Reduction in stress-reactivity in rats reared by high-licking dams appears to be mediated by increased glucocorticoid receptor expression in the hippocampus (Liu et al., 1997 and Weaver et al., 2004) which enhances negative feedback on the HPA axis find more (Sapolsky et al., 1985 and Liu et al., 1997). Recent studies have shown that natural variation in maternal care affects a wide range of outcomes beyond anxiety behavior, including social behaviors. High levels of early maternal grooming are associated with increased play behavior in juvenile male rats (Parent and Meaney, 2008 and Van Hasselt et al., 2012),

increased social interaction in adult offspring of both sexes (Starr-Phillips and Beery, 2014), and altered play dominance rank in adult female rats (Parent et al., 2013). Effects of maternal contact have also been described in other species; for example in prairie voles, maternal care and family structure have been associated with social investigation in adolescence, and changes in parental and mate-directed behaviors in adulthood (Ahern and Young, 2009 and Perkeybile et al., 2013). Early experience of maternal care is sometimes associated with changes in oxytocin and vasopressin system regulation (reviewed in Veenema, 2012), although it is not yet clear whether such changes underlie LBH589 clinical trial the known differences in social behavior. In a synthesis of findings across rodents, primates,

and human studies, Shelly Taylor proposed that in addition to flight-or-flight responses to stress, females show pronounced “tend and befriend” responses to a stressor (Taylor et al., 2000). Taylor related “tending” to parental nurturing behaviors, based on evidence that rat dams lick their pups (tending) following separation, that oxytocin appears to be more

elevated in females following a stressor, and that oxytocin can act both MYO10 as an anxiolytic and to promote affiliative behavior. “Befriending” was related to the adaptive value of social support under stressful conditions, and its particular value for females that might be more vulnerable than males. Whether or not shared history of maternal care-giving and defensive social behaviors best explains distinct female responses to stress, the existence of such sex differences in stress/social behavior interactions has been demonstrated repeatedly. We have discussed several examples in this review; first, we described sex differences in the potency of particular stressors, for example crowding is particularly stressful for males, but is either calming to females or does not have major effects on physiological endpoints ( Brown and Grunberg, 1995 and Kotrschal et al., 2007). Even when the same event is stressful to both males and females, the sequelae of stress exposure may differ, for example stress impairs classical conditioning in females, which is the opposite of the effect found in males ( Wood and Shors, 1998).

43. Of the cases with drusen volume regression, 30.6% (15/49) completely regressed during follow-up, whereas 69.4% (34/49) showed a decreased drusen volume only. In cases of small hard drusen with increased drusen volume, 33.9% (19/56) showed development of new drusen, whereas 66.1% (37/56) of those small hard drusen showed an increased drusen volume. Pointed drusen showed a significant

association with a progression in volume (P = .031; OR 4.89; 95% CI 1.16−20.67), with a chance of 0.80 (95% CI 0.55−0.93) for volume progression. No significant longitudinal changes were observed for dome-shaped and saw-toothed drusen. Drusen with overlying photoreceptor layer or RPE damage showed a statistically significant association with a regression in volume (P = .041; OR 7.67; 95% CI 1.09−54.24 and P = .022; OR 12.38; 95% CI 1.44−106.57), with Afatinib chemical structure similar chances for drusen volume regression (0.86 [95% CI 0.41−0.98] and 0.89 [95% CI 0.49−0.99], respectively). Drusen reflectivity and homogeneity did not appear to have significant impact on drusen change. In this study,

we were able to show that small hard drusen in patients with the basal laminar drusen phenotype are subject to a constant dynamic process of drusen remodeling. The initial drusen morphology seemed to predict the future course of drusen development. Small hard drusen with a decreased reflectivity of overlying RPE or photoreceptor layer were more likely to show a regression in drusen volume, whereas pointed small hard drusen were more Ceritinib purchase likely to show volume progression. Although the exact mechanism of drusen biogenesis in basal laminar drusen as well as in “typical” AMD is still unclear, an identical mechanism in the developmental courses may be expected because of the similar topographic, structural, and compositional features.5 In both drusen types, RPE cell pathology seems to play a major role in drusen development. Cellular remnants and debris

derived from degenerated RPE cells become sequestered between the RPE basal lamina and the inner collagenous layer of Bruch membrane and provoke a chronic inflammatory response with complement activation.34, 35 and 36 Simultaneous with this continuous process of accumulating extracellular debris, there is a process of drusen removal that may be related to at least 2 Parvulin factors. The first is the removal of these drusen constituents by macrophages.5, 10 and 37 Different types of macrophages are present in the normal human choroid.38 In contrast to resident choroidal macrophages, Bruch membrane macrophages are only seen in eyes with drusen, making these macrophages a possible player in the process of drusen regression.39 A role for macrophages in the process of drusen removal is further supported by animal models that suggest that an impaired mobilization of macrophages may prevent the clearance of drusen-like lesions in mice.

