218 research outputs found

    Defending against redirect attacks in mobile IP

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    Research progress on the pathogenesis of arthritis

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    Juvenile Idiopathic Arthritis (JIA) pathogenesis is not very clear, but it may be associated with specific components of various infectious microorganisms as foreign antigens for people with a genetic background, activate immune cells, and trigger an abnormal immune response by directly damaging or secreting cytokines, autoantibodies. Cause damage and degeneration of our own organization. Especially certain bacteria, viruses, special components (such as HSP) can be used as superantigens, T cells are activated directly by binding to T cell receptors (TCR) with a special variable region β chain (chain) structure and stimulate immune damage. Self-tissue denaturing components (endogenous antigens), can also be used as an antigen to trigger an immune response to its own tissue components. Further aggravate the immune damage. Intestinal microbial groups and environmental factors may also play an important role in the pathogenesis of JIA

    Unraveling the therapeutic mechanisms of dichloroacetic acid in lung cancer through integrated multi-omics approaches: metabolomics and transcriptomics

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    Objective: The aim of this study was to investigate the molecular mechanisms underlying the therapeutic effects of dichloroacetic acid (DCA) in lung cancer by integrating multi-omics approaches, as the current understanding of DCA’s role in cancer treatment remains insufficiently elucidated.Methods: We conducted a comprehensive analysis of publicly available RNA-seq and metabolomic datasets and established a subcutaneous xenograft model of lung cancer in BALB/c nude mice (n = 5 per group) treated with DCA (50 mg/kg, administered via intraperitoneal injection). Metabolomic profiling, gene expression analysis, and metabolite-gene interaction pathway analysis were employed to identify key pathways and molecular players involved in the response to DCA treatment. In vivo evaluation of DCA treatment on tumor growth and MIF gene expression was performed in the xenograft model.Results: Metabolomic profiling and gene expression analysis revealed significant alterations in metabolic pathways, including the Warburg effect and citric acid cycle, and identified the MIF gene as a potential therapeutic target in lung cancer. Our analysis indicated that DCA treatment led to a decrease in MIF gene expression and an increase in citric acid levels in the treatment group. Furthermore, we observed a potential interaction between citric acid and the MIF gene, suggesting a novel mechanism underlying the therapeutic effects of DCA in lung cancer.Conclusion: This study underscores the importance of integrated omics approaches in deciphering the complex molecular mechanisms of DCA treatment in lung cancer. The identification of key metabolic pathways and the novel finding of citric acid elevation, together with its interaction with the MIF gene, provide promising directions for the development of targeted therapeutic strategies and improving clinical outcomes for lung cancer patients

    Defending against redirect attacks in mobile IP

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    A new approach for anonymous password authentication

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    A*STA

    Double symmetry breaking of solitons in one-dimensional virtual photonic crystals

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    We demonstrate that spatial solitons undergo two consecutive spontaneous symmetry breakings (SSBs), with the increase of the total power, in nonlinear photonic crystals (PhCs) built as arrays of alternating linear and nonlinear stripes, in the case when maxima of the effective refractive index coincide with minima of the self-focusing coefficient, and vice versa, i.e.,the corresponding linear and nonlinear periodic potentials are in competition. This setting may be induced, as a virtual PhC, by means of the EIT (electromagnetically-induced-transparency) technique, in a uniform optical medium. It may also be realized as a Bose-Einstein condensate (BEC) subject to the action of combined periodic optical potential and periodically modulated Feshbach resonance. The first SSB happens at the center of a linear stripe, pushing a broad low-power soliton into an adjacent nonlinear stripe and gradually suppressing side peaks in the soliton's shape. Then, the soliton restores its symmetry, being pinned to the midpoint of the nonlinear stripe. The second SSB occurs at higher powers, pushing the narrow soliton off the center of the nonlinear channel,while the soliton keeps its internal symmetry. The results are obtained by means of numerical and analytical methods. They may be employed to control switching of light beams by means of the varying power.Comment: 8 pages, 5 figures, Phys. Rev. A, in pres

    Evolutionary Enhancement of Zika Virus Infectivity in Aedes aegypti Mosquitoes

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    Zika virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013-2014) and South America (2015-2016). Phylogenetic studies have shown that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV was responsible for the recent epidemics in the Americas. However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are unclear. Non-structural protein 1 (NS1) facilitates flavivirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes. Here we show that NS1 antigenaemia determines ZIKV infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have higher NS1 antigenaemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at residue 188 in NS1. ZIKV infectivity was enhanced by this amino acid substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viraemic C57BL/6 mouse deficient in type I and II interferon (IFN) receptors (AG6 mouse). Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased NS1 antigenaemia. Enhancement of NS1 antigenaemia in infected hosts promotes ZIKV infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent ZIKV epidemics
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