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The current Internet is facing serious scalability problems and the overloading of Internet Protocol (IP) addresses is regarded as an important reason. The Locator/ID Separation Protocol (LISP) is proposed as a network-based solut...
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The current Internet is facing serious scalability problems and the overloading of Internet Protocol (IP) addresses is regarded as an important reason. The Locator/ID Separation Protocol (LISP) is proposed as a network-based solution that separates IP addresses into Routing Locators (RLOCs) and Endpoint Identifiers (EIDs) to address the routing scalability problems. It is a critical challenge for LISP to design a scalable and efficient mapping system. In this paper, we propose a hierarchical mapping system (HMS). HMS consists of two levels with the bottom level maintaining the EID-to-RLOC mappings in an Autonomous System (AS) and the upper level storing the mappings between EID-prefixes and ASs in the global network. We adopt one-hop Distributed Hash Table (DHT) to organize EID-to-RLOC mappings in the bottom level and use a protocol like Border Gateway Protocol (BGP) to propagate EID-prefix-to-AS mappings in the upper level. HMS aggregates the prefixes in an AS and decreases the global mapping entries in the upper level. The evaluation results show that the number of mapping entries in HMS grows slower than the routing table size, which makes HMS scalable. In addition, the mobility in HMS does not cause mapping changes in the upper level. It makes HMS efficient in supporting host mobility. We estimate the map-requests sent to the mapping system, which show the load on HMS is small. Last, we compare HMS with LISP-TREE and LISP+ALT by quantitative analysis, in terms of resolution cost, and qualitative analysis. The results show that HMS has a good performance.
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Because virtual computing platforms are dynamically changing, it is difficult to build high-quality intrusion detection system. In this paper, we present an automated approach to intrusions detection in order to maintain sufficien...
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Because virtual computing platforms are dynamically changing, it is difficult to build high-quality intrusion detection system. In this paper, we present an automated approach to intrusions detection in order to maintain sufficient performance and reduce dependence on execution environment. We discuss a hidden Markov model strategy for abnormality detection using frequent system call sequences, letting us identify attacks and intrusions automatically and efficiently. We also propose an automated mining algorithm, named AGAS, to generate frequent system call sequences. In our approach, the detection performance is adaptively tuned according to the execution state every period. To improve performance, the period value is also under self-adjustment.
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The disposal of apoptotic bodies by professional phagocytes is crucial to effective inflammation resolution. Our ability to improve the disposal of apoptotic bodies by professional phagocytes is impaired by a limited understanding...
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The disposal of apoptotic bodies by professional phagocytes is crucial to effective inflammation resolution. Our ability to improve the disposal of apoptotic bodies by professional phagocytes is impaired by a limited understanding of the molecular mechanisms that regulate the engulfment and digestion of the efferocytic cargo. Macrophages are professional phagocytes necessary for liver inflammation, fibrosis, and resolution, switching their phenotype from proinflammatory to restorative. Using sterile liver injury models, we show that the STAT3–IL-10–IL-6 axis is a positive regulator of macrophage efferocytosis, survival, and phenotypic conversion, directly linking debris engulfment to tissue repair. Copyright ? 2018 by The American Association of Immunologists, Inc.
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Angiogenesis and lymphangiogenesis participate in many inflammatory diseases, and their reversal is thought to be beneficial. However, the extent of reversibility of vessel remodeling is poorly understood. We exploited the potent ...
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Angiogenesis and lymphangiogenesis participate in many inflammatory diseases, and their reversal is thought to be beneficial. However, the extent of reversibility of vessel remodeling is poorly understood. We exploited the potent anti-inflammatory effects of the corticosteroid dexamethasone to test the preventability and reversibility of vessel remodeling in Mycoplasma pulmonis-infected mice using immunohistochemistry and quantitative RT-PCR. In this model robust immune responses drive rapid and sustained changes in blood vessels and lymphatics. In infected mice not treated with dexamethasone, capillaries enlarged into venules expressing leukocyte adhesion molecules, sprouting angiogenesis and lymphangiogenesis occurred, and the inflammatory cytokines tumor necrosis factor and interleukin-1 increased. Concurrent dexamethasone treatment largely prevented the remodeling of blood vessels and lymphatics. Dexamethasone also significantly reduced cytokine expression, bacterial burden, and leukocyte influx into airways and lungs over 4 weeks of infection. In contrast, when infection was allowed to proceed untreated for 2 weeks and then was treated with dexamethasone for 4 weeks, most blood vessel changes reversed but lymphangiogenesis did not, suggesting that different survival mechanisms apply. Furthermore, dexamethasone significantly reduced the bacterial burden and influx of lymphocytes but not of neutrophils or macrophages or cytokine expression. These findings show that lymphatic remodeling is more resistant than blood vessel remodeling to corticosteroid-induced reversal. We suggest that lymphatic remodeling that persists after the initial inflammatory response has resolved may influence subsequent inflammatory episodes in clinical situations.
