Punishing Warmongers for Their “Mad and Criminal Projects” – Bismarck’s Proposal for an International Criminal Court to Assign Responsibility for the Franco‑Prussian War

The idea of punishing aggressive war is routinely presented as having been first conceived of in the wake of the First World War. This conventional narrative is incorrect; the intellectual seed for the project had begun to take root long before, in the reactions to the interstate conflicts of the nineteenth century. This article explores one of the most significant moments from aggression’s unappreciated ‘pre-history’; Chancellor Bismarck’s pursuit of a trial before an international criminal court of the Franco-Prussian War’s (1870-1) French ‘intellectual originators and instigators.’ Although the proposal ultimately failed to attract the political and public support necessary for its implementation, it prompted in its own time an unprecedented discussion on the viability of international criminal responsibility for aggression and international criminal courts. The proposal later took on new life as both a precedent and an anti-precedent as these ideas resurfaced periodically after 1870. The goal of this paper is to restore Bismarck’s proposal to its rightful place in the story of the crime’s development. At stake is more than historic fidelity; contemporary expectations of what international criminal law can accomplish, what circumstances should or could accompany international criminal law’s invocation, and what the parameters of the crime of aggression should be are shaped by such histories. As the 2010 Kampala Amendments to the Rome Statute are now a single accession away from accumulating the requisite number of ratifications to come into effect, raising the prospect that the International Criminal Court will imminently be tasked with adjudicating the first aggression case in over seventy years, the need for reflection on these issues has taken on unusual salience

Questioning the UN\u27s Immunity in the Dutch Courts: Unresolved Issues in the Mothers of Srebrenica Litigation

The Article discusses the court case Mothers of Srebrenica v. the Netherlands & the United Nations regarding the mandate of the United Nations on the prevention of the 1995 attacks against the Muslims of Bosnia at Srebrenica and the failure of the Dutch troops to act upon the situation. The decision of the International Court of Justice and former Yugoslavia\u27s International Criminal Tribunal regarding the case is also presented

Genetic determinants of the response to bezafibrate treatment in the lower extremity arterial disease event reduction (LEADER) trial.

Genetic determinants of baseline levels and the fall in plasma triglyceride and fibrinogen levels in response to bezafibrate treatment were examined in 853 men taking part in the lower extremity arterial disease event reduction (LEADER) trial. Three polymorphisms in the peroxisome proliferator activated receptor alpha (PPARalpha) gene were investigated (L162V, G>A in intron 2 and G>C in intron 7), two in the apolipoprotein CIII (APOC3) gene (-482C>T and -455T>C) and one in the beta-fibrinogen (FIBB) gene (-455G>A). The presence of diabetes (n=158) was associated with 15% higher triglyceride levels at baseline compared to non-diabetics (n=654) (PC substitution. In the non-diabetic patients, the PPARalpha V162 allele was significantly associated with 9% higher baseline triglyceride levels (P<0.03) and a similar, but non-significant trend was seen for the intron 7 polymorphism. Overall, triglyceride levels fell by 26% with 3 months of bezafibrate treatment, and current smokers showed a poorer response compared to ex/non-smokers (23% fall compared to 28% P=0.03), but none of the genotypes examined had a significant influence on the magnitude of response. Carriers of the -455A polymorphism of the FIBB gene had, as expected, marginally higher baseline fibrinogen levels, 3.43 versus 3.36 g/l (P=0.055), but this polymorphism did not affect response to treatment. Overall, fibrinogen levels fell by 12%, with patients with the highest baseline fibrinogen levels showing the greatest decrease in response to bezafibrate. For both the intron 2 and the L162V polymorphisms of the PPARalpha gene there was a significant interaction (both P<0.01) between genotype and baseline levels of fibrinogen on the response of fibrinogen levels to bezafibrate, such that individuals carrying the rare alleles in the lowest tertile showed essentially no overall decrease compared to a 0.18 g/l fall in homozygotes for the common allele. Thus while these genotypes are a minor determinant of baseline triglyceride and fibrinogen levels, there is little evidence from this study that the magnitude of response to bezafibrate treatment in men with peripheral vascular disease is determined by variation at these loci

