These reactants included many cytokines and other biochemical substances; the increased Factor VIII, and fibrinogen levels increased blood coagulability. Vasdekis and colleagues (2013) in their review identify many potential reactants (opioids, nitric oxide, adenosine, bradykinin, catecholamines, heat shock proteins, heme oxygenase, tumor necrosis factors – α (TNF-α), angiotensin, prostaglandins, hydrogen sulfide, nitrous oxide, and interleukins). This list reads like the usual suspects proffered to explain features of most neurological

conditions. Animal studies have shown that these agents are active in ischemic models. Ischemic Inhibitors,research,lifescience,medical Preconditioning Studies in Humans The review of Vasdekis et al. contains extensive data about the studies performed to date (Vasdekis et al. 2013). Most often the preconditioning involved causing transient upper or lower limb selleck chemicals llc ischemia shortly before a procedure or surgery. The preconditioning Inhibitors,research,lifescience,medical was targeted for an acute short-term effect. The procedures studied were (1) open heart surgery in infants, children, and adults in whom heart, lung, and kidney protection

from injury was studied; (2) before coronary artery stenting in which the extent of myocardial damage was monitored; (3) angiography in patients with kidney disease and before renal transplantation – the target organ studied was the kidney; (4) before aortic aneurysm repair Inhibitors,research,lifescience,medical – targeting renal, myocardial, and intestinal injuries. Only two studies involved patients Inhibitors,research,lifescience,medical with neck or intracranial stenotic lesions. One sought an acute effect – transient limb ischemia was induced before carotid endarterectomy in order to reduce the frequency and extent of intraoperative hypotension. Only one study had a more chronic and persistent brain protection target and, unlike all of the other studies, involved patients who were known to have brain ischemia. This was a randomized clinical trial in which 68 Inhibitors,research,lifescience,medical Chinese patients who recently had a stroke or TIA attributable to intracranial

arterial stenosis were studied (Meng et al. 2012). Upper limb ischemic preconditioning was performed among 38 patients. The preconditioning protocol was five cycles of bilateral upper limb ischemia for 5 min followed by reperfusion for another 5 min, performed twice a day for a total of 300 consecutive days. An electronic autocontrol device was used in the preconditioning. The frequency of stroke, TIAs, and cerebral perfusion were compared with 30 patients who had the same inclusion Dacomitinib criteria but no preconditioning. The use of antiplatelets, lipid control agents, and antidiabetic drugs was the same in both groups. The incidence of recurrent stroke with positive brain selleck Afatinib imaging at 90 and 300 days was 5% and 7.9% in those preconditioned and 23.3% and 26.7% in the control group, respectively (P = 0.01 each). The frequency of TIAs was also less in the preconditioned group. Brain perfusion was studied using single photon emission computed tomography; 31.

It was reported that 20% multiple trauma patients died in this period.[1] A multidisciplinary task force for advanced bleeding care in trauma was formed in 2005 with the aim of developing a guideline for the management of bleeding following severe injury.

This group published the first and an updated version of guideline in 2007 and 2010 respectively, which provides an evidence-based multidisciplinary approach to the management of critically injured bleeding trauma patients based on a systematic review of published literature. The newest 2010 guideline[1]include new www.selleckchem.com/products/ganetespib-sta-9090.html recommendations on coagulation support and monitoring and the appropriate Inhibitors,research,lifescience,medical use of local haemostatic measures, tourniquets, calcium and desmopressin in the bleeding trauma patient. Holeomb reported that identified and corrects coagulopathy can increase rescue success rate.[4] In our study, we also found that the patients with coagulopathy were more likely to die. Different to traditional management of injured bleeding trauma Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical patients which centered upon correction of acidosis and hypotension with crystalloids. Damage control resuscitation (DCR), a new resuscitation strategy, is permissive hypotension

and early hemostatic resuscitation combined identified and corrects coagulopathy with fresh-frozen plasma (FFP), restricting use of crystalloids.[5,6] In our hospital, doctors now maintain patients’ blood pressure around (90-80)/(60-50) mmHg before bleeding was controlled. The trauma patients who received blood transfusion, such as packed red blood cells, fresh-frozen plasma, platelet, cryoprecipitate, Inhibitors,research,lifescience,medical rFVII2 and tranexamic acid, seemed have a better outcome. 80.5% trauma patients recovered, which is a great deal higher than before. Conclusions In conclusion, immediately find out and treat the life-threatening bleeding and hypotension, identify and correct coagulopathy, damage control resuscitation are helpful to manage critically injured bleeding trauma patients. Inhibitors,research,lifescience,medical In order to improve patient outcomes, this evidence-based approach is worthy of further practice