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The complement C5b-9 complexes can result in cell apoptosis, but the mechanism of sublytic C5b-9-mediated glomerular mesangial cell (GMC) apoptosis in Thy-1 nephritis (Thy-1N) remains largely unclear. The Gadd45 gene is involved i...
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The complement C5b-9 complexes can result in cell apoptosis, but the mechanism of sublytic C5b-9-mediated glomerular mesangial cell (GMC) apoptosis in Thy-1 nephritis (Thy-1N) remains largely unclear. The Gadd45 gene is involved in the cellular response to DNA damage and can promote cell apoptosis. In this study, both Gadd45 gamma expression patterns and pathologic changes of renal tissue were examined in rat Thy-1N. Both Gadd45 gamma expression and GMC apoptosis were significantly decreased in Thy-1N rats upon the depletion of complement with cobra venom factor. Our in vitro studies showed that Gadd45 gamma over-expression increased sublytic C5b-9-induced GMC apoptosis, while Gadd45 gamma gene knockdown by siRNA greatly reduced GMC apoptosis. Moreover, Gadd45 gamma gene silencing in vivo markedly inhibited the pathologic changes in the renal tissue of Thy-1N rats. These data suggest that Gadd45 gamma gene expression is involved in regulating GMC apoptosis mediated by sublytic C5b-9 in Thy-1N.
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The complement C5b-9 complexes can result in cell apoptosis, but the mechanism of sublytic C5b-9-mediated glomerular mesangial cell (GMC) apoptosis in Thy-1 nephritis (Thy-1N) remains largely unclear. The Gadd45 gene is involved i...
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The complement C5b-9 complexes can result in cell apoptosis, but the mechanism of sublytic C5b-9-mediated glomerular mesangial cell (GMC) apoptosis in Thy-1 nephritis (Thy-1N) remains largely unclear. The Gadd45 gene is involved in the cellular response to DNA damage and can promote cell apoptosis. In this study, both Gadd45 gamma expression patterns and pathologic changes of renal tissue were examined in rat Thy-1N. Both Gadd45 gamma expression and GMC apoptosis were significantly decreased in Thy-1N rats upon the depletion of complement with cobra venom factor. Our in vitro studies showed that Gadd45 gamma over-expression increased sublytic C5b-9-induced GMC apoptosis, while Gadd45 gamma gene knockdown by siRNA greatly reduced GMC apoptosis. Moreover, Gadd45 gamma gene silencing in vivo markedly inhibited the pathologic changes in the renal tissue of Thy-1N rats. These data suggest that Gadd45 gamma gene expression is involved in regulating GMC apoptosis mediated by sublytic C5b-9 in Thy-1N.
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In this paper, humic acid bonded silica (HAAS) stationary phase was prepared through the spacer of aminoalkyl silanes. The high performance liquid chromatographic behavior of several polar compounds, including four alkaloids and c...
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In this paper, humic acid bonded silica (HAAS) stationary phase was prepared through the spacer of aminoalkyl silanes. The high performance liquid chromatographic behavior of several polar compounds, including four alkaloids and clenbuterol, was studied on HAAS. The effect of mobile phase variables such as organic solvent content, buffer pH, and ionic strength on their chromatographic behavior was investigated. The retention mechanism of tested compounds on the stationary phase was elucidated. The results indicate that the HAAS stationary phase behaved as hydrophilic interaction chromatographic packing, using high content organic solvent as mobile phase, and the stationary phase showed good separation selectivity for four alkaloids and clenbuterol.
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Polyvinyl caprolactam-polyvinyl acetate-polyethylene glycol graft copolymer, or Soluplus? is a relatively new copolymer and a promising carrier of amorphous solid dispersions. Knowledge on the inherent properties of Soluplus?(e.g....
