significantly increased in the aged group, compared with those in the young group (P < 0.01). Furthermore, almost all ssDNA-positive cells in young and aged groups co-localized with NeuN and nestin staining. Ex vivo studies revealed that neurospheres, which differentiated into neurons and glia in culture, could only be isolated from injured brain tissue in young and aged groups at 3 days after TBI. These results indicate that, although there were fewer NSCs that have the potential to differentiate into neurons and glia, these NSCs escaped free radical-induced degeneration around the damaged area after TBI in the aged rat brain.
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- 2013
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7. Increased apoptotic neuronal cell death and cognitive impairment at early phase after traumatic brain injury in aged rats.
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Itoh T, Imano M, Nishida S, Tsubaki M, Mizuguchi N, Hashimoto S, Ito A, and Satou T
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- 8-Hydroxy-2'-Deoxyguanosine, Age Factors, Aldehydes metabolism, Animals, Antigens, Nuclear metabolism, Behavior, Animal, Brain metabolism, Brain Injuries metabolism, Brain Injuries pathology, Brain Injuries psychology, Cognition Disorders metabolism, Cognition Disorders pathology, Cognition Disorders psychology, DNA Breaks, Single-Stranded, DNA, Single-Stranded metabolism, Deoxyguanosine analogs & derivatives, Deoxyguanosine metabolism, Disease Models, Animal, Immunohistochemistry, Lipid Peroxidation, Male, Malondialdehyde metabolism, Maze Learning, Motor Activity, Nerve Tissue Proteins metabolism, Neurons metabolism, Oxidative Stress, Rats, Rats, Wistar, Reactive Oxygen Species metabolism, Time Factors, Apoptosis, Brain pathology, Brain Injuries complications, Cognition, Cognition Disorders etiology, Neurons pathology
- Abstract
Progressive age-associated increases in cerebral dysfunction have been shown to occur following traumatic brain injury (TBI). Moreover, levels of neuronal mitochondrial antioxidant enzymes in the aged brain are reduced, resulting in free radical-induced cell death. It was hypothesized that cognitive impairment after TBI in the aged progresses to a greater degree than in younger individuals, and that damage involves neuronal degeneration and death by free radicals. In this study, we investigated the effects of free radicals on neuronal degeneration, cell death, and cognitive impairment in 10-week-old (young group) and 24-month-old rats (aged group) subjected to TBI. Young and aged rats received TBI with a pneumatic controlled injury device. At 1, 3 and 7 days after TBI, immunohistochemistry, lipid peroxidation and behavioral studies were performed. At 1, 3 and 7 days post-TBI, the number of 8-hydroxy-2'-deoxyguanosine-, 4-hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells, and the levels of malondialdehyde around the damaged area after TBI significantly increased in the aged group when compared with the young group (P < 0.05). In addition, the majority of ssDNA-positive cells in both groups co-localized with neuronal cells around the damaged area. There was a significant decrease in the number of surviving neurons and an increase in cognitive impairment after TBI in the aged group when compared with the young group (P < 0.05). These results indicate that following TBI, high levels of free radicals are produced in the aged rat brain, which induces neuronal degeneration and apoptotic cell death around the damaged area, resulting in cognitive impairment.
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- 2013
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8. (-)-Epigallocatechin-3-gallate increases the number of neural stem cells around the damaged area after rat traumatic brain injury.
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Itoh T, Imano M, Nishida S, Tsubaki M, Mizuguchi N, Hashimoto S, Ito A, and Satou T
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- Animals, Brain Injuries metabolism, Catechin pharmacology, Cell Proliferation drug effects, Immunohistochemistry, Male, Rats, Rats, Wistar, Brain Injuries pathology, Catechin analogs & derivatives, Lipid Peroxidation drug effects, Neural Stem Cells drug effects, Neuroprotective Agents pharmacology
- Abstract
A major component of green tea is (-)-epigallocatechin gallate (EGCG), which has strong antioxidant properties. Here, we investigated the effect of EGCG on neural stem cell (NSC) proliferation around the damaged area following traumatic brain injury (TBI). In this study, male Wistar rats that had access to normal drinking water, or water containing 0.1% (w/v) EGCG, ad libitum received TBI at 10 weeks of age. Immunohistochemistry revealed that the number of nestin-positive cells around the damaged area after TBI in the EGCG treatment group increased significantly compared with the normal water group (P < 0.05). However, the number of 8-hydroxy-2'-deoxyguanosine-, 4-hydroxy-2-nonenal-, single-stranded DNA (ssDNA)-positive cells and the level of peroxidation around the damaged area after TBI significantly decreased in the EGCG treatment group when compared with the water group (P < 0.05). Furthermore, in contrast to the EGCG group, almost all ssDNA-positive cells in the water group co-localized with NeuN and nestin-staining. Ex vivo studies revealed that spheres could only be isolated from injured brain tissue in the water group at 3 days following TBI. However, in the EGCG group, spheres could be isolated at both 3 and 7 days following TBI. A greater number of spheres could be isolated from the EGCG group, which differentiated into neurons and glia in culture without basic fibroblast growth factor. These results indicate that consumption of water containing EGCG pre- and post-TBI inhibits free radical-induced degradation of NSCs, which have the potential to differentiate into neurons and glia around the area of damage following TBI.
