当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い
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700 ジャーナル と 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得
Paul Whitesman
In an attempt to create a model of Parkinson’s disease (PD) eighty-three proteins were extracted from the Swiss- Prot protein database that had some casual mention of PD. These were split up into various subsets of proteins of which three are focused on here: PARK, made up of proteins that had some indication that polymorphisms in the protein might increase a person’s susceptibility to develop PD; MITOCHOND, proteins which had some association with the mitochondria; and MT-C1D, proteins that were implicated in mitochondrial complex 1 deficiency. The PARK subset had 21 out of 83 proteins (21/83); MITOCHOND 33 out of 83 proteins (33/83); and MT-C1D 17 out of 83 proteins (17/83). The results could be used to build up a basic model of PD creating phenotypes based on sets of proteins. The main phenotypes established here are; non-mitochondrial PD (50/83) and mitochondrial PD (33/83). Further division is possible dependant on whether proteins have polymorphisms which increase susceptibility to develop PD. MT-C1D seems to be independent of the PARK set. This is a very simplistic attempt at trying to model Parkinson’s disease at the proteomic level and will need further work to build up the more complex and realistic PD proteomic disease model.