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Myopia (nearsightedness) is the most common eye disorder, which is rapidly becoming one of the leading causes of vision loss in several parts of the world because of a recent sharp increase in prevalence. Nearwork, which produces hyperopic optical defocus on the retina, has been implicated as one of the environmental risk factors causing myopia in humans. Experimental studies have shown that hyperopic defocus imposed by negative power lenses placed in front of the eye accelerates eye growth and causes myopia, whereas myopic defocus imposed by positive lenses slows eye growth and produces a compensatory hyperopic shift in refractive state. The balance between these two optical signals is thought to regulate refractive eye development; however, the ability of the retina to recognize the sign of optical defocus and the composition of molecular signaling pathways guiding emmetropization are the subjects of intense investigation and debate. We found that the retina can readily distinguish between imposed myopic and hyperopic defocus, and identified key signaling pathways underlying retinal response to the defocus of different signs. Comparison of retinal transcriptomes in common marmosets exposed to either myopic or hyperopic defocus for 10 days or 5 weeks revealed that the primate retina responds to defocus of different signs by activation or suppression of largely distinct pathways. We also found that 29 genes differentially expressed in the marmoset retina in response to imposed defocus are localized within human myopia quantitative trait loci (QTLs), suggesting functional overlap between genes differentially expressed in the marmoset retina upon exposure to optical defocus and genes causing myopia in humans. These findings identify retinal pathways involved in the development of myopia, as well as potential new strategies for its treatment.

Studying the temporal integration of visual signals is crucial to understand how time spent on different visual tasks can affect emmetropization and refractive error development. In this study we assessed the effect of interrupting positive and negative lens-imposed defocus with brief periods of unrestricted vision or darkness. A total of forty-six marmosets were treated monocularly with soft contact lenses for 4 weeks from 10 weeks of age (OD: + 5D or − 5D; OS: plano). Two control groups wore + 5D (n = 5) or − 5D (n = 13) lenses continuously for 9 h/day. Two experimental groups had lens-wear interrupted for 30 min twice/day at noon and mid-afternoon by removing lenses and monitoring vision while marmosets sat at the center of a viewing cylinder (normal vision interruption, + 5D: n = 7; − 5D: n = 8) or while they were in the dark (dark interruption, + 5D: n = 7; − 5D: n = 6). The interruption period (30 min/day) represented approx. 10% of the total stimulation time (9 h/day). On-axis refractive error (RE) and vitreous chamber depth (VCD) were measured using an autorefractor and high frequency A-scan ultrasound at baseline and after treatment. Wearing + 5D lenses continuously 9 h/day for 4 weeks induced slowed eye growth and hyperopic shifts in RE in treated relative to contralateral control eyes (relative change, VCD: − 25 ± 11 μm, p > 0.05; RE: + 1.24 ± 0.58 D, p > 0.05), whereas − 5D lens wear resulted in larger and myopic eyes (relative change, VCD: + 109 ± 24 μm, p < 0.001; RE: − 2.03 ± 0.56 D, p < 0.05), significantly different from those in the + 5D lens-treated animals (p < 0.01 for both). Interrupting lens induced defocus with periods of normal vision or darkness for approx. 10% of the treatment time affected the resulting compensation differently for myopic and hyperopic defocus. Interrupting defocus with unrestricted vision reduced − 5D defocus compensation but enhanced + 5D defocus compensation (− 5D, VCD: + 18 ± 33 μm; RE: − 0.93 ± 0.50 D, both p > 0.05; + 5D, VCD: − 86 ± 30 μm; RE: + 1.93 ± 0.50 D, both p < 0.05). Interrupting defocus with darkness also decreased − 5D defocus compensation, but had little effect on + 5D defocus compensation (− 5D, VCD: + 73 ± 34 μm, RE: − 1.13 ± 0.77 D, p > 0.05 for both; + 5D, VCD: − 10 ± 28 μm, RE: + 1.22 ± 0.50 D, p > 0.05 for both). These findings in a non-human primate model of emmetropization are similar to those described in other species and confirm a non-linear model of visual signal integration over time. This suggests a mechanism that is conserved across species and may have clinical implications for myopia management in school-aged children.

