Evolution over time of heavy vehicle volume in toll roads: A dynamic panel data to identify key explanatory variables in Spain

Improving the knowledge of demand evolution over time is a key aspect in the evaluation of transport policies and in forecasting future investment needs. It becomes even more critical for the case of toll roads, which in recent decades has become an increasingly common device to fund road projects. However, literature regarding demand elasticity estimates in toll roads is sparse and leaves some important aspects to be analyzed in greater detail. In particular, previous research on traffic analysis does not often disaggregate heavy vehicle demand from the total volume, so that the specific behavioral patternsof this traffic segment are not taken into account. Furthermore, GDP is the main socioeconomic variable most commonly chosen to explain road freight traffic growth over time. This paper seeks to determine the variables that better explain the evolution of heavy vehicle demand in toll roads over time. To that end, we present a dynamic panel data methodology aimed at identifying the key socioeconomic variables that explain the behavior of road freight traffic throughout the years. The results show that, despite the usual practice, GDP may not constitute a suitable explanatory variable for heavy vehicle demand. Rather, considering only the GDP of those sectors with a high impact on transport demand, such as construction or industry, leads to more consistent results. The methodology is applied to Spanish toll roads for the 1990?2011 period. This is an interesting case in the international context, as road freight demand has experienced an even greater reduction in Spain than elsewhere, since the beginning of the economic crisis in 2008.

New QR Survey Methodologies to Analyze User Perception of Service Quality in Public Transport: The Experience of Madrid

Customer Satisfaction Surveys (CSS) have become an important tool for public transport planners, as improvements in the perceived quality of service lead to greater use of public transport and lower traffic pollution. Until now, Intelligent Transportation System (ITS) enhancements in public transport have traditionally included fleet management systems based on Automatic Vehicle Location (AVL) technologies, which can be used to optimize routing and scheduling, and to feed real-time information into passenger information channels. However, surveys of public transport users could also benefit from the new information technologies. As most customers carry their smartphones when traveling, Quick Response (QR) codes open up the possibility of conducting these surveys at a lower cost.This paper contributes to the limited existing literature by developing the analysis of QR codes applied to CSS in public transport and highlighting their importance in reducing the cost of data collection and processing. The added value of this research is that it provides the first assessment of a real case study in Madrid (Spain) using QR codes for this purpose. This pilot experience was part of a research project analyzing bus service quality in the same case study, so the QR code survey (155 valid questionnaires) was validated using a conventional face-to-face survey (520 valid questionnaires). The results show clearly that, after overcoming a few teething troubles, this QR code application will ultimately provide transport management with a useful tool to reduce survey costs

Understanding how to reduce road transport emissions : modelling the impact of eco-driving

