Did Producer Hedging Opportunities in the Live Hog Contract Decline?

The paper assesses the usefulness of selective hedging strategies when combined with forecast techniques in the live hog contract. The use of routine futures and options hedging is not attractive relative to a cash-only strategy. However, forecasting and hedging can contribute to price risk management improvement for risk-averse producers. Consistent with previous research, the results indicate that the live hog contract continues to offer producers attractive pricing opportunities. The findings suggests that the success of the new lean value carcass contract may depend on its ability to attract trading volume from outside the traditional production sector.hedging, forecasting, risk management, live hog futures, lean hog futures

CROP INSURANCE VALUATION UNDER ALTERNATIVE YIELD DISTRIBUTIONS

Considerable disagreement exists about the most appropriate characterization of farm-level yield distributions. Yet, the economic importance of alternate yield distribution specifications on insurance valuation, product designs and farm-level risk management has not been investigated or documented. The results of this study demonstrate that large differences in expected payments from popular crop insurance products can arise solely from the parameterization chosen to represent yields. The results suggest that the frequently unexamined yield distribution specification may lead to incorrect conclusions in important areas of insurance and risk management research such as policy rating, and assessment of expected payments from policies.Risk and Uncertainty,

ESTIMATING FARM-LEVEL YIELD DISTRIBUTIONS FOR CORN AND SOYBEANS IN ILLINOIS

Many yield modeling approaches have been developed in attempts to provide accurate characterizations of farm-level yield distributions due to the importance of yield uncertainty in crop insurance design and rating, and for managing farm-level risk. Competing existing models of crop yields accommodate varying skewness, kurtosis, and other departures from normality including features such as multiple modes. Recently, the received view of crop yield modeling has been challenged by Just and Weninger who indicate that there is insufficient evidence to reject normality given data limitations and potential methodological shortcomings in controlling for deterministic components (trend) in yields. They point out that past empirical efforts to estimate and validate specific-farm distributional characterizations have been severely hampered by data limitations. As a result, they argue in favor of normality as an appropriate parameterization of crop yields. This paper investigates alternate representations of farm-level crop yield distributions using a unique data set from the University of Illinois Endowment farms, containing same-site yield observations for a relatively long period of time, and under conditions that closely mirror actual farm conditions in Illinois. Results from alternate econometric model specifications controlling for trend effects suggest that a linear trend provides an adequate representation of crop yields at the farm level during the period covered by the estimations. Specification tests based on a linear-trend model suggest significant heteroskedasticity is present in only a few farms, and that the residuals are white noise. With these data, Jarque-Bera normality test results indicate that normality of detrended yield residuals is rejected by a far greater number of fields than would be explained due to randomness. Thus, to further clarify the issue of yield distribution characterizations, more complete goodness-of-fit measures are compared across a larger set of candidate distributions. The results indicate that the Weibull distribution consistently ranks better than the normal distribution both in fields where normality is rejected and in fields where normality is not rejected. The results highlight the fact that failing to reject normality is not the same as identifying normality as a "best" parameterization, and provide guidance for progressing toward better representations of farm-level crop yields.Productivity Analysis, Research Methods/ Statistical Methods, Teaching/Communication/Extension/Profession,

An agonistic anti-CD137 antibody disrupts lymphoid follicle structure and T-cell-dependent antibody responses

CD137 is a costimulatory receptor expressed on natural killer cells, T cells, and subsets of dendritic cells. An agonistic monoclonal antibody (mAb) against CD137 has been used to reduce tumor burden or reverse autoimmunity in animal models and clinical trials. Here, we show that mice treated with an agonistic anti-CD137 mAb have reduced numbers of germinal center (GC) B cells and follicular dendritic cells (FDCs) in lymphoid tissues, which impair antibody responses to multiple T-cell-dependent antigens, including infectious virus, viral proteins, and conjugated haptens. These effects are not due to enhanced apoptosis or impaired proliferation of B cells but instead correlate with changes in lymphoid follicle structure and GC B cell dispersal and are mediated by CD137 signaling in CD

An agonistic anti-CD137 antibody disrupts lymphoid follicle structure and T-cell-dependent antibody responses

CD137 is a costimulatory receptor expressed on natural killer cells, T cells, and subsets of dendritic cells. An agonistic monoclonal antibody (mAb) against CD137 has been used to reduce tumor burden or reverse autoimmunity in animal models and clinical trials. Here, we show that mice treated with an agonistic anti-CD137 mAb have reduced numbers of germinal center (GC) B cells and follicular dendritic cells (FDCs) in lymphoid tissues, which impair antibody responses to multiple T-cell-dependent antigens, including infectious virus, viral proteins, and conjugated haptens. These effects are not due to enhanced apoptosis or impaired proliferation of B cells but instead correlate with changes in lymphoid follicle structure and GC B cell dispersal and are mediated by CD137 signaling in CD

