How Agricultural Economists Increase the Value of Agribusiness Research

Historically, there has been declining cooperation between agribusiness firms and agricultural economists. In new product marketing research, firms' tend to conduct their own analyses, partially due to confidentiality, usually consisting of simple univariate or bivariate statistics such as chi-squared tests of independence. The primary objective of this paper is to demonstrate, through a case study, one way in which agricultural economists can add value to agribusiness firms research. Results from the econometric model offer a richer explanation of consumer behavior and may be more useful to agribusiness firms.Teaching/Communication/Extension/Profession,

Choice in Computer-Mediated Environments

In the last several years, the increased diffusion of computer andtelecommunications technologies in businesses and homes has produced newways for organizations to connect with their customers. These computermediated environments (CMEs) such as the World Wide Web raise new researchquestions. In this paper, we examine the potential research issuesassociated with CMEs in five areas: (1) decision processes, (2) advertisingand communications, (3) brand choice, (4) brand communities, and (5)pricing.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47229/1/11002_2004_Article_138117.pd

Prevention, health care Access & Risk Taking in Young people - evidence for ‘youth friendly’ interventions in primary care

APHCRI Conversations was a regular program of presentations held at the Department of Health to facilitate exchange between APHCRI Network researchers and Department policymakers. Topics are developed jointly with the Department of Health and involve a range of speakers from APHCRI, including CRE invited experts, CRE Chief Investigators and stream project Chief Investigator

Deaths in young people after contact with the youth justice system: a retrospective data linkage study

Introduction Young people who have contact with the youth justice system are distinguished by a high prevalence of complex, co-occurring health problems, including known risk factors for preventable mortality. However, almost nothing is known about health outcomes for these young people after separation from the youth justice system. Objectives and Approach We aimed to examine the incidence, timing, causes and risk factors for death in justice-involved young people. We linked youth justice records in Queensland, Australia 1993-2016 (N=48,963) with adult correctional records and the National Death Index. We split the cohort into three subgroups: those who had ever been in detention (n=7,643), those supervised in the community but never detained (n=12,953), and those charged with an offence but never convicted (n=28,367). We calculated all-cause and cause-specific crude mortality rates (CMRs), and indirectly standardised mortality ratios (SMRs). We used Cox regression to identify static and time-varying risk factors for death. Results During a median of 13.6 years of follow-up there were 1,452 deaths (3.0%). The all-cause CMR was 2.2 (95%CI 2.1-2.3) per 1000 person-years, and the all-cause SMR was 3.1 (95%CI 3.0-3.3). The leading external causes of death were suicide (32% of all deaths), transport accidents (16%), accidental drug-related causes (13%), and violence (3%). In adjusted analyses, independent risk factors for all-cause mortality included being male (HR=1.4, 95%CI 1.2-1.6) and older (>=15 vs. vs. charge only; HR=1.6, 95%CI 1.2-2.0) and subsequent incarceration as an adult (HR=1.8, 95%CI 1.4-2.4). Conclusion/Implications Young people who have contact with the youth justice system are at markedly increased risk of preventable death, after separation from that system. Efforts to improve long-term health outcomes for justice-involved youth have the potential to reduce preventable deaths in these highly vulnerable young people

What’s Next for Acute Heart Failure Research?

Each year over one million patients with acute heart failure (AHF) present to a United States emergency department (ED). The vast majority are hospitalized for further management. The length of stay and high postdischarge event rate in this cohort have changed little over the past decade. Therapeutic trials have failed to yield substantive improvement in postdischarge outcomes; subsequently, AHF care has changed little in the past 40 years. Prior research studies have been fragmented as either “inpatient” or “ED-based.” Recognizing the challenges in identification and enrollment of ED patients with AHF, and the lack of robust evidence to guide management, an AHF clinical trials network was developed. This network has demonstrated, through organized collaboration between cardiology and emergency medicine, that many of the hurdles in AHF research can be overcome. The development of a network that supports the collaboration of acute care and HF researchers, combined with the availability of federally funded infrastructure, will facilitate more efficient conduct of both explanatory and pragmatic trials in AHF. Yet many important questions remain, and in this document our group of emergency medicine and cardiology investigators have identified four high-priority research areas

Clinical and Research Considerations for Patients with Hypertensive Acute Heart Failure

Management approaches for patients in the emergency department (ED) who present with acute heart failure (AHF) have largely focused on intravenous diuretics. Yet, the primary pathophysiologic derangement underlying AHF in many patients is not solely volume overload. Patients with hypertensive AHF (H-AHF) represent a clinical phenotype with distinct pathophysiologic mechanisms that result in elevated ventricular filling pressures. To optimize treatment response and minimize adverse events in this subgroup, we propose that clinical management be tailored to a conceptual model of disease based on these mechanisms. This consensus statement reviews the relevant pathophysiology, clinical characteristics, approach to therapy, and considerations for clinical trials in ED patients with H-AHF

Massive migration from the steppe is a source for Indo-European languages in Europe