Entre los problemas medioambientales más trascendentales para la sociedad, se encuentra el del cambio climático así como el de la calidad del aire en nuestras áreas metropolitanas. El transporte por carretera es uno de los principales causantes, y como tal, las administraciones públicas se enfrentan a estos problemas desde varios ángulos: Cambios a modos de transporte más limpios, nuevas tecnologías y combustibles en los vehículos, gestión de la demanda y el uso de tecnologías de la información y la comunicación (ICT) aplicadas al transporte. En esta tesis doctoral se plantea como primer objetivo el profundizar en la comprensión de cómo ciertas medidas ICT afectan al tráfico, las emisiones y la propia dinámica de los vehículos. El estudio se basa en una campaña de recogida de datos con vehículos flotantes para evaluar los impactos de cuatro medidas concretas: Control de velocidad por tramo, límites variables de velocidad, limitador de velocidad (control de crucero) y conducción eficiente (eco‐driving). Como segundo objetivo, el estudio se centra en la conducción eficiente, ya que es una de las medidas que más ahorros de combustible presenta a nivel individual. Aunque estas reducciones están suficientemente documentadas en la literatura, muy pocos estudios se centran en estudiar el efecto que los conductores eficientes pueden tener en el flujo de tráfico, y cuál sería el impacto si se fuera aumentando el porcentaje de este tipo de conductores. A través de una herramienta de microsimulación de tráfico, se han construido cuatro modelos de vías urbanas que se corresponden con una autopista urbana, una arteria, un colector y una vía local. Gracias a los datos recogidos en la campaña de vehículos flotantes, se ha calibrado el modelo, tanto el escenario base como el ajuste de parámetros de conducción para simular la conducción eficiente. En total se han simulado 72 escenarios, variando el tipo de vía, la demanda de tráfico y el porcentaje de conductores eficientes. A continuación se han calculado las emisiones de CO2 and NOx mediante un modelo de emisiones a nivel microscópico. Los resultados muestran que en escenarios con alto porcentaje de conductores eficientes y altas demandas de tráfico las emisiones aumentan. Esto se debe a que las mayores distancias de seguridad y las aceleraciones y frenadas suaves hacen que aumente la congestión, produciendo así mayores emisiones a nivel global. Climate change and the reduced air quality in our metropolitan areas are two of the main environmental problems that the society is addressing currently. Being road transportation one of the main contributors, public administrations are facing these problems from different points of view: shift to cleaner modes, new fuels and vehicle technologies, demand management and the use of information and communication technologies (ICT) applied to transportation. The first objective of this thesis is to understand how certain ICT measures affect traffic, emissions and vehicle dynamics. The study is based on a data collection campaign with floating vehicles to evaluate the impact of four specific measures: section speed control, variable speed limits, cruise control and eco‐driving. The second objective of the study focuses on eco‐driving, as it is one of the measures that present the largest fuel savings at an individual level. Although these savings are well documented in the literature, few studies focus on how ecodrivers affect the surrounding vehicles and the traffic, and what would be the impact in case of different eco‐drivers percentage. Using a traffic micro‐simulation tool, four models in urban context have been built, corresponding to urban motorway, urban arterial, urban collector and a local street. Both the base‐case and the parameters setting to simulate eco‐driving have been calibrated with the data collected through floating vehicles. In total 72 scenarios were simulated, varying the type of road, traffic demand and the percentage of eco‐drivers. Then, the CO2 and NOx emissions have been estimated through the use of an emission model at microscopic level. The results show that in scenarios with high percentage of co‐drivers and high traffic demand the emissions rise. Higher headways and smooth acceleration and decelerations increase congestion, producing higher emissions globally.

The Transport Disruption Ontology

Postprint

TravelBot: Journey Disruption Alerts Utilising Social Media and Linked Data

Postprint

Broken symmetry and critical transport properties of random metals

Recent experimental data on the conductivity σ+(T), T → 0, on the metallic side of the metal–insulator transition in ideally random (neutron transmutation-doped) 70Ge:Ga have shown that σ+(0) ∝ (N − Nc)μ with μ = ½, confirming earlier ultra-low-temperature results for Si:P. This value is inconsistent with theoretical predictions based on diffusive classical scaling models, but it can be understood by a quantum-directed percolative filamentary amplitude model in which electronic basis states exist which have a well-defined momentum parallel but not normal to the applied electric field. The model, which is based on a new kind of broken symmetry, also explains the anomalous sign reversal of the derivative of the temperature dependence in the critical regime.

