Design of the freeform V-cut optics in the cell phone backlight system

2004-2005 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Mercury profiles in sediments of the Pearl River Estuary and the surrounding coastal area of South China

Author name used in this publication: Carman C. M. Ip2009-2010 > Academic research: refereed > Publication in refereed journalAccepted ManuscriptPublishe

Periodic pattern formation in reaction-diffusion systems -an introduction for numerical simulation

The aim of the present review is to provide a comprehensive explanation of Turing reaction–diffusion systems in sufficient detail to allow readers to perform numerical calculations themselves. The reaction–diffusion model is widely studied in the field of mathematical biology, serves as a powerful paradigm model for self-organization and is beginning to be applied to actual experimental systems in developmental biology. Despite the increase in current interest, the model is not well understood among experimental biologists, partly because appropriate introductory texts are lacking. In the present review, we provide a detailed description of the definition of the Turing reaction–diffusion model that is comprehensible without a special mathematical background, then illustrate a method for reproducing numerical calculations with Microsoft Excel. We then show some examples of the patterns generated by the model. Finally, we discuss future prospects for the interdisciplinary field of research involving mathematical approaches in developmental biology

Effects of Excess Brain-Derived Human α-Synuclein on Synaptic Vesicle Trafficking

α-Synuclein is a presynaptic protein that regulates synaptic vesicle trafficking under physiological conditions. However, in several neurodegenerative diseases, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy, α-synuclein accumulates throughout the neuron, including at synapses, leading to altered synaptic function, neurotoxicity, and motor, cognitive, and autonomic dysfunction. Neurons typically contain both monomeric and multimeric forms of α-synuclein, and it is generally accepted that disrupting the balance between them promotes aggregation and neurotoxicity. However, it remains unclear how distinct molecular species of α-synuclein affect synapses where α-synuclein is normally expressed. Using the lamprey reticulospinal synapse model, we previously showed that acute introduction of excess recombinant monomeric or dimeric α-synuclein impaired distinct stages of clathrin-mediated synaptic vesicle endocytosis, leading to a loss of synaptic vesicles. Here, we expand this knowledge by investigating the effects of native, physiological α-synuclein isolated from the brain of a neuropathologically normal human subject, which comprised predominantly helically folded multimeric α-synuclein with a minor component of monomeric α-synuclein. After acute introduction of excess brain-derived human α-synuclein, there was a moderate reduction in the synaptic vesicle cluster and an increase in the number of large, atypical vesicles called “cisternae.” In addition, brain-derived α-synuclein increased synaptic vesicle and cisternae sizes and induced atypical fusion/fission events at the active zone. In contrast to monomeric or dimeric α-synuclein, the brain-derived multimeric α-synuclein did not appear to alter clathrin-mediated synaptic vesicle endocytosis. Taken together, these data suggest that excess brain-derived human α-synuclein impairs intracellular vesicle trafficking and further corroborate the idea that different molecular species of α-synuclein produce distinct trafficking defects at synapses. These findings provide insights into the mechanisms by which excess α-synuclein contributes to synaptic deficits and disease phenotypes

Optical design of freeform lens for LED streetlight

2008-2009 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

An integrated bidirectional multi-channel opto-electro arbitrary waveform stimulator for treating motor neurone disease

This paper presents a prototype integrated bidirectional stimulator ASIC capable of mixed opto-electro stimulation and electrophysiological signal recording. The development is part of the research into a fully implantable device for treating motor neurone disease using optogenetics and stem cell technology. The ASIC consists of 4 stimulator units, each featuring 16-channel optical and electrical stimulation using arbitrary current waveforms with an amplitude up to 16 mA and a frequency from 1.5 Hz to 50 kHz, and a recording front-end with a programmable bandwidth of 1 Hz to 4 kHz, and a programmable amplifier gain up to 74 dB. The ASIC was implemented in a 0.18μm CMOS technology. Simulated performance in stimulation and recording is presented

Maintaining hard disk integrity with digital legal professional privilege (LPP) data

published_or_final_versio

Observation of the Zero Doppler Effect

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material.National Basic Research Program (973) of China (No. 2011CB922001), and National Natural Science Foundation of China (No. 11234010)

Hemodynamic, Functional, and Clinical Responses to Pulmonary Artery Denervation in Patients With Pulmonary Arterial Hypertension of Different Causes: Phase II Results From the Pulmonary Artery Denervation-1 Study

Background—The mechanisms underlying pulmonary arterial hypertension (PAH) are multifactorial. The efficacy of pulmonary artery denervation (PADN) for idiopathic PAH treatment has been evaluated. This study aimed to analyze the hemodynamic, functional, and clinical responses to PADN in patients with PAH of different causes. Methods and Results—Between April 2012 and April 2014, 66 consecutive patients with a resting mean pulmonary arterial pressure ≥25 mmHg treated with PADN were prospectively followed up. Target drugs were discontinued after the PADN procedure. Hemodynamic response and 6-minute walk distance were repeatedly measured within the 1 year post PADN follow-up. The clinical end point was the occurrence of PAH-related events at the 1-year follow-up. There were no PADNrelated complications. Hemodynamic success (defined as the reduction in mean pulmonary arterial pressure by a minimal 10% post PADN) was achieved in 94% of all patients, with a mean absolute reduction in systolic pulmonary arterial pressure and mean pulmonary arterial pressure within 24 hours of −10 mmHg and −7 mmHg, respectively. The average increment in 6-minute walk distance after PADN was 94 m. Worse PAH-related events occurred in 10 patients (15%), mostly driven by the worsening of PAH (12%). There were 8 (12%) all-cause deaths, with 6 (9%) PAH-related deaths. Conclusions—PADN was safe and feasible for the treatment of PAH. The PADN procedure was associated with significant improvements in hemodynamic function, exercise capacity, and cardiac function and with less frequent PAH-related events and death at 1 year after PADN treatment. Further randomized studies are required to confirm the efficacy of PADN for PAH