221 research outputs found

    Privacy in Internet of Things: A Model and Protection Framework

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    AbstractA new form of computation is being evolved to include massive number of diverse set of conventional computing systems, sensors, devices, equipments, software and information services and apps. This new form of computing environment is known as the “Internet-of-Things” (IoT). The adoption of IoT is fast and the “things” are becoming integral part of people day-to-day life as well as essential elements in the businesses everyday activities and processes. Open characteristics of IoT environments raises privacy concern as “things” are autonomous with some degree of authority to sharing their capabilities and knowledge to fulfil their individual or collective tasks. As such privacy becomes central and an inherit computational aspect of the “things”. The work presented here is based on modelling IoT as Cooperative Distributed Systems (CDS). It proposes a novel approach of analysing and modelling privacy concepts and concerns. Privacy protection is captured as a form of “sensitive information” management at the interaction level. A privacy protection management framework for CDS at the interaction level is proposed. The application of the framework has been demonstrated by extending Contract Net Protocol (CNP) to support privacy protection for CDS

    A rearrangement-based approach to secondary difluorophosphonates

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    [3,3]-Claisen rearrangements allowed the conversion of a readily available allylic difluorophosphonate to nucleic acid and inositol phosphate-related products via epoxide cyclisation or ring closing metathesis respectively

    Isolation and Characterization of Alkalophilic Xylanase Producing Bacteria MS-2-1 from Marine Water Sample

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    A novel marine bacterium was isolated from Pichavaram mangrove forest located near Chidambaram, Tamil Nadu and designated as MS-2-1. Morphological, cultural, physiological characteristics as well as 16S rRNA gene sequence based phylogenetic analysis confirmed taxonomic affiliation of MS 2 as Marinobacter aquaeolei. The optimum pH and temperature for maximum production of xylanase was observed at pH 8.0 and 30ºC

    AGE-modified basement membrane cooperates with Endo180 to promote epithelial cell invasiveness and decrease prostate cancer survival

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    Biomechanical strain imposed by age-related thickening of the basal lamina and augmented tissue stiffness in the prostate gland coincides with increased cancer risk. Here we hypothesized that the structural alterations in the basal lamina associated with age can induce mechanotransduction pathways in prostate epithelial cells (PECs) to promote invasiveness and cancer progression. To demonstrate this, we developed a 3D model of PEC acini in which thickening and stiffening of basal lamina matrix was induced by advanced glycation end-product (AGE)-dependent non-enzymatic crosslinking of its major components, collagen IV and laminin. We used this model to demonstrate that antibody targeted blockade of CTLD2, the second of eight C-type lectin-like domains in Endo180 (CD280, CLEC13E, KIAA0709, MRC2, TEM9, uPARAP) that can recognize glycosylated collagens, reversed actinomyosin-based contractility [myosin-light chain-2 (MLC2) phosphorylation], loss of cell polarity, loss of cell–cell junctions, luminal infiltration and basal invasion induced by AGE-modified basal lamina matrix in PEC acini. Our in vitro results were concordant with luminal occlusion of acini in the prostate glands of adult Endo180ΔEx2–6/ΔEx2–6 mice, with constitutively exposed CTLD2 and decreased survival of men with early (non-invasive) prostate cancer with high epithelial Endo180 expression and levels of AGE. These findings indicate that AGE-dependent modification of the basal lamina induces invasive behaviour in non-transformed PECs via a molecular mechanism linked to cancer progression. This study provides a rationale for targeting CTLD2 in Endo180 in prostate cancer and other pathologies in which increased basal lamina thickness and tissue stiffness are driving factors

    Maternal deaths in Pakistan : intersection of gender, class and social exclusion.

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    Background: A key aim of countries with high maternal mortality rates is to increase availability of competent maternal health care during pregnancy and childbirth. Yet, despite significant investment, countries with the highest burdens have not reduced their rates to the expected levels. We argue, taking Pakistan as a case study, that improving physical availability of services is necessary but not sufficient for reducing maternal mortality because gender inequities interact with caste and poverty to socially exclude certain groups of women from health services that are otherwise physically available. Methods: Using a critical ethnographic approach, two case studies of women who died during childbirth were pieced together from information gathered during the first six months of fieldwork in a village in Northern Punjab, Pakistan. Findings: Shida did not receive the necessary medical care because her heavily indebted family could not afford it. Zainab, a victim of domestic violence, did not receive any medical care because her martial family could not afford it, nor did they think she deserved it. Both women belonged to lower caste households, which are materially poor households and socially constructed as inferior. Conclusions: The stories of Shida and Zainab illustrate how a rigidly structured caste hierarchy, the gendered devaluing of females, and the reinforced lack of control that many impoverished women experience conspire to keep women from lifesaving health services that are physically available and should be at their disposal

    Uneventful Disappearance of a Large Left Atrial Ball Thrombus with Enoxaparin in a Patient with Mitral Stenosis Associated with Pregnancy

