研究者詳細 - 森實　祐基

論文 - 森實　祐基

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黄斑色素を含んだ黄斑上膜を伴う層状黄斑円孔に対する新しい硝子体手術手技

白潟ゆかり, 白神史雄, 高須逸平, 福田恒輝, 藤田智純, 山下彩奈, 廣岡一行, 森實祐基, 藤原篤之

日本眼科学会雑誌 117 ( 臨増 ) 284 - 284 2013年3月

マウス網膜色素上皮細胞の細胞遊走におけるAMP依存性キナーゼの役割

森實祐基, 竹内侯雄, 鈴木潤, 吉村武, 塚本真啓, 木村修平, Viollet Benoit, Miller Joan, Vavvas Demetrios

日本眼科学会雑誌 117 ( 臨増 ) 347 - 347 2013年3月

ARPE-19の細胞増殖におけるAMP依存性キナーゼの役割

塚本真啓, 木村修平, 米澤朋子, 小阪淳, 森實祐基

日本眼科学会雑誌 117 ( 臨増 ) 352 - 352 2013年3月

Aminoimidazole carboxamide ribonucleotide (AICAR) inhibits the growth of retinoblastoma in vivo by decreasing angiogenesis and inducing apoptosis. 国際誌

Sofia Theodoropoulou, Katarzyna Brodowska, Maki Kayama, Yuki Morizane, Joan W Miller, Evangelos S Gragoudas, Demetrios G Vavvas

PloS one 8 ( 1 ) e52852 2013年

記述言語：英語掲載種別：研究論文（学術雑誌）

5-Aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR), an analog of AMP is widely used as an activator of AMP-kinase (AMPK), a protein that regulates the responses of the cell to energy change. Recently, we showed that AICAR-induced AMPK activation inhibits the growth of retinoblastoma cells in vitro by decreasing cyclins and by inducing apoptosis and S-phase arrest. In this study, we investigated the effects of AMPK activator AICAR on the growth of retinoblastoma in vivo. Intraperitoneal injection of AICAR resulted in 48% growth inhibition of Y79 retinoblastoma cell tumors in mice. Tumors isolated from mice treated with AICAR had decreased expression of Ki67 and increased apoptotic cells (TUNEL positive) compared with the control. In addition, AICAR treatment suppressed significantly tumor vessel density and macrophage infiltration. We also showed that AICAR administration resulted in AMPK activation and mTOR pathway inhibition. Paradoxically observed down-regulation of p21, which indicates that p21 may have a novel function of an oncogene in retinoblastoma tumor. Our results indicate that AICAR treatment inhibited the growth of retinoblastoma tumor in vivo via AMPK/mTORC1 pathway and by apoptogenic, anti-proliferative, anti-angiogenesis mechanism. AICAR is a promising novel non-chemotherapeutic drug that may be effective as an adjuvant in treating Retinoblastoma.

DOI： 10.1371/journal.pone.0052852

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広範囲の網膜分離を伴った成人発症型卵黄様黄斑ジストロフィの1例

細木三佳, 井澤優子, 高畠まゆみ, 森實祐基, 高須逸平

眼科臨床紀要 5 ( 10 ) 963 - 964 2012年10月

水晶体皮質が融解・自然吸収した1例

平野雅幸, 森實祐基, 熊瀬文明, 高畠隆, 木村修平, 塚本真啓, 大月洋

臨床眼科 66 ( 9 ) 1359 - 1361 2012年9月

記述言語：日本語出版者・発行元：(株)医学書院

目的:炎症所見を伴わない水晶体皮質融解の症例の報告。症例:62歳女性が内科でWegener肉芽腫症と診断され,精査のため紹介され受診した。所見と経過:矯正視力は右1.0,左指数弁で,眼圧は正常範囲にあった。左眼では水晶体皮質の大部分が消失し,水晶体嚢と茶褐色の核のみがあった。前房に炎症所見はなかった。水晶体乳化吸引術,水晶体嚢切除,眼内レンズの嚢外固定を行い,6ヵ月後に0.6の視力を得た。眼底に異常所見はなかった。結論:無症状の水晶体皮質融解に対して水晶体再建術を行い,良好な結果を得た。(著者抄録)

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Aminoimidazole carboxamide ribonucleotide ameliorates experimental autoimmune uveitis. 国際誌