and popularization. Declarations This article has been published as part of BMC Emergency Medicine Volume 13 Supplement 1, 2013: Proceedings of the 2012 Emergency Medicine Annual Congress. Entinostat The full contents of the supplement are available online at http://www.biomedcentral.com/bmcemergmed/supplements/13/S1. The publication costs for this article was funded by Xijing Hospital, the Fourth Military Medical University.
Ninety-four AECOPD patients selleck chemicals Bicalutamide admitted into the intensive care unit (ICU) of our hospital from June 2008 to March 2012 were included, all of whom in accordance with the criteria of COPD guideline constituted by Chinese Society of Respiratory Diseases in 2007 and the diagnosis standard of pulmonary encephalopathy[2,3].

Increasing the stiffness of these scientific study particles by increasing hydrogel crosslink density can reduce the elimination half-life 30-fold and change the accumulation of these particles from the spleen to the lungs and liver. These two studies highlight the importance that flexible control of particle size, shape, and chemistry affords drug delivery vehicles. Additionally, the PRINT

manufacturing process has been demonstrated at Lapatinib chemical structure scales relevant Inhibitors,research,lifescience,medical to support preclinical and clinical studies. Liquidia Technologies has initiated a Phase I clinical study of a PRINT vaccine candidate, demonstrating the production of GMP pharmaceutical materials using this novel nanofabrication process, at a scale relevant to clinical development [16]. The outcome of implementing this particle engineering approach for dry powder fabrication is improved aerosol Inhibitors,research,lifescience,medical performance applicable to respiratory drug delivery, demonstrated by incorporation of a variety of pharmaceutically relevant compounds. In vitro results demonstrate that PRINT particle aerosols possess high respirable dose, high fine particle fraction, and tunable particle aerodynamic diameter. In vivo canine deposition studies demonstrate the ability to influence dry powder delivery as a function of particle geometry. These results suggest that this tunable particle engineering approach is a versatile platform for Inhibitors,research,lifescience,medical enabling next-generation Inhibitors,research,lifescience,medical respiratory drug

delivery. We also highlight some of the utility of PRINT for the production of particles for small molecule, protein, and oligonucleotide drug delivery, which demonstrates that PRINT is a versatile formulation approach

and should find applicability in oral, parenteral, and topical dosage forms for multiple disease indications. 2. Methods 2.1. Fabrication of Particles for Drug Delivery Using PRINT Technology PRINT is an adaptation of micro- and nanomolding technologies, rooted in the microelectronics industry, that is used to fabricate monodisperse particles of controlled sizes and shapes using roll-to-roll manufacturing processes. It allows for the Inhibitors,research,lifescience,medical fabrication of monodisperse particles with Dacomitinib precise control over size, shape, composition, and surface functionalization. Unlike many other particle fabrication techniques, the PRINT method is versatile and gentle enough to be compatible with the multitude of next-generation therapeutic and diagnostic agents, including small molecules, protein biologics, siRNA, and bioabsorbable and hydrophilic polymer matrix materials with embedded pharmaceutical cargo. An overview of the PRINT process is outlined in Figure 1. As mentioned previously, the particles produced using the PRINT process are templated using polymeric micromolds. The molds themselves arise from replication of a silicon master template (Figure 1(a)), which is fabricated using advanced lithographic techniques.

Loving http://www.selleckchem.com/products/Romidepsin-FK228.html kindness is practiced by directed well wishing,

typically supported by silent repetition of phrases such as “may X be happy.” In so doing, practitioners cultivate openness, present-centered awareness, and selfless love, toward themselves and others (Salzberg 1995). Loving kindness and related practices such as compassion meditation have been found Inhibitors,research,lifescience,medical to enhance positive and diminish negative emotional states, and have shown preliminary utility in the treatment of depression, social anxiety, and stress, among others (for review see Hofmann et al. 2011). Yet little is known about the neural substrate of loving kindness meditation. Related studies have assessed the effects of loving kindness or compassion meditation on the neural response to cognitive or affective tasks. For Inhibitors,research,lifescience,medical example, a recent study (Lee et al. 2012) reported that loving kindness meditation led to changes in the neural response to viewing emotional faces, in brain regions implicated in emotion processing, including the left ventral anterior cingulate cortex, right Erlotinib mechanism of action inferior frontal

