Consensus Reaching Process for Traditional Group Decision Making in View of the Optimal Adjustment Mechanism.

Consensus reaching process (CRP) is a key topic in the area of group decision making (GDM). When the consensus level is not high enough, it becomes necessary to adjust the original opinions of decision makers (DMs). To offer the adjustment reference for DMs, we build the programming models to determine the minimum modification to be carried out from the individual and global perspectives. Meanwhile, all DMs are divided into two subgroups: DMs with acceptable and unacceptable consensus levels. If some DMs with unacceptable consensus level do not accept the relevant modifications, the Nash bargaining game-based programming model is built for the fairness and efficiency of modifications. When some DMs refuse to make any modifications or tend to modify the opinions in their way, with respect to different group consensus situations, we make the minimum hybrid penalty mechanism by the Nash bargaining game-based programming models. For each case, we determine the corresponding optimal modification mechanism in view of the fixed individual total modification and the maximum consensus level. Furthermore, we study the arrangements of weights of DMs according to their cardinal and ordinal consensus contributions. Based on these results, we present a new algorithm and illustrate its application by a numerical example. Moreover, we carry out the sensitivity and comparison analysis. We summarize the conclusions and future research directions in the end. The main originality of the new method includes: the fairness and efficiency of modifications, and the determination of the hybrid penalty mechanism.

A large-scale group decision making method to select the ideal mobile health application for the hospital.

Mobile health, which is not limited by time and space, can effectively alleviate the imbalance of medical resources. Currently, more and more hospitals begin to pay attention to online medical care and actively expand their mobile channels. Among of which, the cooperation with the third-party platform is an effective way to expand the online services of most hospitals. With the increasing number of mobile health applications (mHealth apps), it is difficult to select the ideal application. Most of the existing studies on mHealth app selection are conducted from the perspective of users who have health needs, which is insufficient. The views of multiple stakeholders should be taken into account. mHealth app selection can be regarded as a large-scale group decision making (LSGDM) problem. In this paper, a hybrid LSGDM method is proposed to select the mHealth app with the highest user satisfaction. First, the weights of criteria are obtained based on quality function deployment and 2-additive measure. Furthermore, a consensus model that considers cooperative and non-cooperative behaviors of decision makers is applied to select the ideal mHealth app. Finally, an illustrative example is implemented to exhibit the utility and validity of the proposed model.

Optimal Interaction Priority Calculation From Hesitant Fuzzy Preference Relations Based on the Monte Carlo Simulation Method for the Acceptable Consistency and Consensus.

To address the situation where the complete consistency is unnecessary, a stepwise optimization model-based method for testing the acceptably additive consistency (AAC) of hesitant fuzzy preference relations (HFPRs) is introduced. Then, an AAC concept for HFPRs is defined. Meanwhile, incomplete HFPRs (iHFPRs) are discussed and a series of optimization models to acquire complete HFPRs is constructed. If the consistency is unacceptable, an optimization model for revising unacceptably consistent HFPRs under the conditions of the AAC and maximizing the ordinal consistency (OC) is offered. Subsequently, a model for minimizing the number of adjusted variables is presented. Considering the weighting information and the consensus for group decision making (GDM), the weights of fuzzy preference relations (FPRs) obtained from each individual HFPR and the decision makers (DMs) are determined using the distance measure. With regard to the consensus, two models for reaching the consensus requirement and minimizing the amount of revised variables are separately constructed, which are both based on the analysis of maximizing the OC. Furthermore, the thresholds of the additive consistency and the consensus are studied using the Monte Carlo simulation method. A GDM algorithm with HFPRs is offered. Finally, an example and comparison are provided to show the efficiency of the new procedure.

Fiber grating sensing interrogation system based on a modulated grating Y-branch tunable laser for core-and-cladding-integrated fiber Bragg grating temperature measurement.