Jun Suzuki, Takeru Yoshimura, Marina Simeonova, Kimio Takeuchi, Yusuke Murakami, Yuki Morizane, Joan W Miller, Lucia Sobrin, Demetrios G Vavvas

Investigative ophthalmology & visual science 53 ( 7 ) 4158 - 69 2012年6月

記述言語：英語掲載種別：研究論文（学術雑誌）

PURPOSE: To investigate the anti-inflammatory effect of an adenosine monophosphate (AMP) analog, aminoimidazole carboxamide ribonucleotide (AICAR), in experimental autoimmune uveoretinitis (EAU). METHODS: C57BL/6 mice were injected daily with AICAR (200 mg/kg, intraperitoneally [IP]) from day 0, the day of interphotoreceptor retinoid-binding protein (IRBP) immunization, until day 21. The severity of uveitis was assessed clinically and histopathologically. T-cell proliferation and cytokine production of IFN-γ, IL-17, and IL-10 in response to IRBP stimulation were determined. In addition, regulatory T-cell (Treg) populations were measured. Co-stimulatory molecule expression (CD40, 80, 86, and I-Ab) on dendritic cells (DCs) in EAU and on bone marrow-derived dendritic cells (BMDCs) treated with AICAR was measured. RESULTS: AICAR treatment significantly reduced clinical and histologic severity of EAU as well as ocular cytokine production. An anti-inflammatory effect associated with the inhibition of T-cell proliferation and Th1 and Th17 cytokine production was observed. Increases in the Th2 response and Treg population were not observed with AICAR treatment. AICAR did significantly inhibit BMDC maturation by reducing co-stimulatory molecule expression. CONCLUSIONS: AICAR attenuates EAU by preventing generation of Ag-specific Th1 and Th17 cells. Impaired DC maturation may be an underlying mechanism for this anti-inflammatory effect observed with AICAR.

DOI： 10.1167/iovs.11-9323

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Evidence for baseline retinal pigment epithelium pathology in the Trp1-Cre mouse. 国際誌

Aristomenis Thanos, Yuki Morizane, Yusuke Murakami, Andrea Giani, Dimosthenis Mantopoulos, Maki Kayama, Mi In Roh, Norman Michaud, Basil Pawlyk, Michael Sandberg, Lucy H Young, Joan W Miller, Demetrios G Vavvas

The American journal of pathology 180 ( 5 ) 1917 - 27 2012年5月

記述言語：英語掲載種別：研究論文（学術雑誌）

The increasing popularity of the Cre/loxP recombination system has led to the generation of numerous transgenic mouse lines in which Cre recombinase is expressed under the control of organ- or cell-specific promoters. Alterations in retinal pigment epithelium (RPE), a multifunctional cell monolayer that separates the retinal photoreceptors from the choroid, are prevalent in the pathogenesis of a number of ocular disorders, including age-related macular degeneration. To date, six transgenic mouse lines have been developed that target Cre to the RPE under the control of various gene promoters. However, multiple lines of evidence indicate that high levels of Cre expression can be toxic to mammalian cells. In this study, we report that in the Trp1-Cre mouse, a commonly used transgenic Cre strain for RPE gene function studies, Cre recombinase expression alone leads to RPE dysfunction and concomitant disorganization of RPE layer morphology, large areas of RPE atrophy, retinal photoreceptor dysfunction, and microglial cell activation in the affected areas. The phenotype described herein is similar to previously published reports of conditional gene knockouts that used the Trp1-Cre mouse, suggesting that Cre toxicity alone could account for some of the reported phenotypes and highlighting the importance of the inclusion of Cre-expressing mice as controls in conditional gene targeting studies.

DOI： 10.1016/j.ajpath.2012.01.017

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Inhibitory effect of aminoimidazole carboxamide ribonucleotide (AICAR) on endotoxin-induced uveitis in rats. 国際誌

Jun Suzuki, Akrivi Manola, Yusuke Murakami, Yuki Morizane, Kimio Takeuchi, Maki Kayama, Joan W Miller, Lucia Sobrin, Demetrios G Vavvas

Investigative ophthalmology & visual science 52 ( 9 ) 6565 - 71 2011年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