Biofeedback training has been used to access autonomically-controlled body functions through visual or acoustic signals to manage conditions like anxiety and hyperactivity. Here we examined the use of auditory biofeedback to improve accommodative responses to near visual stimuli in patients wearing single vision (SV) and multifocal soft contact lenses (MFCL). MFCLs are one evidence-based treatment shown to be effective in slowing myopia progression in children. However, previous research found that the positive addition relaxed accommodation at near, possibly reducing the therapeutic benefit. Accommodation accuracy was examined in 18 emmetropes and 19 myopes while wearing SVCLs and MFCLs (centre-distance). Short periods of auditory biofeedback training to improve the response (reduce the lag of accommodation) was performed and accommodation re-assessed while patients wore the SVCLs and MFCLs. Significantly larger accommodative lags were measured with MFCLs compared to SV. Biofeedback training effectively reduced the lag by ≥0.3D in individuals of both groups with SVCL and MFCL wear. The training was more effective in myopes wearing their habitual SVCLs. This study shows that accommodation can be changed with short biofeedback training independent of the refractive state. With this proof-of-concept, we hypothesize that biofeedback training in myopic children wearing MFCLs might improve the treatment effectiveness.

The purpose of this study was to evaluate the effect of interrupting negative lens wear for short periods early or late during the development of lens-induced myopia in marmosets. Sixteen marmosets were reared with a −5D contact lens on their right eye (plano on contralateral eye) for 8 weeks. Eight marmosets had lenses removed for 30 mins twice/day during the first four weeks (early interruption) and eight during the last four weeks (late interruption). Data were compared to treated controls that wore lenses continuously (N = 12) and untreated controls (N = 10). Interocular differences (IOD) in vitreous chamber (VC) depth and central and peripheral mean spherical refractive error (MSE) were measured at baseline and after four (T 4 ) and eight (T 8 ) weeks of treatment. Visual experience during the interruptions was monitored by measuring refraction while marmosets were seated at the center of a 1 m radius viewing cylinder. At T 4 the eyes that were interrupted early were not different from untreated controls (p = 0.10) and at T 8 had grown less and were less myopic than those interrupted later (IOD change from baseline, VC: +0.07 ± 0.04 mm vs +0.20 ± 0.03 mm, p < 0.05; MSE: −1.59 ± 0.26D vs −2.63 ± 0.60D, p = 0.13). Eyes interrupted later were not different from treated controls (MSE, p = 0.99; VC, p = 0.60) and grew at the same rate as during the first four weeks of uninterrupted lens wear (T 4  − T 0 : 3.67 ± 1.1 µm/day, T 8  − T 4 : 3.56 ± 1.3 µm/day p = 0.96). Peripheral refraction was a predictive factor for the amount of myopia developed only when the interruption was not effective. In summary, interrupting hyperopic defocus with short periods of myopic defocus before compensation occurs prevents axial myopia from developing. After myopia develops, interruption is less effective.

The spatial and temporal pattern of cone packing during marmoset foveal development was explored to understand the variables involved in creating a high acuity area. Retinal ages were between fetal day (Fd) 125 and 6 years. Cone density was determined in wholemounts using a new hexagonal quantification method. Wholemounts were labeled immunocytochemically with rod markers to identify reliably the foveal center. Cones were counted in small windows and density was expressed as cones × 103/mm2 (K). Two weeks before birth (Fd 125–130), cone density had a flat distribution of 20–30 K across the central retina encompassing the fovea. Density began to rise at postnatal day 1 (Pd 1) around, but not in, the foveal center and reached a parafoveal peak of 45–55 K by Pd 10. Between Pd 10 and 33, there was an inversion such that cone density at the foveal center rose rapidly, reaching 283 K by 3 months and 600 K by 5.4 months. Peak foveal density then diminished to 440 K at 6 months and older. Counts done in sections showed the same pattern of low foveal density up to Pd 1, a rapid rise from Pd 30 to 90, followed by a small decrease into adulthood. Increasing foveal cone density was accompanied by 1) a reduction in the amount of Müller cell cytoplasm surrounding each cone, 2) increased stacking of foveal cone nuclei into a mound 6–10 deep, and 3) a progressive narrowing of the rod-free zone surrounding the fovea. Retaining foveal cones in a monolayer precludes final foveal cone densities above 60 K. However, high foveal adult cone density (300 K) can be achieved by having cone nuclei stack into columns and without reducing their nuclear diameter. Marmosets reach adult peak cone density by 3–6 months postnatal, while macaques and humans take much longer. Early weaning and an arboreal environment may require rapid postnatal maturation of the marmoset fovea.

