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Rural four-lane roadways provide important transportation accessibility and mobility to populations in rural areas. It is a challenge for practitioners to determine cross-section types when both benefits and costs need to be considered. Crash Modification Factors (CMFs) are developed to evaluate the safety effectiveness of alternative designs. However, safety effectiveness could vary significantly across contexts. Thus, this study aims to estimate CMFs for alternative cross sections of rural four-lane roadways under different contexts characterized by traffic volume, truck percentage, and access point density. Using Georgia state-wide crash data, this study developed Safety Performance Functions (SPFs) to predict crash frequencies for different contexts. Considering linearity and independence assumptions of traditional negative binomial SPFs, this study adopts Bayesian generalized negative binomial modeling approaches to relax those assumptions and only follows the Bayes rule to form SPFs for CMF estimation. This study focuses on four typical cross-sections including: (1) non-traversable medians; (2) two-way-left-turn lanes; (3) 4-ft flush medians; and (4) undivided roadways with double-yellow lines (the base cross-section design). The results show that CMFs vary significantly across different contexts. Compared with the base cross-section design, safety benefits of the other three designs can be either positive or negative under different traffic or road conditions. For example, 4-ft flush medians are found to have positive safety benefits (CMF 1) under greater average daily traffic volumes (e.g., ≥ 15,000). The findings suggest that, to enhance roadway safety, practitioners should vary cross-section designs for different rural contexts.

Background and aims Itaconate, a metabolite of the tricarboxylic acid cycle, plays anti-inflammatory roles in macrophages during endotoxemia. The mechanisms underlying its anti-inflammatory roles have been shown to be mediated by the modulation of oxidative stress, an important mechanism of hepatic ischemia-reperfusion (I/R) injury. However, the role of itaconate in liver I/R injury is unknown. Approach and results We found that deletion of immune-responsive gene 1 (IRG1), encoding for the enzyme producing itaconate, exacerbated liver injury and systemic inflammation. Furthermore, bone marrow adoptive transfer experiments indicated that deletion of IRG1 in both hematopoietic and nonhematopoietic compartments contributes to the protection mediated by IRG1 after I/R. Interestingly, the expression of IRG1 was up-regulated in hepatocytes after I/R and hypoxia/reoxygenation-induced oxidative stress. Modulation of the IRG1 expression levels in hepatocytes regulated hepatocyte cell death. Importantly, addition of 4-octyl itaconate significantly improved liver injury and hepatocyte cell death after I/R. Furthermore, our data indicated that nuclear factor erythroid 2-related factor 2 (Nrf2) is required for the protective effect of IRG1 on mouse and human hepatocytes against oxidative stress-induced injury. Our studies document the important role of IRG1 in the acute setting of sterile injury induced by I/R. Specifically, we provide evidence that the IRG1/itaconate pathway activates Nrf2-mediated antioxidative response in hepatocytes to protect liver from I/R injury. Conclusions Our data expand on the importance of IRG1/itaconate in nonimmune cells and identify itaconate as a potential therapeutic strategy for this unfavorable postsurgical complication.

Tunnels are critical areas for highway safety because the severity of crashes in tunnels tends to be more serious. Controlling vehicle speed is regarded as a feasible measure to reduce the accident rate in the tunnel entrance and exit areas. This paper aims to evaluate the effectiveness of three types of speed reduction markings (SRMs) in tunnel entrance and exit zones by conducting a driving simulation experiment. For this study, 25 drivers completed the driving tasks in the day and night scenarios. The vehicle speed and acceleration data were collected for analysing and the relative speed contrast, time mean speed and acceleration were adopted as indices to evaluate the effectiveness of SRMs. The repeated ANOVA test results revealed that SRMs have a significant effect in reducing vehicle speed, especially in the exit zone. Colour Anti-skid Markings (CASMs) produced a more obvious deceleration in the entrance zone. In the entrance zone, a similar downward trend was performed in the situation of NSRMs and SRMs, but a lower speed occurred in case of SRMs. Besides, CASMs work better and cause an obvious gap of 10 km/h in daytime and 5 km/h at night compared to the speed without SRMs. In the exit zone, the present study supports the conclusion that the drivers are prone to accelerate. Our results showed that the drivers accelerated in case of NSRMs, while they slowed down in case of SRMs. Thus, SRMs are necessarily implemented in the highway tunnel entrance and exit zones. Our study also indicates that though CASMs result in lower speed at night, the Transverse Speed Reduction Markings(TSRMs) have a better performance than CASMs in daytime. The investigation provides essential information for developing a new marking design criterion and intelligent driver support systems in the highway tunnel zones.

