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This book serves as an introduction to the ongoing political debate about the relationship of capitalism and democracy. In recent years, the ideological battles between advocates of free markets and minimal government, on the one hand, and adherents of greater democratic equality and some form of the welfare state, on the other hand, have returned in full force. Anyone who wants to make sense of contemporary American politics and policy battles needs to have some understanding of the divergent beliefs and goals that animate this debate. In Capitalism and Democracy , Thomas A. Spragens, Jr., examines the opposing sides of the free market versus welfare state debate through the lenses of political economy, moral philosophy, and political theory. He asks: Do unchecked markets maximize prosperity, or do they at times produce wasteful and damaging outcomes? Are market distributions morally appropriate, or does fairness require some form of redistribution? Would a society of free markets and minimal government be the best kind of society possible, or would it have serious problems? After leading the reader through a series of thought experiments designed to compare and clarify the thought processes and beliefs held by supporters of each side, Spragens explains why there are no definitive answers to these questions. He concludes, however, that some answers are better than others, and he explains why his own judgement is that a vigorous free marketplace provides great benefits to a democratic society, both economically and politically, but that it also requires regulation and supplementation by collective action for a society to maximize prosperity, to mitigate some of the unfairness of the human condition, and to be faithful to important democratic purposes and ideals. This engaging and accessible book will interest students and scholars of political economy, democratic theory, and theories of social justice. It will also appeal to general readers who are seeking greater clarity and understanding of contemporary debates about government's role in the economy.

The epidemic of opioid abuse is related in part to incomplete understanding of pain-relief management, opioid tolerance, and opioid addiction. Among the prevention strategies are more widespread sharing of data about opioid neuropharmacology and opioid-use patterns. Chronic pain not caused by cancer is among the most prevalent and debilitating medical conditions but also among the most controversial and complex to manage. The urgency of patients’ needs, the demonstrated effectiveness of opioid analgesics for the management of acute pain, and the limited therapeutic alternatives for chronic pain have combined to produce an overreliance on opioid medications in the United States, with associated alarming increases in diversion, overdose, and addiction. Given the lack of clinical consensus and research-supported guidance, physicians understandably have questions about whether, when, and how to prescribe opioid analgesics for chronic pain without increasing public . . .

ABSTRACT To infer adaptation of plant material, restoration practitioners often consider only surrogate geographic or climatic information. However, empirical biomass data could assist in deciding what material to use where. To test this approach, we transplanted seven bluebunch wheatgrass (BBWG; Pseudoroegneria spicata) and five Snake River wheatgrass (SRWG; Elymus wawawaiensis) populations to three sites ranging from low to high precipitation (LPPT, MPPT, and HPPT). We measured establishment‐year (2011) biomass at all sites and 2012–16 biomass at MPPT and HPPT. When data were standardized by site, P‐7 and Anatone produced the most BBWG biomass across sites and Wahluke the least in both 2011 and 2012–16, while E‐58X produced the most SRWG biomass and Secar and E‐49X the least in 2011 and 2012–16, respectively. Among BBWG populations in 2011, relative performance of P‐7 (G6 generation) and Goldar increased and Whitmar decreased at wetter sites, while Columbia was stable (high) and Wahluke was stable (low) over sites. Among SRWG populations in 2011, Secar, Secar78, and E‐58X increased at drier sites and Discovery at wetter sites. However, once established, populations of both species were much more similar for trend. In 2012–16, trend somewhat increased for five BBWG populations from MPPT to HPPT, was stable for Wahluke, but declined for Columbia, while all five SRWG populations declined at HPPT. These results suggest that, once established, BBWG is mostly stable across sites, while SRWG is less adapted to wetter sites. In 2012–16, BBWG populations originating at drier (or wetter) sites mostly performed relatively better at MPPT (or HPPT), suggesting adaptation to site. However, in the establishment year (2011), this relationship did not hold, suggesting seedling vigor and immature growth rate play a stronger role than precipitation at the site of origin. Plant materials can be characterized for adaptation to various potential restoration environments through prior testing. This may be more predictive than surrogate site measures of geographical, climatic, or soils data.

