ORCID Profile
0000-0003-2218-9951
Current Organisations
Centre for Eye Research Australia
,
University of Melbourne
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Publisher: Springer Science and Business Media LLC
Date: 27-04-2023
DOI: 10.1186/S12909-023-04252-X
Abstract: Early- and mid-career academics in medicine, dentistry and health sciences are integral to research, education and advancement of clinical professions, yet experience significant illbeing, high attrition and limited advancement opportunities. Identify and synthesise published research investigating challenges and opportunities related to ersity and inclusion, as experienced by early and mid-career academics employed in medicine, dentistry and health sciences disciplines. Rapid review. OVID Medline, Embase, APA PsycInfo, CINAHL and Scopus. We systematically searched for peer reviewed published articles within the last five years, investigating challenges and opportunities related to ersity and inclusion, as experienced by early and mid-career academics employed in medicine, dentistry and health sciences. We screened and appraised articles, then extracted and synthesised data. Database searches identified 1162 articles, 11 met inclusion criteria. Studies varied in quality, primarily reporting concepts encompassed by professional identity. There were limited findings relating to social identity, with sexual orientation and disability being a particularly notable absence, and few findings relating to inclusion. Job insecurity, limited opportunities for advancement or professional development, and a sense of being undervalued in the workplace were evident for these academics. Our review identified overlap between academic models of wellbeing and key opportunities to foster inclusion. Challenges to professional identity such as job insecurity can contribute to development of illbeing. Future interventions to improve wellbeing in academia for early- and mid-career academics in these fields should consider addressing their social and professional identity, and foster their inclusion within the academic community. Open Science Framework ( 0.17605/OSF.IO/SA4HX ).
Publisher: Frontiers Media SA
Date: 12-10-2017
Publisher: Association for Research in Vision and Ophthalmology (ARVO)
Date: 29-07-2016
DOI: 10.1167/TVST.5.4.8
Publisher: Public Library of Science (PLoS)
Date: 03-11-2014
Publisher: Association for Research in Vision and Ophthalmology (ARVO)
Date: 21-09-2018
DOI: 10.1167/TVST.7.5.9
Publisher: Association for Research in Vision and Ophthalmology (ARVO)
Date: 21-12-2018
DOI: 10.1167/TVST.7.6.26
Publisher: MDPI AG
Date: 02-2021
Abstract: Glaucoma is a leading cause of blindness worldwide. In glaucoma, a progressive dysfunction and death of retinal ganglion cells occurs, eliminating transfer of visual information to the brain. Currently, the only available therapies target the lowering of intraocular pressure, but many patients continue to lose vision. Emerging pre-clinical and clinical evidence suggests that metabolic deficiencies and defects may play an important role in glaucoma pathophysiology. While pre-clinical studies in animal models have begun to mechanistically uncover these metabolic changes, some existing clinical evidence already points to potential benefits in maintaining metabolic fitness. Modifying diet and exercise can be implemented by patients as an adjunct to intraocular pressure lowering, which may be of therapeutic benefit to retinal ganglion cells in glaucoma.
Publisher: Wiley
Date: 20-12-2015
DOI: 10.1111/OPO.12174
Abstract: To assess ocular blood flow responses to acute IOP stress following 4 weeks of chronic IOP elevation in streptozotocin (STZ)-induced diabetic and control rats. We hypothesise that chronic IOP elevation for 4 weeks will further impair blood flow regulation in STZ-induced diabetic rats eyes. Two weeks following citrate buffer or STZ-injections chronic IOP elevation was induced in Long Evans rats via fortnightly intracameral injections of microspheres (15 μm) suspended in 5% polyethylene glycol. IOP was monitored daily. Electroretinography (ERG, -6.79-2.07 log cd s m(-2) ) was undertaken at Week 4 to compare photoreceptor (RmPIII ), ON-bipolar cell (Vmax ) and ganglion cell dominant ERG [scotopic threshold response (STR)] components. 4 weeks post-chronic IOP induction, ocular blood flow (laser Doppler flowmetry) was measured in response to acute IOP challenge (10-100 mmHg, in 5 mmHg steps, each 3 min). Four weeks of chronic IOP (mean ± S.E.M., citrate: 24.0 ± 0.3 to 30.7 ± 1.3 and STZ-diabetes: 24.2 ± 0.2 to 31.1 ± 1.2 mmHg) was associated with reduced photoreceptor litude in both groups (-25.3 ± 2.2% and -17.2 ± 3.0%, respectively). STZ-diabetic eyes showed reduced photoreceptor sensitivity (citrate: 0.5 ± 1.8%, STZ-diabetic: -8.1 ± 2.4%). Paradoxically ON-bipolar cell sensitivity was increased, particularly in citrate control eyes (citrate: 166.8 ± 25.9%, STZ-diabetic: 64.8 ± 18.7%). The ganglion cell dominant STR was not significantly reduced in STZ-diabetic rats. Using acute IOP elevation to probe autoregulation, we show that STZ-diabetes impaired autoregulation compared with citrate control animals. The combination of STZ-diabetes and chronic IOP elevation further impaired autoregulation. STZ-diabetes and chronic IOP elevation appear to be additive risk factors for impairment of ocular blood flow autoregulation.
Publisher: Springer Science and Business Media LLC
Date: 17-09-2019
DOI: 10.1038/S41467-019-12242-1
Abstract: Studies of rodent models of Alzheimer’s disease (AD) and of human tissues suggest that the retinal changes that occur in AD, including the accumulation of amyloid beta (Aβ), may serve as surrogate markers of brain Aβ levels. As Aβ has a wavelength-dependent effect on light scatter, we investigate the potential for in vivo retinal hyperspectral imaging to serve as a biomarker of brain Aβ. Significant differences in the retinal reflectance spectra are found between in iduals with high Aβ burden on brain PET imaging and mild cognitive impairment ( n = 15), and age-matched PET-negative controls ( n = 20). Retinal imaging scores are correlated with brain Aβ loads. The findings are validated in an independent cohort, using a second hyperspectral camera. A similar spectral difference is found between control and 5xFAD transgenic mice that accumulate Aβ in the brain and retina. These findings indicate that retinal hyperspectral imaging may predict brain Aβ load.
Publisher: Proceedings of the National Academy of Sciences
Date: 13-12-2021
Abstract: This work identifies a role for microglia, the innate immune cells of the CNS, in the local control of the retinal vasculature and identifies deficits early in diabetes. Microglia contact neurons and vasculature and express several vasoactive agents. Activation of microglial fractalkine-Cx3cr1 signaling leads to capillary constriction and blocking the renin-angiotensin system (RAS) with candesartan abolishes microglial-mediated vasoconstriction in the retina. In early diabetes, reduced retinal blood flow is coincident with capillary constriction, increased microglial–vessel association, loss of microglial–capillary regulation, and altered microglial expression of the RAS pathway. While candesartan restores retinal capillary diameter early in diabetes, targeting of microglial–vascular regulation is required to prevent coincident dilation of large retinal vessels and reduced retinal blood flow.
Publisher: Elsevier BV
Date: 08-2023
Publisher: Wiley
Date: 09-2022
DOI: 10.1111/CEO.14169
Publisher: Elsevier BV
Date: 07-2018
DOI: 10.1016/J.PRETEYERES.2018.04.001
Abstract: Retinal ganglion cell (RGC) degeneration causes vision loss in patients with glaucoma, and this has been generally considered to be irreversible due to RGC death. We question this assertion and summarise accumulating evidence that points to visual function improving in glaucoma patients with treatment, particularly in the early stages of disease. We propose that prior to death, RGCs enter periods of dysfunction but can recover with relief of RGC stress. We first summarise the clinical evidence for vision improvement in glaucoma and then detail our experimental work that points to the underlying processes that underpin clinical improvement. We show that functional recovery can occur following a prolonged course of RGC dysfunction and demonstrate how the capacity for recovery can be modified. Detecting RGC dysfunction and augmenting recovery of such 'comatosed' RGCs holds clinical potential to improve early detection of glaucoma and improve visual function.