PURPOSE. To investigate the anti-inflammatory effect of aminoimidazole carboxamide ribonucleotide (AICAR), an analog of adenosine monophosphate (AMP), in endotoxin-induced uveitis (EIU). METHODS. EIU was induced by subcutaneous injection of lipopolysaccharide (LPS) (200 μg) in Lewis rats. AICAR (50 mg/kg, intraperitoneally) was given 6 hours prior and at the same time as LPS injection. Clinical uveitis scores, number of anterior chamber (AC) infiltrating cells, anterior chamber protein concentration, retinal vessel leukocyte adhesion, and protein leakage were measured 24 hours later. Protein levels of C-C chemokine ligand-2 (CCL-2)/monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) in aqueous humor and retina and nuclear translocation of nuclear factor-κB (NF-κB) in the retina were determined by enzyme-linked immunosorbent assay (ELISA). Both mRNA and protein levels of CD14 in peripheral blood mononuclear cells were also measured. RESULTS. AICAR treatment significantly reduced EIU clinical severity as well as inflammatory cell infiltration and protein concentration in aqueous humor. Similarly, the number of retinal vessel-adherent leukocytes and protein leakage were decreased by AICAR treatment. Protein levels of TNF-α, CCL-2/MCP-1, and ICAM-1 in aqueous humor and CCL-2/MCP-1 and ICAM-1 levels in retina were suppressed with AICAR treatment. AICAR also reduced NF-κB translocation and CD14 expression. CONCLUSIONS. AICAR reduces systemic LPS susceptibility and attenuates intraocular inflammation in a rat EIU model by limiting infiltration of leukocytes, suppressing inflammatory mediators, and inhibiting the NF-κB pathway.

DOI： 10.1167/iovs.11-7331

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AMP-activated protein kinase suppresses matrix metalloproteinase-9 expression in mouse embryonic fibroblasts. 国際誌

Yuki Morizane, Aristomenis Thanos, Kimio Takeuchi, Yusuke Murakami, Maki Kayama, George Trichonas, Joan Miller, Marc Foretz, Benoit Viollet, Demetrios G Vavvas

The Journal of biological chemistry 286 ( 18 ) 16030 - 8 2011年5月

記述言語：英語掲載種別：研究論文（学術雑誌）

Matrix metalloproteinase-9 (MMP-9) plays a critical role in tissue remodeling under both physiological and pathological conditions. Although MMP-9 expression is low in most cells and is tightly controlled, the mechanism of its regulation is poorly understood. We utilized mouse embryonic fibroblasts (MEFs) that were nullizygous for the catalytic α subunit of AMP-activated protein kinase (AMPK), which is a key regulator of energy homeostasis, to identify AMPK as a suppressor of MMP-9 expression. Total AMPKα deletion significantly elevated MMP-9 expression compared with wild-type (WT) MEFs, whereas single knock-out of the isoforms AMPKα1 and AMPKα2 caused minimal change in the level of MMP-9 expression. The suppressive role of AMPK on MMP-9 expression was mediated through both its activity and presence. The AMPK activators 5-amino-4-imidazole carboxamide riboside and A769662 suppressed MMP-9 expression in WT MEFs, and AMPK inhibition by the overexpression of dominant negative (DN) AMPKα elevated MMP-9 expression. However, in AMPKα(-/-) MEFs transduced with DN AMPKα, MMP-9 expression was suppressed. AMPKα(-/-) MEFs showed increased phosphorylation of IκBα, expression of IκBα mRNA, nuclear localization of nuclear factor-κB (NF-κB), and DNA-binding activity of NF-κB compared with WT. Consistently, selective NF-κB inhibitors BMS345541 and SM7368 decreased MMP-9 expression in AMPKα(-/-) MEFs. Overall, our results suggest that both AMPKα isoforms suppress MMP-9 expression and that both the activity and presence of AMPKα contribute to its function as a regulator of MMP-9 expression by inhibiting the NF-κB pathway.

DOI： 10.1074/jbc.M110.199398

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Distribution of α(IV) collagen chains in the ocular anterior segments of adult mice. 国際誌

Kenji Saito, Tomoko Yonezawa, Jun Minaguchi, Masae Kurosaki, Shiho Suetsugu, Ai Nakajima, Hiroyuki Nomoto, Yuki Morizane, Yoshikazu Sado, Manabu Sugimoto, Shozo Kusachi, Yoshifumi Ninomiya

