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Dive into the research topics where Nina Sagara is active.

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Featured researches published by Nina Sagara.


Retina-the Journal of Retinal and Vitreous Diseases | 2007

Plasmin-assisted vitrectomy for management of proliferative membrane in proliferative diabetic retinopathy: a pilot study.

Akira Hirata; Akiomi Takano; Yasuya Inomata; Naoko Yonemura; Nina Sagara; Hidenobu Tanihara

Purpose: To demonstrate the feasibility of autologous plasmin for treatment of proliferative diabetic retinopathy. Methods: The study examined prospectively six patients with bilateral proliferative diabetic retinopathy. Comparisons of the surgical time and the incidence of retinal tears were made between the eyes treated with autologous plasmin and their respective opposite eyes, which were treated without plasmin. Results: All eyes treated with autologous plasmin required significantly less surgical time (68 versus 89 minutes, P = 0.04, paired t-test). In the plasmin group, no additional surgical procedures for removing the proliferative membrane were needed, including membrane delamination or segmentation. Moreover, with plasmin pretreatment, there were no retinal tears, which was in contrast to the control group, where three eyes with retinal tears were observed. There was no significant difference found between the two groups for final visual outcomes. Conclusion: Autologous plasmin may be beneficial in the surgical management of proliferative diabetic retinopathy.


Current Eye Research | 2010

Suppression of Choroidal Neovascularization by N-Acetyl-Cysteine in Mice

Ryuhei Hara; Yasuya Inomata; Takahiro Kawaji; Nina Sagara; Masaru Inatani; Mikiko Fukushima; Hidenobu Tanihara

Purpose: N-acetyl-cysteine (NAC) is a potent antioxidant known to be a precursor of glutathione. The purpose of this study was to investigate the role of NAC in the development of choroidal neovascularization (CNV). Methods: CNV was induced in C57BL/6 mice by laser photocoagulation of the ocular fundus. Mice were injected intraperitoneally with NAC or vehicle alone. The levels of 4-hydoroxy-2-nonenal (4-HNE)-modified protein and nucleus factor (NF)-κB were determined by wester blotting. The recruitment of macrophages and neutrophils after laser injury was analyzed immunohistochemically and in myeloperoxidase (MPO) assays. Enzyme-linked immunosorbent assays (ELISA) were used to measure monocyte chemotactic protein (MCP)-1, CXCL1, vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1, and VEGFR-2. The extent of CNV was evaluated 7 d after laser injury by lectin staining. Results: In NAC-treated mice with laser-induced injuries, the induction of 4-HNE-modified protein after 3 hr and the activation of NF-κB in nuclear extracts after 6 hr were markedly suppressed compared to vehicle-treated mice. Macrophage and neutrophil recruitment were inhibited and the levels of MCP-1, CXCL1, VEGF, and VEGFR-1 were also lower in NAC-treated mice compared to vehicle-treated mice. Furthermore, the extent of CNV induced was significantly lower in NAC-treated compared to vehicle-treated mice (p = 0.027). Conclusions: Our results clearly showed that NAC inhibited indicators of oxidative stress and the activation of NF-κB induced by laser injury, and, consequently, suppressed macrophage and neutrophil infiltration and the development of CNV. This suggests novel preventative and interventional therapeutic strategies for age-related macular degeneration.


Current Eye Research | 2007

Pitavastatin: Protection against Neuronal Retinal Damage Induced by Ischemia-Reperfusion Injury in Rats

Takahiro Kawaji; Yasuya Inomata; Akiomi Takano; Nina Sagara; Masaru Inatani; Mikiko Fukushima; Hidenobu Tanihara; Megumi Honjo

Purpose: To evaluate the neuroprotective effects of pitavastatin against neuronal retinal damage induced by ischemia-reperfusion injury in rats. Methods and Results: Ischemia-reperfusion injury was induced in Sprague-Dawley rats using ocular hypertension. Pitavastatin (0.1, 0.5, or 1.0 mg/kg) was given intravenously 12 hr or 5 min before, or 12 or 24 hr after the induction of ischemia-reperfusion injury. Morphometric and retrograde labeling analyses revealed neuroprotective effects when pitavastatin (0.5 mg/kg) was administered 5 min before—even 12 and 24 hr—after induction of ischemia-reperfusion injury. These effects depended on dose; protection was noted at pitavastatin concentrations of 0.5 and 1 mg/kg but not 0.1 mg/kg. Furthermore, preadministration of pitavastatin (0.5 mg/kg) reduced expression of P-selectin and intercellular adhesion molecule-1 at 12 and 24 hr after induction of ischemia-reperfusion injury. Conclusions: As pitavastatin was efficacious in preventing retinal neuronal death, it may be a novel therapeutic modality for ischemic retinal diseases.


