University of Toronto

About: University of Toronto is a education organization based out in Toronto, Ontario, Canada. It is known for research contribution in the topics: Population & Health care. The organization has 126067 authors who have published 294940 publications receiving 13536856 citations. The organization is also known as: UToronto & U of T.

Phenotypic plasticity in the interactions and evolution of species.

Abstract: When individuals of two species interact, they can adjust their phenotypes in response to their respective partner, be they antagonists or mutualists. The reciprocal phenotypic change between individuals of interacting species can reflect an evolutionary response to spatial and temporal variation in species interactions and ecologically result in the structuring of food chains. The evolution of adaptive phenotypic plasticity has led to the success of organisms in novel habitats, and potentially contributes to genetic differentiation and speciation. Taken together, phenotypic responses in species interactions represent modifications that can lead to reciprocal change in ecological time, altered community patterns, and expanded evolutionary potential of species.

Implicit and explicit memory for new associations in normal and amnesic subjects.

Abstract: Two experiments examined whether repetition priming effects on a word completion task are influenced by new associations between unrelated word pairs that were established during a single study trial. On the word completion task, subjects were presented with the initial three letters of the response words from the study list pairs and they completed these fragments with the first words that came to mind. The fragments were shown either with the paired words from the study list (same context) or with other words (different context). Both experiments showed a larger priming effect in the same-context condition than in the different-context condition, but only with a study task that required elaborative processing of the word pairs. This effect was observed with college students and amnesic patients, suggesting that word completion performance is mediated by implicit memory for new associations that is independent of explicit recollection.

Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms

Abstract: In patients with spinal cord injury, the primary or mechanical trauma seldom causes total transection, even though the functional loss may be complete. In addition, biochemical and pathological changes in the cord may worsen after injury. To explain these phenomena, the concept of the secondary injury has evolved for which numerous pathophysiological mechanisms have been postulated. This paper reviews the concept of secondary injury with special emphasis on vascular mechanisms. Evidence is presented to support the theory of secondary injury and the hypothesis that a key mechanism is posttraumatic ischemia with resultant infarction of the spinal cord. Evidence for the role of vascular mechanisms has been obtained from a variety of models of acute spinal cord injury in several species. Many different angiographic methods have been used for assessing microcirculation of the cord and for measuring spinal cord blood flow after trauma. With these techniques, the major systemic and local vascular effects of acute spinal cord injury have been identified and implicated in the etiology of secondary injury. The systemic effects of acute spinal cord injury include hypotension and reduced cardiac output. The local effects include loss of autoregulation in the injured segment of the spinal cord and a marked reduction of the microcirculation in both gray and white matter, especially in hemorrhagic regions and in adjacent zones. The microcirculatory loss extends for a considerable distance proximal and distal to the site of injury. Many studies have shown a dose-dependent reduction of spinal cord blood flow varying with the severity of injury, and a reduction of spinal cord blood flow which worsens with time after injury. The functional deficits due to acute spinal cord injury have been measured electrophysiologically with techniques such as motor and somatosensory evoked potentials and have been found proportional to the degree of posttraumatic ischemia. The histological effects include early hemorrhagic necrosis leading to major infarction at the injury site. These posttraumatic vascular effects can be treated. Systemic normotension can be restored with volume expansion or vasopressors, and spinal cord blood flow can be improved with dopamine, steroids, nimodipine, or volume expansion. The combination of nimodipine and volume expansion improves posttraumatic spinal cord blood flow and spinal cord function measured by evoked potentials. These results provide strong evidence that posttraumatic ischemia is an important secondary mechanism of injury, and that it can be counteracted.