Implications for the U.S. of Anglo-French Defense Cooperation

The paper analyzes, from a predominantly UK perspective, the implications for the U.S. of the November 2, 2010, Anglo-French Defence Cooperation Treaty. The current pressures on British and French defence budgets were the primary driving force behind this cooperative effort. London and Paris have made steps toward improving joint efforts in a number of areas, with defence acquisition and industrial cooperation being prominent. In the UK, there appears to be strong political support at the highest levels, which has permeated to lower levels in the bureaucracy, while the UK defence industry appears to be cautiously optimistic about future business opportunities. The impact of enhanced Anglo-French cooperation on the U.S. would appear to be largely favourable for Washington. Rather than providing a basis for weakened UK attention to the U.S., as some fear, the efforts by London and Paris will potentially generate greater national military capability from scarce resources and could serve as a vehicle for broader European efforts to enhance their defence capabilities. While multinational European military development projects are viewed with scepticism in the UK, the Anglo-French arrangement could strengthen the prospects for bilateral projects in which other European states may elect to participate

Campus Vol VIII N 1

Howard Studio. Chris Doner . Picture. 0. Hawk, Pete and Don Shackelford. Prose. 2. Lefevre, Ioe. A Matter Of Propriety. Prose. 3. Porter, Bob. And, In Just 7 Days-You Too Can Be a Freshman! . Picture. 4. Martin, Lyn. And, In Just 7 Days-You Too Can Be a Freshman! . Prose. 4. Clapp, joy. Resignation . Prose. 6. Hawk, Pete. Mile Faces Life: A Case History . Prose. 8. Cook, Mike. A Definition of modernity . Poem. 9.; Miller, Ted. Untitled. Poem.9. Moore, Jules. On Picnics . Poem. 9. Emmet, June. Untitled. Poem. 9. Jacobs, Edward R. Orson Got Angry Again . Prose. 10. Ski-U-Mah. Contemporary Humor . Prose. 13. Pine Needle. Untitled. Prose. 13.; Anonymous. Untitled. Prose. 13

Somatic mutations and clonal dynamics in healthy and cirrhotic human liver.

The most common causes of chronic liver disease are excess alcohol intake, viral hepatitis and non-alcoholic fatty liver disease, with the clinical spectrum ranging in severity from hepatic inflammation to cirrhosis, liver failure or hepatocellular carcinoma (HCC). The genome of HCC exhibits diverse mutational signatures, resulting in recurrent mutations across more than 30 cancer genes1-7. Stem cells from normal livers have a low mutational burden and limited diversity of signatures8, which suggests that the complexity of HCC arises during the progression to chronic liver disease and subsequent malignant transformation. Here, by sequencing whole genomes of 482 microdissections of 100-500 hepatocytes from 5 normal and 9 cirrhotic livers, we show that cirrhotic liver has a higher mutational burden than normal liver. Although rare in normal hepatocytes, structural variants, including chromothripsis, were prominent in cirrhosis. Driver mutations, such as point mutations and structural variants, affected 1-5% of clones. Clonal expansions of millimetres in diameter occurred in cirrhosis, with clones sequestered by the bands of fibrosis that surround regenerative nodules. Some mutational signatures were universal and equally active in both non-malignant hepatocytes and HCCs; some were substantially more active in HCCs than chronic liver disease; and others-arising from exogenous exposures-were present in a subset of patients. The activity of exogenous signatures between adjacent cirrhotic nodules varied by up to tenfold within each patient, as a result of clone-specific and microenvironmental forces. Synchronous HCCs exhibited the same mutational signatures as background cirrhotic liver, but with higher burden. Somatic mutations chronicle the exposures, toxicity, regeneration and clonal structure of liver tissue as it progresses from health to disease.This work was supported by a Wellcome Trust and Cancer Research UK (CRUK) Grand Challenge Award (C98/A24032). P.J.C. is a Wellcome Trust Senior Clinical Fellow (WT088340MA); S.F.B. was supported by the Swiss National Science Foundation (P2SKP3-171753 and P400PB-180790); M.A.S. is supported by a Rubicon fellowship from NWO (019.153LW.038); the Cambridge Human Research Tissue Bank is supported by the NIHR Cambridge Biomedical Research Centre; and M.H. is supported by a CRUK Clinician Scientist Fellowship (C52489/A19924)