gyrus (IFG), and right precuneus for happy faces, and the left caudate and middle frontal gyrus for sad faces. Another study (Lutz et al. 2008) found that compassion meditation led to increased Inhibitors,research,lifescience,medical activation in brain regions involved in affective processing in response to emotional sounds, including the dorsal anterior cingulate cortex (dACC) and insula. Another recent study (Weng et al. 2013) found that compassion meditation training led to increased altruistic behavior outside of the training context, and associated changes in the neural response to suffering during

post-pre functional magnetic resonance imaging (fMRI) in brain regions Inhibitors,research,lifescience,medical involved in social cognition and emotion regulation, including the inferior parietal cortex and dorsolateral prefrontal cortex. These neuroimaging studies provide evidence that loving kindness and related meditation practices can alter emotional or affective processing, Inhibitors,research,lifescience,medical yet do not describe the neural underpinnings of loving kindness meditation without a concurrent task. Thus, the aim of this study was to assess the neural substrate of loving kindness meditation. A prior study from our research group, which was designed to test for common neural activation patterns across three meditation types (Brewer et al. 2011), found that loving Dacomitinib kindness led to reduced blood oxygen level-dependent (BOLD) signal in clusters in the inferior temporal gyrus/uncus/amygdala, posterior cingulate cortex/precuneus (PCC/PCu), and the inferior parietal lobule, in experienced meditators as compared to novices. Moreover, relatively reduced BOLD signal in meditators in the PCC/PCu—a hub of the default mode network (DMN) involved in self-related processing and mind wandering (Northoff et al. 2006)—was common across all three meditation types. This study investigates the neural substrate of loving kindness meditation in a larger sample size of meditators and novices.

In addition, we have found that chronic rolipram

administration increases neurogenesis in adult hippocampus.46,58 Second, viral expression of CREB in the hippocampus of rat produces an antidepressant response in the forced swim and learned helplessness selleck kinase inhibitor models of depression.59 However, further studies demonstrated that the effects of CREB are dependent on the brain region where it is expressed. For example, expression of CREB in the nucleus accumbens produces a prodepressant effect, while expression of a dominant, Inhibitors,research,lifescience,medical negative mutant of CREB results in an antidepressant response in the forced swim test.60 Transgenic expression of dominant negative CREB in the nucleus accumbens is consistent with this effect.61 The different behavioral effects of CREB can be currently explained by different target genes in the hippocampus (ic, BDNF) versus the nucleus accumbens (ie,prodynorphin). Regulation of neurotrophic factors Inhibitors,research,lifescience,medical and depression The regulation of CREB by antidepressant treatment indicates that regulation of gene expression also plays a role in the actions of antidepressants. There have been many gene targets identified for antidepressants,51,52 but BDNF is one that has gained attention and is relevant to neural plasticity responses to Inhibitors,research,lifescience,medical antidepressant medications. Studies to identify additional gene targets and gene profiles using gene microarray analysis are currently being conducted. Antidepressant treatment upregulates BDNF Neurotrophic

factors were originally

identified and studied for their role in development, and neuronal survival. However, it is now clear that these factors are expressed in the adult brain, arc dynamically regulated by neuronal activity, and are Inhibitors,research,lifescience,medical critical for the survival and function of adult neurons. On the basis of these considerations, it is clear why decreased expression of BDNF could have serious consequences for the function of limbic brain Inhibitors,research,lifescience,medical structures that control mood and cognition. In contrast, antidepressant treatment results in significant upregulation of BDNF in the hippocampus and cerebral cortex of rodents.28,53,54 Increased expression of BDNF is dependent on chronic treatment, and is observed with different classes of antidepressants, but not other psychotropic drugs. The induction of BDNF would be expected to protect neurons from damage resulting from stress, elevated glucocorticoids, or other types of neuronal insult. BDNF has antidepressant effects in behavioral models of depression Batimastat The possibility that BDNF contributes to the actions of antidepressant treatment is supported by behavioral studies of recombinant BDNF and transgenic mouse models. Microinfusions of BDNF into the hippocampus produce an antidepressant-like response in the learned helplessness and forced swim models of depression.62 The antidepressant, effect of BDNF is observed after a single infusion, compared with repeated administration of a. chemical antidepressant, and is relatively long-lasting (up to 10 days after infusion).