Numerous studies have addressed various methods to interrogate fiber Bragg gratings (FBGs). However, conventional methods are ineffective for multipeak FBG demodulation. A core-and-cladding-integrated fiber Bragg grating (FBG) temperature-interrogation system, based on a modulated grating Y-branch (MG-Y) tunable laser and home-built FBG, is proposed in this study. The sensing system comprises an MG-Y tunable laser interrogation system, a 3-dB optical fiber coupler, a core-and-cladding-integrated FBG, a heating platform, and a personal computer. The core-and-cladding-integrated FBG with two reflection peaks is sampled by the designed MG-Y laser. The FBG has a period of 534 nm and a grating length of 2000 µm. It is fabricated in a single-mode fiber by femtosecond-laser writing through the fiber coating. The interrogator is suitable for temperature measurement via the core-and-cladding-integrated FBG. In tests of the temperature-interrogation system, a temperature change from 30 to 100 °C generates spectral shifts toward longer wavelengths for both the core and cladding reflection peaks. For the core and cladding, temperature sensing sensitivities of 111 and 113 pm/°C with linearities of 0.993 and 0.99, respectively, during heating and 117 and 120 pm/°C with linearity coefficients of 0.994 and 0.99, respectively, during cooling are achieved.

Characterization of metallic-packaging fiber Bragg grating sensors with coated and bare fibers.

Metallic packaging of fiber Bragg grating (FBG) sensors is developed using the ultrasonic welding method. Both polyimide-coated fiber and bare fiber could be bonded well to aluminum alloy substrate using Sn-Bi alloy. Two kinds of metal-packaged FBG sensors, coated FBG and bare FBG, are characterized for studying the thermal sensitivity, strain response, short-term creep, and temporal temperature response. Both FBG sensors showed increasing sensitivity with temperature from -40°C to 80°C. The metal-packaged coated FBG sensor displayed relative strengths in strain stability, repeatability, creep, spectra shape, and temperature response when compared with the bare one. Moreover, the boundaries between optical fiber and metal alloy are intact, and cross-sectional scanning electron microscope micrographs clearly illustrated that metal alloy coated well with the coated and bare fiber.

MiR-145 inhibited lipopolysaccharide-induced apoptosis of gastric mucosal via up-regulating JNK-mediated cytoprotective autophagy.

It has been reported that specific microRNA could inhibit apoptosis of gastric mucosa. Our study was designed to investigate the effect and mechanisms of miR-145 in gastric mucosa. Gastric mucosal cells (GES-1) were treated with null-vector or miR-145 over expression plasmid. Cell viability was determined by CCK-8 assay and detection of apoptosis by flow cytometry. Autophagic and apoptosis protein expression and c-Jun NH2-terminal kinase (JNK) phosphorylation were determined by Western blotting. Autophagy response and JNK activities were inhibited by specific inhibitor, 3MA or SP600125, respectively. LDH release assay was used to detect cytotoxicity. We confirmed that miR-145 triggered an autophagic response in GES-1 cells and depended on JNK activation. Blocking autophagy or JNK activation with specific inhibitor, 3MA or SP600125, potentiated cell death and caspase-3 activation. Furthermore, we confirmed that miR-145 enhanced the viability of GES-1 cells, phosphorylation of JNK and inhibited apoptosis of gastric mucosal miR-145 inhibited apoptosis of gastric mucosal via up-regulating JNK-mediated cytoprotective autophag.

Incorporation of iloprost in phospholipase-resistant phospholipid scaffold enhances its barrier protective effects on pulmonary endothelium.

Correction of barrier dysfunction and inflammation in acute lung injury (ALI) represents an important problem. Previous studies demonstrate barrier-protective and anti-inflammatory effects of bioactive lipid prostacyclin and its stable analog iloprost (ILO). We generated a phospholipase resistant synthetic phospholipid with iloprost attached at the sn-2 position (ILO-PC) and investigated its biological effects. In comparison to free ILO, ILO-PC caused sustained endothelial cell (EC) barrier enhancement, linked to more prolonged activation of Rap1 and Rac1 GTPases and their cytoskeletal and cell junction effectors: cortactin, PAK1, p120-catenin and VE-cadherin. ILO and ILO-PC equally efficiently suppressed acute, Rho GTPase-dependent EC hyper-permeability caused by thrombin. However, ILO-PC exhibited more sustained barrier-protective and anti-inflammatory effects in the model of chronic EC dysfunction caused by bacterial wall lipopolysacharide (LPS). ILO-PC was also more potent inhibitor of NFκB signaling and lung vascular leak in the murine model of LPS-induced ALI. Treatment with ILO-PC showed more efficient ALI recovery over 3 days after LPS challenge than free ILO. In conclusion, this study describes a novel synthetic phospholipid with barrier-enhancing and anti-inflammatory properties superior to existing prostacyclin analogs, which may be used as a prototype for future development of more efficient treatment for ALI and other vascular leak syndromes.