Charge transfer and transport in DNA

We explore charge migration in DNA, advancing two distinct mechanisms of charge separation in a donor (d)–bridge ({Bj})–acceptor (a) system, where {Bj} = B1,B2, … , BN are the N-specific adjacent bases of B-DNA: (i) two-center unistep superexchange induced charge transfer, d*{Bj}a → d∓{Bj}a±, and (ii) multistep charge transport involves charge injection from d* (or d+) to {Bj}, charge hopping within {Bj}, and charge trapping by a. For off-resonance coupling, mechanism i prevails with the charge separation rate and yield exhibiting an exponential dependence ∝ exp(−βR) on the d-a distance (R). Resonance coupling results in mechanism ii with the charge separation lifetime τ ∝ Nη and yield Y ≃ (1 + δ̄ Nη)−1 exhibiting a weak (algebraic) N and distance dependence. The power parameter η is determined by charge hopping random walk. Energetic control of the charge migration mechanism is exerted by the energetics of the ion pair state d∓B1±B2 … BNa relative to the electronically excited donor doorway state d*B1B2 … BNa. The realization of charge separation via superexchange or hopping is determined by the base sequence within the bridge. Our energetic–dynamic relations, in conjunction with the energetic data for d*/d− and for B/B+, determine the realization of the two distinct mechanisms in different hole donor systems, establishing the conditions for “chemistry at a distance” after charge transport in DNA. The energetic control of the charge migration mechanisms attained by the sequence specificity of the bridge is universal for large molecular-scale systems, for proteins, and for DNA.

Topoisomerase II drives DNA transport by hydrolyzing one ATP

DNA topoisomerase II is a homodimeric molecular machine that couples ATP usage to the transport of one DNA segment through a transient break in another segment. In the presence of a nonhydrolyzable ATP analog, the enzyme is known to promote a single turnover of DNA transport. Current models for the enzyme’s mechanism based on this result have hydrolysis of two ATPs as the last step, used only to reset the enzyme for another round of reaction. Using rapid-quench techniques, topoisomerase II recently was shown to hydrolyze its two bound ATPs in a strictly sequential manner. This result is incongruous with the models based on the nonhydrolyzable ATP analog data. Here we present evidence that hydrolysis of one ATP by topoisomerase II precedes, and accelerates, DNA transport. These results indicate that important features of this enzyme’s mechanism previously have been overlooked because of the reliance on nonhydrolyzable analogs for studying a single reaction turnover. A model for the mechanism of topoisomerase II is presented to show how hydrolysis of one ATP could drive DNA transport.

The maturity-onset diabetes of the young (MODY1) transcription factor HNF4α regulates expression of genes required for glucose transport and metabolism

Hepatocyte nuclear factor 4α (HNF4α) plays a critical role in regulating the expression of many genes essential for normal functioning of liver, gut, kidney, and pancreatic islets. A nonsense mutation (Q268X) in exon 7 of the HNF4α gene is responsible for an autosomal dominant, early-onset form of non-insulin-dependent diabetes mellitus (maturity-onset diabetes of the young; gene named MODY1). Although this mutation is predicted to delete 187 C-terminal amino acids of the HNF4α protein the molecular mechanism by which it causes diabetes is unknown. To address this, we first studied the functional properties of the MODY1 mutant protein. We show that it has lost its transcriptional transactivation activity, fails to dimerize and bind DNA, implying that the MODY1 phenotype is because of a loss of HNF4α function. The effect of loss of function on HNF4α target gene expression was investigated further in embryonic stem cells, which are amenable to genetic manipulation and can be induced to form visceral endoderm. Because the visceral endoderm shares many properties with the liver and pancreatic β-cells, including expression of genes for glucose transport and metabolism, it offers an ideal system to investigate HNF4-dependent gene regulation in glucose homeostasis. By exploiting this system we have identified several genes encoding components of the glucose-dependent insulin secretion pathway whose expression is dependent upon HNF4α. These include glucose transporter 2, and the glycolytic enzymes aldolase B and glyceraldehyde-3-phosphate dehydrogenase, and liver pyruvate kinase. In addition we have found that expression of the fatty acid binding proteins and cellular retinol binding protein also are down-regulated in the absence of HNF4α. These data provide direct evidence that HNF4α is critical for regulating glucose transport and glycolysis and in doing so is crucial for maintaining glucose homeostasis.

