| 1. |
Fukuda Y, Notomi S, Shiose S, Kano K, Hashimoto S, Fujiwara K, Akiyama M, Ishikawa K, Hisatomi T, Sonoda KH, Differences in central and peripheral choroidal thickness among the subtypes of age-related macular degeneration in an Asian population , J Clin Med, 2023.08. |
| 2. |
Nagata J, Shiose S, Ishikawa K, Fukui T, Kano K, Mori K, Nakama T, Notomi S, Sonoda KH, Clinical characteristics of neovascular age-related macular degeneration eyes with retinal pigment epithelium tears, J Clin Med., 2023.08. |
| 3. |
Wada I, Nakao S, Fukuda Y, Shiose S, Takeda A, Kannan R, Sonoda KH, Persistence of vascular empty sleeves in choroidal neovascularization after VEGF therapy in both animal models and humans, Graefes Arch Clin Exp Ophthalmol. , 2023.03. |
| 4. |
Fukui T, Ishikawa K, Shiose S, Kano K, Mori K, Notomi S, Sonoda KH, Spatial pattern of retinal pigment epithelium tear development and progression after anti-vascular endothelial growth factor therapy for neovascular age-related macular degeneration , Retin Cases Brief Rep., 2022.11. |
| 5. |
Notomi S, Shiose S, Fukuda Y, Mori K, Hashimoto S, Kano K, Ishikawa K, Sonoda KH, Characteristics of retinal pigment epithelium elevations preceding exudative age-related macular degeneration in Japanese., Ophthalmic Research, 2022.08. |
| 6. |
Fukuda Y, Nakao S, Kohno RI, Ishikawa K, Shimokawa S, Shiose S, Takeda A, Morizane Y, Sonoda KH, Postoperative follow‐up of submacular hemorrhage displacement treated with vitrectomy and subretinal injection of tissue plasminogen activator, Jpn J Ophthalmol, 2022.05. |
| 7. |
Notomi S, Shiose S, Kohno RI, Shimokawa S, Ishikawa K, Kano K, Mori K, Wada I, Fukuda Y, Nakatake S, Yamaguchi M, Sonoda KH, A case of bullous central serous chorioretinopathy treated with surgical removal of submacular fibrin and subsequent photodynamic therapy under silicone oil , Case Rep Ophthalmol. , 2022.05. |
| 8. |
Nakamura S, Nakao S, Shiose S, Kohno RI, Hasegawa E, Sonoda KH, Optical Coherence Tomography Angiography of Choroidal Neovascularization in Immune Choroiditis Following Acute Retinal Necrosis, Eur J Ophthalmol , 2020.11. |
| 9. |
Ishikawa K, Fukui T, Nakao S, Shiose S, Sonoda KH, Vitrectomy with peripapillary internal limiting membrane peeling for macular retinoschisis associated with normal-tension glaucoma, Am J Ophthalmol Case Rep., 2020.03. |
| 10. |
Iori Wada, Yuji Oshima, Satomi Shiose, Kumiko Kano, Shintaro Nakao, Yoshihiro Kaizu, Shigeo Yoshida, Tatsuro Ishibashi, Koh hei Sonoda, Five-year treatment outcomes following intravitreal ranibizumab injections for neovascular age-related macular degeneration in Japanese patients, Graefe's Archive for Clinical and Experimental Ophthalmology, 10.1007/s00417-019-04361-8, 257, 7, 1411-1418, 2019.07, Purpose: To assess the real-world 5-year treatment outcomes of ranibizumab therapy in Japanese patients with neovascular age-related macular degeneration (AMD). Methods: This was a retrospective, observational, and open-label effectiveness study that included 295 eyes. The participants were patients with treatment-naïve neovascular AMD who received intravitreal ranibizumab (IVR) monthly injection at least three times as the loading phase, followed by further injections as needed (pro re nata (PRN)) and follow-up assessments for 5 years. Outcomes were determined at least 5 years after the first ranibizumab injection. Results: Mean logMAR best-corrected visual acuity (BCVA) at baseline was 0.52. The mean BCVA significantly improved after three loading injections; however, it declined gradually. The BCVA at 1 year was significantly better than the baseline BCVA, whereas the 3-year, 4-year, and 5-year BCVA values were significantly lower than the baseline values. The average central foveal thickness improved significantly from 366 ± 125 μm to 268 ± 134 μm (p |
| 11. |
Hoshiyama K, Nakao S, Shiose S, Yoshikawa H, Kano K, Kaizu Y, Murata T, Sonoda KH, Optical Coherence Tomography Angiography Detects Choriocapillaris Loss in Decalcification of Choroidal Osteoma, J Vitreoretin Dis. , 2019.07. |
| 12. |
Ken Ichi Takaki, Hiroshi Yoshikawa, Mika Tanabe, Satomi Shiose, Masayuki Murata, Minako Fujiwara, Koh Hei Sonoda, A case of AIDS-related Kaposi sarcoma in the eyelid, Japanese Journal of Clinical Ophthalmology, 72, 6, 781-786, 2018.06, Purpose: To report a case of AIDS-related Kaposi sarcoma in the eyelid. Case: A 35-year-old man had noted a tumor in the lower eyelid since 6 months before. It gradually increased in size following transconjunctival incision and curettage. Multiple foci in the lung were detected during health check-up 4 months before. He was diagnosed with AIDS at the Department of Internal Medicine of Kyushu University. He was referred to us regarding the eyelid tumor. Findings and Clinical Course: A painful, dark red mass was present in the right lower eyelid. Another red mass was present in the left bulbar conjunctiva. The tumor in eye right eyelid was resected and proved to be Kaposi sarcoma. Metastatic lesions were present in the lung and gastrointestinal tract. He was treated with highly active antiretroviral therapy (ART) and six courses of liposomal doxorubicin. Tumors in the eyes, lung, and gastrointestinal tract disappeared 6 months after end of treatment. Conclusion: This case illustrates that a tumor in the eyelid may be initial clinical manifestation of AIDS-related Kaposi sarcoma.. |
