No description available.

Speech perception is challenging because the acoustic input is extremely variable. This variability partially stems from differences in how talkers pronounce words. For example, Voice Onset Time (VOT) is the primary cue that distinguishes /b/ from /p/. Women tend to use longer Voice Onset Times (VOTs) than men. A VOT of 20 msec could thus be a /b/ spoken by a woman and a /p/ spoken by a man. A critical question is how listeners deal with this variability. Previous research shows that listeners use these regularities (e.g., the systematic relationship between gender and VOT) to compensate for variability. For example, listeners adjust their phoneme category boundary based on talker gender. However, it is unclear the exact mechanisms by which talker gender information influences speech processing. Talker gender could influence only later stages of speech processing, like phoneme categorization. Alternatively, talker gender could modulate the earliest stage: acoustic cue encoding. I use event-related potentials, eye-tracking in the visual world paradigm, and electrocorticography to isolate the specific role of talker gender in speech perception. The results show that the auditory system influences the earliest stage of speech perception by allowing cues to be encoded relative to prior expectations about gender and that gender is integrated with acoustic cues during lexical activation. These experiments give insight into how the brain deals effectively with variability during categorization.

No description available.

No description available.

Adult neurogenesis is defined as the generation of new nerve cells in the adult central nervous system (CNS). Stimulating neurogenesis may potentially offer a therapeutic approach for neurodegenerative diseases such as Parkinson???s disease. However, it is not clear why neurogenesis does not normally replace neurons lost in these diseases. As a first step to address this problem it is necessary to identify mechanisms that regulate adult neurogenesis in the normal and diseased brain and further, determine if manipulating these mechanisms may offer therapeutic potential. In this thesis, we identify activin A, a member of the transforming growth factor ?? (TGF??) superfamily, as a significant regulator of neurogenesis. We demonstrate that mRNA encoding activin A is expressed after a KA injury, and that inhibition of this activin A profoundly impairs neurogenesis in the hippocampus. Further we demonstrate that activin A impairs gliosis and also has potent anti-inflammatory effects in the injured hippocampus. Finally, we provide evidence that the majority of activin A???s neurogenic effect results from its potent anti-inflammatory actions. Our study draws a clear link between neurogenesis and inflammation in the CNS and is the first to provide evidence that this process is regulated through activin signalling. Since inflammation is now believed to be an important component of many neurological diseases we suggest that therapeutic compounds that enhance activin A signalling may offer a therapeutic approach for treating these diseases by suppressing inflammation and stimulating neurogenesis.

Adult neurogenesis is defined as the generation of new nerve cells in the adult central nervous system (CNS). Stimulating neurogenesis may potentially offer a therapeutic approach for neurodegenerative diseases such as Parkinson???s disease. However, it is not clear why neurogenesis does not normally replace neurons lost in these diseases. As a first step to address this problem it is necessary to identify mechanisms that regulate adult neurogenesis in the normal and diseased brain and further, determine if manipulating these mechanisms may offer therapeutic potential. In this thesis, we identify activin A, a member of the transforming growth factor ?? (TGF??) superfamily, as a significant regulator of neurogenesis. We demonstrate that mRNA encoding activin A is expressed after a KA injury, and that inhibition of this activin A profoundly impairs neurogenesis in the hippocampus. Further we demonstrate that activin A impairs gliosis and also has potent anti-inflammatory effects in the injured hippocampus. Finally, we provide evidence that the majority of activin A???s neurogenic effect results from its potent anti-inflammatory actions. Our study draws a clear link between neurogenesis and inflammation in the CNS and is the first to provide evidence that this process is regulated through activin signalling. Since inflammation is now believed to be an important component of many neurological diseases we suggest that therapeutic compounds that enhance activin A signalling may offer a therapeutic approach for treating these diseases by suppressing inflammation and stimulating neurogenesis.

Adult neurogenesis is defined as the generation of new nerve cells in the adult central nervous system (CNS). Stimulating neurogenesis may potentially offer a therapeutic approach for neurodegenerative diseases such as Parkinson???s disease. However, it is not clear why neurogenesis does not normally replace neurons lost in these diseases. As a first step to address this problem it is necessary to identify mechanisms that regulate adult neurogenesis in the normal and diseased brain and further, determine if manipulating these mechanisms may offer therapeutic potential. In this thesis, we identify activin A, a member of the transforming growth factor ?? (TGF??) superfamily, as a significant regulator of neurogenesis. We demonstrate that mRNA encoding activin A is expressed after a KA injury, and that inhibition of this activin A profoundly impairs neurogenesis in the hippocampus. Further we demonstrate that activin A impairs gliosis and also has potent anti-inflammatory effects in the injured hippocampus. Finally, we provide evidence that the majority of activin A???s neurogenic effect results from its potent anti-inflammatory actions. Our study draws a clear link between neurogenesis and inflammation in the CNS and is the first to provide evidence that this process is regulated through activin signalling. Since inflammation is now believed to be an important component of many neurological diseases we suggest that therapeutic compounds that enhance activin A signalling may offer a therapeutic approach for treating these diseases by suppressing inflammation and stimulating neurogenesis.

Many 3D objects in the world around us are strongly constrained. For instance, not only cultural artifacts but also many natural objects are bilaterally symmetric. Thoretical arguments suggest and psychophysical experiments confirm that humans may be better in the recognition of symmetric objects. The hypothesis of symmetry-induced virtual views together with a network model that successfully accounts for human recognition of generic 3D objects leads to predictions that we have verified with psychophysical experiments.

Thesis (M.A.)--York University, 2004. Graduate Programme in Psychology. / Typescript. Includes bibliographical references (leaves 146-156). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: LINK NOT YET AVAILABLE.

Thesis (Ph. D.)--University of Alberta, 2009. / Title from pdf file main screen (viewed on Dec. 21, 2009). "A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Physiology, Cell Biology and Developmental Biology, Department of Biological Sciences, University of Alberta." Includes bibliographical references.