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Author

Agnes M. F. Wong

Other affiliations: York University, University Health Network, McMaster University  ...read more
Bio: Agnes M. F. Wong is an academic researcher from University of Toronto. The author has contributed to research in topics: Binocular vision & Strabismus. The author has an hindex of 29, co-authored 137 publications receiving 2826 citations. Previous affiliations of Agnes M. F. Wong include York University & University Health Network.


Papers
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Journal ArticleDOI
08 Jan 2010-Cell
TL;DR: It is demonstrated that normal TUBB3 is required for axon guidance and maintenance in mammals and it is shown that the disease-associated mutations can impair tubulin heterodimer formation in vitro, although folded mutant heterodimers can still polymerize into microtubules.

519 citations

Journal ArticleDOI
TL;DR: There is increasing recognition that both humoral and cell mediated immune mechanisms are involved in the pathogenesis of opsoclonus, and further studies are needed to further elucidate its immunopathogenesis and pathophysiology in order to develop novel and efficacious therapy.
Abstract: Purpose of reviewThe aim of this article is to review opsoclonus, with particular emphasis on its immunopathogenesis and pathophysiology.Recent findingsInfections (West Nile virus, Lyme disease), neoplasms (non-Hodgkin's lymphoma, renal adenocarcinoma), celiac disease, and allogeneic hematopoietic s

141 citations

Journal ArticleDOI
TL;DR: Computer simulation of a model of the saccadic system indicated that disinhibition of the oculomotor region of the fastigial nucleus (FOR) in the cerebellum can generate opsoclonus, consistent with damage to afferent projections to the FOR, as determined by the model.

138 citations

Journal ArticleDOI
TL;DR: Today's neuroimaging findings that show how amblyopia affects various brain regions and how it disrupts the interactions among these brain regions are examined, and current concepts of brain plasticity and their implications for novel therapeutic strategies that may be beneficial for both children and adults with amblyopic are reviewed.
Abstract: Amblyopia is a visual impairment secondary to abnormal visual experience (eg, strabismus, anisometropia, form deprivation) during early childhood that cannot be corrected immediately by glasses alone It is the most common cause of monocular blindness globally Patching remains the mainstay of treatment, but it is not always successful and there are also compliance and recurrence issues Because amblyopia is a neural disorder that results from abnormal stimulation of the brain during the critical periods of visual development, it is essential to understand the neural mechanisms of amblyopia in order to devise better treatment strategies In this review, I examine our current understanding of the neural mechanisms that underlie the characteristic deficits associated with amblyopia I then examine modern neuroimaging findings that show how amblyopia affects various brain regions and how it disrupts the interactions among these brain regions Following this, I review current concepts of brain plasticity and their implications for novel therapeutic strategies, including perceptual learning and binocular therapy, that may be beneficial for both children and adults with amblyopia

123 citations

Journal ArticleDOI
TL;DR: Deficits in spatiotemporal vision in amblyopia are associated with poor PS, and PS of amblyopic and fellow eyes is differentially affected depending on viewing condition.
Abstract: PURPOSE. We investigated whether the sensory impairments of amblyopia are associated with a decrease in eye position stability (PS). METHODS. The positions of both eyes were recorded simultaneously in three viewing conditions: binocular, monocular fellow eye viewing (right eye for controls), and monocular amblyopic eye viewing (left eye for controls). For monocular conditions, movements of the covered eye were also recorded (open-loop testing). Bivariate contour ellipses (BCEAs), representing the region over which eye positions were found 68.2% of the time, were calculated and normalized by log transformation. RESULTS. For controls, there were no differences between eyes. Binocular PS (log10BCEA ¼� 0.88) was better than monocular PS (log10BCEA¼� 0.59) indicating binocular summation, and the PS of the viewing eye was better than that of the covered eye (log10BCEA ¼� 0.33). For patients, the amblyopic eye exhibited a significant decrease in PS during amblyopic eye (log10BCEA ¼� 0.20), fellow eye (log10BCEA ¼ 0.0004), and binocular (log10BCEA ¼� 0.44) viewing. The PS of the fellow eye depended on viewing condition: it was comparable to controls during binocular (log10BCEA ¼ � 0.77) and fellow eye viewing (log10BCEA ¼� 0.52), but it decreased during amblyopic eye viewing (log10BCEA ¼ 0.08). Patients exhibited binocular summation during fellow eye viewing, but not during amblyopic eye viewing. Decrease in PS in patients was mainly due to slow eye drifts.

