Disabled Laborers And The Equal Employment Opportunity Commission’s (EEOCs) Nightmare

In 2012, EEOC v. Henry’s Turkey Service was one of the largest disability settlements in American history.  Henry’s Turkey Service was ordered to pay $240 million for paying mentally disabled workers with I.Q.s estimated in the 60-70 range, 41 cents per hour and housing them in unsafe housing and health conditions (Hsieh, 2013).  Over forty years, Henry’s Turkey Service relocated hundreds of mentally disabled workers from Texas to Iowa where they were subjected to horrendous living conditions with unlawful, minimal pay—about$65.00 per month, while they worked at a local turkey processing factory in West Liberty, Iowa.  The actual case shows a pattern of violations of the Fair Labor Standards Act of 1938 and Americans with Disability Act, 1990. After a raid of the bright blue, florescent colored, century old school house in Atalissa, Iowa, these employers were brought to justice.  This case study is about one of the largest EEOC settlements in the history of the United States; yet due to federal damage caps was cut to $1.6 million for all of the men and their estates. The graphic account of the inhumane treatment and degradation of the labors presented in this study is not provided for gratuitous or salacious purposes; rather, it places into context what can occur when governmental regulations and laws go unheeded, unenforced and when authorities are apprised of wrongdoing possibilities stand idly by and in this case, do nothing for 35 years.

The MHV68 M2 Protein Drives IL-10 Dependent B Cell Proliferation and Differentiation

Murine gammaherpesvirus 68 (MHV68) establishes long-term latency in memory B cells similar to the human gammaherpesvirus Epstein Barr Virus (EBV). EBV encodes an interleukin-10 (IL-10) homolog and modulates cellular IL-10 expression; however, the role of IL-10 in the establishment and/or maintenance of chronic EBV infection remains unclear. Notably, MHV68 does not encode an IL-10 homolog, but virus infection has been shown to result in elevated serum IL-10 levels in wild-type mice, and IL-10 deficiency results in decreased establishment of virus latency. Here we show that a unique MHV68 latency-associated gene product, the M2 protein, is required for the elevated serum IL-10 levels observed at 2 weeks post-infection. Furthermore, M2 protein expression in primary murine B cells drives high level IL-10 expression along with increased secretion of IL-2, IL-6, and MIP-1α. M2 expression was also shown to significantly augment LPS driven survival and proliferation of primary murine B cells. The latter was dependent on IL-10 expression as demonstrated by the failure of IL10−/− B cells to proliferate in response to M2 protein expression and rescue of M2-associated proliferation by addition of recombinant murine IL-10. M2 protein expression in primary B cells also led to upregulated surface expression of the high affinity IL-2 receptor (CD25) and the activation marker GL7, along with down-regulated surface expression of B220, MHC II, and sIgD. The cells retained CD19 and sIgG expression, suggesting differentiation to a pre-plasma memory B cell phenotype. These observations are consistent with previous analyses of M2-null MHV68 mutants that have suggested a role for the M2 protein in expansion and differentiation of MHV68 latently infected B cells—perhaps facilitating the establishment of virus latency in memory B cells. Thus, while the M2 protein is unique to MHV68, analysis of M2 function has revealed an important role for IL-10 in MHV68 pathogenesis—identifying a strategy that appears to be conserved between at least EBV and MHV68

Normal and abnormal development of the intrapericardial arterial trunks in humans and mice

The definitive cardiac outflow channels have three components: the intrapericardial arterial trunks; the arterial roots with valves; and the ventricular outflow tracts (OFTs). We studied the normal and abnormal development of the most distal of these, the arterial trunks, comparing findings in mice and humans. Using lineage tracing and three-dimensional visualization by episcopic reconstruction and scanning electron microscopy, we studied embryonic day 9.512.5 mouse hearts, clarifying the development of the OFTs distal to the primordia of the arterial valves. We characterize a transient aortopulmonary (AP) foramen, located between the leading edge of a protrusion from the dorsal wall of the aortic sac and the distal margins of the two outflow cushions. The foramen is closed by fusion of the protrusion, with its cap of neural crest cells (NCCs), with the NCC-filled cushions; the resulting structure then functioning transiently as an AP septum. Only subsequent to this closure is it possible to recognize, more proximally, the previously described AP septal complex. The adjacent walls of the intrapericardial trunks are derived from the protrusion and distal parts of the outflow cushions, whereas the lateral walls are formed from intrapericardial extensions of the pharyngeal mesenchyme derived from the second heart field. We provide, for the first time, objective evidence of the mechanisms of closure of an AP foramen that exists distally between the lumens of the developing intrapericardial arterial trunks. Our findings provide insights into the formation of AP windows and the variants of common arterial trun