479 research outputs found

    Determining the Impact of Food Price and Income Changes on Obesity

    Get PDF
    Despite the significant rise in obesity in the U.S., economic research on obesity is still in its infancy. This paper employs a microeconomic approach to investigate the effects of price and income changes on weight in an effort to determine how a high-calorie food tax, a low-calorie food subsidy, and/or an income changes affect body weight. Although raising the price of high-calorie food typically will likely lead to decreased demand for such goods; it is not clear that such an outcome will actually reduce weight. The model developed in this paper identifies conditions under which price and income changes are mostly likely to actually result in a weight loss. The model is easily implemented using data on own-and cross-price elasticities that are often readily available from extant literature. This is important because survey data that contain both economic information, such as food prices, and weight are extremely rare. Information on relationship between price and weight is critical in developing appropriate public policy and in determining when and where fat taxes, thin subsidies or income re-distribution will achieve the desired objective of reducing obesity.Health Economics and Policy,

    The Relative Importance of Preferences for Country-of-Origin in China, France, Niger and the United States

    Get PDF
    Country-of-origin (COO) is an increasingly politicized credence attribute in the globalizing food system. While international policy development in this area is geographically far-reaching, the benefits of country-of-origin labels (COOL) to producers and consumers from countries in different locations and levels of economic development are not clear. Previous work investigates the importance of COO to consumers, but is typically limited in scope to consumers in one nation. In addition, little is known about the importance of COO information relative to other credence attributes, especially in non-meat food products. This study measures the benefits of COOL to an internationally diverse set of consumers (in developed and developing countries) and estimates their priority rank in policy development. The paper draws upon research in the management literature suggesting consumer information needs are not based on quality alone, but also relate to affective (emotional) and normative (social acceptance) needs. A conjoint experiment is conducted in China, France, Niger and the United States to elicit consumer preferences for COO information, organic production, and genetic modification. The results indicate COO information is not as important as genetically modified content information (France, the United States, and Niger) or organic production information (China). Findings reveal individuals with quality and food safety information needs place higher importance on genetically modified and organic food information than COO information.country-of-origin, genetic modification, organic, conjoint, onion, information, food policy, International Relations/Trade, Q13, Q18, Q17,

    A Multidimensional Homo Economicus: Cultural Dimensions of Economic Preferences in Four Countries

    Get PDF
    Previous work in experimental economics reveals specific differences in economic behavior, especially reciprocity and free-riding behavior, across cultures. We expand the possible pallet of cross-cultural behavioral differences that may exist. We hypothesize that different kinds of strategic interaction and individual decision-making behaviors differ across locations. The variety of experiments we use allow us to report multidimensional rather than just single dimensional differences in behavior across locations. In order to build a broad Homo Economicus we conducted economic experiments in four dissimilar locations: Hangzhou, China; Niamey, Niger; Grenoble, France; Manhattan, Kansas; and West Lafayette, Indiana. Each subject completed an ultimatum bargaining game experiment, Voluntary Contribution Mechanism experiment, time preference experiment, and risk preference experiment. Results indicate economic behavior is not independent of location. Location differences are greatest for strategic interaction behavior and less prevalent for individual decision-making behavior.Time preference, risk preference, voluntary contribution mechanism, Ultimatum bargaining game, cultural, China, France, Niger, Kansas, Indiana, US, Institutional and Behavioral Economics,

    Preliminary catalog of pictures taken on the lunar surface during the Apollo 15 mission

    Get PDF
    Catalog of all pictures taken from lunar module or lunar surface during Apollo 15 missio

    Sustained release formulation of an anti-tuberculosis drug based on para-amino salicylic acid-zinc layered hydroxide nanocomposite

