Ignite: A Promotional Magazine for Liberty University

For my senior thesis I received special permission to do a project instead of a paper. I named my magazine Ignite, and it is a promotional magazine. The magazine target audience is primarily high school juniors and seniors who are interested in attending Liberty University in Lynchburg, Virginia. I completely designed the magazine from beginning to end, with the exception of the photographs. The photographs used are ones approved by the Liberty University Marketing Department that the author has permission to reprint. This way, if Liberty University decides to add this publication to their line of products the school already has the copyrights to the images. All graphic design elements and writings are the sole creation of the author. The goal of this magazine is to help Liberty University and to help prospective students as they are going through their college selection process. I want this magazine to be something that Liberty can use for years to come with bits of updating throughout the years as the school sees fit. I believe this magazine can be used to create interest in Liberty University and will be something that few other colleges can offer to students. It is something I would like to give back to the school for the experiences I have been blessed to have here

Mitophagy and Parkinson's disease: The PINK1–parkin link

The study of rare, inherited mutations underlying familial forms of Parkinson's disease has provided insight into the molecular mechanisms of disease pathogenesis. Mutations in these genes have been functionally linked to several key molecular pathways implicated in other neurodegenerative disorders, including mitochondrial dysfunction, protein accumulation and the autophagic-lysosomal pathway. In particular, the mitochondrial kinase PINK1 and the cytosolic E3 ubiquitin ligase parkin act in a common pathway to regulate mitochondrial function. In this review we discuss the recent evidence suggesting that the PINK1/parkin pathway also plays a critical role in the autophagic removal of damaged mitochondria–mitophagy. This article is part of a Special Issue entitled Mitochondria: the deadly organelle

PINK1 deficiency in β-cells increases basal insulin secretion and improves glucose tolerance in mice

The Parkinson's disease (PD) gene, PARK6, encodes the PTEN-induced putative kinase 1 (PINK1) mitochondrial kinase, which provides protection against oxidative stress-induced apoptosis. Given the link between glucose metabolism, mitochondrial function and insulin secretion in β-cells, and the reported association of PD with type 2 diabetes, we investigated the response of PINK1-deficient β-cells to glucose stimuli to determine whether loss of PINK1 affected their function. We find that loss of PINK1 significantly impairs the ability of mouse pancreatic β-cells (MIN6 cells) and primary intact islets to take up glucose. This was accompanied by higher basal levels of intracellular calcium leading to increased basal levels of insulin secretion under low glucose conditions. Finally, we investigated the effect of PINK1 deficiency in vivo and find that PINK1 knockout mice have improved glucose tolerance. For the first time, these combined results demonstrate that loss of PINK1 function appears to disrupt glucose-sensing leading to enhanced insulin release, which is uncoupled from glucose uptake, and suggest a key role for PINK1 in β-cell function

Loss of PINK1 Increases the Heart's Vulnerability to Ischemia-Reperfusion Injury.

Mutations in PTEN inducible kinase-1 (PINK1) induce mitochondrial dysfunction in dopaminergic neurons resulting in an inherited form of Parkinson's disease. Although PINK1 is present in the heart its exact role there is unclear. We hypothesized that PINK1 protects the heart against acute ischemia reperfusion injury (IRI) by preventing mitochondrial dysfunction

"It's making contacts" : notions of social capital and implications for widening access to medical education

Acknowledgements Our thanks to the Medical Schools Council (MSC) of the UK for funding Study A; REACH Scotland for funding Study B; and Queen Mary University of London, and to the medical school applicants and students who gave their time to be interviewed. Our thanks also to Dr Sean Zhou and Dr Sally Curtis, and Manjul Medhi, for their help with data collection for studies A and B respectively. Our thanks also to Dr Lara Varpio, Uniformed Services University of the USA, for her advice and guidance on collating data sets and her comments on the draft manuscript.Peer reviewedPublisher PD

Epidemiology of basal and cutaneous squamous cell carcinoma in the U.K. 2013–15:a cohort study

BACKGROUND: Basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC), together known as keratinocyte cancers (KCs), are the commonest cancer in white ethnic populations. Recent improvements to registry data collection in England has allowed more accurate analysis of the epidemiology of BCC and cSCC and for the first time we are able to provide an accurate (representative) tumour burden for KC in the U.K. OBJECTIVES: To estimate the incidence of BCC and cSCC in the U.K. METHODS: A cohort of patients with KCs between 2013 and 2015 were identified using linkage to diagnostic codes derived from pathology reports collected into the national cancer registry. Data from England's cancer registry were combined with data from Scotland, Northern Ireland and Wales. European age-standardized incidence rates (EASRs) of the first BCC and cSCC per patient per annum (PPPA) were calculated. RESULTS: In the U.K, the EASR of the first BCC and cSCC PPPA in 2013-15 were 285 and 77 per 100 000 person years, respectively (211 120 KCs total in 2015). The mean annual percentage increase was 5% between 2013 and 2015 for both BCC and cSCC. By counting the first KC PPPA, we include an additional 51% KCs compared with the previous reporting technique which counts only the first BCC and cSCC in a patient's lifetime, yet it represents a probable underestimation of 5-11% of the true tumour count. CONCLUSIONS: Based on an improved methodology, a more representative incidence of KC is presented, which is essential to healthcare planning and will lead to improved understanding of the epidemiology of KC. What's already known about this topic? Keratinocyte cancers (KCs) are the most common cancers affecting white ethnic populations. The incidence of basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC) is increasing worldwide including the U.K., most commonly in elderly male Caucasian patients. These cancers are traditionally substantially underreported and frequently excluded from national cancer statistics. What does this study add? Using improved data collection methods in England and validated tumour-reporting techniques, we report the most accurate BCC and cSCC incidence data for the U.K. ever published. Identifying the first BCC and cSCC per patient per annum, the incidence of BCC and cSCC in the U.K. (excluding Wales) was 285 and 77 per 100 000 person years, respectively, between 2013 and 2015, with more than 210 000 KCs in the U.K. in 2015