A new species, Blumea htamanthii Y.L. Peng, C.X. Yang & Y. Luo from Myanmar is described. The new species is distinguished from B. bifoliata by its leaves with short petioles, abaxially purple, leaf blade with papillary hair and sparse multicellular villous, capitula with 1–4 heads, glabrous florets and usually unbranched stems. A key to Blumea species in Myanmar is provided.

In this work, we describe a new species, Ainsliaea daheishanensis Y.L.Peng, C.X.Yang & Y.Luo, based on morphological traits. The new species was discovered in the mountains of Yunnan, near the border between Myanmar and China. The new species differs from the phenotypically closely-related Ainsliaea foliosa Handel-Mazzetti in the morphology of the leaf veins and phyllaries, those having a protruding abaxial reticulate pattern in the lower and median part of stem with white hairs and narrow inner phyllaries. A key to the three closed Ainsliaea species occurring in China is provided.

Safety Performance Functions (SPFs) can be used to predict the number of crashes for highway facilities by site characteristics, including traffic exposures and other specific site factors. The traditional approach to developing SPFs relies on factors that are observed in the data and has an unstated assumption that the relationships between safety performance and observed factors are stationary. However, there might be factors that are not captured by the data but also have significant impacts on roadway safety performance. These factors can lead to significant unobserved heterogeneity in safety performance at different sites. Failure to capture such unobserved heterogeneity in developing SPFs may result in biases and decrease the predictive accuracy. Given the interactions between highway traffic and roadway environments, the unobserved heterogeneity is likely related to the geographic space of the highway network. This study employs a spatial modeling approach, namely Geographically Weighted Negative Binomial Regression (GWNBR), to incorporate spatial heterogeneity into SPF model estimation. The GWNBR model can generate a local SPF for every site instead of a global SPF for one entire jurisdiction (e.g., a state) from the traditional approach. Local SPFs (or l-SPFs) are high-resolution and may be difficult for practitioners to use. To support the implementation of l-SPFs, this study proposes a method to aggregate l-SPFs to various geographic levels. This study first uses the 2014-2018 geo-referenced crash data from Alabama to develop l-SPFs for two-way STOP-controlled (TWST) three-leg intersections on rural two-lane two-way (TLTW) roadways in the state. The results show that l-SPFs vary substantially across Alabama. For example, the coefficients of traffic volume (AADT) on major roads range from 0.126 to 1.203 across different areas of the state. Then, an aggregation method based on K-means clustering is demonstrated to aggregate l-SPFs to various geographic levels of interest. The l-SPFs and their aggregation provide geographic flexibility in developing countermeasures and allocating funds to improve traffic safety considering local conditions.

Accidents involving electric bicycles, a popular means of transportation in China during peak traffic periods, have increased. However, studies have seldom attempted to detect the unique crash consequences during this period. This study aims to explore the factors influencing injury severity in electric bicyclists during peak traffic periods and provide recommendations to help devise specific management strategies. The random-parameters logit or mixed logit model is used to identify the relationship between different factors and injury severity. The injury severity is divided into four categories. The analysis uses automobile and electric bicycle crash data of Xi’an, China, between 2014 and 2019. During the peak traffic periods, the impact of low visibility significantly varies with factors such as areas with traffic control or without streetlights. Furthermore, compared with traveling in a straight line, three different turnings before the crash reduce the likelihood of severe injuries. Roadside protection trees are the most crucial measure guaranteeing riders’ safety during peak traffic periods. This study reveals the direction, magnitude, and randomness of factors that contribute to electric bicycle crashes. The results can help safety authorities devise targeted transportation safety management and planning strategies for peak traffic periods.