4 years for the bivalent vaccine with 100% seropositivity maintained and at least 5 years for the quadrivalent vaccine with 98.8% seropositivity PF-2341066 maintained

[24]. The bivalent vaccine induces sustained antibody titres for HPV18 several fold higher than after natural infection, 8.4 years after initial vaccination with 100% seropositivity maintained. However, for the quadrivalent vaccine, 18 months after first vaccination, the induced antibody titres for HPV18 return to the level of natural infection, with a reduction in seropositivity over time [42]. A correlate for protection has not yet been established and further studies will determine whether these decreasing antibody levels are linked to reduced effectiveness. The immunogenicity of the bivalent and quadrivalent vaccine was Selleck BMN-673 compared in a head-to-head trial. Neutralising antibodies (nAbs) against HPV16 and HPV18 were 3.7 and 7.3-fold higher, respectively for the bivalent vaccine compared to the quadrivalent vaccine in women of age 18–26 years old at month 7 after receiving the first dose [43]. These differences remained similar in older age groups. After 24 months of follow-up, the GMTs of nAbs were 2.4–5.8-fold higher for HPV16 and 7.7–9.4-fold higher for HPV-18 with the bivalent versus the quadrivalent vaccine [24] and [44]. This observation remained similar up to 48 months of follow-up: GMTs of nAbs were consistently

higher in those receiving the bivalent vaccine across all age strata: 2.0–5.2-fold higher for HPV16 and 8.6–12.8-fold higher for HPV18 [45]. The use of different adjuvants in the vaccines might explain these differences in immunogenicity [46]. The difference in immune response observed at month 7 between the two vaccines was sustained up to month 48. However, the long-term clinical implications of these

observed differences in antibody response need to be determined. An anamnestic response was observed after the administration of a fourth dose after 5 years for the quadrivalent vaccine [47] and after 7 years for the bivalent vaccine [48]. In a phase I/II study in South Africa, the bivalent HPV vaccine was shown to PDK4 be immunogenic and well tolerated in HIV-infected women up to 12 months after vaccination. All subjects, both HIV-positive and HIV-negative were seropositive at month 2, 7 and 12, although antibody titers were lower in HIV-positive children [49]. Similar results were observed with the quadrivalent vaccine [50]. Several studies are currently on-going in HIV-positive adolescent girls and young women to evaluate the safety and immunogenicity of HPV vaccines [17]. Both HPV vaccines have some cross-protection against types that are not included in the vaccines, possibly explained by phylogenetic similarities between L1 genes from vaccine and non-vaccine types: HPV16 is phylogenetically related to HPV types 31, 33, 52 and 58 (A9 species); and HPV18 is related to HPV45 (A7 species).

, 2001). Intra-LC administration of a CRF antagonist during the stress prevented the stress-induced excitation and revealed a greater post-stress inhibition that is naloxone-sensitive (Valentino and Wehby, 1988a and Curtis et al., Dolutegravir 2001). Additionally, LC administration of naloxone alone increased the time taken for LC excitation

to recover to pre-stress levels. This study suggested that opioid inhibition was important in recovery of LC activity from this physiological stressor. Together these findings support a model whereby acute stressors engage both CRF and opioid inputs to the LC (Fig. 2A). CRF is the predominant afferent and shifts LC discharge to a high tonic mode that favors

increased arousal, scanning attention and behavioral flexibility, effects that would be adaptive coping responses to an acute threat. At the same time endogenous opioid afferents that have opposing actions are engaged. These function to restrain the CRF excitation and to promote recovery after stressor termination. These CRF/opioid interactions adjust the activity and reactivity of LC neurons so that level of arousal selleck and processing of sensory stimuli are optimized to facilitate adaptive behavioral responses to stressors. The protective effects of opioids are apparent in the many studies documenting that morphine administration shortly after a single traumatic event reduces the incidence of PTSD (Bryant et al., 2009 and Holbrook et al., 2010). During acute stress MOR regulation of the LC serves as an adaptive counterbalance that curbs the excitatory effects of CRF and protects against the consequences of a hyperactive