122 citations


Cited by
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Journal ArticleDOI
TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
Abstract: Irrespective of the morphological features of end-stage cell death (that may be apoptotic, necrotic, autophagic, or mitotic), mitochondrial membrane permeabilization (MMP) is frequently the decisive event that delimits the frontier between survival and death. Thus mitochondrial membranes constitute the battleground on which opposing signals combat to seal the cell's fate. Local players that determine the propensity to MMP include the pro- and antiapoptotic members of the Bcl-2 family, proteins from the mitochondrialpermeability transition pore complex, as well as a plethora of interacting partners including mitochondrial lipids. Intermediate metabolites, redox processes, sphingolipids, ion gradients, transcription factors, as well as kinases and phosphatases link lethal and vital signals emanating from distinct subcellular compartments to mitochondria. Thus mitochondria integrate a variety of proapoptotic signals. Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria. These catabolic enzymes as well as the cessation of the bioenergetic and redox functions of mitochondria finally lead to cell death, meaning that mitochondria coordinate the late stage of cellular demise. Pathological cell death induced by ischemia/reperfusion, intoxication with xenobiotics, neurodegenerative diseases, or viral infection also relies on MMP as a critical event. The inhibition of MMP constitutes an important strategy for the pharmaceutical prevention of unwarranted cell death. Conversely, induction of MMP in tumor cells constitutes the goal of anticancer chemotherapy.

3,340 citations

01 Aug 2001
TL;DR: The study of distributed systems which bring to life the vision of ubiquitous computing systems, also known as ambient intelligence, is concentrated on in this work.
Abstract: With digital equipment becoming increasingly networked, either on wired or wireless networks, for personal and professional use alike, distributed software systems have become a crucial element in information and communications technologies. The study of these systems forms the core of the ARLES' work, which is specifically concerned with defining new system software architectures, based on the use of emerging networking technologies. In this context, we concentrate on the study of distributed systems which bring to life the vision of ubiquitous computing systems, also known as ambient intelligence.

2,774 citations

01 Jan 2010
TL;DR: In this paper, the authors describe a scenario where a group of people are attempting to find a solution to the problem of "finding the needle in a haystack" in the environment.
Abstract: 中枢神経系疾患の治療は正常細胞(ニューロン)の機能維持を目的とするが,脳血管障害のように機能障害の原因が細胞の死滅に基づくことは多い.一方,脳腫瘍の治療においては薬物療法や放射線療法といった腫瘍細胞の死滅を目標とするものが大きな位置を占める.いずれの場合にも,細胞死の機序を理解することは各種病態や治療法の理解のうえで重要である.現在のところ最も研究の進んでいる細胞死の型はアポトーシスである.そのなかで重要な位置を占めるミトコンドリアにおける反応および抗アポトーシス因子について概要を紹介する.

2,716 citations

Journal ArticleDOI
01 Feb 2001-Brain
TL;DR: Once ischaemia has occurred, treatment regimens such as a combination of induced hypertension and hypervolaemia, or transluminal angioplasty, are plausible, but of unproven benefit.
Abstract: The incidence of subarachnoid haemorrhage (SAH) is stable, at around six cases per 100 000 patient years. Any apparent decrease is attributable to a higher rate of CT scanning, by which other haemorrhagic conditions are excluded. Most patients are <60 years of age. Risk factors are the same as for stroke in general; genetic factors operate in only a minority. Case fatality is approximately 50% overall (including pre-hospital deaths) and one-third of survivors remain dependent. Sudden, explosive headache is a cardinal but non-specific feature in the diagnosis of SAH: in general practice, the cause is innocuous in nine out of 10 patients in whom this is the only symptom. CT scanning is mandatory in all, to be followed by (delayed) lumbar puncture if CT is negative. The cause of SAH is a ruptured aneurysm in 85% of cases, non-aneurysmal perimesencephalic haemorrhage (with excellent prognosis) in 10%, and a variety of rare conditions in 5%. Catheter angiography for detecting aneurysms is gradually being replaced by CT angiography. A poor clinical condition on admission may be caused by a remediable complication of the initial bleed or a recurrent haemorrhage in the form of intracranial haematoma, acute hydrocephalus or global brain ischaemia. Occlusion of the aneurysm effectively prevents rebleeding, but there is a dearth of controlled trials assessing the relative benefits of early operation (within 3 days) versus late operation (day 10-12), or that of endovascular treatment versus any operation. Antifibrinolytic drugs reduce the risk of rebleeding, but do not improve overall outcome. Measures of proven value in decreasing the risk of delayed cerebral ischaemia are a liberal supply of fluids, avoidance of antihypertensive drugs and administration of nimodipine. Once ischaemia has occurred, treatment regimens such as a combination of induced hypertension and hypervolaemia, or transluminal angioplasty, are plausible, but of unproven benefit.

1,208 citations