Isoform‐specific upregulation of FynT kinase expression is associated with tauopathy and glial activation in Alzheimer’s disease and Lewy body dementias

This is the author accepted manuscript. The final version is available from Wiley via the DOI in this record Cumulative data suggest the involvement of Fyn tyrosine kinase in progression of Alzheimer's disease (AD). Previously, our group has shown increased immunoreactivities of the FynT isoform in AD neocortex (with no change in the alternatively spliced FynB isoform) which associated with neurofibrillary degeneration and reactive astrogliosis. Since both the aforementioned neuropathological features are also frequently found in Lewy Body dementias (LBD), we investigated potential perturbations of Fyn expression in the postmortem neocortex of patients with AD, as well as those having one of the two main subgroups of LBD: Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB). We found selective upregulation of FynT expression in AD, PDD and DLB which also correlated with cognitive impairment. Furthermore, increased FynT expression correlated with hallmark neuropathological lesions, soluble β-amyloid and phosphorylated tau, as well as markers of microglia and astrocyte activation. In line with the human postmortem studies, cortical FynT expression in aged mice transgenic for human P301S tau was upregulated and correlated with accumulation of aggregated phosphorylated tau as well as with microglial and astrocytic markers. Our findings point to FynT being an important mediator of disease progression in neurodegenerative dementias, likely via effects on tauopathy and neuroinflammation.National Medical Research Council, Singapor

The detector system of the Daya Bay reactor neutrino experiment

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Career Self-efficacy, School Connectedness, and Academic Achievement: Sex Differences and Implications for Counselling High School Adolescents..

Conference titled: Coming Together of Neighbour

CpG/CpNpG motifs in the coding region are preferred sites for mutagenesis in the breast cancer susceptibility genes

The range of BRCA1/BRCA2 gene mutations is diverse and the mechanism accounting for this heterogeneity is obscure. To gain insight into the endogenous mutational mechanisms involved, we evaluated the association of specific sequences (i.e. CpG/CpNpG motifs, homonucleotides, short repeats) and mutations within the genes. We classified 1337 published mutations in BRCA1 (1765 BRCA2 mutations) for each specific sequence, and employed computer simulation combined with mathematical calculations to estimate the true underlying tendency of mutation occurrence. Interestingly, we found no mutational bias to homonucleotides and repeats in deletions/insertions and substitutions but striking bias to CpG/CpNpG in substitutions in both genes. This suggests that methylation-dependent DNA alterations would be a major mechanism for mutagenesis. © 2007 Federation of European Biochemical Societies.link_to_subscribed_fulltex

Preservation of cortical histamine H3 receptors in ischemic vascular and mixed dementias

Aim: Histamine H3 receptor antagonists have been proposed as a novel therapeutic approach for the symptomatic treatment of Alzheimer's disease (AD). However, it is unclear whether there is a neurochemical basis for extending their potential use in vascular and mixed dementias. In this study, we measured cortical H3 receptors in patients with subcortical ischemic vascular dementia (SIVD) and mixed SIVD/AD (MIX). Materials and methods: Radioligand binding assays using [3H]GSK189254 were used to measure H3 receptors in the postmortem frontal cortex, anterior cingulate gyrus and hippocampus of a cohort of longitudinally assessed SIVD, MIX and age-matched controls. Results: H3 receptor levels were unchanged in SIVD and MIX in all areas studied. Furthermore, frontal H3 receptor densities negatively correlated with predeath assessment of cognition using Mini-Mental State Examination (MMSE) scores. Conclusion: Our data suggest that H3 receptors are preserved in SIVD and MIX, thus supporting further assessments of H3 antagonists as potential therapeutics in these dementias. © 2011 Elsevier B.V. All rights reserved

Joint linkage device

Inventor name used in this publication: 汤启宇Tong Kai YuInventor name used in this publication: 宋嵘Inventor name used in this publication: 林昭凯, Lam Chiu HoiInventor name used in this publication: 谭惠民, Tam Wai Man,Inventor name used in this publication: 邝国权Inventor name used in this publication: 彭民杰·彼得Inventor name used in this publication: 陈茂华, Chan Mau WahInventor name used in this publication: 梁焕方·华莱士Title in Traditional Chinese: 關節聯動裝置ChinaVersion of Recor

Robotic training system with multi-orientation module

US8540652; US8540652 B2; US8540652B2; US8,540,652; US 8,540,652 B2; 8540652; Appl. No. 11/802,267Inventor name used in this publication: Kai Yu TongInventor name used in this publication: Chiu Hoi LamInventor name used in this publication: Wai Man TamUSVersion of Recor

Multiple joint linkage device

US7854708; US7854708 B2; US7854708B2; US7,854,708; US 7,854,708 B2; 7854708; Appl. No. 11/802,273Inventor name used in this publication: Kai Yu TongInventor name used in this publication: Chiu Hoi LamInventor name used in this publication: Wai Man TamInventor name used in this publication: Kwok Kuen KwongInventor name used in this publication: Tak Chi LeeInventor name used in this publication: Mau Wah ChanInventor name used in this publication: Woon Fong Wallace LeungUSVersion of Recor