Aidin Safvati
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Project: Mediators of neovascularisation and the hypoxic cornea.
While the latest generation of contact lenses have increased the amount of available oxygen for optimal corneal health, the optometry field and industry continues to work towards developing lenses that lead to an absolute minimum of adverse responses by the eye.
Neovascularisation is a serious, sight–threatening condition that can result from a reduction in oxygen availability to the cornea and is regulated by mediators of angiogenesis. Contact lens wear is among the most frequent causes of corneal angiogenesis (the growth of new blood vessels into the cornea that can disrupt vision).
The aim of Aidin’s project is to investigate the mechanisms by which corneal hypoxia leads to angiogenesis and establish the expression levels and mechanism of action of the mediators of neovascularisation in the cornea and during contact lens wear and to determine the threshold for their induction by hypoxia.
Research has demonstrated that angiogenin, VEGF and HIF-1α show different patterns of time-dependent upregulation by hypoxia in immortalised human corneal epithelial cells. While studies also indicate involvement of yet unidentified factors, VEGF and angiogenin are potentially capable of being used as markers of severe hypoxia in the human cornea.
These results are being further investigated by applying cell-free supernatants from hypoxic human corneal epithelial cells onto human microvascular endothelial cells. Inhibition of individual angiogenic components and signalling pathways will be studied to elucidate the mechanisms of the observed changes. The results will be further tested by measuring the levels of these mediators in human tears collected after brief periods of hydrogel and silicone hydrogel contact lens wear.
Aidin’s project has involved investigations into the long standing question of how much oxygen does the cornea need to remain healthy during contact lens wear? While researchers in the past have approached this question in several different ways, there is no consensus about the level of oxygen below which the human cornea starts sending out warning signals of hypoxia. Hypothetically, a new way of approaching this question would be to find the levels of oxygen above which the cornea stops producing the main mediators of neovascularisation.
Aidin graduated from the Beheshti University of Medical Sciences in Tehran, Iran with a BSc Optometry Honours degree in 1992. He spent nine years as a lecturer / tutor at the University while operating his private optometry practice and practicing in eye hospitals. At the end of this time, together with a large team of his students, he was involved in hosting the Global Centenary of Optometry conference in Iran in 2001. An important result of the conference was the initiation of the Vision 2020 agenda in Iran.
In 2002, he began working as a Professional Services Manager with CIBA Vision in seven countries in the Persian Gulf region, focusing on educating practitioners in the area of prescription and use of contact lenses. This assignment allowed Aidin to enjoy nearly three years of extensive collaboration with optometrists and ophthalmologists in the region, while promoting the concept of frequent replacement of contact lenses and introducing silicone hydrogel contact lenses in these countries.
These experiences led to a growing interest in the adverse events that can occur with contact lens wear, particularly hypoxia. In 2005, Aidin was awarded the Brien A Holden Scholarship which enabled him to undertake his doctoral thesis through the Vision CRC and School of Optometry and Vision Science, UNSW. His poster at Asia ARVO 2009 was short-listed for a rapid fire presentation and brought him the Best Poster Prize. He aspires to continue research in corneal stem cells and communication between cell types in the human cornea and to contribute further to contact lens care and vision, with special focus on the communities around the Persian Gulf region and the Middle East.
Supervisors: Professor Mark Willcox; Dr Emma Hume.
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