Search

The defect classification of knitted fabrics is a challenging area of research. Most of the defect detection works in India; Bangladesh is being carried by manually trained inspectors. The long working hours and the working environment at the company induces the fatigue, lack of concentration, and triteness to the workers due to this they may not able to detect the defects on the clothes after it is manufactured. To overcome this problem, a computer-aided defect detection system is being developed using digital image processing and artificial neural Network methods. The two types of artificial neural networks were applied to compare the results obtained. The networks were: a back propagation based feed forward neural network and the other was Levenberg–Marquardt (LM) algorithm based back propagation network. Experimental results predicted detection of a high degree of variety of fabric defects. [ABSTRACT FROM AUTHOR]

Low power devices have always been important in all electronics and computer devices. In this paper, a proposed design has been implemented for the full adder circuit with significant modifications in the existing hybrid GDI (Gate Diffusion Input) based full adder. All the results are implemented using CADENCE tool at 45nm scale and 0.4V. Existing hybrid GDI based adder design delivers 7.135x10-9 watt power dissipation. The proposed hybrid GDI-PTL design delivers a significant reduction in power dissipation equal to 6.70x10-9 watt. Further, this power dissipation has been reduced to 6.55x10-9 watt by using high Vth (threshold voltage) PMOS transistor in the proposed hybrid GDI-PTL design for one-bit full adder. [ABSTRACT FROM AUTHOR]

In the backdrop of the UNESCO's endeavor to promote cultural industries in Asia-Pacific region, India's enthusiasm can be conspicuously seen in hosting the symposium which finalized the background document for a holistic development of the sector. The agenda set by this document is multipronged; however, 'income generation' and 'wealth creation' appear to be more significant. This document has identified different slots for different markers of culture amongst which 'crafts' are also marked as a separate slot. However UNESCO's proposal cannot ignore Frankfurt School critiques. Overall, there has been a critique of over-administered culture that promises an 'integral freedom' but gets fragmented into high art and products of culture industry that never sum up to what they promise (Adorno, 1991). Cultural sociologists have taken a neutral stand and analyze them just as other important institutions, engaged in creative processes of cultural production (Santoro, 2008). Nevertheless, the critiques of culture industries remain relevant. Culture industries define themselves on the criteria of 'creativity', 'cultural knowledge' and 'intellectual property'. They will have to be accommodated with each other on these issues and explore other kinds of relationships that pertain to art, communities and religion rather than only to the pecuniary ones. In crafts communities, art and religion are very significant, yet we have modern knowledge and technology which have been posing as challenges to be reconciled. Aesthetics of crafts are a mélange of the above mentioned forces, and the neglect of even a single phenomenon would be an injustice to the crafts at large. [ABSTRACT FROM AUTHOR]

Foodborne transmission of bovine spongiform encephalopathyencephalopathy (BSE) to humans as variant Creutzfeldt-Jakob disease (CJD) has affected over 100 individuals, and probably millions of others have been exposed to BSE-contaminated food substances. Despite these obvious public health concerns, surprisingly little is known about the mechanism by which PrP-scrapie (PrpSc), the most reliable surrogate marker of infection in BSE-contaminated food, crosses the human intestinal epithelial cell barrier. Here we show that digestive enzyme (DE) treatment of sporadic CJD brain homogenate generates a C-terminal fragment similar to the proteinase K-resistant PrPSc core of 27-30 kDa implicated in prion disease transmission and pathogenesis. Notably, DE treatment results in a PrP Sc-protein complex that is avidly transcytosed in vesicular structures across an in vitro model of the human intestinal epithelial cell barrier, regardless of the amount of endogenous PrPC expression. Unexpectedly, PrPSc is cotransported with ferritin, a prominent component of the DE-treated PrP Sc-protein complex. The transport of PrPSc-ferritin is sensitive to low temperature, brefeldin-A, and nocodazole treatment and is inhibited by excess free ferritin, implicating a receptor- or transporter-mediated pathway. Because ferritin shares considerable homology across species, these data suggest that PrP Sc-associated proteins, in particular ferritin, may facilitate PrP Sc uptake in the intestine from distant species, leading to a carrier state in humans. [ABSTRACT FROM AUTHOR]

Prion diseases or transmissible spongiform encephalopathies are neurodegenerative disorders that are genetic, sporadic, or infectious. The pathogenetic event common to all prion disorders is a change in conformation of the cellular prion protein (PrPC) to the scrapie isoform (PrPSc), which, unlike PrPC, aggregates easily and is partially resistant to protease digestion. Although PrPSc is believed to be essential for the pathogenesis and transmission of prion disorders, the mechanism by which PrPSc deposits cause neurodegeneration is unclear. It has been proposed that in some cases of prion disorders, a transmembrane form of PrP, termed CtmPrP may be the mediator of neurodegenerative changes rather than PrPSc per se. In order to understand the underlying cellular processes by which PrPSc mediates neurodegeneration, we have investigated the mechanism of neurotoxicity by a beta-sheet rich peptide of PrP in a cell model. We show that exposure of human neuronal cell lines NT-2 and M17 to the prion peptide 106-126 (PrP106-126) catalyzes the aggregation of endogenous cellular prion protein (PrPC) to an amyloidogenic form that shares several characteristics with PrPSc. Intracellular accumulation of these PrPSc-like forms upregulates the synthesis of CtmPrP, which is proteolytically cleaved in the endoplasmic reticulum and the truncated C-terminal fragment is transported to the cell surface. In addition, we have isolated mutant NT-2 and neuroblastoma cells that are resistant to toxicity by PrP106-126 to facilitate further characterization of the biochemical pathways of PrP106-126 neurotoxicity. The PrP106-126-resistant phenotype of these cells could result from aberrant binding or internalization of the peptide, or due to an abnormality in the downstream pathway(s) of neuronal toxicity. Thus, our data suggest that PrPSc aggregation occurs by a process of 'nucleation' on a pre-existing 'seed' of PrP. Furthermore, the PrP106-126-resistant cells reported here will provide a unique opportunity for identifying the cellular and biochemical pathways that mediate neurotoxicity by PrPSc.