11 results on '"Hiromi Kuma"'
Search Results
2. The Posterolaterally Oriented and Laterally Downward Sloping Facet Joint Is a Risk Factor for Degenerative Cervical Spondylolisthesis and Myelopathy
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Hiromi Kumamaru, Keiichiro Iida, Takeyuki Saito, Shingo Yoshizaki, Yasuharu Nakashima, and Katsumi Harimaya
- Subjects
cervical degenerative spondylolisthesis ,computed tomography ,facet joint ,myelopathy ,Surgery ,RD1-811 - Abstract
Introduction: Facet joints are anatomical structures that are known to be crucial for determining spinal biomechanical motion; however, the potential relationship between facet orientation and the development of cervical spondylolisthesis remains unclear. Thus, in this study, we aimed to explore the relationship between facet orientation and cervical spondylolisthesis as well as myelopathy. Methods: Facet orientation in the cervical spine was investigated using computed tomography in 103 patients with cervical myelopathy, and facet inclination was measured on axial, coronal, and sagittal reconstructed images. Patients were divided into anterolisthesis, retrolisthesis, and no spondylolisthesis groups at each intervertebral level (C2/3-C6/7 levels). Results: Facet joints in the anterolisthesis and retrolisthesis groups tended to slope posterolaterally and downward laterally compared with those in the no spondylolisthesis group at C3/4, C4/5, and C5/6 levels (P
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- 2022
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3. Early maternal deprivation induces alterations in brain-derived neurotrophic factor expression in the developing rat hippocampus
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Yoshiki Takeuchi, Takashi Kusaka, Hanayo Okamoto, Takanori Miki, Kuldip S. Bedi, Toshifumi Yokoyama, Hiromi Kuma, Hong-Peng Li, Yoshiki Matsumoto, He Gu, Shoju Onishi, Hiroshi Suwaki, and Irawan Satriotomo
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Brain-derived neurotrophic factor ,Maternal deprivation ,medicine.medical_specialty ,Brain-Derived Neurotrophic Factor ,Maternal Deprivation ,General Neuroscience ,Period (gene) ,Central nervous system ,Gene Expression Regulation, Developmental ,Hippocampal formation ,Hippocampus ,Rats ,Real-time polymerase chain reaction ,Endocrinology ,medicine.anatomical_structure ,Animals, Newborn ,Pregnancy ,Neurotrophic factors ,Internal medicine ,medicine ,Animals ,Hippocampus (mythology) ,Female ,Rats, Wistar ,Psychology - Abstract
The effects of maternal deprivation (MD) during early postnatal life on the brain-derived neurotrophic factor (BDNF) level were investigated in the present study. Wistar rats were assigned to either maternal deprivation or mother-reared control (MRC) groups. MD manipulation was achieved by separating rat pups from their mothers for 3 h a day during postnatal days (PND) 10-15. At 16, 20, 30, and 60 days of age, the level of BDNF mRNA in the hippocampal formation of each group was determined using real-time PCR analysis. Early postnatal maternal deprivation of rat pups resulted in a significant increase in body weight at 60 days of age. The expression of BDNF mRNA in the hippocampus was significantly decreased at 16 days of age, and increased at 30 and 60 days of age. These data indicate that even a brief period of maternal deprivation during early postnatal life can affect hippocampal BDNF expression.
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- 2004
4. Early postnatal ethanol exposure induces fluctuation in the expression of BDNF mRNA in the developing rat hippocampus
- Author
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Takanori, Miki, Hiromi, Kuma, Toshifumi, Yokoyama, Kazunori, Sumitani, Yoshiki, Matsumoto, Takashi, Kusaka, Katsuhiko, Warita, Zhi-Yu, Wang, Naohisa, Hosomi, Tomohiro, Imagawa, Kuldip, S Bedi, Susumu, Itoh, Yu, Nakamura, and Yoshiki, Takeuchi
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Ethanol ,Pregnancy ,Reverse Transcriptase Polymerase Chain Reaction ,Brain-Derived Neurotrophic Factor ,Body Weight ,Animals ,Central Nervous System Depressants ,Female ,RNA, Messenger ,Rats, Wistar ,Hippocampus ,Rats - Abstract
Effects of early postnatal ethanol exposure on brain-derived neurotrophic factor (BDNF) mRNA expression in the rat hippocampus were investigated. Wistar rats were assigned to either ethanol treatment (ET) separation control (SC) or mother-reared control (MRC) groups. Ethanol exposure was achieved by a vapor inhalation method for 3 hours a day between postnatal days (PND) 1015. On PND 16, 20, 30, and 60, the expression of BDNF mRNA in the hippocampus was determined using real-time RT-PCR analysis. There was a significant age-related increase in the BDNF mRNA expression between PND 3060 in MRC animals. The BDNF mRNA expression in ET rats was increased at both PND 16 and 20 and thereafter decreased at PND 60 compared to SC animals. Such age-related fluctuation in the expression of BDNF mRNA differed from that of MRC animals. The exact functional implications, if any, of these ethanol-induced changes in BDNF mRNA expression remain unknown although it can be speculated that they may have an effect on the behaviors known to be influenced by the hippocampal formation.
