Confusions of Cantonese tones in teenagers with sensorineural hearing impairment

A dissertation submitted in partial fulfilment of requirements for the Bachelor of Science (Speech and Hearing Sciences), University of Hong Kong, April 30, 1992.Thesis (B.Sc)--University of Hong Kong, 1992Also available in print.published_or_final_versionSpeech and Hearing SciencesBachelorBachelor of Science in Speech and Hearing Science

Community Engagement Is Difficult for Immigrants

Being involved in community activities is important for the social well-being of a person and a community. However, engagement is low among immigrants in communities that are growing in diversity. There are specific barriers that prevent them from joining in social activities. These include language, time, knowledge and money barriers. These barriers can be eased if service organizations and the government address the challenges faced by newcomers when they first settle.York's Knowledge Mobilization Unit provides services and funding for faculty, graduate students, and community organizations seeking to maximize the impact of academic research and expertise on public policy, social programming, and professional practice. It is supported by SSHRC and CIHR grants, and by the Office of the Vice-President Research & Innovation. [email protected] www.researchimpact.c

Forebrain Origins of Glutamatergic Innervation to the Rat Paraventricular Nucleus of the Hypothalamus: Differential Inputs to the Anterior Versus Posterior Subregions

The hypothalamic paraventricular nucleus (PVN) regulates numerous homeostatic systems and functions largely under the influence of forebrain inputs. Glutamate is a major neurotransmitter in forebrain, and glutamate neurosignaling in the PVN is known to mediate many of its functions. Previous work showed that vesicular glutamate transporters (VGluTs; specific markers for glutamatergic neurons) are expressed in forebrain sites that project to the PVN; however, the extent of this presumed glutamatergic innervation to the PVN is not clear. In the present study retrograde FluoroGold (FG) labeling of PVN-projecting neurons was combined with in situ hybridization for VGluT1 and VGluT2 mRNAs to identify forebrain regions that provide glutamatergic innervation to the PVN and its immediate surround in rats, with special consideration for the sources to the anterior versus posterior PVN. VGluT1 mRNA colocalization with retrogradely labeled FG neurons was sparse. VGluT2 mRNA colocalization with FG neurons was most abundant in the ventromedial hypothalamus after anterior PVN FG injections, and in the lateral, posterior, dorsomedial, and ventromedial hypothalamic nuclei after posterior PVN injections. Anterograde tract tracing combined with VGluT2 immunolabeling showed that 1) ventromedial nucleus-derived glutamatergic inputs occur in both the anterior and posterior PVN; 2) posterior nucleus-derived glutamatergic inputs occur predominantly in the posterior PVN; and 3) medial preoptic nucleus-derived inputs to the PVN are not glutamatergic, thereby corroborating the innervation pattern seen with retrograde tracing. The results suggest that PVN subregions are influenced by varying amounts and sources of forebrain glutamatergic regulation, consistent with functional differentiation of glutamate projections. J. Comp. Neurol. 519:1301–1319, 2011. © 2010 Wiley-Liss, Inc

Peroxisome Proliferator-Activated Receptor-γ Promotes Adipogenic Changes in Growth Plate Chondrocytes In Vitro

Chondrocytes and adipocytes are two differentiated cell types which are both derived from mesenchymal cells. The purpose of this study was to investigate whether peroxisome proliferator-activated receptor-γ (PPARγ), a transcription factor involved in lineage determination during adipogenesis, is able to induce adipogenic differentiation in growth plate chondrocytes. Isolated epiphyseal chondrocytes were infected with a PPARγ adenovirus or treated with the PPARγ agonist ciglitazone. Both of these treatments resulted in lipid droplet accumulation and expression of the adipogenic markers aP2, lipoprotein lipase, and adipsin in chondrocytes. Proteoglycan matrix synthesis was decreased in the PPARγ-infected cells, as was the expression of the chondrogenic genes Col2a1 and aggrecan. Growth plate cells transfected with a PPARγ expression plasmid under the control of the collagen α1(II) promoter also demonstrated a similar adipogenic changes. Terminal differentiation of growth plate chondrocytes induced by thyroid hormone was also inhibited by overexpression of PPARγ and ciglitazone treatment, with decreased expression of alkaline phosphatase and Runx2/Cbfa1 genes. These in vitro data suggest that PPARγ is able to promote adipogenic differentiation in growth plate chondrocytes, while negatively regulating chondrogenic differentiation and terminal differentiation

Disruption of nNOS-NOS1AP protein-protein interactions suppresses neuropathic pain in mice