Peroxisome Proliferator-activated receptor alpha gene variation influences age of onset and progression of type 2 diabetes

Dysregulation of fatty acid metabolism is important in the pathogenesis of type 2 diabetes. Peroxisome proliferator-activated receptor (PPAR) is a master regulator of fatty acid catabolism, and PPAR activators delay the onset of type 2 diabetes. We examined association between three PPAR gene polymorphisms (an AC variant in intron 1, the L162V variant, and the intron 7 GC variant) and age at diagnosis of type 2 diabetes in 912 Caucasian type 2 diabetic subjects. Individually, PPAR gene variants did not influence age at diagnosis, but in combination, the rare alleles of both the intron 1 AC (P < 0.001) and intron 7 GC (P = 0.025) variants synergistically lowered age at diagnosis (interaction P < 0.001). Overall, the PPAR haplotype signficantly influenced age at diagnosis (P = 0.027), with the C-L-C and C-V-C haplotypes (intron 1-L162V-intron 7) accelerating onset of diabetes by 5.9 (P = 0.02) and 10 (P = 0.03) years, respectively, as compared with the common A-L-G haplotype, and was associated with an odds ratio for early-onset diabetes (age at diagnosis 45 years) of 3.75 (95% CI 1.65–8.56, P = 0.002). Intron 1 C-allele carriers also progressed more rapidly to insulin monotherapy (AA 9.4 ± 1.5 and AC + CC 5.3 ± 1.1 years, P = 0.002). These data indicate that PPAR gene variation influences the onset and progression of type 2 diabetes

Apolipoprotein AIV gene variant S347 is associated with increased risk of coronary heart disease and lower plasma apolipoprotein AIV levels

The impact of common variants in the apolipoprotein gene cluster (APOC3-A4-A5) on prospective coronary heart disease (CHD) risk was examined in healthy UK men. Of the 2808 men followed over 9 years, 187 had a clinically defined CHD event. Examination of 9 single nucleotide polymorphisms (SNPs) in this group revealed that homozygotes for APOA4 S347 had significantly increased risk of CHD [hazard ratio (HR) of 2.07 (95%CI 1.04 to 4.12)], whereas men homozygous for APOC3 1100T were protected [HR 0.28 (95%CI 0.09 to 0.87)]. In stepwise multiple regression analysis, after entering all the variants and adjusting for established risk factors APOA4 T347S alone remained in the model. Using all nine SNPs, the highest risk-estimate haplotypes carried APOA4 S347 and rare alleles of the two flanking intergenic markers. The protective effect of APOC3 1100T could be explained by negative linkage disequilibrium with these alleles. To determine the association of APOA4 T347S with apoAIV levels, the relationship was examined in 1600 healthy young European men and women. S347 homozygotes had significantly lower apoAIV plasma levels (13.64±0.59 mg/dL) compared with carriers of the T347 allele (14.90±0.12 mg/dL) (P=0.035). These results demonstrate that genetic variation in and around APOA4, independent of the effects of triglyceride, is associated with risk of CHD and apoAIV levels, supporting an antiatherogenic role for apoAIV