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- 2012
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9. Exercise inhibits neuronal apoptosis and improves cerebral function following rat traumatic brain injury.
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Itoh T, Imano M, Nishida S, Tsubaki M, Hashimoto S, Ito A, and Satou T
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- Animals, Male, Neurons metabolism, Neurons pathology, Random Allocation, Rats, Rats, Wistar, Recovery of Function physiology, Apoptosis physiology, Brain Injuries pathology, Brain Injuries physiopathology, Brain Injuries rehabilitation, Exercise Therapy methods, Nerve Degeneration pathology, Nerve Degeneration physiopathology, Nerve Degeneration rehabilitation, Physical Conditioning, Animal physiology
- Abstract
Exercise is reported to inhibit neuronal apoptotic cell death in the hippocampus and improve learning and memory. However, the effect of exercise on inhibition of neuronal apoptosis surrounding the area of damage after traumatic brain injury (TBI) and the improvement of cerebral dysfunction following TBI are unknown. Here, we investigate the effect of exercise on morphology and cerebral function following TBI in rats. Wistar rats received TBI by a pneumatic controlled injury device were randomly divided into two groups: (1) non-exercise group and (2) exercise group. The exercise group ran on a treadmill for 30 min/day at 22 m/min for seven consecutive days. Immunohistochemical and behavioral studies were performed following TBI. The number of single-stranded DNA (ssDNA)-positive cells around the damaged area early after TBI was significantly reduced in the exercise group compared with the non-exercise group (P < 0.05). Furthermore, most ssDNA-positive cells in the non-exercise group co-localized with neuronal cells. However, in the exercise group, a few ssDNA-positive cells co-localized with neurons. In addition, there was a significant increase in neuronal cell number and improvement in cerebral dysfunction after TBI in the exercise group compared with the non-exercise group (P < 0.05). These results indicate that exercise following TBI inhibits neuronal degeneration and apoptotic cell death around the damaged area, which results in improvement of cerebral dysfunction. In summary, treadmill running improved cerebral dysfunction following TBI, indicating its potential as an effective clinical therapy. Therefore, exercise therapy (rehabilitation) in the early phase following TBI is important for recuperation from cerebral dysfunction.
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- 2011
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10. Exercise increases neural stem cell proliferation surrounding the area of damage following rat traumatic brain injury.
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Itoh T, Imano M, Nishida S, Tsubaki M, Hashimoto S, Ito A, and Satou T
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- Animals, Brain Injuries pathology, Cell Differentiation physiology, Cell Proliferation, Fluorescent Antibody Technique, Immunohistochemistry, Male, Rats, Rats, Wistar, Brain Injuries physiopathology, Neural Stem Cells cytology, Neural Stem Cells physiology, Physical Conditioning, Animal physiology
- Abstract
Exercise enhances neuronal stem cell (NSC) proliferation and neurogenesis. However, the effect of exercise on NSC proliferation surrounding the area of damage after traumatic brain injury (TBI) is unknown. Here, we investigate the effect of running on NSC proliferation following TBI in the rat. Wistar rats received TBI and were randomly divided into two groups: (1) non-exercise group and (2) exercise group. The exercise group ran on a treadmill for 30 min/day at 22 m/min for 7 consecutive days. Immunohistochemistry was used to monitor NSC proliferation around the damaged area, and ex vivo techniques were used to isolate NSCs from the damaged region in both groups. The number of nestin- and Ki67-positive cells observed at 3 and 7 days after TBI was significantly greater in the exercise group than in the non-exercise group (P < 0.01). Furthermore, most nestin-positive cells in the exercise group co-localized with Ki67-positive cells. In ex vivo studies, spheres could be isolated from injured brain tissue from the exercise group at 3 and 7 days following TBI, but at only 3 days in the non-exercise group. The number of spheres isolated from injured brain tissue was greater in the exercise group than in the non-exercise group. Spheres were immunopositive for nestin and comprised NSCs that could differentiate into neurons and glia. Exercise increases the proliferation of NSCs around the damaged area following TBI. Therefore, exercise therapy (rehabilitation) in the early phase following TBI is important for recuperation from cerebral dysfunction induced by TBI.
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- 2011
- Full Text
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