British Journal of Ophthalmology | 2009

Macular hole formation after macular haemorrhage associated with rupture of retinal arterial macroaneurysm

Nina Sagara; Takahiro Kawaji; Yasuo Koshiyama; Yasuya Inomata; Mikiko Fukushima; Hidenobu Tanihara

Aim: To investigate the frequency and risk factors of macular hole (MH) formation after rupture of a retinal arterial macroaneurysm. Methods: Fifty-six eyes from 56 patients with rupture of a retinal arterial macroaneurysm with or without an MH (MH and non-MH groups, respectively) were reviewed. Frequency and risk factors related to MH formation were assessed, with risk factors including age; sex; distance from the macroaneurysm to the fovea; incidence of haemorrhages involving the macula such as preretinal, subinternal limiting membrane (sub-ILM), subretinal and vitreous; and vitreous surgery. MH formation in these patients was recorded and analysed. Results: Of the 56 eyes reviewed, seven (12.5%) had an MH after rupture of the retinal arterial macroaneurysm. The incidence of subretinal and sub-ILM haemorrhages involving the macula was significantly greater in the MH group than in the non-MH group (p = 0.037 and 0.045, respectively). Conclusion: These results suggest that the presence of subretinal and sub-ILM haemorrhages after rupture of a retinal arterial macroaneurysm may contribute to formation of an MH.


British Journal of Ophthalmology | 2008

Trans-Tenon's retrobulbar triamcinolone acetonide injection for macular oedema related to branch retinal vein occlusion.

Takahiro Kawaji; Akiomi Takano; Yasuya Inomata; Nina Sagara; Keiichiro Iwao; Masaru Inatani; Mikiko Fukushima; Hidenobu Tanihara

Background: The aim of the study was to evaluate the safety and effectiveness of trans-Tenon’s retrobulbar triamcinolone acetonide (TA) injection for macular oedema associated with branch retinal vein occlusion (BRVO). Methods: We reviewed the medical records of 50 consecutive patients with macular oedema associated with BRVO who were treated with trans-Tenon’s retrobulbar TA injection (20 mg) as initial treatment for a follow-up period of at least 12 months. Foveal thickness determined by optical coherence tomography, visual acuity, intraocular pressure (IOP) and cataract progression were measured. Results: The mean duration between oedema onset and TA injection was 4.9 months. Foveal thickness decreased significantly at 3 months after injection (p<0.0001). Furthermore, the percentage reduction in foveal thickness in eyes with posterior vitreous detachment (PVD; n = 23) was significantly greater than that without PVD (n = 27, p = 0.003). Improved visual acuity by at least 0.20 log minimum angle of resolution (logMAR) was seen in 22 eyes (44%; 11 eyes with PVD and 11 eyes without PVD). After completion of the 3-month follow-up, 29 eyes (58%) needed additional treatment including TA injections or pars plana vitrectomy (PPV). PPV seemed to be effective for macular oedema resistant to TA. IOP elevation and cataract progression occurred in less than 10% of all patients. Conclusions: Trans-Tenon’s retrobulbar TA injection appeared safe and relatively effective for macular oedema associated with BRVO. In eyes resistant to TA injection, PPV may be effective as an adjunctive treatment.


Investigative Ophthalmology & Visual Science | 2006

Posterior Vitreous Detachment Induced by Nattokinase (Subtilisin NAT): A Novel Enzyme for Pharmacologic Vitreolysis

Akiomi Takano; Akira Hirata; Kazuya Ogasawara; Nina Sagara; Yasuya Inomata; Takahiro Kawaji; Hidenobu Tanihara


Experimental Eye Research | 2007

Effect of pitavastatin on experimental choroidal neovascularization in rats

Nina Sagara; Takahiro Kawaji; Akiomi Takano; Yasuya Inomata; Masaru Inatani; Mikiko Fukushima; Hidenobu Tanihara


Graefes Archive for Clinical and Experimental Ophthalmology | 2010

Photodynamic therapy alone versus combined with intravitreal bevacizumab for neovascular age-related macular degeneration without polypoidal choroidal vasculopathy in Japanese patients

Ryuhei Hara; Takahiro Kawaji; Yasuya Inomata; Jin Tahara; Nina Sagara; Mikiko Fukushima; Hidenobu Tanihara


Investigative Ophthalmology & Visual Science | 2006

Pitavastatin Inhibits Experimental Choroidal Neovascularization in the Rat

Nina Sagara; Takahiro Kawaji; Akiomi Takano; Yasuya Inomata; Hidenobu Tanihara


Investigative Ophthalmology & Visual Science | 2005

Effects and Safety of Subtilisin NAT (Nattokinase) as a Novel Enzyme for Pharmacological Vitrectomy

Akiomi Takano; Akira Hirata; Yasuya Inomata; Takahiro Kawaji; Naoko Yonemura; Nina Sagara; K. Ogasawara; Hidenobu Tanihara

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