Table of contents O1 Changes in peripheral refraction associated with decreased ocular axial growth rate in marmosets Alexandra Benavente-Perez, Ann Nour, Tobin Ansel, Kathleen Abarr, Luying Yan, Keisha Roden, David Troilo O2 PPARα activation suppresses myopia development by increasing scleral collagen synthesis--a new drug target to suppress myopia development Chanyi Lu, Miaozhen Pan, Min Zheng, Jia Qu, Xiangtian Zhou O3 Evidence and possibilities for local ocular growth regulating signal pathways Christine F Wildsoet O4 Myopia researches at Eye Hospital of Wenzhou Medical University Fan Lu, Xiangtian Zhou, Jie Chen, Jinhua Bao, Liang Hu, Qinmei Wang, Zibing Jin, Jia Qu O5 Color, temporal contrast and myopia Frances Rucker, Stephanie Britton, Stephan Hanowsky, Molly Spatcher O6 The impact of atropine usage on visual function and reading performance in myopic school children in Taiwan Hui-Ying Kuo, Ching-Hsiu Ke, I-Hsin Kuo, Chien-Chun Peng, Han-Yin Sun O7 Increased time outdoors prevents the onset of myopia: evidence from randomised clinical trials Ian G Morgan O8 Environmental risk factors and gene-environment interactions for myopia in the ALSPAC cohort Jeremy A. Guggenheim, Rupal L. Shah, Cathy Williams O9 Retinal metabolic profiling identifies declines in FP receptor-linked signaling as contributors to form-deprived myopic development in guinea pigs Jinglei Yang, Peter S. Reinach, Sen Zhang, Miaozhen Pan, Wenfeng Sun, Bo Liu, Xiangtian Zhou O10 The study of peripheral refraction in moderate and high myopes after one month of wearing orthokeratology lens Jun Jiang, Haoran Wu, Fan Lu O11 Axial length of school children around the earth’s equatorial area and factors affecting the axial length Kazuo Tsubota, Hiroko Ozawa, Hidemasa Torii, Shigemasa Takamizawa, Toshihide Kurihara, Kazuno Negishi O12 Processing of defocus in the chicken retina by retinal ganglion cells Klaus Graef, Daniel Rathbun, Frank Schaeffel O13 Blue SAD light protects against form deprivation myopia in chickens, by local signaling within the retina Ladan Ghodsi, William K. Stell O14 Contributions of ON and OFF pathways to emmetropization and form deprivation myopia in mice Machelle T. Pardue, Ranjay Chakraborty, Han na Park, Curran S. Sidhu, P. Michael Iuvone O15 Response of the human choroid to defocus Michael J Collins O16 What can RNA sequencing tell us about myopic sclera? Nethrajeith Srinvasalu, Sally A McFadden, Paul N Baird O17 Overview of dopamine, retinal function, and myopia P. Michael Iuvone O18 The eye as a \"robust\" optical system and myopia Pablo Artal O19 Effect of discontinuation of orthokeratology lens wear on axial elongation in children Pauline Cho, SW Cheung O20 Myopia prevention in Taiwan Pei-Chang Wu O21 Alternatives to ultraviolet light and riboflavin for in vivo crosslinking of scleral collagen Quan V. Hoang, Sally A. McFadden O22 Absence of intrinsically photosensitive retinal ganglion cells (ipRGC) alters normal refractive development in mice Ranjay Chakraborty, Duk C. Lee, Erica G. Landis, Michael A. Bergen, Curran Sidhu, Samer Hattar, P. Michael Iuvone, Richard A. Stone, Machelle T. Pardue O23 Scleral micro-RNAs in myopia development and their potential as therapeutic targets Ravi Metlapally O24 Effects of the long-wavelength filtered continuous spectrum on emmetropization in juvenile guinea pigs Ruiqin Li, Qinglin Xu, Hong Zhon, Chenglin Pan, Weizhon Lan, Xiaoning Li, Ling Chen, Zhikuan Yang O25 Ocular and environmental factors associated with eye growth in childhood Scott A. Read O26 Overview- prevention and