BackgroundThe mechanisms by which moderate tidal volume ventilation (MTV) exacerbates preexisting lung injury are unclear. We hypothesized that systemic endotoxemia via the gut-lung axis would lead to non-canonical and canonical inflammasome activation and pyroptosis in a two-hit model involving polyinosinic-polycytidylic acid (Poly(I:C)), a synthetic analog of dsRNA and MTV and that this would associate with acute lung injury (ALI).MethodsAnesthetized mice were administered Poly(I:C) intratracheally and then 6 h later, they were mechanically ventilated for 4 h with otherwise non-injurious MTV (10ml/kg). Changes in intestinal and alveolar capillary permeability were measured. Further documentation of ALI was assessed by evans blue albumin permeability, protein and IL-1 family concentration in bronchoalveolar lavage fluid (BALF) or plasma, and histopathology in cohorts of wildtype (WT), whole body genetically ablated caspase-11 (caspase-11-/-), caspase-1/caspase-11 double knockout (caspase-1/11-/-), gasdermin D (GSDMD)-/-, nucleotide-binding domain leucine-rich repeat-containing protein 3 (NLRP3)-/- and advanced glycosylation end product-specific receptor (RAGE) -/- mice.ResultsNon-injurious MTV exacerbated the mild lung injury associated with Poly(I:C) administration. This included the disruption of alveolar-capillary barrier and increased levels of interleukin (IL)-6, high mobility group proteins 1 (HMGB-1), IL-1β in BALF and IL-18 in plasma. Combined (Poly(I:C)-MTV) injury was associated with increase in gastrointestinal permeability and endotoxin in plasma and BALF. Poly(I:C)-MTV injury was sensitive to caspase-11 deletion with no further contribution of caspase-1 except for maturation and release of IL-18 (that itself was sensitive to deletion of NLRP3). Combined injury led to large increases in caspase-1 and caspase-11. Genetic ablation of GSDMD attenuated alveolar-capillary disruption and release of cytokines in combined injury model.ConclusionsThe previously noted exacerbation of mild Poly(I:C)-induced ALI by otherwise non-injurious MTV is associated with an increase in gut permeability resulting in systemic endotoxemia. The gut-lung axis resulted in activation of pulmonary non-canonical (cytosolic mediated caspase-11 activation) and canonical (caspase-1) inflammasome (NLRP3) mediated ALI in this two-hit model resulting in GSDMD sensitive alveolar capillary barrier disruption, pyroptosis (alveolar macrophages) and cytokine maturation and release (IL-1β; IL-18). Pharmacologic strategies aimed at disrupting communication between gut and lung, inhibition of inflammasomes or GSDMD in pyroptosis may be useful in ALI.

Background: Neuroblastoma (NB) is the most commonly diagnosed malignancy among pediatric patients with a high level of heterogeneity. NB is rarely seen in adult patients, yet adult-onset NB is associated with poor outcome and distinct clinical features from pediatric NB. Guidelines for the management of adult-onset NB are not yet defined and the treatment is largely dependent on the experience of corresponding oncologists. Previous reports on adult-onset NB have mostly been case reports or case series, without high-quality, population-based cohort study. Our study aims to provide new insights and promotes understanding of adult-onset NB using the data from Surveillance, Epidemiology and End Results (SEER) program.Methods: We extracted data of primary NB patients diagnosed by positive histology during 1975-2016 from the SEER database, and grouped the patients according to the age of diagnosis. Competing-risk model and Kaplan-Meier plot were used to compare survival rates of adult-onset neuroblastoma with pediatric neuroblastoma. Cox proportional hazard regression model was used in univariate and multivariate analysis to identify prognostic factors affecting overall and cancer-specific survival rates in adult patients. A nomogram was developed according to the multivariate model and internally validated using receiver operator curve (ROC) and decision curve analysis (DCA).Results: We found a worsened outcome (Median survival time 31 vs 70 months) and distinct clinical characteristics in adults compared with adolescents. Univariate analysis revealed that age (HR=1.7627, 95%CI: 1.1937-2.6027, p = 0.004), surgery (HR=0.3968, 95%CI: 0.2691-0.5852, p Conclusion: In conclusion, our study provided novel evidence on prognosis of adult-onset NB using large-scale populational database and identified surgical intervention as the most effective treatment toward adult-onset NB. Our nomogram can serve as potential prediction and risk-stratification tool in clinical practice.