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- 2008
5. Effects of chronic ethanol administration on the expression levels of neurotrophic factors in the rat hippocampus
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Toshifumi Yokoyama, Yoshiki Matsumoto, Zhi-Yu Wang, Kyoung-Youl Lee, Takanori Miki, Hiromi Kuma, Ippei Yamaoka, Hong-Peng Li, He Gu, Yu Nakamura, Kazutoshi Fusumada, Tomohiro Imagawa, Yoshiki Takeuchi, and Hanayo Okamoto
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Male ,medicine.medical_specialty ,Central nervous system ,Hippocampus ,Gene Expression ,Hippocampal formation ,Neurotrophic factors ,Internal medicine ,medicine ,Glial cell line-derived neurotrophic factor ,Animals ,Glial Cell Line-Derived Neurotrophic Factor ,RNA, Messenger ,Rats, Wistar ,Brain-derived neurotrophic factor ,biology ,Ethanol ,Reverse Transcriptase Polymerase Chain Reaction ,Brain-Derived Neurotrophic Factor ,Neurotoxicity ,Central Nervous System Depressants ,medicine.disease ,Diet ,Rats ,Disease Models, Animal ,Endocrinology ,medicine.anatomical_structure ,nervous system ,Anesthesia ,biology.protein ,Anatomy ,Alcohol-Related Disorders ,Neurotrophin - Abstract
Chronic ethanol consumption has adverse effects on the central nervous system. Hippocampus is one of the target sites of ethanol neurotoxicity. Hippocampal damage is known to result in impairment of learning and memory. This study was aimed to determine whether chronic ethanol consumption could alter the expression levels of brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF) mRNAs in the hippocampus. Male Wistar rats were given unrestricted access to a liquid diet containing 5% (v/v) ethanol as the sole fluid source for 19 weeks beginning at 10 weeks of age. The expression levels of BDNF and GDNF mRNAs in the hippocampus were analyzed by real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis. The present study revealed that chronic ethanol consumption did not result in significant changes in the expression levels of BDNF and GDNF mRNAs. Our present results showed no significant alteration in the expression of these neurotrophic factors; these results will lead to further studies to examine the possible alterations in the gene expression of various neurotrophins that are related to hippocampal functions including learning and memory.
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- 2006
6. Oligodendrocyte myelin glycoprotein (OMgp) in rat hippocampus is depleted by chronic ethanol consumption
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Yoshiki Takeuchi, Kyoung-Youl Lee, Takanori Miki, Hanayo Okamoto, Kuldip S. Bedi, Yu Nakamura, Satriotomo Irawan, Hong-Peng Li, Hiromi Kuma, Toshifumi Yokoyama, Zhi-Yu Wang, Yoshiki Matsumoto, and He Gu
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Male ,medicine.medical_specialty ,Liquid diet ,Down-Regulation ,Hippocampal formation ,GPI-Linked Proteins ,Hippocampus ,Nerve Fibers, Myelinated ,Myelin ,Alcohol-Induced Disorders, Nervous System ,Neurotrophic factors ,Internal medicine ,medicine ,Glial cell line-derived neurotrophic factor ,Animals ,Glial Cell Line-Derived Neurotrophic Factor ,RNA, Messenger ,Rats, Wistar ,Brain-derived neurotrophic factor ,biology ,Ethanol ,Chemistry ,General Neuroscience ,Brain-Derived Neurotrophic Factor ,Central Nervous System Depressants ,Organ Size ,Oligodendrocyte ,Rats ,Disease Models, Animal ,Myelin-Associated Glycoprotein ,Endocrinology ,medicine.anatomical_structure ,nervous system ,Chronic Disease ,biology.protein ,Neuroglia ,Myelin-Oligodendrocyte Glycoprotein ,Atrophy ,Myelin Proteins ,Demyelinating Diseases - Abstract
The hippocampal formation has been shown to be particularly vulnerable to the neurotoxic effects of chronic ethanol consumption. It was hypothesized that this damage was due to the disruption of the expression of neurotrophic factors and certain other proteins within the hippocampus. By using real-time reverse transcription-polymerase chain reaction (RT-PCR) techniques, this study aimed to determine whether chronic ethanol consumption could alter the mRNA expression level of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), and oligodendrocyte myelin glycoprotein (OMgp) in the hippocampus. Wistar male rats received an unrestricted access to a liquid diet containing 5% (v/v) ethanol as the sole source of fluid from 10 to 29 weeks of age. Control rats had unlimited access to a liquid diet containing an isocaloric amount of sucrose. We found that chronic ethanol consumption did not cause significant changes in the levels of mRNA for BDNF and GDNF. However, OMgp mRNA showed a significant deficit in ethanol-treated animals. It is suggested that this deficit may be related to the demyelination that is commonly observed in human alcoholics and that this may contribute to the functional and cognitive deficits.
