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

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

Predicting Ascospore Release of Monilinia vaccinii-corymbosi of Blueberry with Machine Learning

Mummy berry, caused by Monilinia vaccinii-corymbosi, causes economic losses of highbush blueberry in the U.S. Pacific Northwest (PNW). Apothecia develop from mummified berries overwintering on soil surfaces and produce ascospores that infect tissue emerging from floral and vegetative buds. Disease control currently relies on fungicides applied on a calendar basis rather than inoculum availability. To establish a prediction model for ascospore release, apothecial development was tracked in three fields, one in western Oregon and two in northwestern Washington in 2015 and 2016. Air and soil temperature, precipitation, soil moisture, leaf wetness, relative humidity and solar radiation were monitored using in-field weather stations and Washington State University's AgWeatherNet stations. Four modeling approaches were compared: logistic regression, multivariate adaptive regression splines, artificial neural networks, and random forest. A supervised learning approach was used to train the models on two data sets: training (70%) and testing (30%). The importance of environmental factors was calculated for each model separately. Soil temperature, soil moisture, and solar radiation were identified as the most important factors influencing ascospore release. Random forest models, with 78% accuracy, showed the best performance compared with the other models. Results of this research helps PNW blueberry growers to optimize fungicide use and reduce production costs

A Framework to Reduce Infectious Disease Risk from Urban Poultry in the United States

ObjectivesBackyard poultry ownership is increasingly common in U.S. cities and is regulated at the local level. Human contact with live poultry is a well-known risk for infection with zoonotic pathogens, notably Salmonella, yet the ability of local jurisdictions to reduce the risk of infectious disease transmission from poultry to humans is unstudied. We reviewed urban poultry ordinances in the United States and reported Salmonella outbreaks from backyard poultry to identify regulatory gaps in preventing zoonotic pathogen transmission. Based on this analysis, we propose regulatory guidelines for U.S. cities to reduce infectious disease risk from backyard poultry ownership.MethodsWe assessed local ordinances in the 150 most populous U.S. jurisdictions for content related to noncommercial poultry ownership using online resources and communications with government officials. We also performed a literature review using publicly available data sources to identify human infectious disease outbreaks caused by contact with backyard poultry.ResultsOf the cities reviewed, 93% (n=139) permit poultry in some capacity. Most urban poultry ordinances share common characteristics focused on reducing nuisance to neighbors. Ordinances do not address many pathways of transmission relevant to poultry-to-human transmission of pathogens, such as manure management.ConclusionsTo reduce the risk of pathogen exposure from backyard poultry, urban ordinances should incorporate the following seven components: limited flock size, composting of manure in sealed containers, prohibition of slaughter, required veterinary care to sick birds, appropriate disposal of dead birds, annual permits linked to consumer education, and a registry of poultry owners

Association of WNK1 gene polymorphisms and haplotypes with ambulatory blood pressure in the general population

Background — Blood pressure (BP) is a heritable trait of major public health concern. The WNK1 and WNK4 genes, which encode proteins in the WNK family of serine-threonine kinases, are involved in renal electrolyte homeostasis. Mutations in the WNK1 and WNK4 genes cause a rare monogenic hypertensive syndrome, pseudohypoaldosteronism type II. We investigated whether polymorphisms in these WNK genes influence BP in the general population Methods and Results— Associations between 9 single-nucleotide polymorphisms (SNPs) in WNK1 and 1 in WNK4 with ambulatory BP were studied in a population-based sample of 996 subjects from 250 white European families. The heritability estimates of mean 24-hour systolic BP (SBP) and diastolic BP (DBP) were 63.4% and 67.9%, respectively. We found statistically significant (P<0.05) associations of several common SNPs and haplotypes in WNK1 with mean 24-hour SBP and/or DBP. The minor allele (C) of rs880054, with a frequency of 44%, reduced mean 24-hour SBP and DBP by 1.37 (95% confidence interval, –2.45 to –0.23) and 1.14 (95% confidence interval, –1.93 to –0.38) mm Hg, respectively, per copy of the allele. Conclusions— Common variants in WNK1 contribute to BP variation in the general population. This study shows that a gene causing a rare monogenic form of hypertension also plays a significant role in BP regulation in the general population. The findings provide a basis to identify functional variants of WNK1, elucidate any interactions of these variants with dietary intake or with response to antihypertensive drugs, and determine their impact on cardiovascular morbidity and mortality