Sunnybrook Health Sciences Centre

About: Sunnybrook Health Sciences Centre is a healthcare organization based out in Toronto, Ontario, Canada. It is known for research contribution in the topics: Population & Medicine. The organization has 7689 authors who have published 15236 publications receiving 523019 citations. The organization is also known as: Sunnybrook.

Reduced structural connectivity in ventral visual cortex in congenital prosopagnosia.

Abstract: Prosopagnosics have impaired face recognition, but make relatively normal responses to face stimuli in core brain regions for face recognition. The authors now report that it is the connectivity among these regions that is being disrupted in the disorder. Using diffusion tensor imaging and tractography, we found that a disruption in structural connectivity in ventral occipito-temporal cortex may be the neurobiological basis for the lifelong impairment in face recognition that is experienced by individuals who suffer from congenital prosopagnosia. Our findings suggest that white-matter fibers in ventral occipito-temporal cortex support the integrated function of a distributed cortical network that subserves normal face processing.

Validation of the Hospital Anxiety and Depression Scale for use with multiple sclerosis patients.

Abstract: Detecting clinically significant symptoms of depression and anxiety in medically ill patients using self-report rating scales presents a challenge because of somatic confounders. The Hospital Anxiety and Depression Scale (HADS) was developed with this in mind, but has never been validated for a multiple sclerosis population. Our objective was to validate the HADS for multiple sclerosis patients. Multiple sclerosis patients were interviewed for the presence of major depression (n = 180) and anxiety disorders (n = 140) with the Structured Clinical Interview for DSM-IV disorders. A receiver operating characteristic (ROC) analysis was undertaken to assess which HADS cut-off scores give the best yield with respect to diagnoses of major depression and all anxiety disorders defined by the Structured Clinical Interview for DSM-IV. A threshold score of 8 or greater on the HADS depression subscale provides a sensitivity of 90% and specificity of 87.3% (ROC area under the curve 0.938). The same cut-off score gives a...

EWSR1-ATF1 fusion is a novel and consistent finding in hyalinizing clear-cell carcinoma of salivary gland.

Abstract: Hyalinizing clear-cell carcinoma (HCCC) is a rare, low-grade salivary gland tumor with distinctive clear-cell morphology and pattern of hyalinization as well as focal mucinous differentiation. However, histological overlap exists with other salivary gland tumors, such as epithelial–myoepithelial carcinoma (EMCa), salivary myoepithelial carcinoma, and mucoepidermoid carcinoma (MEC). The potential relationship between HCCC and its morphological mimics has not been yet investigated at the genetic level. In this study, we conducted a molecular analysis for the presence of rearrangements in MAML2, commonly seen in MECs, and EWSR1, involved in “soft tissue myoepithelial tumors” (SMET) by fusion with POU5F1, PBX1, or ZNF444. Fluorescence in situ hybridization (FISH) was performed on 23 HCCC cases for abnormalities in MAML2, EWSR1, FUS, POU5F1, PBX1, and ZNF444. FISH for MAML2 was negative in all cases (0 of 14), including those with mucinous differentiation (0 of 7). An EWSR1 rearrangement was identified in 18 of 22 HCCCs (82%), while no break-apart signals were seen in FUS, POU5F1, PBX1, or ZNF444. 3′RACE on an EWSR1 rearranged HCCC identified an EWSR1-ATF1 fusion, which was confirmed by RT-PCR. ATF1 involvement was further confirmed by FISH analysis in 13 of 14 EWSR1-rearranged HCCC cases (93%). In contrast, all control cases tested, including among others 5 EMCa and 3 MEC with clear cells, were negative for EWSR1 and ATF1 rearrangements. The presence of EWSR1-ATF1 fusion in most HCCCs reliably separates these tumors from its histological mimics. The distinction from MEC is particularly important, as conventional MEC grading schemes overgrade these indolent HCCCs, potentially impacting on treatment. © 2011 Wiley-Liss,Inc.

Microvascular Obstruction and the No-Reflow Phenomenon After Percutaneous Coronary Intervention

Abstract: C ase presentation A: A 50-year-old diabetic man presented to the hospital after 8 hours of continuous chest pain. Because of acute myocardial infarction of the anterior wall, he underwent direct stenting to an occlusion in the left anterior descending coronary artery. Despite revascularization, suboptimal coronary flow was achieved, and he subsequently developed heart failure. Case presentation B: A 77-year-old man underwent elective stenting of a significant stenosis in a degenerated saphenous vein coronary bypass graft. After the procedure, coronary flow in the graft was severely reduced, and he sustained a myocardial infarction in the subtended myocardial territory. The concept of “no reflow” refers to a state of myocardial tissue hypoperfusion in the presence of a patent epicardial coronary artery. The underlying cause of no reflow is microvascular obstruction, which may be produced by various mechanisms. No reflow can be classified according to the duration of the preceding myocardial ischemia (Figure 1). “Reperfusion no reflow” occurs after primary percutaneous coronary intervention (PCI) for reperfusion of an infarct artery in the setting of acute myocardial infarction (AMI) and may be asymptomatic or may present clinically with continued chest pain and ST-segment elevation. Reperfusion no reflow is preceded by ischemic cell injury, is confined to the irreversibly damaged necrotic zone, and may be exacerbated at the time of reperfusion. Reperfusion no reflow is an independent predictor of adverse clinical outcome after AMI regardless of infarct size and is associated with heart failure and increased mortality.1 Figure 1. Schematic illustrating the effect of duration of preceding myocardial ischemia on mechanism of no reflow (NR). “Interventional no reflow” follows noninfarct PCI and affects myocardium that was not subjected to prolonged ischemia before the procedure. Clinically recognized interventional no reflow that complicates PCI is typically sudden in onset, presenting as acute ischemia with chest …