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- 2006
7. The effect of the timing of prenatal X-irradiation on Purkinje cell numbers in rat cerebellum
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Daniel Gonzalez, Takanori Miki, Yoshiki Takeuchi, Irawan Satriotomo, He Gu, Yoshiki Mastumoto, Kuldip S. Bedi, Hiromi Kuma, Hong Peng Li, and Hiroshi Suwaki
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Male ,medicine.medical_specialty ,Cerebellum ,Purkinje cell ,Stereology ,Cell Count ,Biology ,Purkinje Cells ,Developmental Neuroscience ,Cell Movement ,Pregnancy ,Cortex (anatomy) ,Internal medicine ,medicine ,Animals ,Progenitor cell ,Rats, Wistar ,reproductive and urinary physiology ,Stem Cells ,X-Rays ,Body Weight ,Cell Differentiation ,Anatomy ,Organ Size ,Rats ,medicine.anatomical_structure ,Endocrinology ,Animals, Newborn ,Cerebral cortex ,In utero ,Prenatal Exposure Delayed Effects ,embryonic structures ,Female ,Perfusion ,Cell Division ,Developmental Biology - Abstract
Exposure of the developing brain to X-irradiation in utero is known to cause various deleterious consequences. We have previously reported the effects of prenatal X-irradiation on the development of the cerebral cortex in rats. We have now extended this study to examine the effects of such X-irradiation on the development of the cerebellum. Wistar rats were exposed to 1.5 Gy X-irradiation either on days 14, 15 or 16 of gestation (E14, E15, E16). Sham-irradiated animals were used as controls. At seven postnatal weeks of age, male rats from each group were deeply anesthetized and killed by intracardiac perfusion with 2.5% glutaraldehyde in 0.1 M phosphate buffer. The unbiased stereological procedure known as the fractionator method was used to estimate the total number of Purkinje cells in the cerebellum of each animal. Body and cerebellar weights from E14 and E15, but not E16 irradiated rats showed significant deficits compared to control animals. Rats irradiated on E16 and control rats had about 285 100–304 800 Purkinje cells in the cerebellum. There was no significant difference between these values. However, E14 and E15 irradiated animals had about 117 500 and 196 300 Purkinje cells, respectively. These estimates were significantly different from those observed in both control and E16 irradiated rats. Given that the phase of division of Purkinje cell progenitors is mainly between E14–E15 and the phase of differentiation and migration is between E16–E20, it is concluded that the vulnerable period of the Purkinje cells to X-irradiation closely overlaps the phase of division of progenitors.