Connective tissue research 52 ( 2 ) 147 - 56 2011年4月

記述言語：英語掲載種別：研究論文（学術雑誌）

The distribution of the collagen chains from α1(IV) to α6(IV) could serve as a basis for the characterization of type IV collagen. In this study, immunohistochemistry of the ocular anterior segment of adult mice was performed using specific monoclonal antibodies against each chain in the series from α1(IV) to α6(IV). The results show that the components of type IV collagen in vascular basement membranes are α1(IV) and α2(IV) with or without α5(IV) and α6(IV) chains and those in epithelium and muscle basement membranes are α1(IV), α2(IV), α5(IV), and α6(IV) chains. In corneal endothelium, pigmented epithelium of iris and ciliary body, and trabecular meshwork, α3(IV) and α4(IV) chains are also expressed in addition to α1(IV), α2(IV), α5(IV), and α6(IV) chains. Moreover, we investigated the change in molecular composition in ciliary body during postnatal development. α3(IV) and α4(IV) chains were also expressed in addition to α1(IV), α2(IV), α5(IV), and α6(IV) chains in ciliary pigmented epithelium basement membrane from 7 days after birth. This result suggests that the basement membranes gradually change their biochemical features owing to temporal regulation. Taken together, these findings suggest that the different distribution and the developmental expression of α1(IV) to α6(IV) chains are associated with the tissue-specific function of type IV collagen in basement membranes.

DOI： 10.3109/03008207.2010.492062

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Heat shock protein 70 (HSP70) is critical for the photoreceptor stress response after retinal detachment via modulating anti-apoptotic Akt kinase. 国際誌

Maki Kayama, Toru Nakazawa, Aristomenis Thanos, Yuki Morizane, Yusuke Murakami, Sofia Theodoropoulou, Toshiaki Abe, Demetrios Vavvas, Joan W Miller

The American journal of pathology 178 ( 3 ) 1080 - 91 2011年3月

記述言語：英語掲載種別：研究論文（学術雑誌）

Photoreceptor apoptosis is a major cause of vision loss in many ocular diseases. Significant progress has been made to elucidate the molecular pathways involved in this process, yet little is known about proteins counteracting these apoptotic pathways. It is established that heat shock proteins (HSPs) function as molecular helper proteins (chaperones) by preventing protein aggregation and facilitating refolding of dysfunctional proteins, critical to the survival of all organisms. Here, we investigated the role of HSP70 on photoreceptor survival after experimental retinal detachment (RD) in mice and rats. We found that HSP70 was up-regulated after RD and associated with phosphorylated Akt, thereby preventing its dephosphorylation and further activation of cell death pathways. Administration of quercetin, which inhibits HSP70 and suppresses Akt phosphorylation significantly increased photoreceptor apoptosis. Similarly, RD-induced photoreceptor apoptosis was augmented in mice carrying hypomorphic mutations of the genes encoding HSP70. On the other hand, administration of geranylgeranylacetone, which induces an increase in HSP70 significantly decreased photoreceptor apoptosis after RD through prolonged activation of Akt pathway. Thus, HSP70 may be a favorable potential target to increase photoreceptor cell survival after RD.

DOI： 10.1016/j.ajpath.2010.11.072

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Receptor interacting protein kinases mediate retinal detachment-induced photoreceptor necrosis and compensate for inhibition of apoptosis. 国際誌

George Trichonas, Yusuke Murakami, Aristomenis Thanos, Yuki Morizane, Maki Kayama, Christine M Debouck, Toshio Hisatomi, Joan W Miller, Demetrios G Vavvas

Proceedings of the National Academy of Sciences of the United States of America 107 ( 50 ) 21695 - 700 2010年12月

記述言語：英語掲載種別：研究論文（学術雑誌）

Apoptosis has been shown to be a significant form of cell loss in many diseases. Detachment of photoreceptors from the retinal pigment epithelium, as seen in various retinal disorders, causes photoreceptor loss and subsequent vision decline. Although caspase-dependent apoptotic pathways are activated after retinal detachment, caspase inhibition by the pan-caspase inhibitor Z-VAD fails to prevent photoreceptor death; thus, we investigated other pathways leading to cell loss. Here, we show that receptor interacting protein (RIP) kinase-mediated necrosis is a significant mode of photoreceptor cell loss in an experimental model of retinal detachment and when caspases are inhibited, RIP-mediated necrosis becomes the predominant form of death. RIP3 expression, a key activator of RIP1 kinase, increased more than 10-fold after retinal detachment. Morphological assessment of detached retinas treated with Z-VAD showed decreased apoptosis but significantly increased necrotic photoreceptor death. RIP1 kinase inhibitor necrostatin-1 or Rip3 deficiency substantially prevented those necrotic changes and reduced oxidative stress and mitochondrial release of apoptosis-inducing factor. Thus, RIP kinase-mediated programmed necrosis is a redundant mechanism of photoreceptor death in addition to apoptosis, and simultaneous inhibition of RIP kinases and caspases is essential for effective neuroprotection and may be a novel therapeutic strategy for treatment of retinal disorders.

