What’s Driving Food Prices in 2011?

Agricultural Finance, Demand and Price Analysis, Food Consumption/Nutrition/Food Safety,

Mitochondria Death/Survival Signaling Pathways in Cardiotoxicity Induced by Anthracyclines and Anticancer-Targeted Therapies

Anthracyclines remain the cornerstone of treatment in many malignancies but these agents have a cumulative dose relationship with cardiotoxicity. Development of cardiomyopathy and congestive heart failure induced by anthracyclines are typically dose-dependent, irreversible, and cumulative. Although past studies of cardiotoxicity have focused on anthracyclines, more recently interest has turned to anticancer drugs that target many proteins kinases, such as tyrosine kinases. An attractive model to explain the mechanism of this cardiotoxicity could be myocyte loss through cell death pathways. Inhibition of mitochondrial transition permeability is a valuable tool to prevent doxorubicin-induced cardiotoxicity. In response to anthracycline treatment, activation of several protein kinases, neuregulin/ErbB2 signaling, and transcriptional factors modify mitochondrial functions that determine cell death or survival through the modulation of mitochondrial membrane permeability. Cellular response to anthracyclines is also modulated by a myriad of transcriptional factors that influence cell fate. Several novel targeted chemotherapeutic agents have been associated with a small but worrying risk of left ventricular dysfunction. Agents such as trastuzumab and tyrosine kinase inhibitors can lead to cardiotoxicity that is fundamentally different from that caused by anthracyclines, whereas biological effects converge to the mitochondria as a critical target

ARE ECONOMIC FUNDAMENTALS DRIVING FARMLAND VALUES?

Farmland, Land Value, Agricultural Finance, Land Economics/Use, Q14, Q15,

The Purdue Center for Commercial Agriculture Crop Basis Tool

The Purdue Center for Commercial Agriculture Crop Basis Tool is an open-access web-based tool that provides members of the grain industry with access to weekly historical and contemporaneous corn and soybean basis data for local market regions in the eastern Corn Belt. Previously unavailable to most producers in the region, the information the Crop Basis Tool provides has the potential to greatly improve producers\u27 marketing risk management decisions through improved basis forecasts. In addition, there are a myriad of opportunities for Extension personnel to incorporate the Crop Basis Tool in their marketing risk management education and outlook programming

Widespread Inhibition of Posttranscriptional Splicing Shapes the Cellular Transcriptome following Heat Shock

During heat shock and other proteotoxic stresses, cells regulate multiple steps in gene expression in order to globally repress protein synthesis and selectively upregulate stress response proteins. Splicing of several mRNAs is known to be inhibited during heat stress, often meditated by SRp38, but the extent and specificity of this effect have remained unclear. Here, we examined splicing regulation genome-wide during heat shock in mouse fibroblasts. We observed widespread retention of introns in transcripts from ~1,700 genes, which were enriched for tRNA synthetase, nuclear pore, and spliceosome functions. Transcripts with retained introns were largely nuclear and untranslated. However, a group of 580+ genes biased for oxidation reduction and protein folding functions continued to be efficiently spliced. Interestingly, these unaffected transcripts are mostly cotranscriptionally spliced under both normal and stress conditions, whereas splicing-inhibited transcripts are mostly spliced posttranscriptionally. Altogether, our data demonstrate widespread repression of splicing in the mammalian heat stress response, disproportionately affecting posttranscriptionally spliced genes.Weizmann Institute of Science (Postdoctoral Award for Advancing Women in Science)European Molecular Biology Organization (Long-term Fellowship)Machiah FoundationNational Science Foundation (U.S.) (Grant 0821391)National Institutes of Health (U.S.

Exploring Paradigms of Human Resource Development

This study focused on the issue of paradigms in Human Resource Development (HRD). Its purpose was to validate the HRD Cube as a synthesized model of HRD and to explicate some of the extant paradigms of HRD. The study was carried out by examining the text of articles published in Academy of Human Resource Development (AHRD)-sponsored journals. Purposeful, stratified, and random sampling was used to select 16 articles published in AHRD-sponsored journals. Articles were treated as if they were the representative voice(s) of their author(s). Data units from within each article were identified and coded using two sequential techniques. First, units were axially coded and sorted into one of seven pre-determined categories based on the axioms of theory, research, and practice. Second, units were open coded using the constant comparative method, and themes and sub-themes were developed. Axial coding results identified a heavy emphasis on practice. The accumulation of units representing research and theory were comparatively smaller. Evidence of shared perspectives was found that emphasized the practice axiom. The accumulation of units emphasized research-practice, followed by theory-practice, and concluded with theory-research. Data units were also found that described all three axioms concurrently, theory-research-practice. Open coding results identified representative themes and sub-themes within each of the axiom-based categories of theory, research, and practice. Six themes developed in the theory category, 9 themes and 1 sub-theme developed in the research category, and 6 themes and 10 sub-themes developed in the practice category. The results provide evidence to support the overall construction of the HRD Cube. Theory, research, and practice perspectives of HRD were represented within the 16 articles used. The results also support the components described on each side of the HRD Cube. On the theory side, people, processes, and outcomes, and informing disciplines of HRD, were identified. Post-positive, interpretive, and critical epistemologies were identified on the research side. Individual, group, organizational, national, and global levels were identified on the practice side. Given the initial validation and support of the HRD Cube and of the components described within theory, research, and practice sides, within these 16 articles published in AHRD-sponsored journals, at least 18 prospective paradigms of HRD were identified