Publisher: Association for Research in Vision and Ophthalmology (ARVO)
Date: 21-12-2018
DOI: 10.1167/TVST.7.6.27
Publisher: Wiley
Date: 28-07-2020
DOI: 10.1111/CEO.13818
Publisher: Cold Spring Harbor Laboratory
Date: 29-01-2020
DOI: 10.1101/2020.01.28.20019075
Abstract: Retinal ganglion cells endure significant metabolic stress in glaucoma but maintain capacity to recover function. Nicotinamide, a precursor of NAD + , is low in serum of glaucoma patients and its supplementation provides robust protection of retinal ganglion cells in preclinical models. However, the potential of nicotinamide in human glaucoma is unknown. To determine whether nicotinamide supplementation alongside conventional IOP-lowering therapy improves retinal ganglion cell function in glaucoma. Crossover, double-masked, randomised clinical trial. Participants recruited from two tertiary care centres. Fifty-seven participants, diagnosed and treated for primary glaucoma, enrolled. Participants received oral placebo or nicotinamide and reviewed six-weekly. Participants commenced 6-weeks of 1.5 grams/day then 6 weeks of 3.0 grams/day followed by crossover without washout. Visual function measured using electroretinography and perimetry. Change in inner retinal function, determined by photopic negative response (PhNR) parameters: saturated PhNR litude (Vmax), ratio of PhNR/b-wave litude (Vmax ratio). PhNR Vmax improved beyond 95% coefficient of repeatability (COR) in 23% of participants following nicotinamide versus 9% on placebo. Overall, Vmax improved by 14.8% [95% CI: 2.8%, 26.9%], (p=0.02) on nicotinamide and 5.2% [−4.2%, 14.6%], (p=0.27) on placebo. Vmax ratio improved by 12.6% [5.0%, 20.2%], (p=0.002) following nicotinamide, 3.6% [−3.4%, 10.5%], (p=0.30) on placebo. A trend for improved visual field mean deviation was observed with 27% improving ≥1dB on nicotinamide and fewer deteriorating (4%) compared to placebo (p=0.02). Nicotinamide supplementation can improve inner retinal function in glaucoma. Further studies underway to elucidate the effects of long-term nicotinamide supplementation. ANZCTR trial ID: ACTRN12617000809336 www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=373001
Publisher: Elsevier BV
Date: 07-2017
DOI: 10.1016/J.PHARMTHERA.2017.02.009
Abstract: The retina is an easily accessible out-pouching of the central nervous system (CNS) and thus lends itself to being a biomarker of the brain. More specifically, the presence of neuronal, vascular and blood-neural barrier parallels in the eye and brain coupled with fast and inexpensive methods to quantify retinal changes make ocular biomarkers an attractive option. This includes its utility as a biomarker for a number of cerebrovascular diseases as well as a drug pharmacology and safety biomarker for the CNS. It is a rapidly emerging field, with some areas well established, such as stroke risk and multiple sclerosis, whereas others are still in development (Alzheimer's, Parkinson's, psychological disease and cortical diabetic dysfunction). The current applications and future potential of retinal biomarkers, including potential ways to improve their sensitivity and specificity are discussed. This review summarises the existing literature and provides a perspective on the strength of current retinal biomarkers and their future potential.