Supplemental material, sj-docx-1-trr-10.1177_03611981211007141 for Bayesian Approach to Developing Context-Based Crash Modification Factors for Medians on Rural Four-Lane Roadways by Xiaobing Li, Jun Liu, Chenxuan Yang and Timothy Barnett in Transportation Research Record

Background: The mechanisms by which moderate tidal volume ventilation (MTV) may exacerbate preexisting lung injury remain unclear. We hypothesized that in two hit model (polyinosinic-polycytidylic acid (Poly(I:C)), a synthetic analog of dsRNA and MTV), systemic endotoxemia via gut-lung axis would lead to non-canonical (i.e. caspase-11 dependent) and canonical (caspase-1 dependent) inflammasome activation and programmed necrotic cell death (pyroptosis) contributing to acute lung injury (ALI) in intact mice.Methods: Anesthetized mice were administered Poly(I:C) intratracheally and then 6 h later, they were mechanically ventilated for 4 h with otherwise non-injurious MTV (10ml/kg). Changes in intestinal and alveolar capillary permeability were measured. Further documentation of ALI was assessed by evans blue albumin permeability, protein and IL-1 family concentration in bronchoalveolar lavage fluid (BALF) or plasma, and histopathology in cohorts of wildtype, whole body genetically ablated caspase-11 (caspase-11-/-), caspase-1/caspase-11 double knockout (caspase-1/11-/-), gasdermin D (GSDMD-/-), and NLRP3-/- mice. Results: Non-injurious MTV exacerbated mild Poly(I:C) lung injury including disruption of alveolar-capillary barrier and increased levels of IL-6, HMGB1, IL-1β in BALF and IL-18 in plasma. Combined (Poly(I:C)-MTV) injury was associated with increase in gastrointestinal permeability and endotoxin in plasma and BALF. Poly(I:C)-MTV injury was sensitive to caspase-11 deletion with no further contribution of caspase-1 except for maturation and release of IL-18 (that itself was sensitive to deletion of NLRP3). Combined injury led to large increases in pro-caspase-11 and its cleaved product as well as cleaved product of caspase-1. Genetic ablation of GSDMD attenuated alveolar-capillary disruption and maturation and release of cytokines in combined injury model.Conclusions: The previously noted TLR-4 independent exacerbation of mild Poly(I:C)-induced ALI by otherwise non-injurious MTV is associated with an increase in gut permeability resulting in systemic endotoxemia. The gut-lung axis resulted in activation of pulmonary non-canonical (cytosolic mediated caspase-11 activation) and canonical (caspase-1) inflammasome (NLRP3) mediated ALI in this two hit model resulting in GSDMD sensitive alveolar capillary barrier disruption, pyroptosis (in alveolar macrophages) and cytokine maturation and release (IL-1β; IL-18). Pharmacologic strategies at disrupting communication between gut and lung, inhibition of inflammasomes or effector molecule (GSDMD) in pyroptosis may be useful in ALI.

The connection of a high percentage of renewable energy to the grid is an significant direction in the future research of the power system, but a large number of inverter-based nonsynchronous machine sources may cause complex resonance problems when connected to the microgrid. With the purpose of revealing the resonance characteristics of multi nonsynchronous machine source under grid connection, this paper first considers the current control, voltage feed-forward and pulse width modulation to derive the system impedance mathematical model of the inverter, and based on PSCAD / EMTDC to prove the impedance model. On this basis, the equivalent impedance model considering grid impedance and multi grid-connection inverter is constructed. Based on the impedance analysis, the effects of current regulator control parameters and filter parameters changes on the system resonance characteristics are analyzed in detail. The simulation results show that the filter capacitance take greater effect on the system resonance frequency, while the current regulator control parameters have little impact on the system resonance frequency.