Rab11 Is Required for Trans-Golgi Network–to–Plasma Membrane Transport and a Preferential Target for GDP Dissociation Inhibitor

The rab11 GTPase has been localized to both the Golgi and recycling endosomes; however, its Golgi-associated function has remained obscure. In this study, rab11 function in exocytic transport was analyzed by using two independent means to perturb its activity. First, expression of the dominant interfering rab11S25N mutant protein led to a significant inhibition of the cell surface transport of vesicular stomatitis virus (VSV) G protein and caused VSV G protein to accumulate in the Golgi. On the other hand, the expression of wild-type rab11 or the activating rab11Q70L mutant had no adverse effect on VSV G transport. Next, the membrane association of rab11, which is crucial for its function, was perturbed by modest increases in GDP dissociation inhibitor (GDI) levels. This led to selective inhibition of the trans-Golgi network to cell surface delivery, whereas endoplasmic reticulum–to–Golgi and intra-Golgi transport were largely unaffected. The transport inhibition was reversed specifically by coexpression of wild-type rab11 with GDI. Under the same conditions two other exocytic rab proteins, rab2 and rab8, remained membrane bound, and the transport steps regulated by these rab proteins were unaffected. Neither mutant rab11S25N nor GDI overexpression had any impact on the cell surface delivery of influenza hemagglutinin. These data show that functional rab11 is critical for the export of a basolateral marker but not an apical marker from the trans-Golgi network and pinpoint rab11 as a sensitive target for inhibition by excess GDI.

Uptake and Intracellular Transport of Acidic Fibroblast Growth Factor: Evidence for Free and Cytoskeleton-anchored Fibroblast Growth Factor Receptors

Endocytic uptake and intracellular transport of acidic FGF was studied in cells transfected with FGF receptor 4 (FGFR4). Acidification of the cytosol to block endocytic uptake from coated pits did not inhibit endocytosis of the growth factor in COS cells transfected with FGFR4, indicating that it is to a large extent taken up by an alternative endocytic pathway. Fractionation of the cells demonstrated that part of the growth factor receptor was present in a low-density, caveolin-containing fraction, but we were unable to demonstrate binding to caveolin in immunoprecipitation studies. Upon treatment of the cells with acidic FGF, the activated receptor, together with the growth factor, moved to a juxtanuclear compartment, which was identified as the recycling endosome compartment. When the cells were lysed with Triton X-100, 3-([3-chloramidopropyl]dimethylammonio)-2-hydroxy-1-propanesulfonate, or 2-octyl glucoside, almost all surface-exposed and endocytosed FGFR4 was solubilized, but only a minor fraction of the total FGFR4 in the cells was found in the soluble fraction. The data indicate that the major part of FGFR4 is anchored to detergent-insoluble structures, presumably cytoskeletal elements associated with the recycling endosome compartment.

Evidence for specific nucleocytoplasmic transport pathways used by leucine-rich nuclear export signals

Various proteins with different biological activities have been observed to be translocated from the nucleus to the cytoplasm in an energy- and signal-dependent manner in eukaryotic cells. This nuclear export is directed by nuclear export signals (NESs), typically characterized by hydrophobic, primarily leucine, amino acid residues. Moreover, it has been shown that CRM1/exportin 1 is an export receptor for leucine-rich NESs. However, additional NES-interacting proteins have been described. In particular, eukaryotic initiation factor 5A (eIF-5A) has been shown to be a critical cellular cofactor for the nuclear export of the HIV type 1 (HIV-1) Rev trans-activator protein. In this study we compared the nuclear export activity of NESs of different origin. Microinjection of export substrates into the nucleus of somatic cells in combination with specific inhibitors indicated that specific nuclear export pathways exist for different NES-containing proteins. In particular, inhibition of eIF-5A blocked the nuclear export of NESs derived from the HIV-1 Rev and human T cell leukemia virus type I Rex trans-activators, whereas nucleocytoplasmic translocation of the protein kinase inhibitor-NES was unaffected. In contrast, however, inhibition of CRM1/exportin 1 blocked the nuclear export of all NES-containing proteins investigated. Our data confirm that CRM1/exportin 1 is a general export receptor for leucine-rich NESs and suggest that eIF-5A acts either upstream of CRM1/exportin 1 or forms a complex with the NES and CRM1/exportin 1 in the nucleocytoplasmic translocation of the HIV-1 Rev and human T cell leukemia virus type I Rex RNA export factors.

