Mais à l’évidence, l’un des aspects essentiels est d’évoquer

ce type de problème avec les patients, et les médecins traitants ainsi que les AZD9291 datasheet cardiologues ont là un rôle primordial, notamment parce que les risques cardiovasculaires liés à la pratique de l’activité sexuelle sont globalement peu importants chez les patients bien évalués, stables et avec un traitement adapté. les auteurs déclarent ne pas avoir de conflits d’intérêts en relation avec cet article. “
“Pulmonary artery involvement is frequent in Takayasu arteritis. Pulmonary perfusion scintigraphy could represent an interesting and simple imaging tool to detect pulmonary artery involvement in Takayasu arteritis. “
“Les populations précaires ont des niveaux de consommation de tabac et de dépendance supérieurs à celles de la population générale. Ceci induit une plus forte morbi-mortalité. La perspective temporelle a un impact sur les taux de réussite du sevrage tabagique. “
“La prévention secondaire vise à repérer les jeunes ayant un usage à risque

de substances psycho-actives (SPA) ou à l’origine de dommages. Le lien entre repérage en soins primaires et inhibitors consultations spécialisées reste difficile à créer. “
“La baisse de l’estime de soi des learn more femmes alcoolo-dépendantes par rapport aux hommes alcoolo-dépendants et par rapport à un groupe témoin, sans information sur l’estime de soi des femmes devenues abstinentes. La baisse de l’estime de soi générale, familiale et professionnelle des femmes devenues abstinentes et alcoolo-dépendantes par rapport au groupe témoins. “
“Immune thrombocytopenia idiopathic thrombocytopenic purpura (ITP) occurs mainly in PAK6 young adults, particularly women in their second or third decade, with an overall female to male ratio of 2 to 1, suggesting that sex hormones play a role in the susceptibility to ITP. We analysed 225 patients with ITP. “
“Le score SIGAPS sert à évaluer la production scientifique des établissements hospitaliers et leurs attribuer des financements. Plus les

auteurs sont prolifiques (score SIGAPS élevé), moins ils ont tendance à publier en français ; publier en français ne semble donc pas être le meilleur moyen d’avoir un score SIGAPS élevé. “
“Dans l’article « Rein et infection par le virus de l’immunodéficience humaine » paru dans le numéro de mars 2012 de La Presse Médicale, le tableau I était erroné, voici ci-dessous le tableau I corrigé. Nous remercions le service ICAR (service de néphrologie, hôpital Pitié-Salpêtrière, 75013 Paris, France) pour son apport. Nous prions nos lecteurs de nous excuser pour cette regrettable erreur. “
“La population entrant en prison est usagère de drogues La population détenue interrogée poursuit sa consommation de drogues en détention “
“Au Maroc, malgré l’accès aux thérapies antirétrovirales, le diagnostic de l’infection à VIH se fait à des stades avancés de la maladie.

Some of these parents drew a comparison between the expectation for parents to be aware of the ingredients of foods they give their children, but to accept vaccines with little information on their constituent parts. No parents accepting MMR or taking single vaccines mentioned ingredients. If you spilt the contents of one of the [vaccine] syringes it would be a biohazard, you’d have to severely clear up the room. (P24, no MMR) Only parents rejecting all vaccines questioned vaccine efficacy, suggesting two routes to vaccine failure: immunity wearing off, and atypical Hormones antagonist disease strains increasing to take the place of the vaccinated strains.