    Get PDF
    Background: Tuberculosis (TB), is caused by the bacteria, Mycobacterium tuberculosis and its a threat to humans since centuries. Depending on the type of TB, its treatment can last for 6-24 months which is a major cause for patients non-compliance and treatment failure. Many adverse effects are associated with the currently available TB medicines, and there has been no new anti-tuberculosis drug on the market for more than 50 year, as the drug development is very lengthy and budget consuming process.Development of the biocompatible nano drug delivery systems with the ability to minimize the side effects of the drugs, protection of the drug from enzymatic degradation. And most importantly the drug delivery systems which can deliver the drug at target site would increase the therapeutic efficacy. Nanovehicles with their tendency to release the drug in a sustained manner would result in the bioavalibilty of the drugs in the body for a longer period of time and this would reduce the dosing frequency in drug administration. The biocompatible nanovehicles with the properties like sustained release of drug of the target site, protection of the drug from physio-chemical degradation, reduction in dosing frequency, and prolong bioavailability of drug in the body would result in the shortening of the treatment duration. All of these factors would improve the patient compliance with chemotherapy of TB.Result: An anti-tuberculosis drug, 4-amino salicylic acid (4-ASA) was successfully intercalated into the interlamellae of zinc layered hydroxide (ZLH) via direct reaction with zinc oxide suspension. The X-ray diffraction patterns and FTIR analyses indicate that the molecule was successfully intercalated into the ZLH interlayer space with an average basal spacing of 24 Å. Furthermore, TGA and DTG results show that the drug 4-ASA is stabilized in the interlayers by electrostatic interaction. The release of 4-ASA from the nanocomposite was found to be in a sustained manner. The nanocomposite treated with normal 3T3 cells shows it reduces cell viability in a dose- and time-dependent manner.Conclusions: Sustained release formulation of the nanocomposite, 4-ASA intercalated into zinc layered hydroxides, with its ease of preparation, sustained release of the active and less-toxic to the cell is a step forward for a more patient-friendly chemotherapy of Tuberculosis

    Effects of YM155 on survivin levels and viability in neuroblastoma cells with acquired drug resistance

    Get PDF
    Resistance formation after initial therapy response (acquired resistance) is common in high-risk neuroblastoma patients. YM155 is a drug candidate that was introduced as a survivin suppressant. This mechanism was later challenged, and DNA damage induction and Mcl-1 depletion were suggested instead. Here we investigated the efficacy and mechanism of action of YM155 in neuroblastoma cells with acquired drug resistance. The efficacy of YM155 was determined in neuroblastoma cell lines and their sublines with acquired resistance to clinically relevant drugs. Survivin levels, Mcl-1 levels, and DNA damage formation were determined in response to YM155. RNAi-mediated depletion of survivin, Mcl-1, and p53 was performed to investigate their roles during YM155 treatment. Clinical YM155 concentrations affected the viability of drug-resistant neuroblastoma cells through survivin depletion and p53 activation. MDM2 inhibitor-induced p53 activation further enhanced YM155 activity. Loss of p53 function generally affected anti-neuroblastoma approaches targeting survivin. Upregulation of ABCB1 (causes YM155 efflux) and downregulation of SLC35F2 (causes YM155 uptake) mediated YM155-specific resistance. YM155-adapted cells displayed increased ABCB1 levels, decreased SLC35F2 levels, and a p53 mutation. YM155-adapted neuroblastoma cells were also characterized by decreased sensitivity to RNAi-mediated survivin depletion, further confirming survivin as a critical YM155 target in neuroblastoma. In conclusion, YM155 targets survivin in neuroblastoma. Furthermore, survivin is a promising therapeutic target for p53 wild-type neuroblastomas after resistance acquisition (neuroblastomas are rarely p53-mutated), potentially in combination with p53 activators. In addition, we show that the adaptation of cancer cells to molecular-targeted anticancer drugs is an effective strategy to elucidate a drug's mechanism of action

    Mediated Diasporas: Material Translations of the Philippines in a Globalized World

    Get PDF
    Recent work demonstrates the ways that new media and ICTs both in the Philippines and among Filipino diasporans have become central to contemporary processes of identity formation, altering and enabling the articulation of alternative selves and expanding spatially Filipino national identifications and definitions of ‘home’ (Pertierra 2002, 2006, 2010 Tyner and Kuhlke 2000, Ignacio 2005). While attending to media in the specific sense of particular social technologies of mass communication, we extend that work here drawing together new empirical studies both to demonstrate the various ways that a wide range of differently situated migrants make use of those media and by considering processes of mediation in a much broader sense (Mazzarella 2004), an approach that draws together both an analysis of the ‘materialities of migration’ (Basu and Coleman 2008) and ‘the technics of translation’ (Rafael 2005)

    Ex vivo drug response profiling detects recurrent sensitivity patterns in drug-resistant acute lymphoblastic leukemia