Anti-Inflammatory Effects of OxPAPC Involve Endothelial Cell-Mediated Generation of LXA4.

RATIONALE: Oxidation of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (OxPAPC) generates a group of bioactive oxidized phospholipid products with a broad range of biological activities. Barrier-enhancing and anti-inflammatory effects of OxPAPC on pulmonary endothelial cells are critical for prevention of acute lung injury caused by bacterial pathogens or excessive mechanical ventilation. Anti-inflammatory properties of OxPAPC are associated with its antagonistic effects on Toll-like receptors and suppression of RhoA GTPase signaling. OBJECTIVE: Because OxPAPC exhibits long-lasting anti-inflammatory and lung-protective effects even after single administration in vivo, we tested the hypothesis that these effects may be mediated by additional mechanisms, such as OxPAPC-dependent production of anti-inflammatory and proresolving lipid mediator, lipoxin A4 (LXA4). METHODS AND RESULTS: Mass spectrometry and ELISA assays detected significant accumulation of LXA4 in the lungs of OxPAPC-treated mice and in conditioned medium of OxPAPC-exposed pulmonary endothelial cells. Administration of LXA4 reproduced anti-inflammatory effect of OxPAPC against tumor necrosis factor-α in vitro and in the animal model of lipopolysaccharide-induced lung injury. The potent barrier-protective and anti-inflammatory effects of OxPAPC against tumor necrosis factor-α and lipopolysaccharide challenge were suppressed in human pulmonary endothelial cells with small interfering RNA-induced knockdown of LXA4 formyl peptide receptor-2 (FPR2/ALX) and in mFPR2-/- (mouse formyl peptide receptor 2) mice lacking the mouse homolog of human FPR2/ALX. CONCLUSIONS: This is the first demonstration that inflammation- and injury-associated phospholipid oxidation triggers production of anti-inflammatory and proresolution molecules, such as LXA4. This lipid mediator switch represents a novel mechanism of OxPAPC-assisted recovery of inflamed lung endothelium.

Indoor Air Pollution by Methylsiloxane in Household and Automobile Settings.

This study examines characteristics of atmospheric methylsiloxane pollution in indoor settings where interior renovation/redecoration is being undertaken, in addition to ordinary family homes and inside family cars. Concentrations of atmospheric methylsiloxane in these locations were approximately one order of magnitude higher than that in outdoor areas. The average indoor concentration of methylsiloxane where renovation was being undertaken was 9.4 µg/m3, which is slightly higher than that in an ordinary family home (7.88 µg/m3), while samples from family cars showed lower concentration (3.10 µg/m3). The indoor atmospheric concentration during renovation/redecoration work was significantly positively correlated with the duration of the work. The structure of atmospheric methylsiloxane pollution is basically the same in these three venues. The concentration of annulus siloxane was much higher than that of linear compounds (85% of the total methylsiloxane concentrations). Household dust in average family homes showed total methylsiloxane concentration of 9.5 µg/m3 (average); the structure mainly consisted of linear siloxane (approximately 98% of total concentration), thereby differing from that of atmospheric methylsiloxane pollution. The comparatively high concentration of methylsiloxane in these three venues indicates that interior renovation and decoration work, and even travelling in cars, can involve exposure to more serious siloxane contamination during everyday activities.

Alterations of lung microbiota in a mouse model of LPS-induced lung injury.