In contrast, some parents accepting MMR or single vaccines argued that the only reason vaccination may ‘fail’ is if not enough people take it up. We don’t know are we just going to end up with a load of teenagers who have these illnesses when they’re teenagers or in their early adulthood when it’s much worse? (P20) Libraries immune overload concerns were specific to parents opting to give no vaccines at all, but were related to the immunisation schedule as a whole rather than to combination vaccines. These parents felt the schedule is too full, starts too early (with timing motivated by population accessibility rather than

clinical necessity),

covers diseases too mild or uncommon to warrant vaccination. I can’t quote you the figures but you probably know but the number selleck of jabs they have before their first birthday is loads, shocking you know? And their immune system’s not even developed properly and at that age… it just seems to be so much for a little person to take. (P19, no MMR) Maintaining the recommended four-week gap between vaccines was the most important aspect Endonuclease of the schedule for MMR acceptors, primarily to maximise vaccine effectiveness rather than to minimise immune overload risk. Where vaccine postponement was planned, turning two years old was a common milestone, due to language development, increased disease risk due to increased socialising, and perceived immune system maturity. Accordingly, being confident that their child was developing normally reassured some parents that MMR would be safe for them. I’ll wait till they’re two, that’s my target… a lot of my friends waited till they were two … it seems like a good point, so they start going nurseries and different things. (P17, singles) Parents across decision groups considered taking single vaccines, though many (even some of those who eventually opted for singles) felt that the single vaccines industry exploits parent fear for high profits.

Creamy solid (85%), mp 148–149 °C; C26H22N2O3; IR (KBr) 1627, 1614, 1593,

1552, 1483, 1465, 1434, 1309, 1299, 1271, 1255, 1222 cm−1; 1H NMR δH (CDCl3, 300 MHz): 8.16 (dd, 1H, J = 7.7 & 1.6 Hz, C10-H), 7.50–7.43 (m, 7H, Ar-Hs), 7.39–7.28 (m, 5H, Ar-Hs), 7.0 (d, 1H, J = 7.8 Hz, Ar-H), 4.74 (d, 1H, J = 2.7 Hz, C3H), 4.36 (d, 1H, J = 5.5 Hz, inhibitors C11b-H), 4.22 (d, 1H, J = 11.3 Hz, C4H), 3.85-3.76 (m, 1H, C4H), 3.07 (s, 3H, NCH3), 2.65–2.58 (m, 1H, C3aH); 13C NMR δC (CDCl3, 75 MHz): 174.91 (C O), 158.87 (C5a), 152.65 (C6a), 141.41 (q), 140.36 (q), 131.91 (CH), 129.17 (CH), 128.35 (CH), 127.90 (CH), 127.00 (CH), 126.26 (CH), 126.42 (CH), 125.64 (CH), 124.56 (CH), 122.66 (C10a), 116.18 (C7), 95.95 (C11a), Selleckchem I BET151 82.13 (C3), 60.50 (C11b), 51.32 (C4), 46.19 (NCH3), 44.59 (C3a); m/z (ESI) 433.1 (M+ + Na), 410 (M+). Creamy solid (82%), mp 166–168 °C; C20H17FN2O3; IR (KBr): 2309.2 (s), 1620.09 (s), 1592 (s), 1473.51 (m), 1450.37 (s), 1357.79 (w), 1296.08 (s), 1249.79 (w) cm−1; 1H NMR δH (CDCl3, 300 MHz): 7.79 (dd, 1H, J = 8.4 & 3 Hz, C10H), 7.49–7.43 (m, 4H, Ar-Hs), 7.38–7.31 (m, 3H, Ar-Hs), 7.01 (d, 1H, J = 9 Hz, Ar-H), 4.35 (t, 1H, J = 8.1 Hz, C3H), 4.15 (d, 1H, J = 5.4 Hz, C4H), 4.08 (d, 1H, J = 11.4 Hz, C11b-H),

