A Generative Model of Natural Texture Surrogates

Natural images can be viewed as patchworks of different textures, where the local image statistics is roughly stationary within a small neighborhood but otherwise varies from region to region. In order to model this variability, we first applied the parametric texture algorithm of Portilla and Simoncelli to image patches of 64X64 pixels in a large database of natural images such that each image patch is then described by 655 texture parameters which specify certain statistics, such as variances and covariances of wavelet coefficients or coefficient magnitudes within that patch. To model the statistics of these texture parameters, we then developed suitable nonlinear transformations of the parameters that allowed us to fit their joint statistics with a multivariate Gaussian distribution. We find that the first 200 principal components contain more than 99% of the variance and are sufficient to generate textures that are perceptually extremely close to those generated with all 655 components. We demonstrate the usefulness of the model in several ways: (1) We sample ensembles of texture patches that can be directly compared to samples of patches from the natural image database and can to a high degree reproduce their perceptual appearance. (2) We further developed an image compression algorithm which generates surprisingly accurate images at bit rates as low as 0.14 bits/pixel. Finally, (3) We demonstrate how our approach can be used for an efficient and objective evaluation of samples generated with probabilistic models of natural images.Comment: 34 pages, 9 figure

Japanese Encephalitis Virus Induce Immuno-Competency in Neural Stem/Progenitor Cells

BACKGROUND: The low immunogenicity of neural stem/progenitor cells (NSPCs) coupled with negligible expression of MHC antigens has popularized their use in transplantation medicine. However, in an inflammatory environment, the NSPCs express costimulatory molecules and MHC antigens, and also exhibit certain immunomodulatory functions. Since NSPCs are the cellular targets in a number of virus infections both during postnatal and adult stages, we wanted to investigate the immunological properties of these stem cells in response to viral pathogen. METHODOLOGY/PRINCIPAL FINDINGS: We utilized both in vivo mouse model and in vitro neurosphere model of Japanese encephalitis virus (JEV) infection for the study. The NSPCs residing in the subventricular zone of the infected brains showed prominent expression of MHC-I and costimulatory molecules CD40, CD80, and CD86. Using Flow cytometry and fluorescence microscopy, we observed increased surface expression of co-stimulatory molecule and MHC class I antigen in NSPCs upon progressive JEV infection in vitro. Moreover, significant production of pro-inflammatory cyto/chemokines was detected in JEV infected NSPCs by Cytokine Bead Array analysis. Interestingly, NSPCs were capable of providing functional costimulation to allogenic T cells and JEV infection resulted in increased proliferation of allogenic T cells, as detected by Mixed Lymphocyte reaction and CFSE experiments. We also report IL-2 production by NSPCs upon JEV infection, which possibly provides mitogenic signals to T cells and trigger their proliferation. CONCLUSION/SIGNIFICANCE: The in vivo and in vitro findings clearly indicate the development of immunogenicity in NSPCs following progressive JEV infection, in our case, JEV infection. Following a neurotropic virus infection, NSPCs possibly behave as immunogenic cells and contribute to both the innate and adaptive immune axes. The newly discovered immunological properties of NSPCs may have implications in assigning a new role of these cells as non-professional antigen presenting cells in the central nervous system

Role of toll like receptors in bacterial and viral diseases – A systemic approach

Background: Toll like receptors are key-receptors of the innate immune system, but their role against bacterial and viral infections are yet to be understood.Aim: The present study is aimed to investigate the diversity and frequency distribution of 10 TLR genes among typhoid fever and HIV+ patients. In this study, 44 samples were taken from typhoid patients and 55 samples from HIV+ patients.Patients and methods: Widal test positive samples (>1:80) in case of typhoid and the percentage of CD4+ count in case of HIV+ patient were considered for the PCR-SSP analysis.Results: We found that the frequencies of TLR1 and TLR6 were highest in typhoid patients, whereas the frequencies of TLR8 and TLR9 displayed higher among HIV+ patients. Chi-square values were significant for TLR8 and TLR10 in the case of typhoid patients, whereas in HIV patients significant values were considered for TLR2, TLR4, TLR8 and TLR9 respectively. The odds ratio calculated highest for TLR1 and TLR6 among typhoid patients. TLR4 and TLR9 calculated were highest odd for HIV+ patients. A door line association of TLRs with the disease was found when the relative risk was calculated for TLR2 (1.72), TLR3 (1.21) and TLR10 (1.98) in bacterial infection, whereas in case of viral infection relative risk was calculated for TLR4 (1.62), TLR8 (1.18) and in TLR9 (1.16).Conclusion: This study reports the frequency distribution and association of human TLR genes with the bacterial and viral infection in the North Bengal region of India for the first time. It also signified the gene- disease- environment association study in case of infectious diseases and also the risk factors of bacterial and viral infections in this region. It also depicts the role of TLRs in the recognition of the pathogens

Exploiting the Order of Multiplier Operands: A Low Cost Approach for HCCA Resistance

Horizontal collision correlation analysis (HCCA) imposes a serious threat to simple power analysis resistant elliptic curve cryptosystems involving unified algorithms, for e.g. Edward curve unified formula. This attack can be mounted even in presence of differential power analysis resistant randomization schemes. In this paper we have designed an effective countermeasure for HCCA protection, where the dependency of side-channel leakage from a school-book multiplication with the underling multiplier operands is investigated. We have shown how changing the sequence in which the operands are passed to the multiplication algorithm introduces dissimilarity in the information leakage. This disparity has been utilized in constructing a zero-cost countermeasure against HCCA. This countermeasure integrated with an effective randomization method has been shown to successfully thwart HCCA. Additionally we provide experimental validation for our proposed countermeasure technique on a SASEBO platform. To the best of our knowledge, this is the first time that asymmetry in information leakage has been utilized in designing a side channel countermeasure

ECC on Your Fingertips: A Single Instruction Approach for Lightweight ECC Design in GF (p)

Lightweight implementation of Elliptic Curve Cryptography on FPGA has been a popular research topic due to the boom of ubiquitous computing. In this paper we propose a novel single instruction based ultra-light ECC crypto-processor coupled with dedicated hard-IPs of the FPGAs. We show that by using the proposed single instruction framework and using the available block RAMs and DSPs of FPGAs, we can design an ECC crypto-processor for NIST curve P-256, requiring only 81 and 72 logic slices on Virtes-5 and Spartan-6 devices respectively.To the best of our knowledge, this is the first implementation of ECC which requires less than 100 slices on any FPGA device family

Transforming growth factor-β protein inversely regulates in vivo differentiation of interleukin-17 (IL-17)-producing CD4<SUP>+</SUP> and CD8<SUP>+</SUP> T Cells

TGF-β is a pleiotropic cytokine that predominantly exerts inhibitory functions in the immune system. Unexpectedly, the in vitro differentiation of both Th17 and Tc17 cells requires TGF-β. However, animals that are impaired in TGF-β signaling (TGF-βRIIDN mice) display multiorgan autoimmune disorders. Here we show that CD4+ T cells from TGF-βRIIDN mice are resistant to Th17 cell differentiation and, paradoxically, that CD8+ T cells from these animals spontaneously acquire an IL-17-producing phenotype. Neutralization of IL-17 or depletion of CD8+ T cells dramatically inhibited inflammation in TGF-βRIIDN mice. Therefore, the absence of TGF-β triggers spontaneous differentiation of IL-17-producing CD8+ T cells, suggesting that the in vivo and in vitro conditions that promote the differentiation of IL-17-producing CD8+ T cells are distinct