Notch or STING, which is in charge of CD4 T cell fate?, Dysregulation of T cell apoptosis contributes to the pathogenesis of acute systemic inflammation–induced immunosuppression, as seen in sepsis and trauma. However, the regulatory mechanisms of T cell apoptosis are unclear. Activation of stimulator of interferon genes (STING) has been shown to induce T cell apoptosis. Notch was previously identified as the top negative regulator of STING in macrophages through a kinase inhibitor library screening. However, how Notch signaling regulates STING activation in T cells is unknown. Here, using a γ-secretase inhibitor to block Notch signaling, we found that Notch protected CD4 T cells from STING-mediated apoptosis during endotoxemia. Mechanistically, Notch intracellular domain (NICD) interacted with STING at the cyclic dinucleotide (CDN) binding domain and competed with CDN to inhibit STING activation. In conclusion, our data reveal a previously unidentified role of Notch in negative regulation of STING-mediated apoptosis in CD4 T cells.

Additional file 1: Table S1. Composition of rodent special diets. Table S2. Primer sequence used for RT-PCR.

High-mobility group box-1 (HMGB1), a ubiquitous nuclear protein, acts as a late mediator of lethality when released extracellularly during sepsis. The major source of circulating HMGB1 in sepsis is hepatocytes. However, the mechanism of HMGB1 release of hepatocytes during sepsis is not very clear. We have previously shown that bacterial endotoxin [lipopolysaccharide (LPS)] sensing pathways, including Toll-like receptor (TLR)4 and caspase-11, regulate hepatocyte HMGB1 release in response to LPS. Here, we report the novel function of caspase-11 and gasdermin D (GsdmD) in LPS-induced active HMGB1 released from hepatocytes. HMGB1 release during endotoxemia was caspase-11/GsdmD dependent via an active way in vivo and in vitro. Caspase-11/GsdmD was responsible for HMGB1 translocation from nucleus to the cytoplasm via calcium changing-induced phosphorylation of calcium-calmodulin kinase kinase (camkk)β during endotoxemia. Cleaved GsdmD accumulated on the endoplasmic reticulum, suggesting this may lead to calcium leak and intracellular calcium increase. Furthermore, we investigated that exosome was an important pathway for HMGB1 release from hepatocytes; this process was dependent on TLR4, independent of caspase-11 and GsdmD in vivo and in vitro. These findings provide a novel mechanism that TLR4 signaling results in an increase in caspase-11 expression, as well as increased exosome release, while caspase-11/GsdmD activation/cleavage leads to accumulation of HMGB1 in the cytoplasm through a process associated with the release of calcium from the endoplasmic reticulum and camkkβ activation.

Thymic stromal lymphopoietin (TSLP) is a cytokine mainly released by epithelial cells that plays important roles in inflammation, autoimmune disease, and cancer. While TSLP is expressed in the liver at high levels, the role of TSLP in liver ischemia/reperfusion (I/R) injury remains unknown. Experiments were carried out to determine the role of TSLP in liver I/R injury. Wild-type (WT) and TSLP receptor–knockout (TSLPR(–/–)) mice were subjected to liver partial warm I/R injury. Liver injury was assessed by measuring serum alanine aminotransferase (ALT) level, necrotic areas by liver histology, hepatocyte death, and local hepatic inflammatory responses. Signal pathways were explored in vivo and in vitro to identify possible mechanisms for TSLP in I/R injury. TSLP and TSLPR protein expression increased during liver I/R in vivo and following hepatocyte hypoxia/reoxygenation in vitro. Deletion of TSLPR or neutralization of TSLP with anti-TSLP antibody exacerbated liver injury in terms of serum ALT levels as well as necrotic areas in liver histology. Administration of exogenous recombinant mouse TSLP to WT mice significantly reduced liver damage compared with controls, but failed to prevent I/R injury in TSLPR(–/–) mice. TSLP induced autophagy in hepatocytes during liver I/R injury. Mechanistically, Akt was activated in WT mice during liver I/R injury. The opposite results were observed in TSLPR(–/–) mice. In addition, TSLP could directly induce Akt activation in hepatocytes independent of nonparenchymal cells in vitro. Furthermore, the Akt agonist, insulin-like growth factor-1 (IGF-1), prevented I/R injury in TSLPR(–/–) mice and an Akt inhibitor, LY294002, blocked the protective effects of TSLP in WT mice subjected to I/R. Our data indicate that TSLP protects against liver I/R injury via activation of the PI3K/Akt pathway. Through this pathway, TSLP induces autophagy in hepatocytes. Thus, TSLP is a potent inhibitor of stress-induced hepatocyte necrosis.