3.73–3.65 (m, 2H, C3-H & C4-H), 3.0 (s, 3H, N-CH3), 2.84-2.62 (m, 1H, C3a-H); 13C NMR δC (CDCl3, 75 MHz): 175.27 (C O), 158.84 (C5a), 148.80 (C6a), 141.28 (q), 133.24 (CH), 129.30 (CH), 127.25 (CH), 126.13 (CH), 125.74 (CH), 124.48 (CH), 124.14 (C10a), 117.72 (C7), XL184 mw 92.93 (C11a), 69.33 (C3), 61.18 (11b), 51.39 (C4), 45.07 (N CH3), 38.16 (C3a); m/z (ESI) 375 (M+ + Na). Creamy solid (85%), mp 171–173 °C; C26H21FN2O3; before IR (KBr) 2305 (s), 1620.09 (s), 1542.95 (m), 1473.51 (s), 1450.37 (m), 1427.23 (m), 1311.50 (w), 1249.29 (m), 1188.07 (w) cm−1; 1H NMR δH (CDCl3, 300 MHz): 7.79 (dd, 1H, J = 8.10 & 3 Hz, C10-H), 7.49–7.43 (m,

7H, Ar-Hs), 7.38–7.24 (m, 5H, Ar-Hs), 7.01 (d, 1H, J = 9.0 Hz, Ar-H), 4.75 (d, 1H, J = 2.7 Hz, C3H), 4.35 (d, 1H, J = 5.7 Hz, C11b-H), 4.22 (d, 1H, J = 11.4 Hz, C4H), 3.84–3.78 (m, 1H, C4H), 3.06 (s, 3H, NCH3), 2.72–2.48 (m, 1H, C3aH); 13C NMR δC (CDCl3, 75 MHz): 174.35 (C O), 159.26 (C5a), 148.88 (C6a), 141.35 (q), 140.31 (q), 130.54 (CH), 129.46 (CH), 128.23 (CH), 127.80 (CH), 127.43 (CH), 126.46 (CH), 126.42 (CH), 125.85 (CH), 124.25 (CH), 124.15 (C10a), 118.25 (C7), 96.11 (C11a), 82.31 (C3), 60.66 (C11b), 51.56 (C4), 46.26 (NCH3), 44.86 (C3a); m/z (ESI) 451.1 (M+ + Na).

, 2000 and Craig et al., 2008). This advocated approach to complex health interventions, including childhood obesity prevention programmes, necessitates

a deep understanding of the determinants of the problem in the target communities. The importance of the relationship between context (e.g. socio-cultural structures and practices) and Ipatasertib concentration health, and in particular the relationship between context and individual health-related behaviours has been highlighted in recent years (Frohlich et al., 2001). The work of Bronfenbrenner represents a major contribution to the theoretical understanding of the relationship between a child and the context within which they function. Bronfenbrenner proposed the Ecological Systems (ES) model, which depicts layers of contextual structures that influence a child, and in turn, these are influenced by the child’s actions (Bronfenbrenner, 1977). These structures are termed the microsystems (the relationships between the child and their immediate environments, e.g. home, school), mesosystems GS-1101 in vitro (the interrelationships between these settings), exosystems (settings that have an indirect effect, e.g. neighbourhood), and macrosystems

(cultural and inhibitors societal values that are manifested in the micro-, meso- and exosystems). The ES model articulates the complexity and interactions of the contextual structures that a child is embedded in, and acknowledges the reciprocal nature of the relationships. The model is the basis for ecological health promotion models that attempt to move the focus away from individual behaviour change (McLeroy et al., 1988). Bronfenbrenner’s model has given rise to several conceptual models of childhood obesity.

Davison Dipeptidyl peptidase and Birch’s model depicts child weight status at the centre, surrounded by three concentric circles; child characteristics; parenting styles and family characteristics; and community, demographic and societal characteristics (Davison and Birch, 2001). A further example is the ‘Causal Web’ model for the development of obesity, proposed by the International Obesity Taskforce (IOTF), which schematically represents contextual influences on individual lifestyle ‘choices’ (Kumanyika et al., 2002). This model encompasses national and international factors (media and advertising, urbanisation etc.), akin to Bronfenbrenner’s macrosystems, but does not acknowledge the reciprocity of relationships. In this study, we report the findings from focus groups run with members of UK South Asian communities. South Asians are a particular target group for obesity prevention, as they have higher body fat than other ethnic groups, and are more vulnerable to the health consequences of obesity (Bhopal et al., 1999, Whincup et al., 2002 and WHO expert consultation, 2004). The aim of the focus groups was to access key contextual data to inform the development of an obesity prevention programme targeting South Asian children.

