1,567 research outputs found

    Spring: Risks and Rights

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    A Back-reaction Induced Lower Bound on the Tensor-to-Scalar Ratio

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    There are large classes of inflationary models, particularly popular in the context of string theory and brane world approaches to inflation, in which the ratio of linearized tensor to scalar metric fluctuations is very small. In such models, however, gravitational waves produced by scalar modes cannot be neglected. We derive the lower bound on the tensor-to-scalar ratio by considering the back-reaction of the scalar perturbations as a source of gravitational waves. These results show that no cosmological model that is compatible with a metric scalar amplitude of 105\approx 10^{-5} can have a ratio of the tensor to scalar power spectra less than 108\approx 10^{-8} at recombination and that higher-order terms leads to logarithmic growth for r during radiation domination. Our lower bound also applies to non-inflationary models which produce an almost scale-invariant spectrum of coherent super-Hubble scale metric fluctuations.Comment: 5 pages, version 3, minor changes from version

    Magnetic states of linear defects in graphene monolayers: effects of strain and interaction

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    The combined effects of defect-defect interaction and of uniaxial or biaxial strains of up to 10\% on the development of magnetic states on the defect-core-localized quasi-one-dimensional electronic states generated by the so-called 558 linear extended defect in graphene monolayers are investigated by means of {\it ab initio} calculations. Results are analyzed on the basis of the heuristics of the Stoner criterion. We find that conditions for the emergence of magnetic states on the 558 defect can be tuned by uniaxial tensile parallel strains (along the defect direction) at both limits of isolated and interacting 558 defects. Parallel strains are shown to lead to two cooperative effects that favor the emergence of itinerant magnetism: enhancement of the DOS of the resonant defect states in the region of the Fermi level and tuning of the Fermi level to the maximum of the related DOS peak. A perpendicular strain is likewise shown to enhance the DOS of the defect states, but it also effects a detunig of the Fermi level that shifts away from the maximum of the DOS of the defect states, which inhibts the emergence of magnetic states. As a result, under biaxial strains the stabilization of a magnetic state depends on the relative magnitudes of the two components of strain.Comment: 9 pages 8 figure

    Capturing the Existential Cyber Security Threats from the Sub-Saharan Africa Zone through Literature Database

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    Abstract - The Internet brought about the phenomenon known as Cyber-space which is boundless in nature. It is one of the fastest-growing areas of technical infrastructure development over the past decade. Its growth has afforded everyone the opportunity to carry out one or more transactions for personal benefits. The African continent; often branded as ‘backward’ by the Western press has been able to make substantial inroads into the works of Information and Computer Technology (ICT). This rapid transition by Africans into ICT power has thus opened up the opportunities for Cybercriminal perpetrators to seek and target victims worldwide including America for personal financial gains. This existential threat has been growing in bounds and leaps over the past few years that the news media has been awash with cyber-attacks from African countries including Nigeria, South Africa, Ghana, Zimbabwe, and a host of other African nations. There have been several academic research and articles published on the African cyber-criminal activities by several authors; most of which are in silos and in non-subject specific databases everywhere. Our sponsored summer long project therefore re-analyzed the African style cyber- attacks culminating in the creation of an Access based database that captured the pertinent data about the reported cases through the use of secondary data sources

    Marginal Freedoms: Journalism, Participation and Moral Multiplicity in Odisha, India.

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    This dissertation is an ethnography of the moral worlds of journalists and newspaper workers in Odisha, India. It portrays the ethical dilemmas that media producers confront in daily life as marginalized citizens of the world’s largest democracy. Located on India’s eastern coast, Odisha is an infamously poor state now experiencing rapid but uneven economic growth, out of which have arisen violent conflicts over religious conversion and mining in indigenous territories. The dissertation is based on fourteen months of qualitative research in Odisha’s capital, Bhubaneswar, including newsroom participant-observation, long-form interviews, and the analysis of local newspapers and internet-based news. I argue that Odisha’s journalists live with moral multiplicity, or the coexistence of diverse, often incommensurable evaluations of what counts as ethical action, and that such multiplicity produces double binds in Odisha's civic participation. For example, publications in the local language, Odia, are accessible to the growing literate class and can serve as potent metonyms of “the people,” yet local understandings of language devalue Odia journalism as corrupt in comparison with journalism in English. Such moral conflicts arise from frictions between liberal ideals like free speech and local modes of activism and patronage that have origins in the nineteenth century. This dissertation uses micro-level analyses of how journalists manage moral multiplicity in writing techniques, legal complaints, employee interactions, and social networking to illustrate how Indian media producers live with the macro-level historical transformations of globalization. This research reinvigorates the study of South Asian public life outside of major metropolises and contributes to the descriptive study of communication ethics cross-culturally.PhDAnthropologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/110352/1/kbmartin_1.pd