Gardner argues persuasively that there multiple types of creativity, which he refers to as “multiple intelligences.”5 A key component, of Gardner’s approach is that he disagrees with the common stereotype that makes creativity equivalent to pursuing work in the arts, and ignores the fact that people in fields such as engineering or biology also may be highly creative. inhibitor MG132 Csikszentmihalyi stresses the importance of making original contributions and of being recognized for these contributions

by one’s peers.6 Although there are some differences between those cur rently pursuing research on creativity, a definition that most, would embrace is one that Inhibitors,research,lifescience,medical emphasizes that creativity is the ability to produce something that is novel and also useful or beautiful in a very general sense.7 Some would also emphasize the importance Inhibitors,research,lifescience,medical of having achieved some kind of public recognition for this work, such as a Pulitzer Prize, a listing in Who’s Who

in Art, or a Fields Medal. However, this is a relatively stringent criterion. Given this definition of creativity, how then should an investigator identify a sample to study? One approach is to select a very homogeneous group of creative people, such as a group of writers, or musicians, or mathematicians. Inhibitors,research,lifescience,medical This is perhaps the most common. Another approach

is to sample more broadly and to study a mixture of creative individuals from multiple disciplines. The most difficult aspect, of Inhibitors,research,lifescience,medical this type of research is selleckchem identifying and recruiting the subjects, since creative people tend Inhibitors,research,lifescience,medical to be relatively busy. An alternative approach is to identify a group of people for whom written histories are available and to use this information as the basis for study. Examples of this type of approach are the studies of Ellis, Juda, Post, Ludwig, and Schildkraut.3, 8-11 Although using written historical Batimastat biographical and autobiographical material provides a sample of convenience, an obvious problem is that the information may not be complete or accurate. If the goal of a study is to examine the relationship between creativity and psychopathology, then several other challenges must, also be met. One is to use a standard and widely accepted set of definitions of mental illness, and to assess its presence or absence using a structured interview of some type. Although this seems obvious in the early 21st century, most of the extant literature on creativity and mental illness has not used this approach. It is nearly impossible to map the diagnoses of early investigators, such as Adele Juda, into modern nomenclature, and therefore to interpret the results.

The aim of this paper was to address the entire range of morbidities as early in the course of the disease as is possible with the current data. The data were based on PD diagnoses from the Danish National Patient Registry (NPR). Methods Subject selection All patient hospital contacts in Denmark are recorded in the NPR by type and date of contact. The NPR includes administrative

information, primary and secondary diagnoses, diagnostic procedures, and treatment procedures using the International Inhibitors,research,lifescience,medical Classification of Diseases (ICD-10) and their date. Specific clinical information, such as the UPDRS score and imaging results, is not present in the NPR. The NPR contains diagnoses from private Inhibitors,research,lifescience,medical and public hospitals, but does not record diagnoses from general practice. Using the NPR, we identified all patients at least 20 years of age who were diagnosed with PD between 1997 and 2007. For

the PD diagnoses, we used the code G20.9. The code G20 is not accepted in the NPR, so all PD patients are registered as G20.9 (Paralysis agitans). Hospital doctors report the NPR at the time of diagnosis. Then, using data from Denmark’s Civil Registration System Statistics, we randomly selected citizens of the same age, gender, and marital status as the patients who did not have PD. Parity Inhibitors,research,lifescience,medical of socioeconomic status (SES) was ensured by selecting control subjects from the same part of the country as where the patient lived. The ratio of control subjects to

patients was 4:1. Data from patients and matched control subjects who could not be identified in the Coherent Inhibitors,research,lifescience,medical Social Statistics database were excluded from the sample. More than 99% of the observations in the two groups were successfully matched. Morbidity data from the patients and matched control subjects were gathered from their year of Inhibitors,research,lifescience,medical diagnosis until 2007. Data selleck chemicals llc analysis Data were analyzed by developing a conditional logit model, where the dependent variable was the case–control group and the explanatory variables were dummies for the 21 major ICD10 diagnosis groups, omitting the group with no diagnosis 3 years before diagnosis. A second analysis included dummies for ICD10 diagnosis that occurred in more than 1% of either the case or control group. ICD10 diagnoses accounting for 1% or fewer of the total diagnoses were included in the main diagnosis groups. Only estimates for the ICD10 diagnoses are reported in the results, but the dummies for Batimastat the main groups (including the then remaining diagnoses) were included in the regression. Patients could be classified in more than one diagnostic group or with an ICD10 diagnosis during the 3 years before the diagnosis. Not all patients had a 3-year observation period before the registered diagnosis; for the first 3 years of the period, the patient only had data for 1 or 2 years, but as this was also the case for the control group, we have included these shorter periods in the analysis.