This survey contained questions regarding personal characteristics, running routines, and selleck previous RRI. Also a specific question was included to confirm that runners were injury-free before starting the Modulators follow-ups. All questions and details about the baseline survey are described in Appendix 1 (see eAddenda for Appendix 1) and were published elsewhere (Hespanhol Junior et al 2012). Data collection consisted of six follow-up surveys (Appendix 2, see eAddenda for Appendix 2) sent to the runners by email every 14 days throughout

the 12-week study period. Messages were sent by email every two weeks to remind the participants to complete the online survey for the previous fortnight. A reminder email was sent if the SNS-032 ic50 survey was not completed in three days. If runners had not completed the survey eight days after the initial email, they were then contacted by phone to remind them to complete the survey either online or over the phone. A reminder letter was sent by regular mail with a pre-paid return envelope if none

of the previous reminder attempts was successful. Participants who received a reminder by regular mail could complete a printed survey that had the same questions as the online version. In order to minimise the recall bias in the information collected in these follow-up surveys, we sent all runners a running log by regular mail to help them to record each running session. We requested that participants complete the running log with all relevant information and transfer these data while completing the fortnightly follow-up survey. The follow-up survey contained information about training, the presence of any RRI during the period, motivation to run, and any running races that the participant had competed in over the preceding two weeks. These questions elicited information about the following variables: number of times that the participant had trained; the total distance run (in kilometres); average time for each running session; predominant type of training surface (asphalt,

cement, grass, dirt, sand, gravel); Rolziracetam predominant type of terrain (flat course, uphill, downhill, or mixed); amount of speed training (ie, training sessions that include some bouts of high speed running during a very short period); number of interval training sessions as different running intensities (ie, Fartlek); motivation during training (motivated, neutral, or poorly motivated); amount and type of running races performed; and absence of training due to personal reasons, motivation, or unfavourable weather conditions (eg, rain). Participants were also asked whether they failed to train for at least one session due to the presence of any RRI during the period (see Question 12 in Appendix 2 on the eAddenda for details).

, 2003). However, OLIG2 and NKX2.2 are not tightly colocalized in the pMN domain in the run up to MN-OLP fate switching in mice (Sun et al., 1998 and Richardson et al., 2006), so it is not clear that OLIG2 and NKX2.2 normally work together in OLP specification. In fact, OLPs develop normally

in NKX2.2 null mice, although their subsequent differentiation into OLs is prevented (Qi et al., 2001). Another potential cofactor for OLIG2 is MASH1/ASCL1; initially (∼E12.5) there are reduced numbers of OLPs in MASH1 null spinal cords, but MAPK inhibitor this soon resolves, suggesting that MASH1 is not critical for OLP specification (Sugimori et al., 2008). We found that S147A mutation did not have a noticeable effect on binding of OLIG2 to either NKX2.2 or MASH1 (Figure S2A), so we probably have to look elsewhere for critical determinants of OL lineage specification in the spinal cord. The transcription factor NF1A has been proposed to trigger gliogenesis throughout the neural tube (Deneen et al., 2006), but its physical and functional relationships with OLIG2 have yet to be investigated. Recently, OLIG2 was shown to interact with the bHLH protein E47 to directly activate the Sox10-U2 promoter in the OL lineage ( Küspert et al.,