Acute lung injury (ALI) and the more severe acute respiratory distress syndrome are common responses to a variety of infectious and noninfectious insults. We used a mouse model of ALI induced by intratracheal administration of sterile bacterial wall lipopolysaccharide (LPS) to investigate the changes in innate lung microbiota and study microbial community reaction to lung inflammation and barrier dysfunction induced by endotoxin insult. One group of C57BL/6J mice received LPS via intratracheal injection (n = 6), and another received sterile water (n = 7). Bronchoalveolar lavage (BAL) was performed at 72 h after treatment. Bacterial DNA was extracted and used for qPCR and 16S rRNA gene-tag (V3-V4) sequencing (Illumina). The bacterial load in BAL from ALI mice was increased fivefold (P = 0.03). The community complexity remained unchanged (Simpson index, P = 0.7); the Shannon diversity index indicated the increase of community evenness in response to ALI (P = 0.07). Principal coordinate analysis and analysis of similarity (ANOSIM) test (P = 0.005) revealed a significant difference between microbiota of control and ALI groups. Bacteria from families Xanthomonadaceae and Brucellaceae increased their abundance in the ALI group as determined by Metastats test (P < 0.02). In concordance with the 16s-tag data, Stenotrohomonas maltophilia (Xanthomonadaceae) and Ochrobactrum anthropi (Brucellaceae) were isolated from lungs of mice from both groups. Metabolic profiling of BAL detected the presence of bacterial substrates suitable for both isolates. Additionally, microbiota from LPS-treated mice intensified IL-6-induced lung inflammation in naive mice. We conclude that the morbid transformation of ALI microbiota was attributed to the set of inborn opportunistic pathogens thriving in the environment of inflamed lung, rather than the external infectious agents.

Role of Krev Interaction Trapped-1 in Prostacyclin-Induced Protection against Lung Vascular Permeability Induced by Excessive Mechanical Forces and Thrombin Receptor Activating Peptide 6.

Mechanisms of vascular endothelial cell (EC) barrier regulation during acute lung injury (ALI) or other pathologies associated with increased vascular leakiness are an active area of research. Adaptor protein krev interaction trapped-1 (KRIT1) participates in angiogenesis, lumen formation, and stabilization of EC adherens junctions (AJs) in mature vasculature. We tested a role of KRIT1 in the regulation of Rho-GTPase signaling induced by mechanical stimulation and barrier dysfunction relevant to ventilator-induced lung injury and investigated KRIT1 involvement in EC barrier protection by prostacyclin (PC). PC stimulated Ras-related protein 1 (Rap1)-dependent association of KRIT1 with vascular endothelial cadherin at AJs, with KRIT1-dependent cortical cytoskeletal remodeling leading to EC barrier enhancement. KRIT1 knockdown exacerbated Rho-GTPase activation and EC barrier disruption induced by pathologic 18% cyclic stretch and thrombin receptor activating peptide (TRAP) 6 and attenuated the protective effects of PC. In the two-hit model of ALI caused by high tidal volume (HTV) mechanical ventilation and TRAP6 injection, KRIT1 functional deficiency in KRIT1(+/-) mice increased basal lung vascular leak and augmented vascular leak and lung injury caused by exposure to HTV and TRAP6. Down-regulation of KRIT1 also diminished the protective effects of PC against TRAP6/HTV-induced lung injury. These results demonstrate a KRIT1-dependent mechanism of vascular EC barrier control in basal conditions and in the two-hit model of ALI caused by excessive mechanical forces and TRAP6 via negative regulation of Rho activity and enhancement of cell junctions. We also conclude that the stimulation of the Rap1-KRIT1 signaling module is a major mechanism of vascular endothelial barrier protection by PC in the injured lung.

Oxidized phospholipids protect against lung injury and endothelial barrier dysfunction caused by heat-inactivated Staphylococcus aureus.

Increased endothelial cell (EC) permeability and vascular inflammation along with alveolar epithelial damage are key features of acute lung injury (ALI). Products of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine oxidation (OxPAPC) showed protective effects against inflammatory signaling and vascular EC barrier dysfunction induced by gram-negative bacterial wall lipopolysaccharide (LPS). We explored the more general protective effects of OxPAPC and investigated whether delayed posttreatment with OxPAPC boosts the recovery of lung inflammatory injury and EC barrier dysfunction triggered by intratracheal injection of heat-killed gram-positive Staphylococcus aureus (HKSA) bacteria. HKSA-induced pulmonary EC permeability, activation of p38 MAP kinase and NF-κB inflammatory cascades, secretion of IL-8 and soluble ICAM1, fibronectin deposition, and expression of adhesion molecules ICAM1 and VCAM1 by activated EC were significantly attenuated by cotreatment as well as posttreatment with OxPAPC up to 16 h after HKSA addition. Remarkably, posttreatment with OxPAPC up to 24 h post-HKSA challenge dramatically accelerated lung recovery by restoring lung barrier properties monitored by Evans blue extravasation and protein content in bronchoalveolar lavage (BAL) fluid and reducing inflammation reflected by decreased MIP-1, KC, TNF-α, IL-13 levels and neutrophil count in BAL samples. These studies demonstrate potent in vivo and in vitro protective effects of posttreatment with anti-inflammatory oxidized phospholipids in the model of ALI caused by HKSA. These results warrant further investigations into the potential use of OxPAPC compounds combined with antibiotic therapies as a treatment of sepsis and ALI induced by gram-positive bacterial pathogens.

