The habit-driven life: Accounting for inertia in departure time choices for commuting trips

This paper aims to explicitly account for the impact of inertia (or habit) on departure time decisions, and explore (1) to what extent departure time is influenced by inertia, (2) what influences individuals’ inertia with respect to departure time decisions, and (3) to what extent it impacts transport policies. We estimate an integrated choice and latent variable (ICLV) model using a stated preference survey for morning car commuters in the Greater Copenhagen Area. We interact the rescheduling components in the Scheduling Model (SM) with the latent variable Inertia. The modelling results show that higher levels of inertia yields higher rescheduling penalties and lower willing to shift departure time. Furthermore, we find that inertia in departure time is influenced by gender, presence of children in the household as well as work type. We test the behavioral responses to demand management policies for segments with different inertia, and find that the least inertial segment showed the highest substitution patterns, while the most inertial segment show the lowest substitution patterns. Finally, we compared the ICLV model to a reference model without inertia, and find that the effects of the demand management strategy is overestimated if inertia is neglected

Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo

Dendritic cell (DC) activation is a prerequisite for T cell priming. During infection, activation can ensue from signaling via pattern-recognition receptors after contact with pathogens or infected cells. Alternatively, it has been proposed that DCs can be activated indirectly by signals produced by infected tissues. To address the contribution of tissue-derived signals, we measured DC activation in a model in which radioresistant cells can or cannot respond to lipopolysaccharide (LPS). We report that recognition of LPS by the radioresistant compartment is sufficient to induce local and systemic inflammation characterized by high circulating levels of tumor necrosis factor (TNF) α, interleukin (IL) 1β, IL-6, and CC chemokine ligand 2. However, this is not sufficient to activate DCs, whether measured by migration, gene expression, phenotypic, or functional criteria, or to render DC refractory to subsequent stimulation with CpG-containing DNA. Similarly, acute or chronic exposure to proinflammatory cytokines such as TNF-α ± interferon α/β has marginal effects on DC phenotype in vivo when compared with LPS. In addition, DC activation and migration induced by LPS is unimpaired when radioresistant cells cannot respond to the stimulus. Thus, inflammatory mediators originating from nonhematopoietic tissues and from radioresistant hematopoietic cells are neither sufficient nor required for DC activation in vivo

Efficient and versatile manipulation of the peripheral CD4+ T-cell compartment by antigen targeting to DNGR-1/CLEC9A

DC NK lectin group receptor-1 (DNGR-1, also known as CLEC9A) is a C-type lectin receptor expressed by mouse CD8α+ DC and by their putative equivalents in human. DNGR-1 senses necrosis and regulates CD8+ T-cell cross-priming to dead-cell-associated antigens. In addition, DNGR-1 is a target for selective in vivo delivery of antigens to DC and the induction of CD8+ T-cell and Ab responses. In this study, we evaluated whether DNGR-1 targeting can be additionally used to manipulate antigen-specific CD4+ T lymphocytes. Injection of small amounts of antigen-coupled anti-DNGR-1 mAb into mice promoted MHC class II antigen presentation selectively by CD8α+ DC. In the steady state, this was sufficient to induce proliferation of antigen-specific naïve CD4+ T cells and to drive their differentiation into Foxp3+ regulatory lymphocytes. Co-administration of adjuvants prevented this induction of tolerance and promoted immunity. Notably, distinct adjuvants allowed qualitative modulation of CD4+ T-cell behavior: poly I:C induced a strong IL-12-independent Th1 response, whereas curdlan led to the priming of Th17 cells. Thus, antigen targeting to DNGR-1 is a versatile approach for inducing functionally distinct CD4+ T-cell responses. Given the restricted pattern of expression of DNGR-1 across species, this strategy could prove useful for developing immunotherapy protocols in humans

Reference Model for Improving the Process of Enterprise Software Product in the Ecuasis Company

This research work arose to improve the process of enterprise software products for the creation of software companies, through the development of a reference model based on lean startup proposed methodologies to the effect of selective and comparative study of the main methodologies of the entrepreneurship, the methodology to identify that best suits our purpose to generate the proposed model. Finally, generates and implements the proposed model and check the validity by applying a practical case study

Localized thinning for strain concentration in suspended germanium membranes and optical method for precise thickness measurement

We deposited Ge layers on (001) Si substrates by molecular beam epitaxy and used them to fabricate suspended membranes with high uniaxial tensile strain. We demonstrate a CMOS-compatible fabrication strategy to increase strain concentration and to eliminate the Ge buffer layer near the Ge/Si hetero-interface deposited at low temperature. This is achieved by a two-steps patterning and selective etching process. First, a bridge and neck shape is patterned in the Ge membrane, then the neck is thinned from both top and bottom sides. Uniaxial tensile strain values higher than 3% were measured by Raman scattering in a Ge membrane of 76 nm thickness. For the challenging thickness measurement on micrometer-size membranes suspended far away from the substrate a characterization method based on pump-and-probe reflectivity measurements was applied, using an asynchronous optical sampling technique.EC/FP7/628197/EU/Heat Propagation and Thermal Conductivity in Nanomaterials for Nanoscale Energy Management/HEATPRONAN

Development of a Model for Quality Process Stage Development Software Applied Unit Systems UTMACH

In the present investigation discloses some models or standards focused on system development process. Pretending to give a solution to the user dissatisfaction that causes no profiling to develop quality system. And with reference to the systems unit of the Technical University of Machala and under the investigative process that took place it was detected that there is no order of development in the Unit, the various schedules that are performed many times outside the scope of work team. Due to this circumstance and aims these preliminary detected based on a comparative analysis of the various models or standards applied quality system to create a working environment that allows Systems Unit improve the system development process. Forming itself the quality model system that will engage the Systems Unit

The bile salt glycocholate induces global changes in gene and protein expression and activates virulence in enterotoxigenic Escherichia coli

Pathogenic bacteria use specific host factors to modulate virulence and stress responses during infection. We found previously that the host factor bile and the bile component glyco-conjugated cholate (NaGCH, sodium glycocholate) upregulate the colonization factor CS5 in enterotoxigenic Escherichia coli (ETEC). To further understand the global regulatory effects of bile and NaGCH, we performed Illumina RNA-Seq and found that crude bile and NaGCH altered the expression of 61 genes in CS5 + CS6 ETEC isolates. The most striking finding was high induction of the CS5 operon (csfA-F), its putative transcription factor csvR, and the putative ETEC virulence factor cexE. iTRAQ-coupled LC-MS/MS proteomic analyses verified induction of the plasmid-borne virulence proteins CS5 and CexE and also showed that NaGCH affected the expression of bacterial membrane proteins. Furthermore, NaGCH induced bacteria to aggregate, increased their adherence to epithelial cells, and reduced their motility. Our results indicate that CS5 + CS6 ETEC use NaGCH present in the small intestine as a signal to initiate colonization of the epithelium