2010). The results of our present study suggest that dephosphorylated Regorafenib clinical trial OLIG2S147 might specifically interact with E47 in this context. Epigenetic modifications play an important part in cell fate decisions, including OLP specification. For example, in the absence of histone deacetylases 1 and/or 2 (HDAC1/2), OLP formation in the ventral spinal cord is disrupted (Cunliffe and Casaccia-Bonnefil, 2006, Ye et al., 2009 and Li et al., 2009). It will be important in the future to investigate the potential interactions between OLIG2, HDACs, and other histone modifiers (e.g., methylases) and how these interactions

might be influenced by posttranslational modification. Our study focused on reversible phosphorylation of OLIG2-S147, an evolutionarily conserved site that is predicted to be a PKA target. We provided evidence that OLIG2-S147 can be phosphorylated by PKA in cultured Cos-7 cells and that dnPKA inhibits phosphorylation. Despite this, we cannot conclude that PKA is the only—or even the primary—protein serine kinase to target S147 in vivo. For example, the consensus target sequence for PKA found (R[R/K]X[S/T]) can overlap with that of PKC ([R/K]X[S/T]U[R/K]) (U, hydrophobic). Indeed, PKA and PKC are thought to phosphorylate common acceptor sites on the bHLH proteins HAND1 and HAND2 (Firulli et al., 2003). Nevertheless, the fact that Olig2S147A mice failed to develop MNs suggests that PKA might normally play a positive role in MN development. This seems counter to the popular idea that PKA negatively regulates the SHH pathway ( Li et al., 1995, Ruiz i Altaba, 1999, Epstein et al., 1996, Hammerschmidt et al., 1996 and Jacob and Briscoe, 2003).

The overall concordance rates for genes of the two replication predictions with the original predictions ranged from 64%–96%, and a majority of genes learn more predicted to be enriched in one experiment were also predicted to be enriched in the other (Table 2). All but one of the 39 significant functional differences in Table S6 were changed in the same direction in both replication sets, and 87%

of these, including all disease associations, also had a replicated p value smaller than 0.05 in either dorsal or lateral cortex (Table S6). Most, but not all, genes were similar in patterning between dorsal and lateral cortex (Figure S6), confirming previous observations (Hawrylycz et al., 2010). We next turned to the 1,055 lincRNA loci, expressing 1,879 multiexonic transcripts (see also Belgard et al., 2011), which we identified as being expressed in the cortical cell layers, usually at low levels. A large majority (67%) of these loci were novel, in that they had no overlap with annotated noncoding RNA loci (Rhead et al., 2010), likely because of their low expression. Sequence constraint, an indicator of functionality, for these loci was similar to that seen for other lincRNA locus sets (Marques and Ponting, 2009) (Figure S7; Belgard et al., 2011). These lincRNA loci also exhibited experimental hallmarks of transcribed loci; they significantly overlapped

DNase I hypersensitivity sites and histone methylation marks that are associated with active transcription in neuronal precursor cells (Figure S7). Some lincRNA loci have been predicted (Ponjavic et al., 2009), Aurora Kinase inhibitor and experimentally verified (Ørom et al.,

2010), to act in cis by regulating the expression of genomically proximal protein-coding genes. Some lincRNAs expressed in our cortical samples may also possess such functions, particularly in the regulation of patterns of expression across cortical layers. This is supported by patterned protein-coding gene loci being 39% more likely to be adjacent to one SB-3CT or more of these lincRNA loci than expected by chance (p < 10−4), and lincRNA expression across cortical layers being more often correlated, positively or negatively, with expression of their protein-coding genomic neighbors if these genes were patterned than if they were unpatterned (p < 0.02; see also Supplemental Experimental Procedures and  Belgard et al., 2011). Furthermore, we found a significant enrichment of cortical lincRNA transcription across enhancers defined in in vitro neuronal culture ( Kim et al., 2010) (2-fold increase, p < 10−4). Finally, because Evofold-predicted ( Pedersen et al., 2006) RNA structures were substantially enriched in these transcripts (2-fold increase, p = 2 × 10−3), the activity of some cortical lincRNAs is likely to be mediated by their secondary structures.

