Semi-Automated Creation of Cinemagraphs for the Exhibition Still Moving

This project was inspired by cinemagraphs, a style of animated GIFs made out of a compilation of photographs, and brings my study of computer science and photography together. The aim of the computer science component of the project was to animate specific objects within a set of photographs, while leaving the rest of the frame static. I employed various image processing techniques from computer vision and graphics. This eased and automated some of the repetitive and time consuming portions of the process of generating cinemagraphs. The challenge was to create an algorithm capable of balancing the accuracy of detecting the objects with the speed of processing each frame. The project also explored the limitations and advantages of using Microsoft\u27s Kinect in artistic pursuits. From a photographic standpoint, my aim was to make these cinemagraphs presentable for a photography exhibition, hence the cinemagraphs had to go beyond being eye-catching because of technical trickery. The cinemagraphs had to hold the attention of the onlooker in spite of the novelty of the animated motion within the frame. The exhibition was a platform to explore the boundaries of cinemagraphs as an artistic medium

Identification of genetic modifiers of age-at-onset for familial Parkinson’s disease

Parkinson’s disease (PD) is the most common cause of neurodegenerative movement disorder and the second most common cause of dementia. Genes are thought to have a stronger effect on age-at-onset of PD than on risk, yet there has been a phenomenal success in identifying risk loci but not age-at-onset modifiers. We conducted a genome-wide study for age-at-onset. We analysed familial and non-familial PD separately, per prior evidence for strong genetic effect on age-at-onset in familial PD. GWAS was conducted in 431 unrelated PD individuals with at least one affected relative (familial PD) and 1544 non-familial PD from the NeuroGenetics Research Consortium (NGRC); an additional 737 familial PD and 2363 non-familial PD were used for replication. In familial PD, two signals were detected and replicated robustly: one mapped to LHFPL2 on 5q14.1 (PNGRC = 3E-8, PReplication = 2E-5, PNGRC + Replication = 1E-11), the second mapped to TPM1 on 15q22.2 (PNGRC = 8E-9, PReplication = 2E-4, PNGRC + Replication = 9E-11). The variants that were associated with accelerated onset had low frequencies (<0.02). The LHFPL2 variant was associated with earlier onset by 12.33 [95% CI: 6.2; 18.45] years in NGRC, 8.03 [2.95; 13.11] years in replication, and 9.79 [5.88; 13.70] years in the combined data. The TPM1 variant was associated with earlier onset by 15.30 [8.10; 22.49] years in NGRC, 9.29 [1.79; 16.79] years in replication, and 12.42 [7.23; 17.61] years in the combined data. Neither LHFPL2 nor TPM1 was associated with age-at-onset in non-familial PD. LHFPL2 (function unknown) is overexpressed in brain tumours. TPM1 encodes a highly conserved protein that regulates muscle contraction, and is a tumour-suppressor gene