Publisher: American Medical Association (AMA)
Date: 12-2022
DOI: 10.1001/JAMAOPHTHALMOL.2022.4716
Abstract: Despite persistent inequalities in access to eye care services globally, guidance on a set of recommended, evidence-based eye care interventions to support country health care planning has not been available. To overcome this barrier, the World Health Organization (WHO) Package of Eye Care Interventions (PECI) has been developed. To describe the key outcomes of the PECI development. A standardized stepwise approach that included the following stages: (1) selection of priority eye conditions by an expert panel after reviewing epidemiological evidence and health facility data (2) identification of interventions and related evidence for the selected eye conditions from a systematic review of clinical practice guidelines (CPGs) stage 2 included a systematic literature search, screening of title and abstracts (excluding articles that were not relevant CPGs), full-text review to assess disclosure of conflicts of interest and affiliations, quality appraisal, and data extraction (3) expert review of the evidence extracted in stage 2, identification of missed interventions, and agreement on the inclusion of essential interventions suitable for implementation in low- and middle-income resource settings and (4) peer review. Fifteen priority eye conditions were chosen. The literature search identified 3601 articles. Of these, 469 passed title and abstract screening, 151 passed full-text screening, 98 passed quality appraisal, and 87 were selected for data extraction. Little evidence (≤1 CPG identified) was available for pterygium, keratoconus, congenital eyelid disorders, vision rehabilitation, myopic macular degeneration, ptosis, entropion, and ectropion. In stage 3, domain-specific expert groups voted to include 135 interventions (57%) of a potential 235 interventions collated from stage 2. After synthesis across all interventions and eye conditions, 64 interventions (13 health promotion and education, 6 screening and prevention, 38 treatment, and 7 rehabilitation) were included in the PECI. This systematic review of CPGs for priority eye conditions, followed by an expert consensus procedure, identified 64 essential, evidence-based, eye care interventions that are required to achieve universal eye health coverage. The review identified some important gaps, including a paucity of high-quality, English-language CPGs, for several eye diseases and a dearth of evidence-based recommendations on eye health promotion and prevention within existing CPGs.
Publisher: Cold Spring Harbor Laboratory
Date: 16-06-2020
DOI: 10.1101/2020.06.15.151464
Abstract: Local blood flow control within the CNS is critical to proper function and is dependent on coordination between neurons, glia and blood vessels. Macroglia such as astrocytes and Müller cells, contribute to this neurovascular unit within the brain and retina, respectively. This study explored the role of microglia, the innate immune cell of the CNS, in retinal vasoregulation and highlights changes during early diabetes. Structurally, microglia were found to contact retinal capillaries and neuronal synapses. In the brain and retinal explants, the addition of fractalkine, the sole ligand for monocyte receptor Cx3cr1, resulted in capillary constriction at regions of microglial contact. This vascular regulation was dependent on microglial involvement, since mice lacking Cx3cr1, exhibited no fractalkine-induced constriction. Analysis of the microglial transcriptome identified several vasoactive genes, including angiotensinogen, a constituent of the renin-angiotensin system (RAS). Subsequent functional analysis showed that RAS blockade via candesartan, abolished microglial-induced capillary constriction. Microglial regulation was explored in a rat streptozotocin (STZ) model of diabetic retinopathy. Retinal blood flow was reduced after 4 weeks due to reduced capillary diameter and this was coincident with increased microglial association. Functional assessment showed loss of microglial-capillary response in STZ-treated animals and transcriptome analysis showed evidence of RAS pathway dysregulation in microglia. While candesartan treatment reversed capillary constriction in STZ-treated animals, blood flow remained decreased likely due to dilation of larger vessels. This work shows microglia actively participate in the neurovascular unit, with aberrant microglial-vascular function possibly contributing to the early vascular compromise during diabetic retinopathy. This work identifies a novel role for microglia, the innate immune cells of the CNS, in the local control of the retinal vasculature and identifies deficits early in diabetes. Microglia contact neurons and vasculature and express several vasoactive agents. Activation of microglial fractalkine-Cx3cr1 signalling leads to capillary constriction and blocking the renin-angiotensin system (RAS) with candesartan abolishes microglial-mediated vasoconstriction in the retina. In early diabetes, reduced retinal blood flow is coincident with capillary constriction, increased microglial-vessel association, loss of microglial-capillary regulation and altered microglial expression of the RAS pathway. While candesartan restores retinal capillary diameter early in diabetes, targeting of microglial-vascular regulation is required to prevent coincident dilation of large retinal vessels and reduced retinal blood flow.
Publisher: CABI Publishing
Date: 05-07-2022
DOI: 10.1079/SEARCHRXIV.2022.00083
Abstract: RQ1) What are the characteristics of studies about this topic? RQ2) What instruments have been used to investigate this topic? RQ3) What are the reported experiences and perceptions in the included studies?
No related grants have been discovered for Flora Hui.