A Comparative Study of Disordered and Ordered Protein Folding Dynamics Using Computational Simulation

Folding protein dynamics has been an area of high interest for quite some time, especially given the increased focus on the field of Biophysics. Because folding dynamics occur on such short time scales, empirical techniques developed for more "static" protein events, such as X-ray crystallography, nuclear magnetic resonance, and green fluorescent protein (GFP) labelling, aren't as applicable. Instead, computational methods must often be used to simulate these short lived yet highly dynamic events. One such computational method that is proven to provide much valuable insight into protein folding dynamics is Molecular Dynamics Simulation (MD Simulation). This simulation method is both highly computationally demanding, yet highly accurate in its modelling of a proteins physical behaviour. Besides MD Simulation, simulations in general are quite applicable in the context of these protein events. For example, the simple Gillespie algorithm, a computational technique which can be executed on almost any personal computer, provides quite the robust view into protein dynamics given its computational simplicity. This paper will compare the results of two simulations, an MD simulation of a disordered, six-residue, carcinogenic protein fragment, and a Gillespie algorithm based simulation of an ordered folding protein: the mathematically identical nature of the Gillespie algorithm time series of the asymptotically stochastic hyperbolic tangent dynamics for the wild type predicting the exact behaviour of the carcinogenic protein system time series will show the computational power simulations provide for analyzing both disordered and ordered protein systems.Comment: 13 pages, draft 1, 8 figure

The Concurrent Use of Medical Imaging Modalities and Innovative Treatments to Combat Retinitis Pigmentosa

Retinitis pigmentosa (RP), one of the leading causes of vision loss and blindness globally, is a progressive retinal disease involving the degradation of photoreceptors (7) and/or retinal pigment epithelial cells (14). Affecting approximately 1 in 4000 people, RP is caused by a series of genetic mutations; each specific mutation presents a specific pathological pattern in the patient, with the same mutation even presenting in different phenotypes in different patients (14). RP generally starts with peripheral vision loss, attacking the rods first, causing nyctalopia or night blindness (22). In later stages of the disease, the cones start to atrophy, further narrowing the field of vision and obscuring central vision (22). Luckily, with recent advances in medical imaging techniques and novel therapeutic treatments, both early detection and the overall prognosis of RP in patients have improved dramatically in the past few decades. This review will trace RP's physiological causes, how it affects retinal and ocular physiology, the techniques through which we can diagnose and image it, and the various treatments developed to try to combat it. The medical imaging techniques to be discussed include but are not limited to adaptive optics (AO), OCT including SD-OCT and OCTA, fundus autofluorescence (FAF) and its associated fluorescence lifetime imaging ophthalmoscopy (FLIO), colour Doppler flow imaging (CDFI), microperimetry, and MRI. The treatments to be discussed include stem cell therapy, gene therapy, cell transplantation, pharmacological therapy, and artificial retinal implants. Throughout this review, it will be made evident of not just the severity and diversity through which RP can present, but also the advanced made in medical imaging and innovative treatments designed to combat this pathology.Comment: 39 pages, 23 figure