prediction of myopia and pathologic myopia Seang-Mei Saw O27 New insights into the roles of retinal dopamine in form-deprivation myopia and refractive development in C57BL/6 mice Shi-Jun Weng, Xiao-Hua Wu, Kang-Wei Qian, Yun-Yun Li, Guo-Zhong Xu, Furong Huang, Xiangtian Zhou, Jia Qu, Xiong-Li Yang, Yong-Mei Zhong O28 The effects of the adenosine antagonist, 7-methylxanthine, on refractive development in rhesus monkeys Earl L Smith III, Baskar Arumugam, Li-Fang Hung, Lisa A. Ostrin, Klaus Trier, Monica Jong, Brien A. Holden O29 Application of SWATH™ based next generation proteomics (NGP) in studying eye growth: opportunities and challenges Thomas Chuen Lam, Bing Zuo, Samantha Shan, Sally A. McFadden, Dennis Yan-yin Tse, Jingfang Bian, King-Kit Li, Quan Liu, Chi-ho To O30 How could emmetropization make use of longitudinal chromatic aberration? Timothy J. Gawne, John T. Siegwart Jr., Alexander H. Ward, Thomas T. Norton O31 Balance effect of dopamine D1 and D2 receptor subtype activation on refraction development Xiangtian Zhou O32 BMP gene expression changes in chick rpe in response to visual manipulations Yan Zhang, Yue Liu, Carol Ho, Eileen Phan, Abraham Hang, Emily Eng, Christine Wildsoet

Table of contents O1 Changes in peripheral refraction associated with decreased ocular axial growth rate in marmosets Alexandra Benavente-Perez, Ann Nour, Tobin Ansel, Kathleen Abarr, Luying Yan, Keisha Roden, David Troilo O2 PPAR[alpha] activation suppresses myopia development by increasing scleral collagen synthesis--a new drug target to suppress myopia development Chanyi Lu, Miaozhen Pan, Min Zheng, Jia Qu, Xiangtian Zhou O3 Evidence and possibilities for local ocular growth regulating signal pathways Christine F Wildsoet O4 Myopia researches at Eye Hospital of Wenzhou Medical University Fan Lu, Xiangtian Zhou, Jie Chen, Jinhua Bao, Liang Hu, Qinmei Wang, Zibing Jin, Jia Qu O5 Color, temporal contrast and myopia Frances Rucker, Stephanie Britton, Stephan Hanowsky, Molly Spatcher O6 The impact of atropine usage on visual function and reading performance in myopic school children in Taiwan Hui-Ying Kuo, Ching-Hsiu Ke, I-Hsin Kuo, Chien-Chun Peng, Han-Yin Sun O7 Increased time outdoors prevents the onset of myopia: evidence from randomised clinical trials Ian G Morgan O8 Environmental risk factors and gene-environment interactions for myopia in the ALSPAC cohort Jeremy A. Guggenheim, Rupal L. Shah, Cathy Williams O9 Retinal metabolic profiling identifies declines in FP receptor-linked signaling as contributors to form-deprived myopic development in guinea pigs Jinglei Yang, Peter S. Reinach, Sen Zhang, Miaozhen Pan, Wenfeng Sun, Bo Liu, Xiangtian Zhou O10 The study of peripheral refraction in moderate and high myopes after one month of wearing orthokeratology lens Jun Jiang, Haoran Wu, Fan Lu O11 Axial length of school children around the earth's equatorial area and factors affecting the axial length Kazuo Tsubota, Hiroko Ozawa, Hidemasa Torii, Shigemasa Takamizawa, Toshihide Kurihara, Kazuno Negishi O12 Processing of defocus in the chicken retina by retinal ganglion cells Klaus Graef, Daniel Rathbun, Frank Schaeffel O13 Blue SAD light protects against form deprivation myopia in chickens, by local signaling within the retina Ladan Ghodsi, William K. Stell O14 Contributions of ON and OFF pathways to emmetropization and form deprivation myopia in mice Machelle T. Pardue, Ranjay Chakraborty, Han na Park, Curran S. Sidhu, P. Michael Iuvone O15 Response of the human choroid to defocus Michael J Collins O16 What can RNA sequencing tell us