brain norepinephrine system. However, tipping the balance in favor of a MOR influence incurs alternative costs (Fig. 2B). Like the CRF response to stress, the opposing opioid response must be limited. The persistence of an opioid influence can produce enduring modifications in neural circuits that result in opioid tolerance and dependence. Indeed, this may be an underlying basis for the association between stress and substance abuse. A bias toward opioid regulation of the LC was recently demonstrated to occur with repeated through social stress, which diminishes CRF function and enhances MOR function in the LC (Chaijale et al., 2013). Unlike acute stressors, repeated social stress decreased LC neuronal discharge rate by 48 h after the last stress and this inhibition was naloxone-sensitive indicating that MOR receptors were occupied. Analysis of CRF1 and MOR protein levels and receptor trafficking in the LC demonstrated that this paradoxical stress-induced inhibition is due to both a loss of CRF-elicited excitation as a result of CRF1 internalization and to increased opioid release and MOR signalling (Chaijale et al., 2013).

The sensitivity of the assay was 15.6 mIU/ml and the minimum detection level 31.2 mIU/ml. Results were expressed as log2 units or as reciprocal titres. We defined the protective level of HAI measles antibody as a titre of log2 ≥ 3 which equates to 125 mIU [12]. Ex vivo measles effector cell assays: After separation of blood on Lymphoprep PBMC were used in the ex vivo interferon-gamma (IFN-γ) ELIspot assay as previously described [14]. The cells were infected for 2 h with Edmonston (E-D) wild type measles virus or E-Z measles vaccine virus which had been grown for 3 days on a culture of Vero cells in RPMI/10% Foetal Calf Serum (R10F).

The multiplicity of infection was 0.1

and 1.0 for the two strains respectively. The infected cells were then washed high throughput screening compounds and plated in duplicate at 105 cells/well in R10 with 10% AB serum (R10AB, Sigma). Control PBMC were mock infected with R10F harvested after culture of uninfected Vero cells for 3 days. In addition duplicate wells containing 105 PBMCs were also stimulated with a pool of overlapping 20-mer measles fusion peptides (NMI Peptides) dissolved in normal saline and 0.4% DMSO and used at a final concentration of 2 μg/ml Protein Tyrosine Kinase inhibitor in R10AB. Control cells were incubated in medium containing 0.02% DMSO which was the same concentration as that in the test wells. Phytohemagglutinin (5 μg/ml) was used as a positive control. Spots were counted using the AID ELIspot plate reader (Autoimmune Diagnostika). The mean number of spots in the duplicate wells of the negative control was subtracted from the mean spot count in the positive wells; an assay with a control value of ≥50 spots per well was regarded as invalid. Measles

memory cell assays: As described previously 106 PBMC were cultured for 10 days in R10AB with 105 UV irradiated PBMC infected with measles virus [15] or with pooled measles nucleoprotein or fusion peptides as described above. Controls consisted of PBMC mock infected with Vero cell medium and treated in the same way as above. Intracellular cytokine staining (ICS): Following stimulation, cells were permeabilised and stained for flow cytometry analysis as previously described [13]. The staining panel used at 9 and 9.5 months was anti-CD8 through FITC, anti-CD4 PE, anti-CD69 PerCP and anti-IFN-γ APC. At 18 months, the panel was anti-IFN-γ FITC, anti-CD4 PE, anti-CD8 PerCP and anti-IL-2 APC. All antibodies were supplied by BD Biosciences. Cytokines in plasma or supernatants: Plasma was frozen at −40° C until assayed using the Bio-Plex 200 Suspension Array system (Bio-Rad) according to the manufacturer’s instructions. FOXP3 mRNA expression: RNA was extracted from whole blood collected in Paxgene tubes (PreAnalytix, QIAGEN) and frozen at −40° C until RNA extracted.