    Get PDF
    Drug sensitivity and resistance testing on diagnostic leukemia samples should provide important functional information to guide actionable target and biomarker discovery. We provide proof of concept data by profiling 60 drugs on 68 acute lymphoblastic leukemia (ALL) samples mostly from resistant disease in cocultures of bone marrow stromal cells. Patient-derived xenografts retained the original pattern of mutations found in the matched patient material. Stromal coculture did not prevent leukemia cell cycle activity, but a specific sensitivity profile to cell cycle-related drugs identified samples with higher cell proliferation both in vitro and in vivo as leukemia xenografts. In patients with refractory relapses, individual patterns of marked drug resistance and exceptional responses to new agents of immediate clinical relevance were detected. The BCL2inhibitor venetoclax was highly active below 10 nM in B-cell precursor ALL (BCP-ALL) subsets, including MLL-AF4 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in vivo activity as a single agent and in combination with dexamethasone and vincristine. Unexpected sensitivity to dasatinib with half maximal inhibitory concentration values below 20 nM was detected in 2 independent T-ALL cohorts, which correlated with similar cytotoxic activity of the SRC inhibitor KX2-391 and inhibition of SRC phosphorylation. A patient with refractory T-ALL was treated with dasatinib on the basis of drug profiling information and achieved a 5-month remission. Thus, drug profiling captures disease-relevant features and unexpected sensitivity to relevant drugs, which warrants further exploration of this functional assay in the context of clinical trials to develop drug repurposing strategies for patients with urgent medical needs.Peer reviewe

    Activating mutation in MET oncogene in familial colorectal cancer

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>In developed countries, the lifetime risk of developing colorectal cancer (CRC) is 5%, and it is the second leading cause of death from cancer. The presence of family history is a well established risk factor with 25-35% of CRCs attributable to inherited and/or familial factors. The highly penetrant inherited colon cancer syndromes account for approximately 5%, leaving greater than 20% without clear genetic definition. Familial colorectal cancer has been linked to chromosome 7q31 by multiple affected relative pair studies. The <it>MET </it>proto-oncogene which resides in this chromosomal region is considered a candidate for genetic susceptibility.</p> <p>Methods</p> <p><it>MET </it>exons were amplified by PCR from germline DNA of 148 affected sibling pairs with colorectal cancer. Amplicons with altered sequence were detected with high-resolution melt-curve analysis using a LightScanner (Idaho Technologies). Samples demonstrating alternative melt curves were sequenced. A TaqMan assay for the specific c.2975C <b>></b>T change was used to confirm this mutation in a cohort of 299 colorectal cancer cases and to look for allelic amplification in tumors.</p> <p>Results</p> <p>Here we report a germline non-synonymous change in the <it>MET </it>proto-oncogene at amino acid position T992I (also reported as <it>MET </it>p.T1010I) in 5.2% of a cohort of sibling pairs affected with CRC. This genetic variant was then confirmed in a second cohort of individuals diagnosed with CRC and having a first degree relative with CRC at prevalence of 4.1%. This mutation has been reported in cancer cells of multiple origins, including 2.5% of colon cancers, and in <1% in the general population. The threonine at amino acid position 992 lies in the tyrosine kinase domain of MET and a change to isoleucine at this position has been shown to promote metastatic behavior in cell-based models. The average age of CRC diagnosis in patients in this study is 63 years in mutation carriers, which is 8 years earlier than the general population average for CRC.</p> <p>Conclusions</p> <p>Although the <it>MET </it>p.T992I genetic mutation is commonly found in somatic colorectal cancer tissues, this is the first report also implicating this <it>MET </it>genetic mutation as a germline inherited risk factor for familial colorectal cancer. Future studies on the cancer risks associated with this mutation and the prevalence in different at-risk populations will be an important extension of this work to define the clinical significance.</p

    From old organisms to new molecules: integrative biology and therapeutic targets in accelerated human ageing

    Get PDF
    Understanding the basic biology of human ageing is a key milestone in attempting to ameliorate the deleterious consequences of old age. This is an urgent research priority given the global demographic shift towards an ageing population. Although some molecular pathways that have been proposed to contribute to ageing have been discovered using classical biochemistry and genetics, the complex, polygenic and stochastic nature of ageing is such that the process as a whole is not immediately amenable to biochemical analysis. Thus, attempts have been made to elucidate the causes of monogenic progeroid disorders that recapitulate some, if not all, features of normal ageing in the hope that this may contribute to our understanding of normal human ageing. Two canonical progeroid disorders are Werner’s syndrome and Hutchinson-Gilford progeroid syndrome (also known as progeria). Because such disorders are essentially phenocopies of ageing, rather than ageing itself, advances made in understanding their pathogenesis must always be contextualised within theories proposed to help explain how the normal process operates. One such possible ageing mechanism is described by the cell senescence hypothesis of ageing. Here, we discuss this hypothesis and demonstrate that it provides a plausible explanation for many of the ageing phenotypes seen in Werner’s syndrome and Hutchinson-Gilford progeriod syndrome. The recent exciting advances made in potential therapies for these two syndromes are also reviewed
    corecore