Pig producer perspectives on the use of meat inspection as an animal health and welfare diagnostic tool in the Republic of Ireland and Northern Ireland

peer-reviewedBackground Currently, there is growing interest in developing ante and post mortem meat inspection (MI) to incorporate measures of pig health and welfare for use as a diagnostic tool on pig farms. However, the success of the development of the MI process requires stakeholder engagement with the process. Knowledge gaps and issues of trust can undermine the effective exchange and utilisation of information across the supply chain. A social science research methodology was employed to establish stakeholder perspectives towards the development of MI to include measures of pig health and welfare. In this paper the findings of semi-structured telephone interviews with 18 pig producers from the Republic of Ireland and Northern Ireland are presented. Results Producers recognised the benefit of the utilisation of MI data as a health and welfare diagnostic tool. This acknowledgment, however, was undermined for some by dissatisfaction with the current system of MI information feedback, by trust and fairness concerns, and by concerns regarding the extent to which data would be used in the producers’ interests. Tolerance of certain animal welfare issues may also have a negative impact on how producers viewed the potential of MI data. The private veterinary practitioner was viewed as playing a vital role in assisting them with the interpretation of MI data for herd health planning. Conclusions The development of positive relationships based on trust, commitment and satisfaction across the supply chain may help build a positive environment for the effective utilisation of MI data in improving pig health and welfare. The utilisation of MI as a diagnostic tool would benefit from the development of a communication strategy aimed at building positive relationships between stakeholders in the pig industry.The authors acknowledge the financial support provided by the Irish Government’s National Development Plan 2007–2013 (Department of Agriculture, Food and the Marine’s Competitive Research Programme – RSF 11/S/107)

Human paraoxonase gene cluster polymorphisms as predictors of coronary heart disease risk in the prospective Northwick Park Heart Study II

AbstractThe anti-atherogenic effect of HDL has been suggested to be partly due to the action of HDL-associated paraoxonase (PON). Three distinct enzymes have been identified, encoded by PON1, PON2 and PON3, clustered on chromosome 7q21–q22. Two cSNPs in PON1 (L55M and Q192R) and one in PON2 (S311C) have been implicated as independent risk factors for coronary heart disease (CHD) in some, but not all, studies. A PON3 SNP (A99A) was identified and the effect of these four PON SNPs on HDL levels and CHD risk was examined in the prospective Northwick Park Heart Study II (NPHSII). Genotype frequencies did not differ between cases and controls but the CHD risk associated with smoking was significantly modified by PON1 L55M genotype. Compared to LL non-smokers, LL smokers had a hazard ratio (HR) of 1.30 (95% CI 0.81–2.06) while M-allele carriers had a HR of 1.76 (1.17–2.67). When genotypes were analysed in combination, men with the genotype PON1 55 LM/MM+PON2 311 CC, had HR of 3.54 (1.81–6.93) compared to PON1 LL+PON2 SS/SC men (interaction P=0.004). These effects were independent of classical risk factors. These data demonstrate the importance of stratifying by environmental factors and the use of multiple SNPs for genetic analysis

Control of a fast steering mirror for laser-based satellite communication

Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2006.Includes bibliographical references (p. 259).MIT Lincoln Laboratory has been contracted by NASA to test and build a platform capable of sending and receiving laser communication signals in space from Mars. The two main components of the pointing system on the spacecraft include an inertial reference frame to provide coarse laser control and a Fast Steering Mirror to remove any spacecraft jitter from the optical path. The optical path in the satellite must have no more that 400 nanoradians RMS motion from 1 Hz to 1 kHz. This thesis focuses on the feedback control of this Fast Steering Mirror (FSM). The feedback on the FSM comes from two different set of sensors. On power up, the FSM's angular position is controlled with feedback from local position sensors (KAMAN eddy current sensors). Optical feedback is accomplished with a laser beam and quad cell optical sensor. The optical sensor has an extremely small range of operation, and the mirror must first be pointed onto the active area of the quad cell before the optical feedback can be activated. This thesis investigates the controller being used for this FSM, the feedback loops for the different sensors and the pointing algorithms used to switch between feedback sensors.(cont.) The analog control system in use has a crossover frequency of approximately 1 kHz. MIT Lincoln Laboratory and NASA would like to use an FSM with a closed loop bandwidth as high as possible to lower noise restrictions on other parts of the spacecraft. This thesis investigates the FSM dynamics in detail and applies a different control system to push out the bandwidth as far as possible.by Karry Edward Hawe, II.S.M