Moreover, the rat mesenteric

artery reportedly does not express functional NMDArs (51). (±)Ketamine racemate has been reported to inhibited NR1/NR2A and NR1/NR2B channels with IC50 values of 13.6 ± 8.5 and 17.6 ± 7.2 μM, respectively, whereas S(+)-ketamine inhibited NR1/NR2A and NR1/NR2B with IC50 values of 4.1 ± 2.5 and 3.0 ± 0.3 μM, respectively (52). The IC50 values of (+)MK801 and (−)MK801 for inhibiting channels with the NR1 subunit and various NR2 subunit complexes (NR1/NR2X) ranged Z-VAD-FMK datasheet from 9–38 nM and from 32–354 nM, respectively. These IC50 values for inhibiting NMDArs are distinct from those for inhibiting Kv of RMASMCs. The pKa of MK801 is 8.37, and thus approximately 94% of MK801 exists in its protonated, positively charged form at pH 7.2 (the pH of the pipette solution). The results of this study showed that MK801 inhibition of Kv-channel currents was completely voltage-independent (Fig. 3), which suggests that the MK801-binding site of Kv channels is not affected by the sensing of the transmembrane potential, unlike in the case Paclitaxel of the binding sites for open-pore blocking agents. In this study, we did not examine whether an extra-

or intra-cellular site is responsible for the MK801-Kv channel interaction, which warrants future investigation. As described above, MK801 is a potent NMDAr inhibitor. NMDAr is a glutamate receptor and glutamate is the brain’s primary excitatory neurotransmitter. NMDAr is an ionotropic receptor that, when activated, causes the influx of Ca2+ and other cations. MK801 blocks the NMDAr in a state- and voltage-dependent manner, because the PCP-binding sites in the NMDAr are accessible to MK801 only when the channel is open or activated. Therefore, the mechanism by which MK801 was determined

to inhibit the Kv channels of RMASMCs in this study differs considerably from the mechanism of MK801 inhibition of the NMDAr channel. Because we examined the effect of MK801 on native Kv-channel currents in RMASMCs in this study, the specific target of MK801 remains unknown. Multimeric heteromers of several Kv-channel subunits such as Kv1.1, Kv1.2, Kv1.5, and Kv2.1 have been reported to contribute to the native Kv-channel currents of vascular smooth whatever muscle (53), (54) and (55). Furthermore, certain auxiliary Kv-channel beta subunits have been reported to contribute to the complexity and heterogeneity of native Kv currents (56) and (57). These Kv-channel subunits play critical roles in variety of excitable and non-excitable cells such as those in the cardiovascular system and in the CNS. Therefore, future studies could examine the effect of MK801 on specific Kv-channel subunits expressed in heterologous cell systems. As we stated above, we have observed that MK801 blocked the Kv1.5 expressed in CHO cells. The blockade of Kv1.5 by MK801 was very similar with that the present study.

They upgraded their system in spring 2012 to Crenolanib manufacturer include barcode scanning functionality [19]. CHIP requires staff to enter data through a combination of typing data and drop-down menus ( Fig. 3). For barcoded vaccines, immunizers scanned the vial to populate the client’s record with the vaccine name and lot number; expiry date was not recorded. For non-barcoded vaccines, immunizers used CHIP’s conventional methods (i.e., typing in lot

number and using drop-down menus for vaccine name and other data). Immunization staff were provided with scanners (DS6700, Motorola Ltd., United States, $522) and stands (Intellistand for DS67xx series, Motorola Ltd., Unites, States, $55), as well as a group training session by OKAKI staff to demonstrate the scanning process. After obtaining informed consent from the immunization nurses, we collected the following: (i) Immunization record quality – After the immunizer recorded vaccine data, we audited the record,

examining the completeness and accuracy of the relevant data fields (vaccine name, lot number, and expiry date [the latter for APH only]) compared to the information on the vial. Based on earlier work and information from immunization this website managers, we assumed a 1% data entry error rate with barcode scanning and 5% data entry error rate with the manual method. Collecting data for 666 vaccinations per case study (333 barcoded vials and 333 non-barcoded vials) allowed us to detect this difference in data quality with 80% power and 5% alpha-level. We compared data quality of the immunization records using z-tests, where the proportions of immunization records with one or more errors in the vaccine name, lot number, or expiry date fields for barcoded

vials and non-barcoded vials were compared. We used the t-test to compare the average time required by immunization staff to record vaccine data using barcode scanning and the manual method. We assessed readability of barcode scanning by recording the number of barcoded vials that could not be scanned successfully. Analyses were performed using STATA 10 (StataCorp LP, College Station, United DNA ligase States). The interviews were imported into qualitative analysis software (N-Vivo Version 9.0, QSR International, Burlington, United States) to facilitate data organization, review, coding, analysis, and exploration of themes that emerged from the data. Two team members (JAP and SQ) read each transcript once to get an overall sense of the data, and then again to code. Consensus decision-making was used to arrive at mutually agreed-upon coding. For Study Site 1, we collected data from 282 barcoded vials and 346 non-barcoded vials over 21 immunization clinic days between July 23 and October 4 2012 (Table 2).