We generated genome-wide data from 69 Europeans who lived between 8,000-3,000 years ago by enriching ancient DNA libraries for a target set of almost four hundred thousand polymorphisms. Enrichment of these positions decreases the sequencing required for genome-wide ancient DNA analysis by a median of around 250-fold, allowing us to study an order of magnitude more individuals than previous studies and to obtain new insights about the past. We show that the populations of western and far eastern Europe followed opposite trajectories between 8,000-5,000 years ago. At the beginning of the Neolithic period in Europe, ~8,000-7,000 years ago, closely related groups of early farmers appeared in Germany, Hungary, and Spain, different from indigenous hunter-gatherers, whereas Russia was inhabited by a distinctive population of hunter-gatherers with high affinity to a ~24,000 year old Siberian6 . By ~6,000-5,000 years ago, a resurgence of hunter-gatherer ancestry had occurred throughout much of Europe, but in Russia, the Yamnaya steppe herders of this time were descended not only from the preceding eastern European hunter-gatherers, but from a population of Near Eastern ancestry. Western and Eastern Europe came into contact ~4,500 years ago, as the Late Neolithic Corded Ware people from Germany traced ~3/4 of their ancestry to the Yamnaya, documenting a massive migration into the heartland of Europe from its eastern periphery. This steppe ancestry persisted in all sampled central Europeans until at least ~3,000 years ago, and is ubiquitous in present-day Europeans. These results provide support for the theory of a steppe origin of at least some of the Indo-European languages of Europe

Plasmodium falciparum Rosetting Epitopes Converge in the SD3-Loop of PfEMP1-DBL1α

The ability of Plasmodium falciparum parasitized RBC (pRBC) to form rosettes with normal RBC is linked to the virulence of the parasite and RBC polymorphisms that weaken rosetting confer protection against severe malaria. The adhesin PfEMP1 mediates the binding and specific antibodies prevent sequestration in the micro-vasculature, as seen in animal models. Here we demonstrate that epitopes targeted by rosette disrupting antibodies converge in the loop of subdomain 3 (SD3) which connects the h6 and h7 α-helices of PfEMP1-DBL1α. Both monoclonal antibodies and polyclonal IgG, that bound to epitopes in the SD3-loop, stained the surface of pRBC, disrupted rosettes and blocked direct binding of recombinant NTS-DBL1α to RBC. Depletion of polyclonal IgG raised to NTS-DBL1α on a SD3 loop-peptide removed the anti-rosetting activity. Immunizations with recombinant subdomain 1 (SD1), subdomain 2 (SD2) or SD3 all generated antibodies reacting with the pRBC-surface but only the sera of animals immunized with SD3 disrupted rosettes. SD3-sequences were found to segregate phylogenetically into two groups (A/B). Group A included rosetting sequences that were associated with two cysteine-residues present in the SD2-domain while group B included those with three or more cysteines. Our results suggest that the SD3 loop of PfEMP1-DBL1α is an important target of anti-rosetting activity, clarifying the molecular basis of the development of variant-specific rosette disrupting antibodies

Genetic identification of unique immunological responses in mice infected with virulent and attenuated Francisella tularensis

Francisella tularensis is a category A select agent based on its infectivity and virulence but disease mechanisms in infection remain poorly understood. Murine pulmonary models of infection were therefore employed to assess and compare dissemination and pathology and to elucidate the host immune response to infection with the highly virulent Type A F. tularensis strain Schu4 versus the less virulent Type B live vaccine strain (LVS). We found that dissemination and pathology in the spleen was significantly greater in mice infected with F. tularensis Schu4 compared to mice infected with F. tularensis LVS. Using gene expression rofiling to compare the response to infection with the two F. tularensis strains, we found that there were significant differences in the expression of genes involved in the apoptosis pathway, antigen processing and presentation pathways, and inflammatory response pathways in mice infected with Schu4 when compared to LVS. These transcriptional differences coincided with marked differences in dissemination and severity of organ lesions in mice infected with the Schu4 and LVS strains. Therefore, these findings indicate that altered apoptosis, antigen presentation and production of inflammatory mediators explain the differences in pathogenicity of F. tularensis Schu4 and LVS

Ranking insertion, deletion and nonsense mutations based on their effect on genetic information

<p>Abstract</p> <p>Background</p> <p>Genetic variations contribute to normal phenotypic differences as well as diseases, and new sequencing technologies are greatly increasing the capacity to identify these variations. Given the large number of variations now being discovered, computational methods to prioritize the functional importance of genetic variations are of growing interest. Thus far, the focus of computational tools has been mainly on the prediction of the effects of amino acid changing single nucleotide polymorphisms (SNPs) and little attention has been paid to indels or nonsense SNPs that result in premature stop codons.</p> <p>Results</p> <p>We propose computational methods to rank insertion-deletion mutations in the coding as well as non-coding regions and nonsense mutations. We rank these variations by measuring the extent of their effect on biological function, based on the assumption that evolutionary conservation reflects function. Using sequence data from budding yeast and human, we show that variations which that we predict to have larger effects segregate at significantly lower allele frequencies, and occur less frequently than expected by chance, indicating stronger purifying selection. Furthermore, we find that insertions, deletions and premature stop codons associated with disease in the human have significantly larger predicted effects than those not associated with disease. Interestingly, the large-effect mutations associated with disease show a similar distribution of predicted effects to that expected for completely random mutations.</p> <p>Conclusions</p> <p>This demonstrates that the evolutionary conservation context of the sequences that harbour insertions, deletions and nonsense mutations can be used to predict and rank the effects of the mutations.</p