Role of microtubules in attenuation of PepG-induced vascular endothelial dysfunction by atrial natriuretic peptide.

Apart from control of circulating fluid, atrial natriuretic peptide (ANP) exhibits anti-inflammatory effects in the lung. However, molecular mechanisms of ANP anti-inflammatory effects are not well-understood. Peripheral microtubule (MT) dynamics is essential for agonist-induced regulation of vascular endothelial permeability. Here we studied the role of MT-dependent signaling in ANP protective effects against endothelial cell (EC) barrier dysfunction and acute lung injury induced by Staphylococcus aureus-derived peptidoglican-G (PepG). PepG-induced vascular endothelial dysfunction was accompanied by MT destabilization and disruption of MT network. ANP attenuated PepG-induced MT disassembly, NFκB signaling and activity of MT-associated Rho activator GEF-H1 leading to attenuation of EC inflammatory activation reflected by expression of adhesion molecules ICAM1 and VCAM1. ANP-induced EC barrier preservation and MT stabilization were linked to phosphorylation and inactivation of MT-depolymerizing protein stathmin. Expression of stathmin phosphorylation-deficient mutant abolished ANP protective effects against PepG-induced inflammation and EC permeability. In contrast, siRNA-mediated stathmin knockdown prevented PepG-induced peripheral MT disassembly and endothelial barrier dysfunction. ANP protective effects in a murine model of PepG-induced lung injury were associated with increased phosphorylation of stathmin, while exacerbated lung injury in the ANP knockout mice was accompanied by decreased pool of stable MT. Stathmin knockdown in vivo reversed exacerbation of lung injury in the ANP knockout mice. These results show a novel MT-mediated mechanism of endothelial barrier protection by ANP in pulmonary EC and animal model of PepG-induced lung injury via stathmin-dependent control of MT assembly.

Prostacyclin post-treatment improves LPS-induced acute lung injury and endothelial barrier recovery via Rap1.

Protective effects of prostacyclin (PC) or its stable analog beraprost against agonist-induced lung vascular inflammation have been associated with elevation of intracellular cAMP and Rac GTPase signaling which inhibited the RhoA GTPase-dependent pathway of endothelial barrier dysfunction. This study investigated a distinct mechanism of PC-stimulated lung vascular endothelial (EC) barrier recovery and resolution of LPS-induced inflammation mediated by small GTPase Rap1. Efficient barrier recovery was observed in LPS-challenged pulmonary EC after prostacyclin administration even after 15 h of initial inflammatory insult and was accompanied by the significant attenuation of p38 MAP kinase and NFκB signaling and decreased production of IL-8 and soluble ICAM1. These effects were reproduced in cells post-treated with 8CPT, a small molecule activator of Rap1-specific nucleotide exchange factor Epac. By contrast, pharmacologic Epac inhibitor, Rap1 knockdown, or knockdown of cell junction-associated Rap1 effector afadin attenuated EC recovery caused by PC or 8CPT post-treatment. The key role of Rap1 in lung barrier restoration was further confirmed in the murine model of LPS-induced acute lung injury. Lung injury was monitored by measurements of bronchoalveolar lavage protein content, cell count, and Evans blue extravasation and live imaging of vascular leak over 6 days using a fluorescent tracer. The data showed significant acceleration of lung recovery by PC and 8CPT post-treatment, which was abrogated in Rap1a(-/-) mice. These results suggest that post-treatment with PC triggers the Epac/Rap1/afadin-dependent mechanism of endothelial barrier restoration and downregulation of p38MAPK and NFκB inflammatory cascades, altogether leading to accelerated lung recovery.