| 13. |
Masayoshi Seki, Ken Ichi Takaki, Hiroshi Yoshikawa, Mika Tanabe, Satomi Shiose, Noritaka Komune, Koh Hei Sonoda, A case of orbital apex syndrome dead shortly after the onset, Folia Japonica de Ophthalmologica Clinica, 10, 12, 1004-1006, 2017.12. |
| 14. |
Ken Ichi Takaki, Hiroshi Yoshikawa, Naoyuki Morishige, Shuhei Kawahara, Ryoichi Arita, Satomi Shiose, Tatsuro Ishibashi, Findings of chalazion by noncontact meibography, Japanese Journal of Clinical Ophthalmology, 70, 12, 1785-1788, 2016.11, Purpose: To report characteristic findings of chalazion by noncontact meibography. Cases and Method: This study was made on 67 eyes of chalazion. The series comprised 25 males and 42 females. The age ranged from 1 to 90 years, average 38 years. We used two apparatus to record and analyze the findings: a meibogram (MeiboPen) and a camera for infrared photography eliminating light of wavelength longer than 760 nm. Results: Areas of chalazion showed high infrared reflection in 25 eyes, and low reflection in 42 eyes. Low reflection was present in 44% of cases in whom chalazion persisted for less than 30 days. It was present in 84% of cases in whom chalazion persisted longer than 30 days. The difference was significant (p |
| 15. |
Akiko Maeda, Marcin Golczak, Yu Chen, Kiichiro Okano, Hideo Kohno, Satomi Shiose, Kaede Ishikawa, William Harte, Grazyna Palczewska, Tadao Maeda, Krzysztof Palczewski, Primary amines protect against retinal degeneration in mouse models of retinopathies, Nature Chemical Biology, 10.1038/nchembio.759, 8, 2, 170-178, 2012.02, Vertebrate vision is initiated by photoisomerization of the visual pigment chromophore 11-cis-retinal and is maintained by continuous regeneration of this retinoid through a series of reactions termed the retinoid cycle. However, toxic side reaction products, especially those involving reactive aldehyde groups of the photoisomerized product, all-trans-retinal, can cause severe retinal pathology. Here we lowered peak concentrations of free all-trans-retinal with primary amine-containing Food and Drug Administration (FDA)-approved drugs that did not inhibit chromophore regeneration in mouse models of retinal degeneration. Schiff base adducts between all-trans-retinal and these amines were identified by MS. Adducts were observed in mouse eyes only when an experimental drug protected the retina from degeneration in both short-term and long-term treatment experiments. This study demonstrates a molecular basis of all-trans-retinal-induced retinal pathology and identifies an assemblage of FDA-approved compounds with protective effects against this pathology in a mouse model that shows features of Stargardt's disease and age-related retinal degeneration.. |
| 16. |
Satomi Shiose, Yu Chen, Kiichiro Okano, Sanhita Roy, Hideo Kohno, Johnny Tang, Eric Pearlman, Tadao Maeda, Krzysztof Palczewski, Akiko Maeda, Toll-like receptor 3 is required for development of retinopathy caused by impaired all-trans-retinal clearance in mice, Journal of Biological Chemistry, 10.1074/jbc.M111.228551, 286, 17, 15543-15555, 2011.04, Chronic inflammation is an important component that contributes to many age-related neurodegenerative diseases, including macular degeneration. Here, we report a role for toll-like receptor 3 (TLR3) in cone-rod dystrophy (CORD) of mice lacking ATP-binding cassette transporter 4 (ABCA4) and retinol dehydrogenase 8 (RDH8), proteins critical for all-trans-retinal clearance in the retina. Increased expression of toll-like receptor-signaling elements and inflammatory changes were observed in Rdh8-/- Abca4-/- eyes by RNA expression analysis. Unlike 3-month-old Rdh8-/- Abca4-/- mice that developed CORD, 6-month-old Tlr3-/- Rdh8-/- Abca4-/- mice did not evidence an abnormal retinal phenotype. Light-induced retinal degeneration in Tlr3-/- Rdh8 -/- Abca4-/- mice was milder than that in Rdh8 -/- Abca4-/- mice, and a 2-fold increased TLR3 expression was detected in light-illuminated retinas of Rdh8-/- Abca4 -/- mice compared with nonilluminated retinas. Poly(I-C), a TLR3 ligand, caused caspase-8-independent cellular apoptosis. Whereas poly(I-C) induced retinal cell death in Rdh8-/- Abca4-/- and WT mice both in vivo and ex vivo, this was not seen in mice lacking Tlr3. Far fewer invasive macrophage/microglial cells in the subretinal space and weaker activation of Muller glial cells were exhibited by Tlr3-/- Rdh8 -/- Abca4-/- mice compared with Rdh8-/- Abca4-/- mice at 3 and 6 months of age, indicating that loss of TLR3 inhibits local inflammation in the retina. Both poly(I-C) and endogenous products emanating from dying/dead retinal cells induced NF-κB and IRF3 activation. These findings demonstrate that endogenous products from degenerating retina stimulate TLR3 that causes cellular apoptosis and retinal inflammation and that loss of TLR3 protects mice from CORD.. |