Fibroblastic reticular cells (FRCs), a subpopulation of stromal cells in lymphoid organs and fat-associated lymphoid clusters (FALCs) in adipose tissue, play immune-regulatory roles in the host response to infection and may be useful as a form of cell therapy in sepsis. Here, we found an unexpected major role of TLR9 in controlling peritoneal immune cell recruitment and FALC formation at baseline and after sepsis induced by cecal ligation and puncture (CLP). TLR9 regulated peritoneal immunity via suppression of chemokine production by FRCs. Adoptive transfer of TLR9-deficient FRCs more effectively decreased mortality, bacterial load, and systemic inflammation after CLP than WT FRCs. Importantly, we found that activation of TLR9 signaling suppressed chemokine production by human adipose tissue-derived FRCs. Together, our results indicate that TLR9 plays critical roles in regulating peritoneal immunity via suppression of chemokine production by FRCs. These data form a knowledge basis upon which to design new therapeutic strategies to improve the therapeutic efficacy of FRC-based treatments for sepsis and immune dysregulation diseases.

Gasdermin D (GsdmD) was recently identified as the executioner of pyroptotic inflammatory cell death, and is a substrate for caspases-1 and 11. GsdmD is detrimental in lethal endotoxemia but protective in bacterial sepsis. However, little is known about its role during noninfectious/sterile injuries. In this study, we examined the contribution of GsdmD using WT and GsdmD−/− mice in two models of noninfectious liver injury: hemorrhagic shock with resuscitation (HS/R) and acetaminophen (APAP) overdose. GsdmD−/− mice had significantly increased liver damage at 6 h after HS/R or APAP vs WT, shown by significantly elevated ALT level and extended areas of cell death in liver. Caspase-8, a mediator of multiple cell death pathways, was highly elevated in GsdmD−/− mice after injury. Significantly increased cleavage of caspase-8 and subsequent high levels of apoptosis were found in livers of GsdmD−/− mice after HS/R, a relatively mild ROS-induced liver injury. However, during more severe APAP-mediated ROS-induced liver injury, caspase-8 cleavage in GsdmD−/− liver was inhibited compared with WT, resulting in accumulation of pro-caspase-8 and increased levels of necroptosis. Our findings indicate a novel hepatoprotective role for GsdmD in noninfectious inflammation models via regulation of caspase-8 expression and downstream cell death pathways. The effects of GsdmD protection are likely injury specific and may also depend on injury severity and levels of ROS produced. These data suggest modulation of GsdmD/caspase-8 may be a novel therapeutic option in ROS-mediated liver injury.

Dielectric elastomers (DEs) featured with fast reversible and large deformation excited by an external electric field show promising applications as leading artificial muscle materials in many emerging technologies. It remains a great challenge to synthesize a DE simultaneously with high electromechanical performance (large actuation strain, high energy density, free of pre-stretch and bracing) and excellent mechanical properties (low Tg, low viscous loss, low modulus, and high mechanical strength). Herein, we propose and demonstrate that end-block-curing ABA triblock copolymer elastomer with well-designed structures is a new strategy to address the challenge by taking advantage of the microphase separation nature of the block copolymer. Particularly, poly(styrene-b-butyl acrylate-b-styrene) (SBAS) with post-curable end blocks, i.e. polystyrene (PS) blocks, are designed and synthesized. Different levels of cyclohex-3-enylmethyl acrylate (CEA) that contains two asymmetric vinyl groups with very different reactivity are incorporated into the end blocks for end-block curing while the molecular weight for each block is fixed. It is found that curing the end blocks enhances the strain-hardening effect during stretch and thus significantly increases the electro-mechanical performance. Without pre-stretch, the DE actuator of the end block cured SBAS exhibits a maximum actuation strain up to 72%, dielectric breakdown strength up to 154 kV mm−1, and energy density up to 270 kJ/m3, which are three, four, and almost fourty times that of the SBAS free of CEA, respectively. The maximum energy density is over 30 times that of mammalina skeletal muscle while the maximum actuation strain is 3.4 times. Interestingly, the improvement in eletromechanical performance is fulfilled with little increase in glass transition temperature (Tg), mild increase in modulus, and excellent tensile strength due to the microphase structures. The end-block-cured SBAS retains a low Tg of the rubbery phase around −35 °C, relatively low viscous loss of 0.2 at room temperature, a modulus lower than 1 MPa, and tensile strength around 3 MPa, which are attractive in terms of DE device applications.