Asef controls vascular endothelial permeability and barrier recovery in the lung.

Increased levels of hepatocyte growth factor (HGF) in injured lungs may reflect a compensatory response to diminish acute lung injury (ALI). HGF-induced activation of Rac1 GTPase stimulates endothelial barrier protective mechanisms. This study tested the involvement of Rac-specific guanine nucleotide exchange factor Asef in HGF-induced endothelial cell (EC) cytoskeletal dynamics and barrier protection in vitro and in a two-hit model of ALI. HGF induced membrane translocation of Asef and stimulated Asef Rac1-specific nucleotide exchange activity. Expression of constitutively activated Asef mutant mimicked HGF-induced peripheral actin cytoskeleton enhancement. In contrast, siRNA-induced Asef knockdown or expression of dominant-negative Asef attenuated HGF-induced Rac1 activation evaluated by Rac-GTP pull down and FRET assay with Rac1 biosensor. Molecular inhibition of Asef attenuated HGF-induced peripheral accumulation of cortactin, formation of lamellipodia-like structures, and enhancement of VE-cadherin adherens junctions and compromised HGF-protective effect against thrombin-induced RhoA GTPase activation, Rho-dependent cytoskeleton remodeling, and EC permeability. Intravenous HGF injection attenuated lung inflammation and vascular leak in the two-hit model of ALI induced by excessive mechanical ventilation and thrombin signaling peptide TRAP6. This effect was lost in Asef(-/-) mice. This study shows for the first time the role of Asef in HGF-mediated protection against endothelial hyperpermeability and lung injury.

Asef mediates HGF protective effects against LPS-induced lung injury and endothelial barrier dysfunction.

Increased vascular endothelial permeability and inflammation are major pathological mechanisms of pulmonary edema and its life-threatening complication, the acute respiratory distress syndrome (ARDS). We have previously described potent protective effects of hepatocyte growth factor (HGF) against thrombin-induced hyperpermeability and identified the Rac pathway as a key mechanism of HGF-mediated endothelial barrier protection. However, anti-inflammatory effects of HGF are less understood. This study examined effects of HGF on the pulmonary endothelial cell (EC) inflammatory activation and barrier dysfunction caused by the gram-negative bacterial pathogen lipopolysaccharide (LPS). We tested involvement of the novel Rac-specific guanine nucleotide exchange factor Asef in the HGF anti-inflammatory effects. HGF protected the pulmonary EC monolayer against LPS-induced hyperpermeability, disruption of monolayer integrity, activation of NF-kB signaling, expression of adhesion molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and production of IL-8. These effects were critically dependent on Asef. Small-interfering RNA-induced downregulation of Asef attenuated HGF protective effects against LPS-induced EC barrier failure. Protective effects of HGF against LPS-induced lung inflammation and vascular leak were also diminished in Asef knockout mice. Taken together, these results demonstrate potent anti-inflammatory effects by HGF and delineate a key role of Asef in the mediation of the HGF barrier protective and anti-inflammatory effects. Modulation of Asef activity may have important implications in therapeutic strategies aimed at the treatment of sepsis and acute lung injury/ARDS-induced gram-negative bacterial pathogens.

Attenuation of lipopolysaccharide-induced lung vascular stiffening by lipoxin reduces lung inflammation.

