Here is how we think that Pokemon Go might be utilized to prevent infectious diseases spread: Please bear in mind that it is hypothesis!
“Reducing the connectivity of the Pokémon Go network to limit transmission of infectious diseases. A) In a normal situation, players of Pokémon Go interact in a “small world network”, in which players (blue dots) battle each other at PokéGyms (red dots). Some players become “hubs” in the network by visiting multiple PokéGyms (green dots). B) If an infectious disease breaks out in a specific part of the city (green area), a virtual quarantine could be instituted by strategically modifying which PokéGyms are visible to individual players.”
Please check our recent paper published in Translational Psychiatry in which we showed that DNA repeat polymorphisms in two particular genes, i.e. ATXN7 and TBP, were associated with the risk of lifetime depression in two large and well-characterized Dutch cohorts — the Netherlands Study of Depression and Anxiety (NESDA) and the Netherlands Study of Depression in Older Persons (NESDO) —including 2165 depressed and 1058 non-depressed individuals. We found that carriers of either ATXN7 or TBP alleles with relatively large CAG repeat sizes in both alleles had a substantially increased risk of lifetime depression. I believe that these as well as many other DNA repeat polymophisms could actually account for a substanial degree of ‘missing heritability’, and not only of depression. The paper is open access, so please feel free to disseminate!
Gardiner SL, Van Belzen MJ, Boogaard MW; Van Roon-Mom WM, Rozing MP, Van Hemert AM, Smit JH, Beekman AT, Van Grootheest G, Schoevers RA, Oude Voshaar RC, Comijs HC, Penninx BW, Van der Mast RC, Roos RA, Aziz NA (2017). Large normal-range TBP and ATXN7 CAG repeat lengths are associated with increased lifetime risk of depression. Translational Psychiatry. 7(6): e1143. doi: 10.1038/tp.2017.116.
Recently our research letter was accepted for publication in Brain. In this paper we show for the first time that CAG repeat length variations in genes other than the HTT gene may also affect phenotype in patients with Huntington disease. Interestingly, only two weeks after our paper was accepted for publication, another intriguing paper was published in Nature by David Rubinsztein’s group which could provide a mechanistic basis for interactions among polyglutamine-disease associated genes through polyglutamine-length dependent competitive interactions among the encoded proteins and regulators of autophagy. Fascinating!
A few days ago I posted a preprint of a methodological paper in which I examine the potential value of a new measure grounded in information theory called ‘transfer entropy’ for analyzing observational epidemiological data (Transfer entropy as a tool for inferring causality from observational studies in epidemiology. ). I posted it on ‘bioRxiv’ (dubbed ‘The Preprint Server for Biology’ by the makers) which is a new website very similar to ‘arxiv’ but with a focus on life sciences. I think that the paper needs more polishing for final publication, so please feel free to comment! That is the whole idea behind publishing preprint: To allow peers to review a piece before it gets eternalized.
Thanks for visiting my personal website! On this website you can find information on a wide range of things which are either directly or indirectly of interest to me. And to be honest, I am interested in almost everything, so it is very hard for me to give this website an all encompassing title or theme; ‘Curious Brain’ was, unfortunately, the best I could think of …