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    An atrial thrombus is a relatively common echocardiographic finding in patients with mitral valve stenosis (MVS) and atrial fibrillation (AF). However, a “ball thrombus” or floating thrombus in the left atrium is a rare and specific entity associated with MVS. A 24-year-old woman with rheumatic MVS presented with complaints of progressive dyspnea and inferior limbs edema that began 23 days earlier after a caesarean operation for stillbirth carried out at 8 months of pregnancy. At the time of hospitalization, she was in New York Heart Association functional class III and the ECG showed sinus rhythm. Transthoracic color-flow Doppler echocardiography revealed a thick, stenotic mitral valve with a valvular area of 0.9 cm2, and an echogenic large left-atrial mass diagnosed as a free-floating left-atrial thrombus that was corroborated by transesophageal echocardiography. She refused surgery and was treated medically, and low molecular weight heparin (LMWH) (enoxaparin 80 mg/12 h) was given for 14 days and was discharged uneventfully on coumarin. Two days before discharge, a transthoracic and transesophageal ecocardiography showed disappearance of the ball thrombus uneventfully leaving spontaneous echo contrast inside the left atrium. To the best of our knowledge, this is the first case showing disappearance of a giant left atrial ball thrombus with LMWH treatment in a patient with severe MVS during sinus rhythm associated with pregnancy

    Prediagnostic concentrations of plasma genistein and prostate cancer risk in 1,605 men with prostate cancer and 1,697 matched control participants in EPIC

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    PURPOSE: Data from prospective epidemiological studies in Asian populations and from experimental studies in animals and cell lines suggest a possible protective association between dietary isoflavones and the development of prostate cancer. We examined the association between circulating concentrations of genistein and prostate cancer risk in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition. METHODS: Concentrations of the isoflavone genistein were measured in prediagnostic plasma samples for 1,605 prostate cancer cases and 1,697 matched control participants. Relative risks (RRs) for prostate cancer in relation to plasma concentrations of genistein were estimated by conditional logistic regression. RESULTS: Plasma genistein concentrations were not associated with prostate cancer risk; the multivariate relative risk for men in the highest fifth of genistein compared with men in the lowest fifth was 1.00 (95 % confidence interval: 0.79, 1.27; p linear trend = 0.82). There was no evidence of heterogeneity in this association by age at blood collection, country of recruitment, or cancer stage or histological grade. CONCLUSION: Plasma genistein concentration was not associated with prostate cancer risk in this large cohort of European men

    Genome editing reveals a role for OCT4 in human embryogenesis.

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    Despite their fundamental biological and clinical importance, the molecular mechanisms that regulate the first cell fate decisions in the human embryo are not well understood. Here we use CRISPR-Cas9-mediated genome editing to investigate the function of the pluripotency transcription factor OCT4 during human embryogenesis. We identified an efficient OCT4-targeting guide RNA using an inducible human embryonic stem cell-based system and microinjection of mouse zygotes. Using these refined methods, we efficiently and specifically targeted the gene encoding OCT4 (POU5F1) in diploid human zygotes and found that blastocyst development was compromised. Transcriptomics analysis revealed that, in POU5F1-null cells, gene expression was downregulated not only for extra-embryonic trophectoderm genes, such as CDX2, but also for regulators of the pluripotent epiblast, including NANOG. By contrast, Pou5f1-null mouse embryos maintained the expression of orthologous genes, and blastocyst development was established, but maintenance was compromised. We conclude that CRISPR-Cas9-mediated genome editing is a powerful method for investigating gene function in the context of human development.DW was supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre Programme. NK was supported by the University of Oxford Clarendon Fund. AB was supported by a British Heart Foundation PhD Studentship (FS/11/77/39327). LV was supported by core grant funding from the Wellcome Trust and Medical Research Council (PSAG028). J-SK was supported by the Institute for Basic Science (IBS-R021-D1). Work in the KKN and JMAT labs was supported by the Francis Crick Institute which receives its core funding from Cancer Research UK, the UK Medical Research Council, and the Wellcome Trust (FC001120 and FC001193)

    Association of selenoprotein and selenium pathway gnotypes with risk of colorectal cancer and interaction with selenium status

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    Selenoprotein genetic variations and suboptimal selenium (Se) levels may contribute to the risk of colorectal cancer (CRC) development. We examined the association between CRC risk and genotype for single nucleotide polymorphisms (SNPs) in selenoprotein and Se metabolic pathway genes. Illumina Goldengate assays were designed and resulted in the genotyping of 1040 variants in 154 genes from 1420 cases and 1421 controls within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Multivariable logistic regression revealed an association of 144 individual SNPs from 63 Se pathway genes with CRC risk. However, regarding the selenoprotein genes, only TXNRD1 rs11111979 retained borderline statistical significance after adjustment for correlated tests (PACT = 0.10; PACT significance threshold was P < 0.1). SNPs in Wingless/Integrated (Wnt) and Transforming growth factor (TGF) beta-signaling genes (FRZB, SMAD3, SMAD7) from pathways affected by Se intake were also associated with CRC risk after multiple testing adjustments. Interactions with Se status (using existing serum Se and Selenoprotein P data) were tested at the SNP, gene, and pathway levels. Pathway analyses using the modified Adaptive Rank Truncated Product method suggested that genes and gene x Se status interactions in antioxidant, apoptosis, and TGF-beta signaling pathways may be associated with CRC risk. This study suggests that SNPs in the Se pathway alone or in combination with suboptimal Se status may contribute to CRC development
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