c.i, ii), miR-1 and miR-133a were found to be upregulated in canine hearts c-Kit mutation selleck isolated from animals with chronic HF accompanied by increased left ventricular dimensions and impaired contractility of the left ventricle. 94 These miRNAs were shown to target the mRNA of the PP2A catalytic

subunit of RyR2, which led to increased RyR2 phosphorylation and abnormal spontaneous sarcoplasmic reticulum Ca2+ release, thus contributing to arrythmogenesis. 94 These in vivo findings confirm previous studies in rat CMCs, where miR-1 over-expression was shown to decrease the protein phosphatase PP2A regulatory subunit B56alpha, which in turn resulted in increased phosphorylation of the L-type and RyR2 calcium channels, and ultimately enhanced cardiac excitation-contraction. 125 These observations point to miR-1 and miR-133a as regulators of CMC contractility via modulation of calcium signaling, suggesting their implication in arrhythmia manifestation during HF. The role of miR-1 in calcium signaling has been further investigated in additional rodent models of HF. Studies in the cardiomyocyte-specific

SRF knock-out mouse model of HF revealed that sodium-calcium exchanger 1 (NCX1) and AnxA5 mRNAs are targets of miR-1. 126 This is consistent with previous studies in chronic post-myocardial infarction rat model of HF, where miR-1 expression was restored by SERCA2a gene therapy (AAV9.SERCA2a) in the failing heart and led to normalization of NCX1 expression. 127 Of note, miR-1 expression restoration also resulted in improved cardiac function in this model. 127 Moreover, studies in the mouse model of hypertrophy derived from cardiac-specific Dicer deletion, showed that miR-1 also targets sorcin, which functions as a regulator of calcium signaling and excitation-contraction coupling. 76 With regards to the role of SERCA2a in the failing myocardium, functional screening of 875 miRNAs, identified miR-25 as a suppressor of SERCA2a expression and consequently a potent regulator of intracellular calcium handling. MiRNA-25 has also been found overexpressed in human and experimental HF. Moreover, experiments in cardiomyocyte-like

HL-1 cells demonstrated that miR-25 delayed calcium uptake kinetics, whilst Entinostat AAV9-mediated overexpression in a mouse model of HF led to loss of contractile function. Importantly, inhibition of miR-25 expression via antagomiRs in a mouse model of HF halted the established HF, and improved cardiac function and survival, thereby suggesting that miR-25 may be a novel therapeutic target for HF. 180 These findings suggest that miRNAs, among their many mechanisms of contributing to HF, may also impair different aspects of calcium homeostasis in the cardiomyocytes. miRNAs impact on mitochondrial dysfunction underlying HF Interestingly, recent studies suggest that miRNAs may be implicated in HF development via impairing mitochondrial function.

The drugs used in this approach aim at retarding the formation of the lysosomal substance to a rate at which the residual Gemcitabine synthesis enzyme activity can catabolize stored and incoming lysosomal substance. Two main classes of inhibitors of glycosphingolipid biosynthesis have at present been described. Both inhibit the ceramide-specific glucosyltransferase: the first class of inhibitors is made of analogues of ceramide; the second one of N-alkylated

iminosugars (9). N-butyldeoxynojirimycin Inhibitors,research,lifescience,medical (Miglustat) was approved for patients with mild to moderate type 1 Gaucher disease unwilling or unable to receive ERT (10). The use of hydrophobic iminosugars Cisplatin msds seemed to be promising in mouse models of Tay-Sachs disease, Sandhoff disease, GM1 gangliosidosis and Niemann-Pick disease type C (11, 12). At present many more trails Inhibitors,research,lifescience,medical with miglustat are being carried out in patients with Niemann-Pick disease type C, late-onset Tay-Sachs disease and juvenile Sandhoff disease (GM2