about myopic sclera? Nethrajeith Srinvasalu, Sally A McFadden, Paul N Baird O17 Overview of dopamine, retinal function, and myopia P. Michael Iuvone O18 The eye as a \"robust\" optical system and myopia Pablo Artal O19 Effect of discontinuation of orthokeratology lens wear on axial elongation in children Pauline Cho, SW Cheung O20 Myopia prevention in Taiwan Pei-Chang Wu O21 Alternatives to ultraviolet light and riboflavin for in vivo crosslinking of scleral collagen Quan V. Hoang, Sally A. McFadden O22 Absence of intrinsically photosensitive retinal ganglion cells (ipRGC) alters normal refractive development in mice Ranjay Chakraborty, Duk C. Lee, Erica G. Landis, Michael A. Bergen, Curran Sidhu, Samer Hattar, P. Michael Iuvone, Richard A. Stone, Machelle T. Pardue O23 Scleral micro-RNAs in myopia development and their potential as therapeutic targets Ravi Metlapally O24 Effects of the long-wavelength filtered continuous spectrum on emmetropization in juvenile guinea pigs Ruiqin Li, Qinglin Xu, Hong Zhon, Chenglin Pan, Weizhon Lan, Xiaoning Li, Ling Chen, Zhikuan Yang O25 Ocular and environmental factors associated with eye growth in childhood Scott A. Read O26 Overview- prevention and prediction of myopia and pathologic myopia Seang-Mei Saw O27 New insights into the roles of retinal dopamine in form-deprivation myopia and refractive development in C57BL/6 mice Shi-Jun Weng, Xiao-Hua Wu, Kang-Wei Qian, Yun-Yun Li, Guo-Zhong Xu, Furong Huang, Xiangtian Zhou, Jia Qu, Xiong-Li Yang, Yong-Mei Zhong O28 The effects of the adenosine antagonist, 7-methylxanthine, on refractive development in rhesus monkeys Earl L Smith III, Baskar Arumugam, Li-Fang Hung, Lisa A. Ostrin, Klaus Trier, Monica Jong, Brien A. Holden O29 Application of SWATH[TM] based next generation proteomics (NGP) in studying eye growth: opportunities and challenges Thomas Chuen Lam, Bing Zuo, Samantha Shan, Sally A. McFadden, Dennis Yan-yin Tse, Jingfang Bian, King-Kit Li, Quan Liu, Chi-ho To O30 How could emmetropization make use of longitudinal chromatic aberration? Timothy J. Gawne, John T. Siegwart Jr., Alexander H. Ward, Thomas T. Norton O31 Balance effect of dopamine D1 and D2 receptor subtype activation on refraction development Xiangtian Zhou O32 BMP gene expression changes in chick rpe in response to visual manipulations Yan Zhang, Yue Liu, Carol Ho, Eileen Phan, Abraham Hang, Emily Eng, Christine Wildsoet

The growth of the vertebrate eye achieves a close match between the power of the optics and the length of the eye with the result that images are focused on the retina (emmetropia). The possibility that vision is required for the feedback regulation of eye growth was studied experimentally using domestic chicks (Gallus domesticus) as subjects. The approach was to produce either myopia (nearsightedness) or hyperopia (farsightedness) by manipulating the chick's visual experience just after hatching. After discontinuing the manipulations, the ability of the eye to correct the refractive errors was determined in intact chicks, and in chicks with a severed optic nerve (to test the role of the brain in eye growth regulation) or with lesions of the Edinger-Westphal nucleus (to test the role of ocular accommodation in eye growth regulation). Chicks recovered quickly from induced myopia or hyperopia mainly by adjusting the growth of their vitreous chambers--growth decreased in eyes correcting for myopia and increased in eyes correcting for hyperopia. Because the hyperopic eyes were already larger than normal controls these results indicate that refractive