The prognostic value of derived neutrophil to lymphocyte ratio in oesophageal cancer treated with definitive chemoradiotherapy

Background and purpose The derived neutrophil–lymphocyte ratio (dNLR) is a validated prognostic biomarker for cancer survival but has not been extensively studied in locally-advanced oesophageal cancer treated with definitive chemoradiotherapy (dCRT). We aimed to identify the prognostic value of dNLR in patients recruited to the SCOPE1 trial. Materials and methods 258 patients were randomised to receive dCRT ± cetuximab. Kaplan–Meier’s curves and both univariable and multivariable Cox regression models were calculated for overall survival (OS), progression free survival (PFS), local PFS inside the radiation volume (LPFSi), local PFS outside the radiation volume (LPFSo), and distant PFS (DPFS). Results An elevated pre-treatment dNLR ≥ 2 was significantly associated with decreased OS in univariable (HR 1.74 [95% CI 1.29–2.35], p < 0.001) and multivariable analyses (HR 1.64 [1.17–2.29], p = 0.004). Median OS was 36 months (95% CI 27.8–42.4) if dNLR < 2 and 18.4 months (95% CI 14.1–24.9) if dNLR ≥ 2. All measures of PFS were also significantly reduced with an elevated dNLR. dNLR was prognostic for OS in cases of squamous cell carcinoma with a non-significant trend for adenocarcinoma/undifferentiated tumours. Conclusions An elevated pre-treatment dNLR may be an independent prognostic biomarker for OS and PFS in oesophageal cancer patients treated with definitive CRT. dNLR is a simple, inexpensive and readily available tool for risk-stratification and should be considered for use in future oesophageal cancer clinical trials

Mitochondria death/ survival signaling pathways in cardiotoxicity induced by anthracyclines and anticancer-targeted therapies. Biochem Res Int

Anthracyclines remain the cornerstone of treatment in many malignancies but these agents have a cumulative dose relationship with cardiotoxicity. Development of cardiomyopathy and congestive heart failure induced by anthracyclines are typically dosedependent, irreversible, and cumulative. Although past studies of cardiotoxicity have focused on anthracyclines, more recently interest has turned to anticancer drugs that target many proteins kinases, such as tyrosine kinases. An attractive model to explain the mechanism of this cardiotoxicity could be myocyte loss through cell death pathways. Inhibition of mitochondrial transition permeability is a valuable tool to prevent doxorubicin-induced cardiotoxicity. In response to anthracycline treatment, activation of several protein kinases, neuregulin/ErbB2 signaling, and transcriptional factors modify mitochondrial functions that determine cell death or survival through the modulation of mitochondrial membrane permeability. Cellular response to anthracyclines is also modulated by a myriad of transcriptional factors that influence cell fate. Several novel targeted chemotherapeutic agents have been associated with a small but worrying risk of left ventricular dysfunction. Agents such as trastuzumab and tyrosine kinase inhibitors can lead to cardiotoxicity that is fundamentally different from that caused by anthracyclines, whereas biological effects converge to the mitochondria as a critical target

Widespread Regulation of Translation by Elongation Pausing in Heat Shock

Global repression of protein synthesis is a hallmark of the cellular stress response and has been attributed primarily to inhibition of translation initiation, although this mechanism may not always explain the full extent of repression. Here, using ribosome footprinting, we show that 2 hr of severe heat stress triggers global pausing of translation elongation at around codon 65 on most mRNAs in both mouse and human cells. The genome-wide nature of the phenomenon, its location, and features of protein N termini suggested the involvement of ribosome-associated chaperones. After severe heat shock, Hsp70’s interactions with the translational machinery were markedly altered and its association with ribosomes was reduced. Pretreatment with mild heat stress or overexpression of Hsp70 protected cells from heat shock-induced elongation pausing, while inhibition of Hsp70 activity triggered elongation pausing without heat stress. Our findings suggest that regulation of translation elongation in general, and by chaperones in particular, represents a major component of cellular stress responses.National Institute of General Medical Sciences (U.S.) (NIGMS fellowship number F32GM095060)Machiah FoundationEuropean Molecular Biology Organization (EMBO long-term fellowship)Weitzmann Institute of Science (National Postdoctoral Award Program for Advancing Women in Science