    Serum anti-Müllerian hormone concentrations before and after treatment of an ovarian granulosa cell tumour in a cat

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    Case summary A 15-year-old female cat was presented for investigation of progressive behavioural changes, polyuria, polydipsia and periuria. An ovarian granulosa cell tumour was identified and the cat underwent therapeutic ovariohysterectomy (OHE). The cat’s clinical signs resolved, but 6 months later it was diagnosed as having an anaplastic astrocytoma and was euthanased. Serum anti-Müllerian hormone (AMH) concentration prior to OHE was increased vs a control group of entire and neutered female cats. Following OHE, serum AMH concentration decreased to <1% of the original value. Relevance and novel information Serum AMH measurement may represent a novel diagnostic and monitoring tool for functional ovarian neoplasms in cats

    Elevated hepatocyte growth factor levels in osteoarthritis osteoblasts contribute to their altered response to bone morphogenetic protein-2 and reduced mineralization capacity

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    PURPOSE: Clinical and in vitro studies suggest that subchondral bone sclerosis due to abnormal osteoblasts is involved in the progression of osteoarthritis (OA). Human osteoblasts isolated from sclerotic subchondral OA bone tissue show an altered phenotype, a decreased canonical Wnt/ß-catenin pathway, and a reduced mineralization in vitro as well as in vivo. These alterations were linked with an abnormal response to BMP-2. OA osteoblasts release factors such as the hepatocyte growth factor (HGF) that contribute to cartilage loss whereas chondrocytes do not express HGF. HGF can stimulate BMP-2 expression in human osteoblasts, however, the role of HGF and its effect in OA osteoblasts remains unknown. Here we investigated whether elevated endogenous HGF levels in OA osteoblasts are responsible for their altered response to BMP-2. METHODS: We prepared primary human subchondral osteoblasts using the sclerotic medial portion of the tibial plateaus of OA patients undergoing total knee arthroplasty, or from tibial plateaus of normal individuals obtained at autopsy. The expression of HGF was evaluated by qRT-PCR and the protein production by western blot analysis. HGF expression was reduced with siRNA technique whereas its activity was inhibited using the selective inhibitor PHA665752. Alkaline phosphatase activity (ALPase) and osteocalcin release were measured by substrate hydrolysis and EIA respectively. Canonical Wnt/β-catenin signaling (cWnt) was evaluated both by target gene expression using the TOPflash TCF/lef luciferase reporter assay and western blot analysis of β-catenin levels in response to Wnt3a stimulation. Mineralization in response to BMP-2 was evaluated by alizarin red staining. RESULTS: The expression of HGF was increased in OA osteoblasts compared to normal osteoblasts and was maintained during their in vitro differentiation. OA osteoblasts released more HGF than normal osteoblasts as assessed by western blot analysis. HGF stimulated the expression of TGF-β1. BMP-2 dose-dependently (1 to 100ng/ml) stimulated both ALPase and osteocalcin in normal osteoblasts whereas, it inhibited them in OA osteoblasts. HGF-siRNA treatments reversed this response in OA osteoblasts and restored the BMP-2 response. cWnt is reduced in OA osteoblasts compared to normal, and HGF-siRNA treatments increased cWnt in OA osteoblasts almost to normal. Smad1/5/8 phosphorylation in response to BMP-2, which is reduced in OA osteoblasts, was corrected when these cells were treated with PHA665752. The BMP-2-dependent mineralization of OA osteoblasts, which is also reduced compared to normal, was only partially restored by PHA665752 treatment whereas 28days treatment with HGF reduced the mineralization of normal osteoblasts. CONCLUSION: OA osteoblasts expressed more HGF than normal osteoblasts. Increased endogenous HGF production in OA osteoblasts stimulated the expression of TGF-β1 and reduced their response to BMP-2. Inhibiting HGF expression or HGF signaling restored the response to BMP-2 and Smad1/5/8 signaling. In addition, decreased HGF signaling partly corrects the abnormal mineralization of OA osteoblasts while increased HGF prevents the normal mineralization of normal osteoblasts. In summary, we hypothesize that sustained elevated HGF levels in OA osteoblasts drive their abnormal phenotype and is implicated in OA pathophysiology
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