Key Points Although the type 2 cytokine response has many important host-protective functions, dysregulated, chronic or hyperreactive type 2 immunity can contribute to the development of disease. Type 2 cytokines are crucial to the pathogenesis of many allergic and fibrotic diseases, they suppress the development of protective type 1 immunity to a wide range of viral, bacterial and protozoan pathogens, and they can promote tumorigenesis and tumour cell growth. As dysregulated type 2 immune responses are major drivers of disease, the mechanisms that control the intensity, maintenance and resolution of type 2 immunity are probably important regulators of disease progression. Several endogenous regulatory mechanisms work collaboratively to prevent or to limit the pathological consequences of sustained type 2 immunity. Inflammatory monocytes and tissues macrophages have emerged as important regulators of established type 2 immune responses. Therapeutic strategies that disrupt the recruitment, the expansion or maintenance of crucial myeloid cell populations could emerge as novel therapeutic approaches for a variety of type 2-driven diseases. Interferon-γ- and interleukin-4 (IL-4)- and/or IL-13-activated macrophages antagonize type 2 inflammation and fibrosis by competing with activated myofibroblasts that require the metabolites l-arginine and l-proline for collagen synthesis. IL-4- and/or IL-13-primed macrophages expressing arginase 1 also inhibit IL-13-driven fibrosis by suppressing the proliferation and the expansion of the CD4 + T helper 2 (T H 2) cell population. The IL-13 decoy receptor (IL-13Rα2), the immunosuppressive cytokine IL-10 and type 1 cytokines collaboratively suppress the development of type 2 cytokine-driven disease and immunity. Therapeutic strategies targeting type 2 cytokine signalling pathways, eosinophil development and recruitment, epithelial cell-derived alarmins, prostaglandins and regulatory T (T Reg ) cell activity are at different stages of development for type 2-driven disease. The type 2 cytokine response provides important host-protective functions, but dysregulated type 2 immune responses can contribute to the development of disease. In this Review, the author describes the regulatory mechanisms that limit the pathological consequences of persistent type 2 immunity. Type 2 immune responses are defined by the cytokines interleukin-4 (IL-4), IL-5, IL-9 and IL-13, which can either be host protective or have pathogenic activity. Type 2 immunity promotes antihelminth immunity, suppresses type 1-driven autoimmune disease, neutralizes toxins, maintains metabolic homeostasis, and regulates wound repair and tissue regeneration pathways following infection or injury. Nevertheless, when type 2 responses are dysregulated, they can become important drivers of disease. Type 2 immunity induces a complex inflammatory response characterized by eosinophils, mast cells, basophils, type 2 innate lymphoid cells, IL-4-and/or IL-13-conditioned macrophages and T helper 2 (T H 2) cells, which are crucial to the pathogenesis of many allergic and fibrotic disorders. As chronic type 2 immune responses promote disease, the mechanisms that regulate their maintenance are thought to function as crucial disease modifiers. This Review discusses the many endogenous negative regulatory mechanisms that antagonize type 2 immunity and highlights how therapies that target some of these pathways are being developed to treat type 2-mediated disease.

One of the central aims in Alzheimer’s disease (AD) research is the identification of clinically relevant drug targets. A plethora of potential molecular targets work very well in preclinical model systems both in vitro and in vivo in AD mouse models. However, the lack of translation into clinical settings in the AD field is a challenging endeavor. Although it is long known that N-terminally truncated and pyroglutamate-modified Abeta (AβpE3) peptides are abundantly present in the brain of AD patients, form stable and soluble low-molecular weight oligomers, and induce neurodegeneration in AD mouse models, their potential as drug target has not been generally accepted in the past. This situation has dramatically changed with the report that passive immunization with donanemab, an AβpE3-specific antibody, cleared aymloid plaques and stabilized cognitive deficits in a group of patients with mild AD in a phase II trial. This review summarizes the current knowledge on the molecular mechanisms of generation of AβpE, its biochemical properties, and the intervention points as a drug target in AD.