An inclusive approach to raising standards in general practice: working with a 'community of practice' in Western Australia

<p>Abstract</p> <p>Background</p> <p>In this study we explored the challenges to establishing a community of practice (CoP) to address standards in general practice. We focused on the issue of improving referral letters which are the main form of communication between general practitioners (GPs) and specialists. There is evidence to suggest that the information relayed to specialists at the time of referral could be improved.</p> <p>Methods</p> <p>We aimed to develop a community of practice consisting of GPs in Western Australia to improve the quality of referral letters to six specialty clinics. Three phases included: establishing the CoP, monitoring the progress of the CoP and sustaining and managing the CoP. The CoP's activity centred on referral letters to each of six selected specialties. A local measure for the quality of the referral letters was developed from a survey of participants about specific items of history and weighted for their perceived importance in the referral letter. Referral letters by participants written before and after the benchmarking exercise were scored for quality based on the standards set by the CoP. Feedback to participants regarding the 'quality' of their individual referrals was provided by a nominated member of the CoP, including a comparison of before and after scores.</p> <p>Results</p> <p>15 GPs were recruited. Only five GPs submitted referral letters both before and after benchmarking. The five GPs that participated in both study phases submitted a total of 102 referral letters (53 before and 49 after). There was a 26 point (95% CI 11–41) improvement in the average scores of the second set of letters after taking clustering by speciality into account, indicating the quality of referral letters improved substantially after feedback.</p> <p>Conclusion</p> <p>There are many challenges to forming a CoP to focus on improving a specific issue in general practice. However we were able to demonstrate that those practitioners who participated in all aspects of the project substantially improved the quality of their referral letters. For recruitment it was important to work with a champion for the project from within the practice. The project took several months to complete therefore some GPs became disengaged. Some were very disappointed by their performance when compared to colleagues. This reaction may be an important motivation to change, however it needs to be sensitively handled if participants are not to become disillusioned or disheartened.</p

Assessment of ROS Production in the Mitochondria of Live Cells

Production of reactive oxygen species (ROS) in the mitochondria plays multiple roles in physiology, and excessive production of ROS leads to the development of various pathologies. ROS in the mitochondria are generated by various enzymes, mainly in the electron transporvt chain, and it is important to identify not only the trigger but also the source of free radical production. It is important to measure mitochondrial ROS in live, intact cells, because activation of ROS production could be initiated by changes in extramitochondrial processes which could be overseen when using isolated mitochondria. Here we describe the approaches, which allow to measure production of ROS in the matrix of mitochondria in live cells. We also demonstrate how to measure kinetic changes in lipid peroxidation in mitochondria of live cells. These methods could be used for understanding the mechanisms of pathology in a variety of disease models and also for testing neuro- or cardioprotective chemicals

Response of nuclear track detector CR-39 to low energy muons

The effectiveness of the PolyAllyl Diglycol Carbonate (PADC) etched solid state nuclear track detector (SSNTD), commonly known as CR-39, as a muon detector is assessed. CR-39 is successfully used to detect higher rest mass particles such as neutrons and protons, and is, for example, widely used in neutron dosimetry applications. CR-39 is generally accepted as being less suitable to detect lower rest mass particles such as muons, and especially electrons, due mostly to their reduced momenta and consequently, reduced stopping power. However, there has been some evidence that CR-39 may have application in the detection of cosmic ray muons. Monte Carlo simulations indicate that CR-39 can detect muons with energies up to 2.8 MeV. Experimental data to demonstrate the ability of CR-39 to detect muons was acquired using the MuSR spectrometer station at the ISIS Neutron and Muon Source. Pits deposited in CR-39 generated by positive muons from the beamline have been characterised and compared with pits deposited by protons and neutrons from other sources. The extent to which a CR-39 SSNTD can discriminate muons from particles with different momenta and rest masses is discussed

Dopamine Induced Neurodegeneration in a PINK1 Model of Parkinson's Disease

Parkinson's disease is a common neurodegenerative disease characterised by progressive loss of dopaminergic neurons, leading to dopamine depletion in the striatum. Mutations in the PINK1 gene cause an autosomal recessive form of Parkinson's disease. Loss of PINK1 function causes mitochondrial dysfunction, increased reactive oxygen species production and calcium dysregulation, which increases susceptibility to neuronal death in Parkinson's disease. The basis of neuronal vulnerability to dopamine in Parkinson's disease is not well understood