Reversible changes in lung microstructure accompany lung inflammation, although alterations in tissue micromechanics and their impact on inflammation remain unknown. This study investigated changes in extracellular matrix (ECM) remodeling and tissue stiffness in a model of LPS-induced inflammation and examined the role of lipoxin analog 15-epi-lipoxin A4 (eLXA4) in the reduction of stiffness-dependent exacerbation of the inflammatory process. Atomic force microscopy measurements of live lung slices were used to directly measure local tissue stiffness changes induced by intratracheal injection of LPS. Effects of LPS on ECM properties and inflammatory response were evaluated in an animal model of LPS-induced lung injury, live lung tissue slices, and pulmonary endothelial cell (EC) culture. In vivo, LPS increased perivascular stiffness in lung slices monitored by atomic force microscopy and stimulated expression of ECM proteins fibronectin, collagen I, and ECM crosslinker enzyme, lysyl oxidase. Increased stiffness and ECM remodeling escalated LPS-induced VCAM1 and ICAM1 expression and IL-8 production by lung ECs. Stiffness-dependent exacerbation of inflammatory signaling was confirmed in pulmonary ECs grown on substrates with high and low stiffness. eLXA4 inhibited LPS-increased stiffness in lung cross sections, attenuated stiffness-dependent enhancement of EC inflammatory activation, and restored lung compliance in vivo. This study shows that increased local vascular stiffness exacerbates lung inflammation. Attenuation of local stiffening of lung vasculature represents a novel mechanism of lipoxin antiinflammatory action.

Extra projection data identification method for fast-continuous-rotation industrial cone-beam CT.

Fast-continuous-rotation is an effective measure to improve the scanning speed and decrease the radiation dose for cone-beam CT. However, because of acceleration and deceleration of the motor, as well as the response lag of the scanning control terminals to the host PC, uneven-distributed and redundant projections are inevitably created, which seriously decrease the quality of the reconstruction images. In this paper, we first analyzed the aspects of the theoretical sequence chart of the fast-continuous-rotation mode. Then, an optimized sequence chart was proposed by extending the rotation angle span to ensure the effective 2π-span projections were situated in the stable rotation stage. In order to match the rotation angle with the projection image accurately, structure similarity (SSIM) index was used as a control parameter for extraction of the effective projection sequence which was exactly the complete projection data for image reconstruction. The experimental results showed that SSIM based method had a high accuracy of projection view locating and was easy to realize.

Autoreactive thymic B cells are efficient antigen-presenting cells of cognate self-antigens for T cell negative selection.

The thymus contains a population of B cells that colocalize with dendritic cells and medullary thymic epithelial cells in the thymic medulla. The development and functional significance of these cells are largely unknown. Using recombination-activating gene 2 GFP reporter mice along with parabiosis experiments, we demonstrate that the vast majority of thymic B cells develop from progenitors within the thymus. Thymic B cells express unique phenotypic markers compared with peripheral B cells; particularly they express high levels of MHC class II, suggesting that they are poised to present self-antigens efficiently. Using Ig knock-in and T-cell receptor transgenic mice specific for the self-antigen glucose-6-phosphate isomerase, we show that autoreactive thymic B cells serve as efficient antigen-presenting cells for T cell negative selection even when they are present at low frequencies. Furthermore, the endogenous thymic B-cell repertoire also functions in this capacity. These results suggest that developing thymic B cells could efficiently capture a broad array of autoantigens through their B-cell receptors, presenting peptides derived from those autoantigens to developing thymocytes and eliminating cognate T cells.

[Study on equilibrium adsorption of volatile chlorinated hydrocarbons on humid soils].

Adsorption is one of the principal mechanisms for soil contamination by volatile chlorinated hydrocarbons (VCHs). Dynamic adsorption experiments were carried out to study the equilibrium adsorption of four common VCHs pollutants onto eight typical soils in China. Results showed that dry soils had far greater adsorption capacity than humid soils. The soil adsorption capacity sharply decreased with the increase in the soil water content, and then reached a plateau as the water content rose to 10% or above. The adsorption isotherms of trichloroethylene (TCE), tetrachloroethylene (PCE) and 1,1,1-trichloroethane (MC) could be fitted with Henry's equation, while the adsorption isotherms of 1,1,2-trichloroethane (1,1,2-TCA) could be fitted with Freundlich model. The adsorption capacities of VCHs on humid soils were principally influenced by the content of soil organic carbon (SOC), but sometimes also impacted by the composition of SOC and the polarities of the VCHs molecules. Low polar molecules such as TCE and PCE showed adsorption capacities positively dependent on the SOC content. High polar molecules such as MC and 1,1,2-TCA displayed adsorption behavior not only influenced by SOC content but also by the SOC composition of high SOC content soils such as black soil. An adsorption equilibrium simulation model was developed for TCE and PCE on humid soils, the predicted values correlating well with the measured values (n = 80, R2 = 0.98).