In girls only, significant relationships between maturity and indices

of anaerobic metabolism were noted. The lack of relationship in the boys is likely to have been due to the boys being pre-pubertal or early pubertal. Kuno et al.72 PARP inhibitor studied the responses of 12–15-year-old boys and adults to quadriceps exercise to exhaustion and during recovery. They reported higher values of PCr/(PCr + Pi) and pH at exhaustion in the boys than in the men and concluded that both the trained and untrained boys had, “less glycolytic ability during exercise than adults”. During recovery the PCr kinetics τ was shown to be invariant with age indicating similar oxidative capacity in boys and men. 73 In conflict with these findings Taylor et al. 74 BMS-387032 molecular weight reported a faster re-synthesis of PCr in children during recovery from calf muscle exercise to exhaustion and concluded that the oxidative capacity of skeletal muscle is highest in children. However, the interpretation of recovery data from both of these studies is confounded by the reported low muscle pH values with adult pH values significantly lower than those of children. In

a more recent study involving finger flexion exercise, Ratel et al. 75 reported similar end-exercise pH values in adults and 11-year-old boys but a faster PCr τ in the boys during recovery. In accord with Taylor they concluded that their results clearly illustrated a greater mitochondrial oxidative capacity in the boys than in the men. The effects of maturation

on exercise metabolism were investigated by Petersen et al.76 who evaluated the responses of nine pre-pubertal and nine pubertal swimmers to 2 min of calf exercise at 40% of pre-determined maximal work capacity (MWC) followed by 2 min at 140% of MWC. At end-exercise the Pi/PCr was higher and the pH lower in the pubertal girls but the differences were not statistically significant. This inferred that glycolytic metabolism was not age or maturity dependent but Isotretinoin this conclusion needs to be interpreted cautiously as the difference between the two groups in Pi/PCr at end-exercise was 66% and the high individual variability and small sample size suggest that this might have biological significance. Using an experimental design in which seven pre-pubertal boys and 10 men performed finger flexion exercise against a resistance of 15% of maximal voluntary strength, Tonson et al.77 investigated muscle energetic changes with maturation. They observed the total energy cost to be similar in both groups but the interplay of metabolic pathways to be different. At the onset of exercise the boys exhibited a higher oxidative contribution to ATP re-synthesis and a lower PCr breakdown than the men.

These disorders are synaptopathies (Ehninger and Silva, 2009) in which dysgenesis of dendritic spines is a recurrent anatomical feature (Penzes et al., PD98059 in vivo 2011). Fragile X syndrome (FXS) is the most common form of inherited ID and a frequent monogenic cause of ASD (Belmonte and Bourgeron, 2006, Hatton et al., 2006, Jacquemont et al., 2007 and Turk, 2011). Patients

with FXS display dendritic spine defects (Irwin et al., 2001), neurodevelopmental delay, and autistic-like phenotype (Jacquemont et al., 2007). FXS is due to loss of function of the RNA-binding protein FMRP (Bagni et al., 2012 and Bassell and Warren, 2008), which regulates dendritic targeting of mRNAs (Dictenberg et al., 2008) and controls protein synthesis and mRNA decay in neuronal soma and at synapses (Bassell and Warren, 2008). High-throughput screenings

(Brown et al., 2001, Darnell et al., 2011, BMS-754807 supplier Klemmer et al., 2011, Liao et al., 2008 and Miyashiro et al., 2003) have revealed that a wide array of neuronal mRNAs is targeted by FMRP, suggesting that simultaneous dysregulation of many proteins contributes to FXS. A key functional partner of FMRP is the cytoplasmic FMRP-interacting protein 1, CYFIP1 (Napoli et al., 2008, Schenck et al., 2003 and Schenck et al., 2001) also known as “specific Rac1-activated” (SRA1) protein (Kobayashi et al., 1998). CYFIP1 is located within a hot spot for ASD (chr15q11.2), close to a region critical for two ASD-related syndromes: the Angelman and Prader-Willi syndromes. Microdeletions or microduplications of the region, including CYFIP1 and three other genes, cosegregate with cognitive disabilities and ASD ( Cooper et al.,