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Polyvinyl caprolactam-polyvinyl acetate-polyethylene glycol graft copolymer, or Soluplus? is a relatively new copolymer and a promising carrier of amorphous solid dispersions. Knowledge on the inherent properties of Soluplus?(e.g. cloud points, critical micelle concentrations, and viscosity) in different conditions is relatively inadequate, and the application characteristics of Soluplus?based solid dispersions made by microwave methods still need to be clarified. In the present investigation, the inherent properties of a Soluplus?carrier, including cloud points, critical micelle concentrations, and viscosity, were explored in different media and in altered conditions. Ibuprofen, a BCS class II non-steroidal anti-inflammatory drug, was selected to develop Soluplus?based amorphous solid dispersions using the microwave-quench cooling (MQC) method. Scanning electronic microscopy (SEM), differential scanning calorimetry (DSC), powder X-ray diffraction (PXRD), Raman spectroscopy (RS), and Fourier transform infrared spectroscopy (FT-IR) were adopted to analyze amorphous properties and molecular interactions in ibuprofen/Soluplus?amorphous solid dispersions generated by MQC. Dissolution, dissolution extension, phase solubility, equilibrium solubility, and supersaturated crystallization inhibiting experiments were performed to elucidate the effects of Soluplus?on ibuprofen in solid dispersions. This research provides valuable information on the inherent properties of Soluplus?and presents a basic understanding of Soluplus?as a carrier of amorphous solid dispersions. ?2016 Informa UK Limited, trading as Taylor & Francis Group.
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Effective thermal management for 3D integrated circuits (3D ICs) is becoming increasingly challenging due to the ever-increasing power density and chip design complexity; traditional heat sinks are expected to quickly reach their ...
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Effective thermal management for 3D integrated circuits (3D ICs) is becoming increasingly challenging due to the ever-increasing power density and chip design complexity; traditional heat sinks are expected to quickly reach their limits for meeting the cooling needs of 3D ICs. Alternatively, the integrated liquid-cooled microchannel heat sink has become one of the most effective solutions. In this paper, we present fast multigrid and block tridiagonally preconditioned graphics processing unit (GPU) based thermal simulation algorithms for 3D ICs. Unlike the CPU-based solver development in which existing sophisticated numerical simulation tools (matrix solvers) can be readily adopted and implemented, GPU-based thermal simulation demands more effort in the algorithm and data structure design phase, and requires careful consideration of GPU's thread/memory organization, data access/communication patterns, arithmetic intensity, as well as its hardware occupancies. As shown by various experimental results, our GPU-based 3D thermal simulation solvers can achieve more than $360times$ speedups over the best available direct solvers and more than $35times$ speedups over the CPU-based iterative solvers, without loss of accuracy.
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Cysteinyl leukotrienes (cysLTs) facilitate mucosal type 2 immunopathology by incompletely understood mechanisms. Aspirin-exacerbated respiratory disease, a severe asthma subtype, is characterized by exaggerated eosinophilic respir...
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Cysteinyl leukotrienes (cysLTs) facilitate mucosal type 2 immunopathology by incompletely understood mechanisms. Aspirin-exacerbated respiratory disease, a severe asthma subtype, is characterized by exaggerated eosinophilic respiratory inflammation and reactions to aspirin, each involving the marked overproduction of cysLTs. Here we demonstrate that the type 2 cysLT receptor (CysLT2R), which is not targeted by available drugs, is required in two different models to amplify eosinophilic airway inflammation via induced expression of IL-33 by lung epithelial cells. Endogenously generated cysLTs induced eosinophilia and expanded group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respiratory disease–like Ptges2/2 mice. These responses were mitigated by deletions of either Cysltr2 or leukotriene C4 synthase (Ltc4s). Administrations of either LTC4 (the parent cysLT) or the selective CysLT2R agonist N-methyl LTC4 to allergen sensitized wild-type mice markedly boosted ILC2 expansion and IL-5/ IL-13 generation in a CysLT2R-dependent manner. Expansion of ILC2s and IL-5/IL-13 generation reflected CysLT2R-dependent production of IL-33 by alveolar type 2 cells, which engaged in a bilateral feed-forward loop with ILC2s. Deletion of Cysltr1 blunted LTC4-induced ILC2 expansion and eosinophilia but did not alter IL-33 induction. Pharmacological blockade of CysLT2R prior to inhalation challenge of Ptges2/2 mice with aspirin blocked IL-33–dependent mast cell activation, mediator release, and changes in lung function. Thus, CysLT2R signaling, IL-33–dependent ILC2 expansion, and IL-33–driven mast cell activation are necessary for induction of type 2 immunopathology and aspirin sensitivity. CysLT2R-targeted drugs May interrupt these processes. The Journal of Immunology, 2018, 200: 915–927. Copyright ? 2018 by The American Association of Immunologists, Inc.
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