gangliosidosis). A new therapeutic strategy has been recently undertaken for some LSDs; it is based on the use of “chaperone” substances, that have the function of binding and stabilizing misfolding-prone proteins, thus increasing the residual enzyme activity (7). In particular, it has been proved that the infusion of galactose or certain reversible Inhibitors,research,lifescience,medical competitive inhibitors of α-galactosidase A (such as 1-deoxy-galactonojirimycin) can increase the residual enzyme activity in cultures of fibroblasts from patients with the cardiac variant of Fabry Inhibitors,research,lifescience,medical disease (13). An active site-directed chemical chaperone for α-galactosidase A to treat Fabry disease is currently in phase I clinical trial. Matsuda and coworkers have synthesized a galactose derivative for the chaperone chemical therapy of GM1-gangliosidosis

(14). At present, chemical chaperoning has shown to be effective in increasing Inhibitors,research,lifescience,medical the activity of the highly prevalent N370S and the less common G202R glucocerebrosidase variants, by culturing Gaucher patient’s fibroblasts with a variety of iminosugar compounds (15). Finally, in the last few years, many studies have been carried out in vitro as well as on animal models to evaluate the effectiveness of gene therapy in LSDs. This therapeutic strategy is based GSK-3 on the idea of directly transfering the normal gene into the defective cells in order to supply the active enzyme and, consequently, reduce the intralysosomal undegraded substances. This can be achieved by either ex vivo or direct in vivo gene therapy strategies. Table ​Table33 lists the viral vectors tested so far for in vivo gene transfer (16, 17) and references therein. Table 3 Gene therapy strategies ((16, 17) and references therein). Experiments on animal models have been carried out in Mucopolysaccharidosis I, II, III, VI, VII, in many Lipidoses, such as Gaucher disease, Fabry disease, Metachromatic leukodystrophy, GM1 and GM2 Gangliosidosis, Niemann-Pick disease, Farber disease and Pompe disease.

Map-matching algorithms must perform an extremely challenging task if we consider the large number of possible road segments to match the position of the vehicle, the GNSS errors and the lack of completeness and accuracy of the digital maps [3].The concept of Enhanced Digital maps (EDmaps), also known as Enhanced Maps (Emaps), appeared with the purpose of creating better maps that could satisfy the needs of some vehicular applications with requirements of terms of map accuracy and completeness higher than those offered by standard maps [4]. Emaps are meant to be more complete and accurate than standard maps. To do so, Emaps may store more detailed data or some parameters that are not usual in standard maps based on polylines.Our Emap proposal aims at supporting positioning and map-matching in urban areas, for which it stores information in two different layers:A road layer, dedicated to describe urban road layouts that is flexible enough to model complicated shapes. When developing Emaps, most of the authors focus their efforts on the accuracy of the centerline of the lane and the estimate of the road curvature. However, in this work another relevant aspect of the map is covered: the accurate representation (in our case, at submeter accuracy) of the road borders in an urban environment, which is contrary to the most common approach of depicting the centerlines, the number of lanes and their widths. This allows further possibilities in map-matching algorithms that can benefit from a more complete description of the road, providing more precise allocations of the vehicles, that are not necessarily referred to the centerline.An elevation layer that contains locations and heights of the buildings along the road. This way, when a vehicle is on a given point of the road, it will be feasible to create a visibility map of the GNSS satellites, detecting whether a satellite is in Line-Of-Sight (LOS) or in Non-Line-Of-Sight (NLOS). When solving the calculation of the vehicle positioning, NLOS satellites can be then removed, avoiding the biases introduced by the multipath effects caused by faulty measurements coming from NLOS satellites. Due to the elevation information stored in the map, the model presented in this paper is named Elevation-Enhanced map, or simply EEmap.The rest of the paper goes as follows: Section 2 presents most relevant works published in this field. Section 3 introduces the EEmap concept and model. Next, Section 4 explains the creation process of the EEmap. Section 5 shows some relevant considerations in terms of accuracy and memory use. Finally, Section 6 concludes the paper.2.?Related exactly WorksDue to its benefits, the concept of enhanced road map has been exploited in former works of the authors in order to achieve lane-level positioning [5], lane-change detection [6] or position integrity [7]. This work follows this research line, adding new contributions to this field.