error, rather than eye size per se, guides the growth of the eye toward emmetropia. This growth compensating for induced refractive errors was found in chicks despite either optic-nerve-section or Edinger-Westphal lesion. The treatments differed in that Edinger-Westphal-lesioned chicks attained emmetropia, whereas optic-nerve-sectioned eyes did not, but instead overshot emmetropia and reversed the sign of the initial refractive error. Together these results suggest that: (1) The eye itself can sense the sign of a refractive error and adjust growth accordingly. (2) Accommodation is not necessary for emmetropization. (3) For emmetropia to be achieved an intact optic nerve is required, suggesting that visual pathways in the brain are involved. (4) Adjustment of refractive state by local ocular growth mechanism is probably different from that of the brain-mediated mechanism. Other experiments presented in this dissertation describe the role of cornea and lens in accommodation in chicks, and the local nature of myopia produced by partial deprivation of the visual field.

Behçet’s syndrome (BS) is a rare systemic vasculitis characterized by different clinical manifestations. As no specific laboratory tests exist, the diagnosis relies on clinical criteria, and the differential diagnosis with other inflammatory diseases can be challenging. Indeed, in a relatively small proportion of patients, BS symptoms include only mucocutaneous, articular, gastrointestinal, and non-typical ocular manifestations, which are frequently found also in psoriatic arthritis (PsA). We investigate the ability of serum interleukin (IL)-36α—a pro-inflammatory cytokine involved in cutaneous and articular inflammatory diseases—to differentiate BS from PsA. A cross-sectional study was performed on 90 patients with BS, 80 with PsA and 80 healthy controls. Significantly lower IL-36α concentrations were found in patients with BS as compared to PsA, although in both groups IL-36α was significantly increased compared to healthy controls. An empirical cut-off of 420.6 pg/mL displayed a specificity of 0.93, with a sensitivity of 0.70 (AUC 0.82) in discriminating PsA from BS. This cut-off displayed a good diagnostic performance also in BS patients lacking highly specific BS manifestations. Our results indicate that IL-36α might be involved in the pathogenesis of both BS and PsA, and might be a candidate biomarker to support the differential diagnosis of BS.

The European Eosinophilic Granulomatosis with Polyangiitis (EGPA) study group first gathered in Firenze in December 2018. The discussion was centred around the clinical and therapeutic needs in EGPA which still remain unmet. Indeed, EGPA is a puzzling and rare disease which shares clinical features with other anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAVs) and hypereosinophilic syndromes (HESs). Some of the recommendations published in 2015 are based on data derived from EGPA-related diseases, rather than from EGPA itself, and therefore need to be updated. Thus, the aim of the meeting was to stimulate ongoing research, to promote collaborative European studies and to define the main issues on which future studies should be focused. Current fields of research on EGPA include potential serological biomarkers of disease activity and of specific organ involvement, possible links between different genetic variants and clinical phenotypes, and new therapeutic perspectives. Herein, we give an overview of the meeting with the goal to stimulate an international collaboration and new points of discussion.