Movement disorder clinic registry at Tung Wah Hospital

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Review of trigeminal neuralgia in a regional neurology clinic

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A γA-Crystallin Mouse Mutant Secc with Small Eye, Cataract and Closed Eyelid

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Perception of Cantonese Parkinsonian speech

Abstract no. 1pSC18published_or_final_versio

Think about cryptococcal meningitis

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Cyp26b1 mediates differential regulation of RA signaling in neural progenitor populations along the anteriorposterior axis of the adult spinal cord

Poster Session - Neural Regeneration: no. 64DMM 2011 entitled: Re-engineering Regenerative MedicineNeural stem cells from the adult subventricular zone (SVZ) are highly heterogeneous, with their position of origin being a key factor in determining the neuronal subtype they can give rise to. Whether this diversity extends to other regions in the adult CNS has not been demonstrated. In vitro studies with directed neuronal differentiation of ES cells suggest that subtype specification may be regulated by the positional identity present in the ES‐derived cell, since altering the positional identity leads to corresponding changes in motor neuron subtype. This limited plasticity suggests the position identity of the original stem cell source is a critical factor for the generation of the desired neuronal subtype. The adult spinal cord consists of endogenous stem/progenitor cells which are …postprin

Cyp26b1 mediates differential neurogenicity in axial-specific populations of adult spinal cord progenitor cells

Utilization of endogenous adult spinal cord progenitor cells (SCPCs) for neuronal regeneration is a promising strategy for spinal cord repair. To mobilize endogenous SCPCs for injury repair, it is necessary to understand their intrinsic properties and to identify signaling factors that can stimulate their neurogenic potential. In this study, we demonstrate that adult mouse SCPCs express distinct combinatorial Hox genes and exhibit axial-specific stem cell properties. Lumbar-derived neurospheres displayed higher primary sphere formation and greater neurogenicity compared with cervical- and thoracic-derived neurospheres. To further understand the mechanisms governing neuronal differentiation of SCPCs from specific axial regions, we examined the neurogenic responses of adult SCPCs to retinoic acid (RA), an essential factor for adult neurogenesis. Although RA is a potent inducer of neuronal differentiation, we found that RA enhanced the generation of neurons specifically in cervical- but not lumbar-derived cells. We further demonstrate that the differential RA response was mediated by the RA-degrading enzyme cytochrome P450 oxidase b1 Cyp26b1. Lumbar cells express high levels of Cyp26b1 and low levels of the RA-synthesizing enzyme retinaldehyde dehydrogenase Raldh2, resulting in limited activation of the RA signaling pathway in these cells. In contrast, low Cyp26b1 expression in cervical spinal cord progenitor cells allows RA signaling to be readily activated upon RA treatment. The intrinsic heterogeneity and signaling factor regulation among adult SCPCs suggest that different niche factor regimens are required for site-specific mobilization of endogenous SCPCs from distinct spatial regions of the spinal cord for injury repair.published_or_final_versio

Analysis of craniofacial defects in Six1/Eya1-associated Branchio-Oto-Renal Syndrome

Poster Session I - Morphogenesis: 205/B10117th ISDB 2013 cum 72nd Annual Meeting of the Society for Developmental Biology, 7th Latin American Society of Developmental Biology Meeting and 11th Congreso de la Sociedad Mexicana de Biologia del Desarrollo.Branchio-Oto-Renal (BOR) syndrome patients exhibit craniofacial and renal anomalies as well as deafness. BOR syndrome is caused by mutations in Six1 or Eya1, both of which regulate cell proliferation and differentiation. The molecular mechanism underlying the craniofacial and branchial arch (BA) defects in BOR syndrome is unclear. We have found that Hoxb3 is up-regulated in the second branchial arch (BA2) of Six1-/- mutants. Moreover, Hoxb3 over-expression in transgenic mice leads to BA abnormalities which are similar to the BA defects in Six1-/- or Eya1-/- mutants, suggesting a regulatory relationship among Six1, Eya1 and Hoxb3 genes. The aim of this study is to investigate the molecular mechanism underlying abnormal BA development in BOR syndrome using Six1 and Eya1 mutant mice. Two potential Six1 binding sites were identified on the Hoxb3 gene. In vitro and in vivo Chromatin IP assays showed that Six1 could directly bind to one of the sites specifically. Furthermore, using a chick in ovo luciferase assay we showed that Six1 could suppress gene expression through one of the specific binding sites. On the other hand, in Six1-/- mutants, we found that the Notch ligand Jag1 was up-regulated in BA2. Similarly, in Hoxb3 transgenic mice, ectopic expression of Jag1 could be also detected in BA2. To investigate the activation of Notch signaling pathway, we found that Notch intracellular domain (NICD), a direct indicator of Notch pathway activation, was up-regulated in BAs of Six1-/-; Eya1-/- double mutants. Our results indicate that Hoxb3 and Notch signaling pathway are involved in mediating the craniofacial defects of Six1/Eya1-associated Branchio-Oto-Renal Syndrome.postprin

Using social network analysis to combat counterfeiting

2013-2014 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

Design of an RFID-based inventory control and management system : a case study

Author name used in this publication: Jacky S. L. Ting2011-2012 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe