Killing Kindly: Applying Jens Timmermann\u27s Kantian Ethics of Animal Welfare to the Modern System of Livestock Farming

This essay seeks to contribute to this conversation in an ethically applicable way, addressing specifically the Kantian vein of animal welfare discussed by Dr. Jens Timmermann in his essay When the Tail Wags the Dog: Animal Welfare and Indirect Duty in Kantian Ethics. In Part I, I will examine the work Timmermann undertakes to extend greater protection to animals under Kantian ethics. I will also raise a critical question concerning Timmermann’s unwillingness to apply his advancements to the animal welfare problems in our modern world. In Part II, I will attempt to apply Timmermann’s conclusions to the question of using domesticated animals for food. Therein I will demonstrate that, under Timmermann’s Kantian ethics, the use of sentient animals to meet nutritional needs is morally acceptable. I will also posit an answer to the inquiry raised in Part I. Finally, in Part III I will then expand the applicability of Timmermann’s ethics by stipulating a list of necessary conditions in rearing domesticated livestock, so as to ensure the process is morally permissible

Administrative Law Judge Upholds FTC Complaint Ordering Evanston NorthwesternHealthcare Corporation to Unwind Five-Year-Old Acquisition

On October 21, 2005, the Federal Trade Commission (FTC) announced that Administrative Law Judge Stephen J. McGuire had ordered Evanston Northwestern Healthcare Corporation (ENH) to divest Highland Park Hospital, located in a Chicago suburb. (The decision can be found at http://www.ftc. gov/os/adjpro/d9315/051021idtextversion. pdf.) ENH had acquired Highland Park five years ago for $200 million. In an administrative complaint issued in February 2004, the FTC alleged that the acquisition had resulted in substantially lessened competition and higher prices for insurers and healthcare consumers for general acute care inpatient services sold to managed care organizations. In upholding part of the complaint, Judge McGuire evaluated post-acquisition evidence that ENH exercised its enhanced post-merger market power to obtain price increases significantly above its premerger prices and substantially larger than price increases obtained by other comparison hospitals. (ENH has filed notice that it will appeal the judge’s initial decision to the full Commission.

From pathobiology to targeted treatment in Epstein Barr virus related T cell and Natural Killer cell lymphoproliferative diseases

Epstein Barr virus (EBV), a gamma-1 herpesvirus, establishes a life-long latent infection in the majority of individuals worldwide. Whilst this seemingly innocuous virus is carried as an asymptomatic infection of memory B cells, EBV is paradoxically linked to two pre-malignant lymphoproliferative diseases (LPDs) and up to nine aetiologically distinct human tumours, accounting for up to 200,000 cancers per year. Although these malignancies primarily occur in B cells and epithelial cells, correlating with the natural tropism of the virus, on rare occasions EBV also infects T and NK cells leading to various pre-malignant LPDs, lymphomas and leukaemia. These conditions are often highly aggressive and are associated with hyperinflammation and organ dysfunction leading to substantial mortality. While, in recent years improvements in chemotherapy, especially asparaginase based regimens, have led to improved outcomes for some, these conditions are often intrinsically chemoresistant with allograft often providing the only curative option. In this review, we address the impact of genetic and epigenetic changes on the pathogenesis of the T/NK cell LPDs and bring together an analysis of recent clinical trials attempting to target these processes. We describe the main molecular characteristics across the range of EBV-associated T/NK cell diseases, from somatic mutations effecting epigenetic regulators seen across EBV related T/NK LPD subtypes to the marked dysregulation of the JAK-STAT-MYC axis observed in higher grade disease such as extranodal NK/T lymphoma (ENKTL). We then go on to analyse the novel therapeutic options available including immunomodulation and small molecule inhibitors. While these approaches show promise in early phase trials there is still much scope for improvement and a need to better understand the pathophysiology to design rational combination treatments

Patterns and drivers of nearshore particulate organic matter composition

Suspended particulate organic matter (POM) is a primary food source for benthic and pelagic suspension feeders in aquatic ecosystems. POM is potentially composed of many sources, including phytoplankton, bacteria, zooplankton, and macrophyte (seaweed and seagrass) and terrestrial detritus. The relative importance of these sources to POM consumers is debated, in large part due to differing interpretations of stable isotope and fatty acid biomarkers. We investigated POM composition in the San Juan Archipelago using multiple methods including visual quantification of living and detrital components, multiple stable isotope (MSI) and fatty acid (FA) analyses. Sampling was conducted at multiple temporal and spatial scales to 1) determine the range of variation in POM biomarkers, 2) quantitatively compare δ13C, δ15N, δ34S and FA biomarkers with putative sources and 3) identify drivers of variation in POM composition. Using multivariate multiple regressions, MSI and FA explained 59.6% and 89.7% of the variation in POM composition, respectively. Variation of total FA concentration and proportions, and of δ13C and δ34S were strongly correlated to phytoplankton abundance. When phytoplankton were rare, bacterial FA were proportionally more abundant and corresponded to depletion of δ13C and δ34S and enrichment of δ15N. We observed a similar range of variation in phytoplankton biomass and biomarker composition at tidal (hourly) and seasonal time scales. Underlying the tidal and seasonal were strong correlations of POM composition and total FA concentration to salinity and temperature; decreased salinity was associated with an increase in the contribution marine of marine phytoplankton. These results suggest that temperature and salinity may be useful indicators for assessing marine primary production in the Salish Sea. This multi-scale study showed that POM composition is highly dynamic and largely driven by environmental controls on phytoplankton abundance

Deciphering the roles of myeloid derived suppressor cells in viral oncogenesis

Myeloid derived suppressor cells (MDSCs) are a heterogenous population of myeloid cells derived from monocyte and granulocyte precursors. They are pathologically expanded in conditions of ongoing inflammation where they function to suppress both innate and adaptive immunity. They are subdivided into three distinct subsets: monocytic (M-) MDSC, polymorphonuclear (or neutrophilic) (PMN-) MDSC and early-stage (e-) MDSC that may exhibit differential function in different pathological scenarios. However, in cancer they are associated with inhibition of the anti-tumour immune response and are universally associated with a poor prognosis. Seven human viruses classified as Group I carcinogenic agents are jointly responsible for nearly one fifth of all human cancers. These viruses represent a large diversity of species, including DNA, RNA and retroviridae. They include the human gammaherpesviruses (Epstein Barr virus (EBV) and Kaposi's Sarcoma-Associated Herpesvirus (KSHV), members of the high-risk human papillomaviruses (HPVs), hepatitis B and C (HBV, HCV), Human T cell leukaemia virus (HTLV-1) and Merkel cell polyomavirus (MCPyV). Each of these viruses encode an array of different oncogenes that perturb numerous cellular pathways that ultimately, over time, lead to cancer. A prerequisite for oncogenesis is therefore establishment of chronic infection whereby the virus persists in the host cells without being eradicated by the antiviral immune response. Although some of the viruses can directly modulate the immune response to enable persistence, a growing body of evidence suggests the immune microenvironment is modulated by expansions of MDSCs, driven by viral persistence and oncogenesis. It is likely these MDSCs play a role in loss of immune recognition and function and it is therefore essential to understand their phenotype and function, particularly given the increasing importance of immunotherapy in the modern arsenal of anti-cancer therapies. This review will discuss the role of MDSCs in viral oncogenesis. In particular we will focus upon the mechanisms thought to drive the MDSC expansions, the subsets expanded and their impact upon the immune microenvironment. Importantly we will explore how MDSCs may modulate current immunotherapies and their impact upon the success of future immune-based therapies.</p