Impact of hepcidin antimicrobial peptide on iron overload in tuberculosis patients

Background: Iron acquisition is essential for the growth of Mycobacterium tuberculosis. Hepcidin is known as an antimicrobial peptide and a component of the innate immune response. Hepcidin inhibits M. tuberculosis growth in vitro. In this study, we decided to identify-582A> G variants of the HAMP promoter in patients with tuberculosis (TB) and investigate its effect on serum iron, ferritin, and hepcidin levels. Methods: The sample population consisted of 105 patients with TB and 104 healthy individuals. The-582A> G polymorphism was genotyped using a tetra-primers PCR set. Serum levels of hepcidin were determined using an ELISA kit. Statistical analysis was performed using SPSS software. Results: The G allele is meaningfully associated with TB disease (95% confidence interval = 2-4.8, p G polymorphism genotypes. There was significant reverse correlation between hepcidin and iron (r =-0.849, p = 0.006). Conclusion: A high association was found between serum hepcidin levels and the HAMP-582A> G variants in patients with TB. These observations indicate a hypothetical role of this polymorphism in iron metabolism. Hepcidin could perhaps be an option for the treatment of TB. © 2014 Informa Healthcare

Complex Cellular Composition of Solitary Fibrous Tumor of the Prostate

Solitary fibrous tumors (SFTs) of the prostate are a rare type of spindle cell neoplasm that can demonstrate either a benign or malignant phenotype. SFTs represent a clinical challenge along with other spindle cell lesions of the prostate in terms of both diagnosis and treatment. The present study shows, for the first time, that SFTs of the prostate and other organs can comprise a mixed population of fibroblast, myofibroblast, and smooth muscle cell types. The highly proliferative component demonstrated a fibroblastic phenotype that readily underwent myofibroblast differentiation on exposure to profibrotic stimuli. Consistent with other recent studies, the prostatic SFTs demonstrated NAB2-STAT6 gene fusions that were also present in the fibroblast, myofibroblast, and smooth muscle cell types of the SFT. The results of these studies suggest that benign and malignant prostatic tumors of mesenchymal origin may be distinguished at the molecular and cellular levels, and that delineation of such defining characteristics may help elucidate the etiology and prognosis of such tumors

Security of data science and data science for security

In this chapter, we present a brief overview of important topics regarding the connection of data science and security. In the first part, we focus on the security of data science and discuss a selection of security aspects that data scientists should consider to make their services and products more secure. In the second part about security for data science, we switch sides and present some applications where data science plays a critical role in pushing the state-of-the-art in securing information systems. This includes a detailed look at the potential and challenges of applying machine learning to the problem of detecting obfuscated JavaScripts

Functional Connectivity Evaluation for Infant EEG Signals based on Artificial Neural Network

The employment of the brain signals electroencephalography (EEG) could supply a deep intuitive understanding for infants behaviour and their alertness level within the living environment. The study of human brain through a computer-based approach has increased significantly as it aiming at the understanding of infants’ mind and measure their attention towards the surrounding activities. The artificial neural network achieved a significant level of success in different fields such as pattern classification, decision making, prediction, and adaptive control by learning from a set of data and construct weight matrices to represent the learning patterns. This research study proposes an artificial neural network based approach to predict the rightward asymmetry or leftward asymmetry which reflects higher frontal functional connectivity in the frontal right and frontal left, respectively within infant’s brain. In the traditional methods, the value of asymmetry of the frontal (FA) functional connectivity is used to determine the rightward or the leftward asymmetry. While the proposed approach is trying to predict that without going through all the levels of the calculation complexity. The achieved work will supply a deep understanding into the deployment of the functional connectivity to provide information on the interactions between different brain regions

Antisense oligonucleotide inhibition of Heat Shock Protein (HSP) 47 improves bleomycin-induced pulmonary fibrosis in rats

<p>Abstract</p> <p>Background</p> <p>The most common pathologic form of pulmonary fibrosis arises from excessive deposition of extracellular matrix proteins such as collagen. The 47 kDa heat shock protein 47 (HSP47) is a collagen-specific molecular chaperone that has been shown to play a major role during the processing and/or secretion of procollagen.</p> <p>Objectives</p> <p>To determine whether inhibition of HSP47 could have beneficial effects in mitigating bleomycin-induced pulmonary fibrosis in rats.</p> <p>Methods</p> <p>All experiments were performed with 250–300 g male Wistar rats. Animals were randomly divided into five experimental groups that were administered: 1) saline alone, 2) bleomycin alone, 3) antisense HSP47 oligonucleotides alone, 4) bleomycin + antisense HSP47 oligonucleotides, and 5) bleomycin + sense control oligonucleotides. We investigated lung histopathology and performed immunoblot and immunohistochemistry analyses.</p> <p>Results</p> <p>In rats treated with HSP47 antisense oligonucleotides, pulmonary fibrosis was significantly reduced. In addition, treatment with HSP47 antisense oligonucleotides significantly improved bleomycin-induced morphological changes. Treatment with HSP47 antisense oligonucleotides alone did not produce any significant changes to lung morphology. Immunoblot analyses of lung homogenates confirmed the inhibition of HSP47 protein by antisense oligonucleotides. The bleo + sense group, however, did not exhibit any improvement in lung pathology compared to bleomycin alone groups, and also had no effect on HSP47 expression.</p> <p>Conclusion</p> <p>These findings suggest that HSP47 antisense oligonucleotide inhibition of HSP47 improves bleomycin-induced pulmonary fibrosis pathology in rats.</p