Le classement par rang médian national des disciplines choisies à l’issue des ECN 2012 montre

un attrait des étudiants pour les spécialités chirurgicales Epacadostat mouse comme l’ophtalmologie ou médicales comme la néphrologie ou la médecine interne. “
“La sclérodermie systémique (ScS) est une affection chronique du tissu conjonctif qui se caractérise par l’existence de manifestations vasculaires, au premier rang desquelles le phénomène de Raynaud, et plus rarement des complications viscérales comme l’hypertension artérielle pulmonaire (HTAP) et la crise rénale sclérodermique, par la survenue de manifestations fibrosantes, intéressant avant tout la peau et le poumon, mais pouvant toucher tous les viscères, et par la détection d’auto-anticorps spécifiques de la maladie [1]. Sa prévalence varie de3 à 24 cas pour 100 000 habitants [2] and [3]. Elle est plus élevée aux États-Unis et en Australie qu’en Europe et au Japon. La ScS touche trois femmes pour un homme avec des extrêmes allant de 1 à 15. Elle débute rarement avant l’âge de 20 ans, et on observe un pic de fréquence entre 45 et 60 ans [3]. Plusieurs SP600125 manufacturer critères diagnostiques

ont été proposés. Si longtemps ceux de l’American College of Rheumatology (ACR) [4] sont restés les critères de référence, leur manque de sensibilité a amené à en élaborer de nouveaux, les critères de l’ACR/EULAR qui viennent de paraître [5] and [6]. Ils sont plus sensibles et plus spécifiques que ceux de l’ACR et utilisent des paramètres qui intéressent la main comme les doigts boudinés ou la sclérodactylie (4 points au total), les cicatrices ou dépressions pulpaires (3 points) et les télangiectasies (2 points). Le score total est calculé en ajoutant le poids maximum (score) dans chaque catégorie. Les patients

dont le score total est ≥ 9 sont classés comme ayant une ScS. La main constitue une cible privilégiée de la ScS [7]. La maladie évolue en trois phases consécutives : • à la phase précoce, en particulier dans les formes diffuses, l’œdème des doigts (doigts gonflés) et des mains prédomine, souvent associé ADP ribosylation factor ou pouvant précéder la survenue du phénomène de Raynaud (figure 1). Au cours de cette période, des arthralgies impliquant les articulations des doigts sont souvent présentes, constituant quelquefois la plainte majeure du patient. L’œdème limite l’amplitude du mouvement des articulations métacarpo-phalangiennes (MCP) et inter-phalangiennes proximales (IPP), et des manifestations du phénomène de Raynaud peuvent entraîner la survenue d’ulcères digitaux (UD) dès cette phase très précoce [8]. Ces UD, associés aux autres anomalies, contribuent à la survenue de douleurs et d’une perte de la fonction de la main [1]. À ce stade très précoce, les crissements tendineux peuvent déjà être observés [9] ; Figure 1.  Phénomène de Raynaud. Phase cyanique La main est une cible privilégiée au cours de la ScS. Toutes les structures anatomiques peuvent être touchées [12].

The challenge is that several studies have shown more than 30% of women with pelvic floor dysfunction are not able to contract the pelvic floor muscles correctly even after thorough individual teaching and feedback (Benvenuti et al 1987, Bump et al 1991, Bø et al 1988). The most common errors

are to bear down or to use hip adductor, gluteal, or abdominal muscles instead of the pelvic floor http://www.selleckchem.com/products/Methazolastone.html muscles (Bump et al 1991, Bø et al 1988). Group training of pelvic floor muscles has been shown in several randomised controlled trials to be effective, but these programs included individual instruction and feedback of the contraction (Bø et al 1990, Bø et al 1999, Mørkved and Bø 1997, Mørkved et al 2003). It is not yet known whether it is possible to teach buy Baf-A1 women participating in a general group-based exercise class to contract the pelvic floor muscles. Culligan et al (2010) concluded, on the basis of their finding that Pilates training produced similar strength gains to pelvic floor muscle