VIP17/MAL, a lipid raft-associated protein, is involved in apical transport in MDCK cells

Apical proteins are sorted and delivered from the trans-Golgi network to the plasma membrane by a mechanism involving sphingolipid–cholesterol rafts. In this paper, we report the effects of changing the levels of VIP17/MAL, a tetraspan membrane protein localized to post-Golgi transport containers and the apical cell surface in MDCK cells. Overexpression of VIP17/MAL disturbed the morphology of the MDCK cell layers by increasing apical delivery and seemingly expanding the apical cell surface domains. On the other hand, expression of antisense RNA directed against VIP17/MAL caused accumulation in the Golgi and/or impaired apical transport of different apical protein markers, i.e., influenza virus hemagglutinin, the secretory protein clusterin (gp80), the transmembrane protein gp114, and a glycosylphosphatidylinositol-anchored protein. However, antisense RNA expression did not affect the distribution of E-cadherin to the basolateral surface. Because VIP17/MAL associates with sphingolipid–cholesterol rafts, these data provide functional evidence that this protein is involved in apical transport and might be a component of the machinery clustering lipid rafts with apical cargo to form apical transport carriers.

Transport of uncharged organic solutes in Xenopus oocytes expressing red cell anion exchangers (AE1s)

When expressed in Xenopus oocytes, the trout red cell anion exchanger tAE1, but not the mouse exchanger mAE1, elicited a transport of electroneutral solutes (sorbitol, urea) in addition to the expected anion exchange activity. Chimeras constructed from mAE1 and tAE1 allowed us to identify the tAE1 domains involved in the induction of these transports. Expression of tAE1 (but not mAE1) is known to generate an anion conductance associated with a taurine transport. The present data provide evidence that (i) the capacity of tAE1 and tAE1 chimeras to generate urea and sorbitol permeability also was associated with an anion conductance; (ii) the same inhibitors affected both the permeability of solutes and anion conductance; and (iii) no measurable water transport was associated with the tAE1-dependent conductance. These results support the view that fish red blood cells, to achieve cell volume regulation in response to hypotonic swelling, activate a tAE1-associated anion channel that can mediate the passive transport of taurine and electroneutral solutes.

Modulation of N-methyl-d-aspartate receptor function by glycine transport

The recent discovery of glycine transporters in both the central nervous system and the periphery suggests that glycine transport may be critical to N-methyl-d-aspartate receptor (NMDAR) function by controlling glycine concentration at the NMDAR modulatory glycine site. Data obtained from whole-cell patch–clamp recordings of hippocampal pyramidal neurons, in vitro, demonstrated that exogenous glycine and glycine transporter type 1 (GLYT1) antagonist selectively enhanced the amplitude of the NMDA component of a glutamatergic excitatory postsynaptic current. The effect was blocked by 2-amino-5-phosphonovaleric acid and 7-chloro-kynurenic acid but not by strychnine. Thus, the glycine-binding site was not saturated under the control conditions. Furthermore, GLYT1 antagonist enhanced NMDAR function during perfusion with medium containing 10 μM glycine, a concentration similar to that in the cerebrospinal fluid in vivo, thereby supporting the hypothesis that the GLYT1 maintains subsaturating concentration of glycine at synaptically activated NMDAR. The enhancement of NMDAR function by specific GLYT1 antagonism may be a feasible target for therapeutic agents directed toward diseases related to hypofunction of NMDAR.