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1.
J Curr Glaucoma Pract ; 13(1): 42-44, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31496561

RESUMO

A 79-year-old man underwent phacoemulsification (phaco) with TORIC intraocular lens (IOL) insertion combined with Kahook dual blade (KDB) goniotomy of the right eye several months after a stand-alone phaco in the fellow eye. He had significant against-the-rule astigmatism in both eyes (2.41D @ 10° right, 2.40D @ 160° left) preoperatively. Postoperatively, nearly all corneal astigmatism disappeared in the right eye (0.60D @ 37°), while it remained the same in the left eye (2.00D @ 167°). Ophthalmologists should be aware that KDB may have an unreported effect of altering corneal astigmatism, which should be considered when inserting TORIC IOL. HOW TO CITE THIS ARTICLE: Hirabayashi MT, McDaniel LM, et al. Reversal of Toric Intraocular Lens-corrected Corneal Astigmatism after Kahook Dual Blade Goniotomy. J Curr Glaucoma Pract 2019;13(1):42-44.

2.
PLoS One ; 13(3): e0192145, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29554088

RESUMO

Vision impairment from corneal fibrosis is a common consequence of irregular corneal wound healing after injury. Intermediate-conductance calmodulin/calcium-activated K+ channels 3.1 (KCa3.1) play an important role in cell cycle progression and cellular proliferation. Proliferation and differentiation of corneal fibroblasts to myofibroblasts can lead to corneal fibrosis after injury. KCa3.1 has been shown in many non-ocular tissues to promote fibrosis, but its role in corneal fibrosis is still unknown. In this study, we characterized the expression KCa3.1 in the human cornea and its role in corneal wound healing in vivo using a KCa3.1 knockout (KCa3.1-/-) mouse model. Additionally, we tested the hypothesis that blockade of KCa3.1 by a selective KCa3.1 inhibitor, TRAM-34, could augment a novel interventional approach for controlling corneal fibrosis in our established in vitro model of corneal fibrosis. The expression of KCa3.1 gene and protein was analyzed in human and murine corneas. Primary human corneal fibroblast (HCF) cultures were used to examine the potential of TRAM-34 in treating corneal fibrosis by measuring levels of pro-fibrotic genes, proteins, and cellular migration using real-time quantitative qPCR, Western blotting, and scratch assay, respectively. Cytotoxicity of TRAM-34 was tested with trypan blue assay, and pro-fibrotic marker expression was tested in KCa3.1-/-. Expression of KCa3.1 mRNA and protein was detected in all three layers of the human cornea. The KCa3.1-/- mice demonstrated significantly reduced corneal fibrosis and expression of pro-fibrotic marker genes such as collagen I and α-smooth muscle actin (α-SMA), suggesting that KCa3.1 plays an important role corneal wound healing in vivo. Pharmacological treatment with TRAM-34 significantly attenuated corneal fibrosis in vitro, as demonstrated in HCFs by the inhibition TGFß-mediated transcription of pro-fibrotic collagen I mRNA and α-SMA mRNA and protein expression (p<0.001). No evidence of cytotoxicity was observed. Our study suggests that KCa3.1 regulates corneal wound healing and that blockade of KCa3.1 by TRAM-34 offers a potential therapeutic strategy for developing therapies to cure corneal fibrosis in vivo.


Assuntos
Córnea/metabolismo , Doenças da Córnea/metabolismo , Modelos Animais de Doenças , Canais de Potássio Ativados por Cálcio de Condutância Intermediária/metabolismo , Animais , Diferenciação Celular/efeitos dos fármacos , Diferenciação Celular/genética , Proliferação de Células/efeitos dos fármacos , Proliferação de Células/genética , Células Cultivadas , Córnea/efeitos dos fármacos , Córnea/patologia , Doenças da Córnea/tratamento farmacológico , Doenças da Córnea/genética , Fibroblastos/metabolismo , Fibrose , Expressão Gênica/efeitos dos fármacos , Humanos , Canais de Potássio Ativados por Cálcio de Condutância Intermediária/antagonistas & inibidores , Canais de Potássio Ativados por Cálcio de Condutância Intermediária/genética , Camundongos Endogâmicos C57BL , Camundongos Knockout , Terapia de Alvo Molecular/métodos , Miofibroblastos/metabolismo , Pirazóis/farmacologia , Cicatrização/efeitos dos fármacos , Cicatrização/genética
3.
Ophthalmic Plast Reconstr Surg ; 33(4): e80-e82, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-27792680

RESUMO

Gold hypersensitivity is a cause of periorbital dermatitis that often presents as a diagnostic challenge for many ophthalmologists. Six female patients are described as presenting with isolated bilateral periorbital dermatitis. Main symptoms included itching (3/6), eyelid redness (3/6), and drooping eyelids (3/6) for an average duration of 16.8 months prior to referral. All 6 patients failed conservative management. Recurrence of symptoms necessitated allergic patch testing, revealing a severe hypersensitivity reaction to gold in all cases. By discontinuing contact with gold, specifically gold jewelry, the allergic periorbital dermatitis completely resolved. No patients required surgical intervention for eyelid malposition. Increased awareness of this reversible cause of allergic periorbital dermatitis may improve patient outcomes.


Assuntos
Dermatite Alérgica de Contato/etiologia , Doenças Palpebrais/etiologia , Ouro/efeitos adversos , Adulto , Dermatite Alérgica de Contato/diagnóstico , Doenças Palpebrais/diagnóstico , Feminino , Humanos , Pessoa de Meia-Idade , Testes do Emplastro
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