Kyushu University · 의학
미츠루 아리마 교수의 연구실은 당뇨병성 망막병증과 선천성 망막질환의 병태생리학적 기전을 규명하고, 그 치료 전략을 개발하는 데 초점을 맞추고 있습니다. 특히 VEGF 외 다수의 염증세포활성화물질이 공통적으로 작용하는 혈망막장벽 파기 메커니즘을 중심으로, 'basigin'과 같은 핵심 분자를 타겟으로 한 새로운 치료법 개발에 주력하고 있습니다. 또한 조산아의 시력 손실을 예방하기 위한 조기 예측 모델 개발과 항VEGF 치료의 장기적 신경발달 영향에 대한 다학제적 연구도 진행 중입니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Approximately 40% of patients with diabetic macular edema (DME) are resistant to anti-vascular endothelial growth factor (VEGF) therapy (rDME). Here, we demonstrate that significant correlations between inflammatory cytokines and VEGF, as observed in naive DME, are lost in patients with rDME. VEGF overexpression in the mouse retina caused delayed inflammatory cytokine upregulation, monocyte/macrophage infiltration (CD11b<sup>+</sup> Ly6C<sup>+</sup> CCR2<sup>+</sup> cells), macrophage/microglia
Administration of IVB may introduce a risk of developmental impairment of interpersonal relationships, socializations, and/or verbal abilities of preterm children. We recommended that preterm infants who received IVB undergo a neurodevelopmental reassessment during their school years or in adulthood.
Despite the advance in medical technology, diabetic retinopathy (DR) is still an intractable disease which leads to the damage of retinal cells and finally the visual loss. Impairment of retinal vascular barrier triggered by an admixture of multiple inflammatory cytokines is a core of pathophysiology of DR. Therefore, the molecules involved commonly in multiple cytokines-induced impairment of vascular barrier would be the targets of curative treatment of DR. Here, we demonstrate that basigin, a
Retinopathy of prematurity (ROP), a vascular proliferative disease affecting preterm infants, is a leading cause of childhood blindness. Various studies have investigated the pathogenesis of ROP. Clinical experience indicates that oxygen levels are strongly correlated with ROP development, which led to the development of oxygen-induced retinopathy (OIR) as an animal model of ROP. OIR has been used extensively to investigate the molecular mechanisms underlying ROP and to evaluate the efficacy of
A contact-type camera is commonly used for paediatric fundus photography. With its use, we can easily photograph the fundus while controlling the eye movement in arbitrary direction. However, it is difficult to use a contact-type camera for infants in poor general condition because ocular compression with the camera lens risks a reduction of vital signs. Furthermore, its continuous use for different infants has a risk to spread infection. Therefore, we attempted to develop a new non-contact-type
Visual loss caused by retinopathy of prematurity (ROP) will be prevented if treatment-requiring ROP (TR-ROP) can be predicted. In this retrospective study including 418 infants with ≤32 weeks of gestational age (GA) and/or ≤1500 grams of birthweight, we attempted to identify useful predictors. We also examined the efficiency of significant predictors compared with existing predictive models, ROPScore and CHOP model. Multivariable logistic regression analyses supported the following factors were
Our study assessed the influence of vascular permeability on vascular flow density (FD)-correlated retinal sensitivity (RS) in DR. In this cross-sectional, prospective, consecutive study, RS in the extrafoveal macula of DR patient was measured by microperimetry. FD was measured in the total, superficial, and deep capillary plexus layers (TCP, SCP, and DCP) by optical coherence tomography angiography. All measurement points were classified into four categories according to intensity of fluorescei
We aimed to verify whether the intravitreal injection of small molecule compounds alone can create photoreceptor cells in mouse models of retinal degeneration. Primary cultured mouse Müller cells were stimulated in vitro with combinations of candidate compounds and the rhodopsin expression was measured on day 7 using polymerase chain reaction and immunostaining. We used 6-week-old N-methyl-N-nitrosourea-treated and 4-week-old rd10 mice as representative in vivo models of retinal degeneration. Th
NCT04621136 and jRCT2071200047.