Elevated N-methyl-D-aspartate receptor (NMDAR) activity is linked to central sensitization and chronic pain. However, NMDAR antagonists display limited therapeutic potential because of their adverse side effects. Novel approaches targeting the NR2B-PSD95-nNOS complex to disrupt signaling pathways downstream of NMDARs show efficacy in preclinical pain models. Here, we evaluated the involvement of interactions between neuronal nitric oxide synthase (nNOS) and the nitric oxide synthase 1 adaptor protein (NOS1AP) in pronociceptive signaling and neuropathic pain. TAT-GESV, a peptide inhibitor of the nNOS-NOS1AP complex, disrupted the in vitro binding between nNOS and its downstream protein partner NOS1AP but not its upstream protein partner postsynaptic density 95 kDa (PSD95). Putative inactive peptides (TAT-cp4GESV and TAT-GESVΔ1) failed to do so. Only the active peptide protected primary cortical neurons from glutamate/glycine-induced excitotoxicity. TAT-GESV, administered intrathecally (i.t.), suppressed mechanical and cold allodynia induced by either the chemotherapeutic agent paclitaxel or a traumatic nerve injury induced by partial sciatic nerve ligation. TAT-GESV also blocked the paclitaxel-induced phosphorylation at Ser15 of p53, a substrate of p38 MAPK. Finally, TAT-GESV (i.t.) did not induce NMDAR-mediated motor ataxia in the rotarod test and did not alter basal nociceptive thresholds in the radiant heat tail-flick test. These observations support the hypothesis that antiallodynic efficacy of an nNOS-NOS1AP disruptor may result, at least in part, from blockade of p38 MAPK-mediated downstream effects. Our studies demonstrate, for the first time, that disrupting nNOS-NOS1AP protein-protein interactions attenuates mechanistically distinct forms of neuropathic pain without unwanted motor ataxic effects of NMDAR antagonists

Mesenchymal to epithelial reverting transition: a key role for re-expression of E-cadherin

Metastasis is a major contributor to breast cancer mortality, as currently available therapies are unable to ensure progression or disease-free survival. Little is known about the molecular pathogenesis of metastasis, and the role of the surrounding microenvironment is only beginning to be understood. In vitro studies have repeatedly shown that epithelial to mesenchymal transition (EMT) and loss of E-cadherin expression are critical events in the initiation of metastasis and can be induced by the microenvironment. However, metastases are often well-differentiated and epithelial in phenotype, suggesting that EMT is reversible. The role of E-cadherin expression and mesenchymal to epithelial reverting transition (MErT) in metastatic colonization of the secondary site remains ill-defined. Evidence for E-cadherin re-expression and partial MErT was observed in metastases of breast and prostate cancer patients, and suggests that MErT is unstable and reversible. MDA-MB-231 breast cancer cells cultured with hepatocytes also resulted in E-cadherin re-expression and partial MErT, suggesting that such phenotypic plasticity can be induced by the microenvironment of the liver, a key site of breast cancer metastases. Re-expression of E-cadherin following hepatocyte coculture not only results in heterotypic ligation between cancer and liver parenchymal cells, but also activates Erk survival signaling and increases resistance to nutrient-deprivation and chemotherapy. Taken together, our results indicate that the distant organ microenvironment may induce E-cadherin re-expression and partial MErT to enhance the survival of metastatic cancer cells at the secondary organ

Making Progress on Mathematical Knowledge for Teaching

Although the field lacks a theoretically grounded, well-defined, and shared conception of mathematical knowledge required for teaching, there appears to be broad agreement that a specialized body of knowledge is vital to improvement. Further, such a construct serves as the foundation for different kinds of studies with different agendas. This article reviews what is known and needs to be known to advance research on mathematical knowledge for teaching. It argues for three priorities: (i) finding common ground for engaging in complementary studies that together advance the field; (ii) innovating and reflecting on method; and (iii) addressing the relationship of such knowledge to mathematical fluency in teaching and to issues of equity and diversity in teaching. It concludes by situating the articles in this special issue within this emerging picture

Conceptualizing Ethics, Authenticity, and Efficacy of Simulations in Teacher Education

This working group was a continuation of working groups in 2019 and 2021 that initially aimed to focus on equity in simulations of practice in mathematics teacher education. We began by discussing our conceptualizations of simulations and equity. Next, we reflected on the lack of work that currently exists at the intersection of simulations and equity as well as our limited collective expertise in this space. We proposed the following areas of potential research: Access,Design, Affective Domains, Teaching Practices, Assessment, Critical Conversations. Attendees self-selected into focus groups and met to discuss their current work and how future work could focus more on equity and access. At the conclusion of our time together we developed a plan for achieving our key goal of disseminating a book that documents the landscape of the field