A multipronged approach to unveil the emerging role of Hsp60 in chronic obstructive pulmonary disease

Inflammation is a major component of chronic obstructive pulmonary disease (COPD) and its cause and mechanisms are still incompletely understood. For example, the role of heat shock proteins (Hsps), many of which are molecular chaperones, has not been explored in detail in COPD, despite the fact that these molecules are known to participate in inflammation in other diseases. It has been shown that extracellular Hsps can signal certain types of T cells, macrophages, dendritic cells, and neutrophils and, thereby, elicit inflammation and immunity. However, these phenomena have not been investigated in COPD despite: a) the increasing awareness of Hsp participation in inflammation and immunity; and b) the fact that this disease is waiting for new knowledge to benefit from effective treatment and continues to be one of the commonest and most serious illnesses in the Western countries. We developed a strategy to study Hsps in COPD involving a multipronged approach, using in vivo and in vitro methods, which would, at least in part, compensate for the limitations inherent to the analysis of human diseases. We determined the levels of six Hsps in bronchial mucosa biopsies, as well as several inflammatory markers, from patients at various stages compared to smoker and non-smoker controls by immunohistochemistry, and found significant increase of Hsp60, Hsp10, and Hsp40 in COPD but no changes for Hsp27, Hsp70 and Hsp90. We also found that the increase in Hsp60 positively correlated with number of neutrophils, and it localized in them. Hsp60 has been implicated in human inflammatory pathology; hence it was pertinent to investigate whether the chaperonin originated only in the neutrophils or also in other cells. In vitro experiments showed that in bronchial epithelial cells submitted to oxidative stress, a characteristic of COPD mucosa, Hsp60 was overexpressed and was released into the extracellular medium. Other measurements indicated that NFkB-p65 was involved in the hsp60-gene upregulation whereas HSF-1 apparently was not. All the data we obtained using a battery of complementary in vivo and in vitro methods coincided to indicate that Hsp60 plays an active role in inflammation in COPD. Hence, one can infer that the chaperonin does contribute to the etiology and/or pathogenesis of COPD and that it is pertinent to investigate this aspect of Hsp60 biology-COPD pathology with renewed intensity. The results could have a significant impact on the developing of strategies for diagnosis, determining prognosis, and treatment that should be centered on Hsp60

CD4+ T Cell Depletion, Immune Activation and Increased Production of Regulatory T Cells in the Thymus of HIV-Infected Individuals

Mechanisms by which HIV affects the thymus are multiple and only partially known, and the role of thymic dysfunction in HIV/AIDS immunopathogenesis remains poorly understood. To evaluate the effects of HIV infection on intra-thymic precursors of T cells in HIV-infected adults, we conducted a detailed immunophenotypic study of thymic tissue isolated from 7 HIV-infected and 10 HIV-negative adults who were to undergo heart surgery. We found that thymuses of HIV-infected individuals were characterized by a relative depletion of CD4+ single positive T cells and a corresponding enrichment of CD8+ single positive T cells. In addition, thymocytes derived from HIV-infected subjects showed increased levels of activated and proliferating cells. Our analysis also revealed a decreased expression of interleukin-7 receptor in early thymocytes from HIV-infected individuals, along with an increase in this same expression in mature double- and single-positive cells. Frequency of regulatory T cells (CD25+FoxP3+) was significantly increased in HIV-infected thymuses, particularly in priorly-committed CD4 single positive cells. Our data suggest that HIV infection is associated with a complex set of changes in the immunophenotype of thymocytes, including a reduction of intrathymic CD4+ T cell precursors, increased expression of activation markers, changes in the expression pattern of IL-7R and enrichment of T regulatory cells generation

Convergent Sets of Data from In Vivo and In Vitro Methods Point to an Active Role of Hsp60 in Chronic Obstructive Pulmonary Disease Pathogenesis

BACKGROUND: It is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses. METHODS AND RESULTS: Bronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between the number of neutrophils and Hsp60 levels. Double-immunostaining showed that Hsp60-positive neutrophils were significantly increased in COPD patients. We then investigated in vitro the effect on Hsp60 expression in bronchial epithelial cells (16HBE) caused by oxidative stress, a hallmark of COPD mucosa, which we induced with H\u2082O\u2082. This stressor determined increased levels of Hsp60 through a gene up-regulation mechanism involving NFkB-p65. Release of Hsp60 in the extracellular medium by the bronchial epithelial cells was also increased after H\u2082O\u2082 treatment in the absence of cell death. CONCLUSIONS: This is the first report clearly pointing to participation of Hsps, particularly Hsp60, in COPD pathogenesis. Hsp60 induction by NFkB-p65 and its release by epithelial cells after oxidative stress can have a role in maintaining inflammation, e.g., by stimulating neutrophils activity. The data open new scenarios that might help in designing efficacious anti-inflammatory therapies centered on Hsp60 and applicable to COP