2011, Doornbos et al., 2009, Leblond et al., 2012, Nishimura et al., 2007, van der Zwaag et al., 2010 and von der Lippe et al., 2010). CYFIP1 messenger RNA (mRNA) is downregulated in a subgroup of FXS patients who have the Prader-Willi phenotype and show severe ASD and obsessive-compulsive Dichloromethane dehalogenase behavior ( Nowicki et al., 2007). In addition, CYFIP1 has recently been linked to schizophrenia (SCZ) ( Tam et al., 2010 and Zhao et al., 2012). Together with FMRP, CYFIP1 represses neuronal protein synthesis: FMRP tethers specific mRNAs to CYFIP1, which in turn sequesters the cap-binding protein eIF4E, thereby preventing initiation of translation (Napoli et al., 2008). Upon activation of the brain-derived neurotrophic factor (BDNF)/NT-3 growth factor receptor (TrkB) or group I metabotropic glutamate receptors (mGluRs), CYFIP1 is released from eIF4E and translation ensues (Napoli et al., 2008). Furthermore, CYFIP1 is part of the Wave Regulatory Complex (WRC), a heteropentamer containing also WAVE1/2/3, ABI1/2, NCKAP1 and HPSC300 (Takenawa and Suetsugu, 2007). The WRC regulates the actin-nucleating activity of the Arp2/3 complex and it can be activated through the small GTPase Rac1, kinases, and phospholipids (Chen et al., 2010, Eden et al., 2002 and Lebensohn and Kirschner, 2009).

A third network concerned with “empathy” is engaged when individuals experience vicarious emotions from observing others PFI-2 ic50 ( de Vignemont and Singer, 2006). Finally, a fourth, “mirror,” network is activated when individuals observe the actions of others and is thought to play a role in learning through observation ( Carr et al., 2003, Rizzolatti and Craighero, 2004 and Spunt and Lieberman, 2012). The empathy and mirror networks are clearly related, and the mentalizing and mirror networks have in fact been combined into more global schemes for a unified model of how we think about other people ( Keysers and Gazzola, 2007). However, there is certainly not unanimous agreement on precisely what the

networks are, on their composition, or on how best to study them ( Barrett and Satpute, 2013). Indeed, it is likely that current beliefs about network architecture are biased, at least in part, by pre-existing theoretical Lapatinib cell line divisions and distinctions in social psychology—as well as limited by data. An alternative data-driven approach that is less biased capitalizes on data mining of the literature to find relationships between the psychological concepts studied and the brain activation patterns

that emerge over several thousand publications (Table 1; Figure 2C) (Yarkoni et al., 2011). Networks derived from these data-driven approaches will need to be compared and combined in some way with networks obtained from specific social neuroscience studies that use concepts from social psychology, as well as with networks obtained from model-based approaches. Yet even a cursory exploration with a data-driven approach (using NeuroSynth, see Figure 2C) yields both a confirmation of known patterns (e.g., several regions, such as medial prefrontal cortex and precuneus, feature in social cognition networks) as well as the discovery of new ones that can be further tested (e.g., the amygdala appears to participate

in many social cognition processes but not mentalizing). The future approach we advocate uses such data mining not as the sole tool but precisely to test results against Fossariinae patterns in the literature and to motivate new hypotheses to be further tested with other approaches (cf. Table 1). One looming question regarding the concept of the “social brain” and its modern network versions is whether any of these networks are specialized for processing social information. Plausibly, all social cognition draws on entirely domain-general processes, only applied to social stimuli. This unresolved question has been discussed in detail before (e.g., Adolphs, 2010) with the recommendation that, for methodological reasons, we should assume the existence of such specialized processes and brain networks (e.g., Kennedy and Adolphs, 2012). This assumption may in time be proved wrong, or wrong for some of the networks (e.g.