HKU's double professional civil engineering and law programme

The scale and complexity of civil engineering projects are increasing exponentially. Coupled with the growing trend of globalisation, the demand for high-calibre civil engineers who are also knowledgeable in legal matters is increasing. Driven by an aspiration to prepare civil engineering graduates with a solid foundation in both civil engineering and law, The University of Hong Kong has developed the first 5-year credit-based double professional degree programme in Hong Kong, which leads to the award of the degrees of Bachelor of Engineering in Civil Engineering (Law) and Bachelor of Laws. The considerations, development process and launching details of the programme are presented in this paper. The students admitted to date perform better academically than other civil engineering students on civil engineering courses. However, they do not perform as well as law students and other law-related double-degree students.published_or_final_versio

Role of epac in the pathogenesis of ischemic stroke

Poster Presentations: Theme 2published_or_final_version15th Research Postgraduate Symposium, Hong Kong, China, 1-2 December 2010. In Abstract - Poste Presentations (Theme II) of 15th Research Postgraduate Symposium, 2010, p. 8

Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy

Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac1 and Epac2, are cAMP mediators playing important roles in maintenance of endothelial barrier and neuronal functions. To investigate the roles of Epacs in the pathogenesis of ischemic retinopathy, transient middle cerebral artery occlusion (tMCAO) was performed on Epac1-deficient (Epac1) mice, Epac2-deficient (Epac2) mice, and their wild type counterparts (Epac1+/+ and Epac2+/+). Two-hour occlusion and 22-hour reperfusion were conducted to induce ischemia/reperfusion injury to the retina. After tMCAO, the contralateral retinae displayed similar morphology between different genotypes. Neuronal loss, retinal edema and increase in immunoreactivity for aquaporin 4 (AQP4), glial fibrillary acidic protein (GFAP), peroxiredoxin 6 (Prx6) were observed in ipsilateral retinae. Epac2 ipsilateral retinae showed more neuronal loss in retinal ganglion cell layer, increased retinal thickness and stronger immunostaining of AQP4, GFAP, and Prx6 than those of Epac2+/+. However, Epac1 ipsilateral retinae displayed similar pathology as those in Epac1+/+ mice. Our observations suggest that Epac2-deficiency led to more severe ischemic retinopathy after retinal ischemia/reperfusion injury.published_or_final_versio

EPAC2-deficiency leads to more severe neurological deficit and larger infarct with higher glial reactivity after transient middle cerebral occlusion

Abstract no. 912INTRODUCTION: Exchange proteins activated by cAMP (Epac1 and Epac2) belong to a family of cAMP-regulated guanine nucleotide exchange factors (cAMPGEFs) for the small GTPases, Rap1 and Rap2[1]. Epac1 was thought to be important in maintenance of tight and adhesion junctions between endothelial cells[2] , suggesting that Epac may play an important role in blood brain barrier (BBB) function. OBJECTIVE: Previously, it was shown that Epac2 mRNA is expressed in the brain[3]. Here, the protein expression of Epac2 was determined and compared to that of Epac1. In addition, the role of Epac2 was determined in the BBB and brain function after ischemia/reperfusion injury. METHOD: Six regions of brain from Epac2 wild type (Epac2+/+) mice was dissected, and proteins were extracted in order to determine the expression of Epac1 and Epac2 under normal and …postprintThe 25th International Symosium on Cerebral Blood Flow, Metabolism, and Function & 10th International Conference on Quantification of Brain Function with PET (BRAIN’11 & BRAINPET’11 ), Barcelona, Spain, 25-28 May 2011

Cognitive impairment in adiponectin-knockout mice

Oral Presentationpublished_or_final_versio

Chronic adiponectin deficiency leads to Alzheimer’s disease-like cognitive impairments and pathologies through AMPK inactivation and cerebral insulin resistance in aged mice