DOI： 10.1073/pnas.1009179107

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Glycocalyx degradation in retinal and choroidal capillary endothelium in rats with diabetes and hypertension.

Fumiaki Kumase, Yuki Morizane, Satoshi Mohri, Ippei Takasu, Aiji Ohtsuka, Hiroshi Ohtsuki

Acta medica Okayama 64 ( 5 ) 277 - 83 2010年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

Endothelial glycocalyx (GCX) has been reported as a protective factor for vascular endothelial cells (VEC) in diabetes and hypertension. However, the involvement of GCX impairment in ocular vasculopathy remains unclear. We evaluated the changes in the GCX thicknesses of the retinal and choroidal capillaries in rats with diabetes and hypertension by cationic colloidal iron staining using a transmission electron microscope. In the control group, the mean (standard error of the mean) thicknesses of retinal and choroidal GCX were 60.2 (1.5) nm and 84.3 (3.1) nm, respectively. The diabetic rats showed a significant decrease of GCX thickness in the retina, but not in the choroid, compared to controls (28.3 (0.3) nm, p<0.01 and 77.8 (1.4) nm, respectively). In the hypertensive rats, both retinal and choroidal GCX were significantly decreased compared to the control values (10.9 (0.4) nm and 13.2 (1.0) nm, respectively, both p<0.01). Moreover, we could visualize the adhesion of leukocytes and platelets on the luminal surface of VEC, at the site where the GCX was markedly degraded. These findings suggest that the GCX prevents adhesion of leukocytes and platelets to the VEC surface, and this impairment may lead to ocular vasculopathy in diabetes and hypertension.

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Retinoblastoma cells are inhibited by aminoimidazole carboxamide ribonucleotide (AICAR) partially through activation of AMP-dependent kinase. 国際誌

Sofia Theodoropoulou, Paraskevi E Kolovou, Yuki Morizane, Maki Kayama, Fotini Nicolaou, Joan W Miller, Evangelos Gragoudas, Bruce R Ksander, Demetrios G Vavvas

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 24 ( 8 ) 2620 - 30 2010年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

5-Aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), an analog of AMP, is widely used as an activator of AMP-kinase (AMPK), a protein that regulates the responses of the cell to energy change. We studied the effects of AICAR on the growth of retinoblastoma cell lines (Y79, WERI, and RB143). AICAR inhibited Rb cell growth, induced apoptosis and S-phase cell cycle arrest, and led to activation of AMPK. These effects were abolished by treatment with dypiridamole, an inhibitor that blocks entrance of AICAR into cells. Treatment with the adenosine kinase inhibitor 5-iodotubericidin to inhibit the conversion of AICAR to ZMP (the direct activator of AMPK) reversed most of the growth-inhibiting effects of AICAR, indicating that some of the antiproliferative effects of AICAR are mediated through AMPK activation. In addition, AICAR treatment was associated with inhibition of the mammalian target of rapamycin pathway, decreased phosphorylation of ribosomal protein-S6 and 4E-BP1, down-regulation of cyclins A and E, and decreased expression of p21. Our results indicate that AICAR-induced activation of AMPK inhibits retinoblastoma cell growth. This is one of the first descriptions of a nonchemotherapeutic drug with low toxicity that may be effective in treating Rb patients.

DOI： 10.1096/fj.09-152546

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Coats病様眼底変化を生じた網膜色素変性症の1例

秋元悦子, 高畠隆, 森實祐基, 岡部泰史, 濱田禎之, 大月洋

臨床眼科 64 ( 6 ) 895 - 898 2010年6月

記述言語：日本語出版者・発行元：(株)医学書院

目的:Coats病に似た眼底を呈し,硝子体出血が生じた網膜色素変性症の症例の報告。症例:61歳男性が左眼視力障害で受診した。13歳で夜盲を自覚し,17歳のときに網膜色素変性症と診断された。兄2人と従兄弟1人に網膜色素変性症がある。4年前に白内障手術を受け,左右とも0.04の視力であった。所見:矯正視力は右0.03,左指数弁で,右眼に網膜色素変性症の所見,左眼に硝子体出血と眼底上方に増殖膜があった。左眼に硝子体手術を行い,器質化した増殖膜と新生血管,毛細血管の拡張蛇行があった。一年後の現在,左右眼とも0.03の矯正視力を維持している。結論:本症例でのCoats病様の網膜血管拡張,新生血管,増殖膜形成は,網膜色素変性症に併発したと解釈され,硝子体手術が有効であった。(著者抄録)

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A novel nonradioactive method to evaluate vascular barrier breakdown and leakage. 国際誌

George Trichonas, Akrivi Manola, Yuki Morizane, Aristomenis Thanos, Xanthi Koufomichali, Thanos D Papakostas, Sandra Montezuma, Lucy Young, Joan W Miller, Evangelos Gragoudas, Demetrios Vavvas

Investigative ophthalmology & visual science 51 ( 3 ) 1677 - 82 2010年3月

記述言語：英語掲載種別：研究論文（学術雑誌）

PURPOSE: To identify a novel, sensitive, nonradioactive leakage assay that can be used in the assessment of retinal vascular permeability in rats and mice. METHODS: Breakdown of the vascular barrier was induced by vascular endothelial growth factor (VEGF), lipopolysaccharide (LPS), or diabetes. Biotinylated bovine serum albumin (bBSA) was administered as a tracer. After perfusion with lactated Ringer's solution, extravasated bBSA was detected with immunoprecipitation and Western blot analysis or sandwich ELISA. The results were then normalized against the final bBSA plasma concentration, the circulation time, and the protein concentration of the tissue. RESULTS: Six hours after VEGF injection, BRB breakdown was quantified in the injected eye and was 2.5-fold higher than in the contralateral phosphate-buffered saline (PBS)-injected eye (n = 6 rats, P < 0.01). Intravitreal LPS injection induced severe inflammation in the directly injected eye and moderate inflammation in the contralateral untreated eye. Leakage was six- and threefold higher, respectively, compared with that in the untreated control animals (n = 5 rats, P < 0.01). Nine-month diabetic rats had a threefold increase in vascular leakage compared with age-matched control animals (n = 6 retinas, P < 0.05). Twenty-four hours after intraperitoneal administration of LPS in mice, the animals showed increased vascular leakage in all tissue organs examined (retina, 1.7-fold; brain, 1.5-fold; and kidney, 1.3-fold). CONCLUSIONS: bBSA can serve as an effective alternative to the current methods used for quantitating vascular leakage and especially the blood-retinal barrier breakdown. It is reasonably easy to perform, low in cost, and adaptable to experiments in mice.

DOI： 10.1167/iovs.09-4193

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胎児ヘモグロビン変換率測定による未熟児網膜症発症リスク評価法の開発

森實祐基

医科学応用研究財団研究報告 27 151 - 154 2010年2月

記述言語：日本語出版者・発行元：(公財)鈴木謙三記念医科学応用研究財団

未熟児網膜症は、低体重出生児への全身管理の際に酸素投与が過剰であった場合に、網膜への酸素供給が必要以上に多くなり、酸素投与を中止したときの変化によって網膜の相対的低酸素状態が惹起され、病的な血管新生によって起こる網膜剥離が原因とされている。本症を起こしやすいリスクファクターは二つに大別され、一つは血管組織側(網膜微小血管)の反応性が高いこと、もう一つは酸素投与時と中止時の末梢酸素供給量の変化が大きいことであると考えられる。本研究では、このうち後者について取り上げ、酸素供給量の変化を規定する赤血球に着目し、ヘモグロビンの酸素親和度と血管の拡張に寄与する一酸化窒素との結合能の生後変化の評価法を確立することを試みた。さらに、酸素運搬体としての赤血球の性質と未熟児網膜症との関係を明らかにするための計測系確立とその応用について展望した。

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光線力学療法再施行時におけるトリアムシノロン硝子体内注射の併用効果

森實祐基, 高畠隆, 岡部泰史, 岡本和夫, 中山雅雄

眼科臨床紀要 1 ( 10 ) 1018 - 1018 2008年10月

網膜芽細胞腫に対する放射線治療14年後に網膜剥離を生じた1例

岡部泰史, 森實祐基, 高畠隆, 岡本和夫, 中山雅雄

眼科臨床紀要 1 ( 10 ) 1029 - 1029 2008年10月

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