training, that their results may ‘lead to widespread use of Pilates-based exercise programs to treat and prevent pelvic floor dysfunction’. In our opinion that conclusion is premature because no randomised trials have demonstrated benefical effects of Pilates exercise on clinically important outcomes (continence) in a sample of incontinent women. Indeed, observational data suggest that this is not the case: a study on group fitness instructors showed that the prevalence of incontinence was the same amongst female yoga and Pilates instructors as in the general population, suggesting that the exercises did not provide a beneficial effect (Bø et al 2011). The suggestion of an association or causal link between breathing, posture, and pelvic floor muscle dysfunction should

be tested in case-control or cohort studies with blinded assessors. A large cross-sectional study found associations between incontinence, Thymidine kinase low back pain, and respiratory disease (Smith et al 2006), but it is quite possible the associations were confounded, so that while participants had multiple complaints at the same time the conditions were not causally related. Cross-sectional studies usually provide weak evidence of causality. There are two contradictory hypotheses on the effect of general exercise on the pelvic floor, previously described by Bø (2004). One hypothesis holds that general exercise makes pelvic floor muscles co-contract, and thus strengthens pelvic floor muscles and prevents stress urinary incontinence. The other hypothesis is that repetitive or heavy impact on the pelvic floor, such as is caused by heavy lifting or marathon running, may fatigue, stretch, and weaken the muscles.

Les données ont été recueillies sur des cahiers de recueil électroniques, permettant un contrôle de qualité des données instantané, MK-8776 ic50 par des techniciens d’études cliniques envoyés sur les différents sites pendant la période de l’étude. De très nombreuses données ont ainsi été collectées, permettant de caractériser au mieux la typologie des patients et leur mode de prise en charge. Un suivi au long cours centralisé est organisé au sein de la Société française de cardiologie avec le concours de l’unité de recherche clinique URCEST de l’hôpital Saint-Antoine (Paris). FAST-MI 2010 s’inscrit dans la continuité des précédents

registres nationaux d’infarctus, USIK 1995, USIC 2000 et FAST-MI 2005, tous construits sur le même principe d’un recueil ponctuel de données pendant une période d’un mois chez les patients hospitalisés selleck chemicals pour un infarctus récent, quel que soit le type d’établissement hospitalier [2], [3] and [4]. Le registre FAST-MI 2010 a été soutenu par le Collège national des cardiologues des hôpitaux, le Collège national des cardiologues français, la Société française de médecine d’urgence et Samu de France. Le financement de l’étude a été assuré par les laboratoires Merck, l’Alliance Eli-Lilly-Daiichi-Sankyo, AstraZeneca, GSK, sanofi-aventis

et Novartis. Le protocole de l’étude a été approuvé par le comité de protection des personnes de l’hôpital Saint-Louis et par la Commission nationale de l’informatique et des libertés. La moyenne d’âge des patients hospitalisés

pour infarctus avec sus-décalage (STEMI) est très sensiblement inférieure à celle des patients hospitalisés pour infarctus sans sus-décalage (NSTEMI) (63 ± 15 ans versus 69 ± 14 ans) ; parmi les patients de 75 ans et plus, 45,5 % ont un STEMI, alors que la proportion est de 60 % chez les moins de 75 ans (figure 1). De même, l’âge de survenue d’un infarctus est nettement plus élevé chez les femmes que chez les hommes (72 ± 14 ans versus 63 ± 14 ans), et 52 % des femmes hospitalisées pour un infarctus ont plus de 75 ans, contre 23,5 % chez les hommes (figure 2). Dans l’infarctus STEMI, les symptômes initiaux Rebamipide varient largement avec l’âge (tableau I). Si la douleur reste le symptôme majeur (plus de 80 %, quel que soit l’âge), l’insuffisance cardiaque et la syncope sont des symptômes dont la fréquence augmente nettement avec l’âge ; à l’inverse, l’arrêt cardiaque initial est moins souvent retrouvé. L’intensité de la douleur tend à diminuer avec l’âge ; sur une échelle de douleur de 10, la moyenne est de 6,2 pour les moins de 65 ans, tandis qu’elle n’est plus que de 5,1 chez les patients de 85 ans et plus ; la proportion de patients ayant une douleur de 7 ou plus est de 21 % en dessous de 65 ans, de 15 % entre 65 et 74 ans, de 11 % entre 75 et 84 ans et de 4,5 % à partir de 85 ans.