In order to determine a suitable relative location of AHP and H point in the vehicle cab and improve the SAE standard design model, this paper modeled the H point which is suitable for Chinese according to human factor engineering principle. First, this paper optimized the location of H point by theoretical analyzing. It can be found that the dimension parameter of human body had an impact on H point location. Besides this, when compared this relationship with the SAE empirical formula, the reasonable ranges of vertical dimension between H point and AHP point are different. Then JACK was used to create Chinese male’s digital model models and their human percentile was set to 5, 50, and 95% which are representative. These models were used to simulate the location of AHP point and H point by evaluating, Comfort, Vision Zones, and Reach Zones. Least square method was used to process the location data and find the optimal H point. The result showed that the model to design H point for Chinese male in this paper was more reasonable than that in SAE. It can be used to design the driving cab for Chinese vehicles.

Thrombocytopenia impairs host defense and hemostasis in sepsis. However, the mechanisms of how platelets regulate host defense are not fully understood. High-mobility group box 1 (HMGB1), a danger-associated molecular pattern protein, is released during infection and contributes to the pathogenesis of sepsis. Platelets express HMGB1, which is released on activation and has been shown to play a critical role in thrombosis, monocyte recruitment, and neutrophil extracellular trap (NET) production. However, the contribution of platelet HMGB1 to host defense is unknown. To determine the role of platelet HMGB1 in polymicrobial sepsis, platelet-specific HMGB1 knockout (HMGB1 platelet factor 4 [PF4]) mice were generated and were subjected to cecal ligation and puncture (CLP), a clinically relevant intra-abdominal sepsis model. Compared with HMGB1 Flox mice and wild-type (WT) mice, HMGB1 PF4 mice showed significantly higher bacterial loads in the peritoneum and blood, an exaggerated systemic inflammation response, and significantly greater mortality after CLP. Deletion of HMGB1 in platelets was associated with lower platelet-derived chemokines (PF4 and RANTES) in the peritoneal cavity, and a decrease of platelet-neutrophil interaction in the lung after CLP. In vitro, neutrophils cocultured with activated HMGB1 knockout platelets showed fewer platelet-neutrophil aggregates, reduced reactive oxygen species (ROS) burst as compared with control. Taken together, these data reveal an unrecognized role of platelet HMGB1 in the regulation of neutrophil recruitment and activation via modulation of platelet activation during sepsis.

To reduce the torsional vibration of vehicle power transmission system (VPTS), a torsional vibration model with multiple degrees of freedom (MDOF) of VPTS was established. The scheme of equipping torsional vibration dampers (TVDs) on the driveshaft was employed by the calculation of the forced vibration and the free vibration of the VPTS. The energy method was used to optimize the parameters of single-stage, two-stage parallel and two-stage series TVDs based on the principle that balances the damping effect and lightweight design. On the basis of this, the parameters of the models incorporating TVD and elastic couplings were optimized. Results showed that the proposed method can ensure the damping effects of TVD and realize the lightweight design.

This paper proposes a quantitative method to evaluate system resilience. By dividing objects into system level and component level, we present two system resilience indexes (ER and p) based on minimal cut-set and its calculation method under continuous disruptive events, considering the influence of component and system structure on system resilience. In addition, the sensitivities of components to the two indexes are also analyzed using Morris-Method, which provides reference for the design and improvement of system resilience.

In the design and allocation of resilience for complex networks, both the resilient characteristics and the locations of constituent components can affect the overall resilience of networks on different levels. Based on the concepts of resilience, this paper proposes the definitions of structure importance, redundancy importance and reinforcement importance, with comprehensive consideration of performance degradation and recovery time. Considering the resilient and plastic behaviors of different levels of complex networks before and after the disruptions, a Monte-Carlo simulation algorithm is also developed to calculate the resilience-based component importance. The results show the feasibility and effectiveness of our importance measures.

