1,056 research outputs found
Back Pay in Employment Discrimination Cases
This Special Project examines the back pay decisions and analyzes the problems that have confronted the courts dealing with this remedy for employment discrimination in the context of Title VII and section 1981. Because of the enormity of the issues that have arisen in Stage I of the proceedings, however, and the extensive coverage given those problems by the courts and commentators, the Special Project will deal only with the recovery stage, or Stage II, of the litigation. Consequently, the reader should assume that liability for employment discrimination has already been established in each of the cases discussed below. Before reaching the various procedural and substantive issues surrounding back pay awards, however, the Project, in part II, presents an over-view of the statutory authority for back pay including the legislative history of Title VII and section 1981. Part II also discusses the development of the appropriate standard for the exercise of judicial discretion in awarding back pay. Part III examines the parties liable for the payment of back pay. In part IV the Project explores presumptive eligibility for back pay and in part V considers possible grounds on which a defendant may seek to rebut the presumption. Parts VI and VII discuss the proof-of-claim procedure that must be followed by discriminatees claiming back pay and the procedure for determining individual awards. Part VIII then identifies and analyzes the various problems facing courts in allocating the burdens of proof that plaintiffs and defendants must meet before the court can determine individual awards. Following the discussion of the order and allocation of the burdens of proof, part IX outlines the various methods used by the courts to compute individual back pay awards and also discusses other issues such as the elements includable and deductible, the mitigation requirement,and the limitation periods for back pay. In part X the Special Project examines the problems that may arise when the parties agree to a settlement of back pay claims
Evaluating predictive pharmacogenetic signatures of adverse events in colorectal cancer patients treated with fluoropyrimidines
The potential clinical utility of genetic markers associated with response to fluoropyrimidine treatment in colorectal cancer patients remains controversial despite extensive study. Our aim was to test the clinical validity of both novel and previously identified markers of adverse events in a broad clinical setting. We have conducted an observational pharmacogenetic study of early adverse events in a cohort study of 254 colorectal cancer patients treated with 5-fluorouracil or capecitabine. Sixteen variants of nine key folate (pharmacodynamic) and drug metabolising (pharmacokinetic) enzymes have been analysed as individual markers and/or signatures of markers. We found a significant association between TYMP S471L (rs11479) and early dose modifications and/or severe adverse events (adjusted OR = 2.02 [1.03; 4.00], p = 0.042, adjusted OR = 2.70 [1.23; 5.92], p = 0.01 respectively). There was also a significant association between these phenotypes and a signature of DPYD mutations (Adjusted OR = 3.96 [1.17; 13.33], p = 0.03, adjusted OR = 6.76 [1.99; 22.96], p = 0.002 respectively). We did not identify any significant associations between the individual candidate pharmacodynamic markers and toxicity. If a predictive test for early adverse events analysed the TYMP and DPYD variants as a signature, the sensitivity would be 45.5 %, with a positive predictive value of just 33.9 % and thus poor clinical validity. Most studies to date have been under-powered to consider multiple pharmacokinetic and pharmacodynamic variants simultaneously but this and similar individualised data sets could be pooled in meta-analyses to resolve uncertainties about the potential clinical utility of these markers
Magnetothermodynamics of BPS baby skyrmions
The magnetothermodynamics of skyrmion type matter described by the gauged BPS
baby Skyrme model at zero temperature is investigated. We prove that the BPS
property of the model is preserved also for boundary conditions corresponding
to an asymptotically constant magnetic field. The BPS bound and the
corresponding BPS equations saturating the bound are found. Further, we show
that one may introduce pressure in the gauged model by a redefinition of the
superpotential. Interestingly, this is related to non-extremal type solutions
in the so-called fake supersymmetry method. Finally, we compute the equation of
state of magnetized BSP baby skyrmions inserted into an external constant
magnetic field and under external pressure , i.e., , where
is the "volume" (area) occupied by the skyrmions. We show that the BPS baby
skyrmions form a ferromagnetic medium.Comment: Latex, 39 pages, 14 figures. v2: New results and references added,
physical interpretation partly change
<i>Trypanosoma brucei rhodesiense</i> transmitted by a single tsetse fly bite in vervet monkeys as a model of human African trypanosomiasis
Sleeping sickness is caused by a species of trypanosome blood parasite that is transmitted by tsetse flies. To understand better how infection with this parasite leads to disease, we provide here the most detailed description yet of the course of infection and disease onset in vervet monkeys. One infected tsetse fly was allowed to feed on each host individual, and in all cases infections were successful. The characteristics of infection and disease were similar in all hosts, but the rate of progression varied considerably. Parasites were first detected in the blood 4-10 days after infection, showing that migration of parasites from the site of fly bite was very rapid. Anaemia was a key feature of disease, with a reduction in the numbers and average size of red blood cells and associated decline in numbers of platelets and white blood cells. One to six weeks after infection, parasites were observed in the cerebrospinal fluid (CSF), indicating that they had moved from the blood into the brain; this was associated with a white cell infiltration. This study shows that fly-transmitted infection in vervets accurately mimics human disease and provides a robust model to understand better how sleeping sickness develops
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