Attenuation of lung inflammation and fibrosis in CD69-deficient mice after intratracheal bleomycin

<p>Abstract</p> <p>Background</p> <p>Cluster of differentiation 69 (CD69), an early activation marker antigen on T and B cells, is also expressed on activated macrophages and neutrophils, suggesting that CD69 may play a role in inflammatory diseases. To determine the effect of CD69 deficiency on bleomycin(BLM)-induced lung injury, we evaluated the inflammatory response following intratracheal BLM administration and the subsequent fibrotic changes in wild type (WT) and CD69-deficient (CD69^-/-) mice.</p> <p>Methods</p> <p>The mice received a single dose of 3 mg/kg body weight of BLM and were sacrificed at 7 or 14 days post-instillation (dpi). Lung inflammation in the acute phase (7 dpi) was investigated by differential cell counts and cytokine array analyses of bronchoalveolar lavage fluid. In addition, lung fibrotic changes were evaluated at 14 dpi by histopathology and collagen assays. We also used reverse transcription polymerase chain reaction to measure the mRNA expression level of transforming growth factor β1 (TGF-β1) in the lungs of BLM-treated mice.</p> <p>Results</p> <p>CD69^-/-mice exhibited less lung damage than WT mice, as shown by reductions in the following indices: (1) loss of body weight, (2) wet/dry ratio of lung, (3) cytokine levels in BALF, (4) histological evidence of lung injury, (5) lung collagen deposition, and (6) TGF-β1 mRNA expression in the lung.</p> <p>Conclusion</p> <p>The present study clearly demonstrates that CD69 plays an important role in the progression of lung injury induced by BLM.</p

Silencing CD36 gene expression results in the inhibition of latent-TGF-β1 activation and suppression of silica-induced lung fibrosis in the rat

<p>Abstract</p> <p>Background</p> <p>The biologically active form of transforming growth factor-β1 (TGF-β1) plays a key role in the development of lung fibrosis. CD36 is involved in the transformation of latent TGF-β1 (L-TGF-β1) to active TGF-β1. To clarify the role of CD36 in the development of silica-induced lung fibrosis, a rat silicosis model was used to observe both the inhibition of L-TGF-β1 activation and the antifibrotic effect obtained by lentiviral vector silencing of CD36 expression.</p> <p>Methods</p> <p>The rat silicosis model was induced by intratracheal injection of 10 mg silica per rat and CD36 expression was silenced by administration of a lentiviral vector (Lv-shCD36). The inhibition of L-TGF-β1 activation was examined using a CCL-64 mink lung epithelial growth inhibition assay, while determination of hydroxyproline content along with pathological and immunohistochemical examinations were used for observation of the inhibition of silica-induced lung fibrosis.</p> <p>Results</p> <p>The lentiviral vector (Lv-shCD36) silenced expression of CD36 in alveolar macrophages (AMs) obtained from bronchoalveolar lavage fluid (BALF) and the activation of L-TGF-β1 in the BALF was inhibited by Lv-shCD36. The hydroxyproline content of silica+Lv-shCD36 treated groups was significantly lower than in other experimental groups. The degree of fibrosis in the silica+Lv-shCD36-treated groups was less than observed in other experimental groups. The expression of collagen I and III in the silica+Lv-shCD36-treated group was significantly lower than in the other experimental groups.</p> <p>Conclusion</p> <p>These results indicate that silencing expression of CD36 can result in the inhibition of L-TGF-β1 activation in a rat silicosis model, thus further preventing the development of silica-induced lung fibrosis.</p

π→ππ\pi \to \pi\pi results in nuclei

The Crystal Ball ($CB$) collaboration at $BNL$ has recently presented results regarding a study of the $\pi^- A \to \pi^0\pi^0 A^\prime$ reaction on $H, D, C, Al$ and $Cu$, using a nearly 4$\pi$ detector. Similar results, but for the $\pi^+ A \to \pi^+\pi^{\pm} A^\prime$ reaction on $^{2}H$, $^{12}C$, $^{40}Ca$, and $^{208}Pb$, have been published earlier by the $CHAOS$ collaboration at $TRIUMF$. In this Brief Report a comparison of the results of the two measurements is made, which shows that the $CHAOS$ and $CB$ data share relevant common features. In particular, the increase in strength as a function of A seen in the near-threshold $\pi^+ \pi^-$ invariant mass spectra reported by the $CHAOS$ group, is also seen in the $\pi^0 \pi^0$ CB data, when the results from the two groups are compared in a way which accounts for the different acceptances of the two experiments.Comment: 7 pages, 1 figure, accepted for publication in Phy. Rev. C - Brief Repor

Grafting Trees: a Fault Attack against the SPHINCS framework

Because they require no assumption besides the preimage or collision resistance of hash functions, hash-based signatures are a unique and very attractive class of post-quantum primitives. Among them, the schemes of the SPHINCS family are arguably the most practical stateless schemes, and can be implemented on embedded devices such as FPGAs or smart cards. This naturally raises the question of their resistance to implementation attacks. In this paper, we propose the first fault attack against the framework underlying SPHINCS, Gravity-SPHINCS and SPHINCS+. Our attack allows to forge any message signature at the cost of a single faulted message. Furthermore, the fault model is very reasonable and the faulted signatures remain valid, which renders our attack both stealthy and practical. As the attack involves a non-negligible computational cost, we propose a fine-grained trade-off allowing to lower this cost by slightly increasing the number of faulted messages. Our attack is generic in the sense that it does not depend on the underlying hash function(s) used