BACKGROUND: Insulin resistance is the major pathogenesis underlying type 2 diabetes mellitus (T2DM) and these patients have doubled risk of Alzheimer's disease (AD). Increasing evidence suggests that insulin resistance plays an important role in AD pathogenesis, possibly due to abnormal GSK3β activation, causing intra- and extracellular amyloid-beta (Aβ) accumulation. Adiponectin (APN) is an adipokine with insulin-sensitizing and anti-inflammatory effects. Reduced circulatory APN level is associated with insulin resistance and T2DM. The role of APN in AD has not been elucidated. In this study, we aim to examine if adiponectin deficiency would lead to cerebral insulin resistance, cognitive decline and Alzheimer's-like pathology in mice. METHODS: To study the role of adiponectin in cognitive functions, we employed adiponectin-knockout (APN-KO) mice and demonstrated chronic APN deficiency in their CNS. Behavioral tests were performed to study the cognitions of male APN-KO mice. Brains and tissue lysates were collected to study the pathophysiological and molecular changes in the brain of APN-KO mice. SH-SY5Y neuroblastoma cell line was used to study the molecular mechanism upon APN and insulin treatment. RESULTS: Aged APN-deficient mice displayed spatial memory and learning impairments, fear-conditioned memory deficit as well as anxiety. These mice also developed AD pathologies including increased cerebral Aβ42 level, Aβ deposition, hyperphosphorylated Tau proteins, microgliosis and astrogliosis with increased cerebral IL-1β and TNFα levels that associated with increased neuronal apoptosis and reduced synaptic proteins levels, suggesting APN deficiency may lead to neuronal and synaptic loss in the brain. AD pathologies-associated APN-KO mice displayed attenuated AMPK phosphorylation and impaired insulin signaling including decreased Akt induction and increased GSK3β activation in the hippocampus and frontal cortex. Aged APN-KO mice developed hippocampal insulin resistance with reduced pAkt induction upon intracerebral insulin injection. Consistently, APN treatment in SH-SY5Y cells with insulin resistance and overexpressing Aβ induce higher pAkt levels through AdipoR1 upon insulin treatment whereas the induction was blocked by compound C, indicating APN can enhance neuronal insulin sensitivity through AMPK activation. CONCLUSION: Our results indicated that chronic APN deficiency inactivated AMPK causing insulin desensitization and elicited AD-like pathogenesis in aged mice which also developed significant cognitive impairments and psychiatric symptoms.published_or_final_versio

Monitoring cytosolic calcium in the dinoflagellate Crypthecodinium cohnii with calcium orange-AM

Calcium plays several important roles in the signal transduction pathways of dinoflagellates. We describe here the development of calcium orange-AM as an intracellular calcium reporter for the heterotrophic dinoflagellate Crypthecodinium cohnii. We demonstrated with confocal microscopy that by restricting the incubation period to 3045 min, no compartmentalization of the dye occurs in the mitochondria or endoplasmic reticulum. The dye fluorescence responded well to the effects of calcium ionophores and calcium chelators. By calibrating the dye with known calcium concentrations, we determined the intracellular calcium concentration of C. cohnii to be 158 +/- 56 nM, which rose to about 550 nM upon mechanical stimulation

Dopamine yransporter (DAT)-expressing cells specific CR6-interacting factor 1 (DATCrif1) knockout mice as an experimental animal model for study the pathogenesis and discovery of novel treatment of Parkinson's Disease

Poster Presentation - Session 3: no. P3.0

Effect of temperatures on the time-dependent behavior of granite

Heat generated from the waste in the repository will result in an increase in rock temperature and substantially change the stress state of the host rock surrounding a nuclear waste repository. In this study, a series of uniaxial constant loading tests with acoustic emission monitoring has been conducted on wet granite in MTS 815 under different stress levels at room temperature, 50°C and 90°C. The results indicate that temperature under 50°C has no significant effect on the time dependent behavior. When the temperature is raised to 90°C, the crack damage stress, which is related to the long-term strength of granite, decreases to 90% of that at room temperature. The time to failure response decreases accordingly. Effect of temperature on the strain rate and acoustic emission rate under constant loading will also be discussed in the paper. Therefore, rock engineers need to consider the long-term in-situ strength of a rock at different temperatures in the design and construction of excavations in the rock for nuclear waste repositories