- Published
- 2002
8. Activation of Intrinsic Growth State Enhances Host Axonal Regeneration into Neural Progenitor Cell Grafts
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Hiromi Kumamaru, Paul Lu, Ephron S. Rosenzweig, and Mark H. Tuszynski
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Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Abstract
Summary: Axonal regeneration after spinal cord injury (SCI) can be enhanced by activation of the intrinsic neuronal growth state and, separately, by placement of growth-enabling neural progenitor cell (NPC) grafts into lesion sites. Indeed, NPC grafts support regeneration of all host axonal projections innervating the normal spinal cord. However, some host axons regenerate only short distances into grafts. We examined whether activation of the growth state of the host injured neuron would elicit greater regeneration into NPC grafts. Rats received NPC grafts into SCI lesions in combination with peripheral “conditioning” lesions. Six weeks later, conditioned host sensory axons exhibited a significant, 9.6-fold increase in regeneration into the lesion/graft site compared with unconditioned axons. Regeneration was further enhanced 1.6-fold by enriching NPC grafts with phenotypically appropriate sensory neuronal targets. Thus, activation of the intrinsic host neuronal growth state and manipulation of the graft environment enhance axonal regeneration after SCI. : Kumamaru and colleagues demonstrate that activation of intrinsic growth state robustly enhances host sensory axonal regeneration into neural stem cell grafts. Regeneration of lesioned host sensory axons was further enhanced by enriching neural stem cell grafts with phenotypically appropriate sensory neuron targets. Keywords: neural stem cells, spinal cord injury, sensory, regeneration, conditioning lesion, Tlx3, spinal dorsal gray
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- 2018
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9. Injured adult motor and sensory axons regenerate into appropriate organotypic domains of neural progenitor grafts
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Jennifer N. Dulin, Andrew F. Adler, Hiromi Kumamaru, Gunnar H. D. Poplawski, Corinne Lee-Kubli, Hans Strobl, Daniel Gibbs, Ken Kadoya, James W. Fawcett, Paul Lu, and Mark H. Tuszynski
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Science - Abstract
Understanding how transplanted cells interact with the host nervous system will be important for cell based neural regeneration approaches. Here, the authors study the sensory fate of neural progenitor cell grafts transplanted to the injured spinal cord, and show that host axons retain the ability to distinguish appropriate and inappropriate graft targets.
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- 2018
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10. Comprehensive Monosynaptic Rabies Virus Mapping of Host Connectivity with Neural Progenitor Grafts after Spinal Cord Injury
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Andrew F. Adler, Corinne Lee-Kubli, Hiromi Kumamaru, Ken Kadoya, and Mark H. Tuszynski
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transsynaptic ,monosynaptic ,rabies ,spinal cord injury ,grafting ,neural progenitor cells ,cell therapy ,neural regeneration ,Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Abstract
Neural progenitor cells grafted to sites of spinal cord injury have supported electrophysiological and functional recovery in several studies. Mechanisms associated with graft-related improvements in outcome appear dependent on functional synaptic integration of graft and host systems, although the extent and diversity of synaptic integration of grafts with hosts are unknown. Using transgenic mouse spinal neural progenitor cell grafts expressing the TVA and G-protein components of the modified rabies virus system, we initiated monosynaptic tracing strictly from graft neurons placed in sites of cervical spinal cord injury. We find that graft neurons receive synaptic inputs from virtually every known host system that normally innervates the spinal cord, including numerous cortical, brainstem, spinal cord, and dorsal root ganglia inputs. Thus, implanted neural progenitor cells receive an extensive range of host neural inputs to the injury site, potentially enabling functional restoration across multiple systems.
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- 2017
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11. Hospital Staff Shortage after the 2011 Triple Disaster in Fukushima, Japan-An Earthquake, Tsunamis, and Nuclear Power Plant Accident: A Case of the Soso District.
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Sae Ochi, Masaharu Tsubokura, Shigeaki Kato, Shuichi Iwamoto, Shinichi Ogata, Tomohiro Morita, Arinobu Hori, Tomoyoshi Oikawa, Antoku Kikuchi, Zenjiro Watanabe, Yukio Kanazawa, Hiromi Kumakawa, Yoshinobu Kuma, Tetsuo Kumakura, Yoshimitsu Inomata, Masahiro Kami, Ryuzaburo Shineha, and Yasutoshi Saito
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Medicine ,Science - Abstract
In 2011, Fukushima was struck by a triple disaster: an earthquake, tsunamis, and a nuclear accident. In the aftermath, there was much fear among hospital staff members about radiation exposure and many staff members failed to report to work.One objective is to measure this shortage in hospital staff and another is to compare the difference in recovery by hospital types and by categories of hospital staff.The monthly records of the number of staff members from May 2011 to September 2012 were extracted anonymously from the records of 7 local hospitals in the Soso district in Fukushima. Change in the number of staff was analyzed.Staff shortages at hospitals reached a maximum within one month after the disaster (47% reported to work). The shortage of clerks was the most severe (38% reported to work), followed by nurses (48% reported to work). The shortages remained even 18 months after the disaster.After a disaster in which the damage to hospital functions surpasses the structural damage, massive support of human resources in the acute phase and a smaller volume of support in the mid-term phase appear to be required, particularly for non-medical staff.
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- 2016
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