Resilience is generally described as the ability of a system to absorb disturbance and to recover rapidly back to its original state. However, the system may not recover thoroughly after every interruption. This paper defines resilient limit and system plasticity, and proposes an analysis method for system resilience considering plasticity, which provides a comprehensive evaluation for both resilience and plasticity of systems suffering from performance degradation. The resilience and plasticity of an airborne GPS/INS navigation system is then analyzed to illustrate the effectiveness of our method.

Introduction Notch signaling regulates cell communication and fate decisions, though recently implicated in inflammatory responses, its regulation and roles in sepsis are unknown. We aim to study the biology of Notch signaling in endotoxemia. Methods WT (C57BL/6), Myd88−/− , TRIF−/−, TLR4−/−, iNOS−/−mice were injected saline or 5mg/kg LPS i.p, spleen and serum were harvested after 0, 4, 8, 12, 24h. The activation of Notch signaling was assessed as notch intracellular domain (NICD), and apoptosis was measured as cleaved-caspase 3 level by western blot. Results The NICD level in spleen peaked at 8h, decreasing to baseline level at 24 h after LPS injection. Cleaved-caspase 3 level in spleen was inversely correlated to the NICD level. Inhibition of Notch activation using DAPT (5 mg/kg) resulted in an increase of cleaved-caspase-3 at 8h after LPS stimulation, suggesting a critical role of Notch signaling for splenocyte survival after LPS stimulation. The sheddase, TNFα-converting enzyme (TACE/ADAM17) participates in activation of Notch and we have previously shown its activation via TLR4/iNOS/NO pathway in hepatocytes, thus we tested whether the pathway is conserved in spleen. LPS-induced Notch activation was significantly lower in TRIF−/−, Myd88−/− , TLR4−/− and iNOS−/− mice. In vitro treatment of SNAP (200 uM) and cGMP analog 8-pCPT-cGMP(400 uM) increased NICD level in primary splenocytes. Treatment with 1400W, an iNOS inhibitor or TAPI-II (800 nM), a TACE inhibitor, reduced LPS-induced Notch activation in splenocytes while increasing cleaved-caspase3. Conclusion Our data suggests that Notch signaling is activated during endotoxemia under the regulation of iNOS/NO/TACE and plays a critical role in regulating splenocytes survival.

At present, rare earth application in wastewater treatment has become more and more widely, according to the fact that the Ce(IV) has the strong oxidation ability under acid condition, we have studied the application of Ce(IV) in industrial wastewater treatment originally. Results showed that oxidation-reduction reaction occurred between Ce(IV) and the organic compounds or other reducing substances in industrial wastewater, thereby the colority and CODcr reduced effectively. Ce(IV) formed [Ce(OH)x·nH2O](4-x)+ after hydrolyzation and Ce(III) obtained after Ce(IV) reduction formed [Ce(OH)x·nH2O](3-x)+ after hydrolyzation, these hydrate had big specific surface area, could adsorb the suspension substances and removed toxic or harmful ions in industrial wastewater. After treatment by Ce(IV), the analytical results of industrial wastewater are as follows: The CODcr became 58 mg/L from 1646 mg/L, the total COD removal efficiency was more than 95.0%. Turbidity reduced to no more than 10NTU from 87NTU. The chroma became 6 degree from 26 degree, suspension substances content decreased to no more than 2 mg/L from 36 mg/L, and total arsenic and fluorion became

This paper presents an iterative scheme for a combined signal optimization and assignment problem, using a traffic model from the well-known procedure TRANSYT. The signal settings are optimized by means of a group based technique, in which the signal timings are specified by the common cycle time, the start time and duration of the period of right of way for each signal group in the network. The optimization problem was formulated as integer program and solved by a set of heuristics. Given the optimized signal settings determined from the group-based technique, a path-based assignment algorithm is employed to obtain the equilibrium traffic pattern using the sensitivity information for TRANSYT model. Based on the equilibrium flow pattern, the group-based optimization algorithm is then used to determine a better set of signal timings. The procedure is repeated until certain convergence criteria are satisfied. A numerical example is employed to demonstrate the benefits obtained from this iterative scheme.