The Development of a United Nations Counter-Terrorism Policy : A pragmatic approach to the problem of a definition of Terrorism

The primary object of this thesis is to propose a pragmatic solution to the legitimacy problems associated with the absence of a definition of Terrorism within United Nations Counter Terrorism Policy. It contends that the attempts to draft such a definition within the Ad Hoc Committee on Terrorism have now come to a political standstill and are unlikely to result in a strong legal definition of terrorism. Any outcome is likely to be a political compromise in nature. This thesis therefore proposes that the international community should instead be examining other pragmatic alternatives and developments within the already established United Nations Universal Legal Framework against Terrorism. It will suggest that the definition found within Article 2(1) of the International Convention for the Suppression of the Financing of Terrorism 1999, contains a fit for purpose definition of terrorism. This definition has the potential to be used as a tool, to guide States, in the application of United Nations counter terrorism instruments. It also suggests that if this article becomes more widely accepted it has the potential to reach the level of customary international law status as an independent universal definition of terrorism. The definition itself provides a compromise between groups of States with different outlooks on counter terrorism. It supports the current sectoral approach by containing an Annex, which pays homage to the international community’s early counter terrorism instruments. It also however includes a mini-definition of terrorism that accommodates States who are looking for a more all-encompassing definition that outlines the necessary objective and subjective elements. The definition makes important reference to the obstacles that have left the Ad Hoc Committee on Terrorism at a standstill, whilst not limiting State sovereignty, leaving contentious issues up to domestic authorities to deal with. The thesis therefore is aiming to demonstrate that this pragmatic approach to the problem of a definition of terrorism is able to aid in increasing the legitimacy of the further development of the provisions within the United Nations counter terrorism policy, allowing it to continue to provide a sustainable successful response to the problem of international terrorism

The Vehicle, Fall 2003

Table of Contents Blame It on My BirthsignMichael Doizanpage 4 Like a BanjoKaitlyn Kingstonpage 6 A BubbleMaria Santoyopage 7 UntitledLiz Toyntonpage 8 She Said It Was Stuck in the FenceGreg Holdenpage 11 Thanksgiving Table CharactersKrystal Heringpage 12 This Is My LandKorah Winnpage 13 Bleeding HeartsKaitlyn Kingstonpage 14 SoldierEmily Rapppage 17 HomelessLaTasha Harrispage 18 InfinitiLindsey Nawojskipage 19 Gone Until ForeverAndy Whytepage 20 On My WayKristin Bornpage 27 GloryJay Popepage 28 Untitled (1)Trevor Moorepage 29 Nature\u27s MoratoriumMatt McCarthypage 29 Untitled (2)Trevor Moorepage 30 Eternal ChildAmy Towerypage 31 FingersJosh Sopiarzpage 31 She Likes JazzMario Podeschipage 32 Back Alley FarmsScott E. Lutzpage 33 Biographiespage 35https://thekeep.eiu.edu/vehicle/1078/thumbnail.jp

Recurrent PTPRB and PLCG1 mutations in angiosarcoma

Angiosarcoma is an aggressive malignancy that arises spontaneously or secondarily to ionizing radiation or chronic lymphoedema. Previous work has identified aberrant angiogenesis, including occasional somatic mutations in angiogenesis signaling genes, as a key driver of angiosarcoma. Here we employed whole-genome, whole-exome and targeted sequencing to study the somatic changes underpinning primary and secondary angiosarcoma. We identified recurrent mutations in two genes, PTPRB and PLCG1, which are intimately linked to angiogenesis. The endothelial phosphatase PTPRB, a negative regulator of vascular growth factor tyrosine kinases, harbored predominantly truncating mutations in 10 of 39 tumors (26%). PLCG1, a signal transducer of tyrosine kinases, encoded a recurrent, likely activating p.Arg707Gln missense variant in 3 of 34 cases (9%). Overall, 15 of 39 tumors (38%) harbored at least one driver mutation in angiogenesis signaling genes. Our findings inform and reinforce current therapeutic efforts to target angiogenesis signaling in angiosarcoma