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Chrome 26 1410 63 Safari 537 31WordfenceTestMonBot test navigator userAgent addEvent evt handler window addEventListener addEventListener evt handler false else window attachEvent attachEvent orragende Kche mit Produkten aus der eigenen Landwirtschaft Toplage auf 1000m Seehhe 4 STERNE SUPERIOR HOTELDer Lrzerhof ist unser 4 Wellness-Hotel in Untertauern Ob im Sommer beim Wandern oder im Winter beim Langlaufen die ideale Kombination zur Gnadenalm TRUMEN UND GENIEEN Grozgige und komfortabel eingerichtete Zimmer erwarten Sie im 4 Sterne Superior Hotel WELLNESS AUF BER 2500m Das Wellnesshotel fr Genieer mit 7 verschiedenen Saunen und vielen Ruherumen Hallenbad und beheiztem Aussenpool GNADENALM WEBCAMS Bilder von der ALM HIGHLIGHTS Romantische Pferdeschlittenfahrten Rodeln auf der beleuchteten Rodelbahn Obertauern Restaurant Eventlocation im Salzburger Land Obertauern im Sommer UDI EVENT LOCATION BILDER WINTER BILDER SOMMER FERNSEHGARTEN OBERTAUERN WINTER RODELBAHN OBERTAUERN PFERDESCHLITTENFAHRTEN LANGLAUFEN Langlauf Loipe Langlauf Schule Skiworld Obertauern Langlaufen Tipps BIATHLON EISSTOCKSCHIESSEN NATUREISLAUFPLATZ WINTERWANDERN SOMMER ALLES ALMFEST 2015 WANDERUNGEN APPARTEMENT ZIMMERANFRAGE ONLINE BUCHEN OBERTAUERN WEBCAMS WEBCAM GNADENALM 1 LIVECAM GNADENALM WEBCAM UNTERTAUERN und 8211 WELLNESSHOTEL LRZERHOF OBERTAUERN WETTER SCHNEE- LOIPENBERICHT HOTELS und 8211 UNTERKNFTE ANREISE OBERTAUERN BLOG WINTERERLEBNISGNADENALMDEN WINTER ERLEBENOBERTAUERN - WO DER SCHNEE ZU HAUSE ISTGNADENALM OBERTAUERN SALZBURGER LANDSOMMER AUF DER ALMSALZBURGER ALMSOMMERALMSOMMER IN 42px font-weight 700 color eluid7efffc55 tbk subtitle font-size 30px line-height 36px font-weight 300 eluid7efffc55 tbk icon font-size 28px zn section eluida1f86e04 padding-top 60px padding-bottom 0px zn section eluidd50d9c42 padding-top 60px padding-bottom 20px wpadminbar ab-top-menu wpk-kallyas-options-menu-item hover div wpadminbar ab-top-menu wpk-kallyas-options-menu-item active div wpadminbar ab-top-menu wpk-kallyas-options-menu-item focus div wpadminbar ab-top-menu wpk-kallyas-options-menu-item div color eee cursor default background 222 position relative wpadminbar ab-top-menu wpk-kallyas-options-menu-item hover div color 45bbe6 !important wpadminbar ab-top-menu wpk-kallyas-options-menu-i rn bietet viele Produkte aus der eigenen Landwirtschaft Die Alm ist Sommer und Winter geffnet Romantische PferdeschlittenfahrtenPferdeschlittenfahrtenAuf Kuven durch die wunderbare Winterlandschaft auf der Gnadenalm Fr Familen und echte Romantiker ein besonderes Erlebnis Salzburger Almsommer SOMMER AUF DER ALMSalzburger Almsommer in Obertauern - Wandern im Salzburger Land Die Gnadenalm bietet Ihnen zahlreiche Wanderwege und Rundwanderwege Unsere Gnadenalm ist dabei Ziel und Ausgangspunkt fr Wanderungen in alle Himmelsrichtungen Unvergessliche Events in ObertauernEvents und Incentives in ObertauernDie Gnadenalm ist die perfekte Eventlocation in Obertauern Mit der Rodelbahn Biathlon Natureislauf tem ab-item before content f111 top 2px w b async !0 src www gnadenalm comwp-contentpluginswp-rocketincfrontjslazyload 1 4 min getElementsByTagName parentNode insertBefore attachEvent?w attachEvent onload w addEventListener load !1 window s id fjs getElementsByTagName d getElementById id js js id id src connect facebook neten USsdk xfbml 1 und version v2 5 fjs parentNode insertBefore fjs script facebook-jssdk Willkommen im Freizeitzentrum und Restaurant Gnadenalm in Obertauern T 43 6456 7351E-Mail info gnadenalm at Gnadenalm ObertauernGnadenalmstrae 20 5561 Obertauern Salzburger Land Open in Google Maps HOTEL-NEUERFFNUNGab Sommer2016 - The place to be! 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| Gnadenhof Anna - Tierschutz Rheinbach Neukirchen Home Aktuell Gnadenhof-Haustiere Projekt Gnadendorf Spenden Die Regenbogenbrcke Bildergalerie Nachde sind steuerlich absetzbar Haben auch Sie ein Herz fr Tiere untersttzen Sie den Verein durch Ihren Beitrag sei durch eine Spende oder sogar durch ih emacht Tieren die von Ihren und bdquo Besitzern und ldquo ausgesetzt oder weggeworfen wurden eine neue und artgerechte Heimat bieten Viele Tiere die k en sind uerst beschrnkt und stehen keinem Verhltnis den regelmig anfallenden Kosten Wir bitte Sie deshalb herzlich Ihre Untersttzung und sind f re ttige Mitarbeit oder auch durch eine Sachspende Herzliche Gre Ihre und Eure Heike und Bernd Schneider und der Gnadenhof Anna - Heike Schneider 2 der die Grnderin das Gnadenhofs ist eine engagierte Tierlieberhaberin und Tierschtzerin die mittlerweile von einer Vielzahl ebenso engagierten Fraue r jede Hilfe unendlich dankbar Der Verein Gnadenhof ist als gemeinntzig anerkannt und hat die Trgerschaft fr den Gnadenhof bernommen Alle Spenden eine Perspektive auf eine Vermittlung haben sei aus Krankheit oder sog Unvertrglichkeit genieen dort ihre letzten Tage Heike Hink heute Heike Schnei nkliches Pressespiegel Links Kontakt Impressum Rheinbach-Neukirchen liegt der Leben gerufene und bdquo Gnadenhof Anna und ldquo hat sich zur Aufgabe g n und Mnner untersttzt wird Der Gnadenhof ist dringend auf Ihre Untersttzung jeglicher Art angewiesen denn die Mglichkeiten Einnahmen erwirtschaft

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Sex xXx fick Erotik sexy hardcore | | edoms even more important now than they were Nowadays the free software movement goes far beyond developing the GNU system See the Free Software Foundation web site for more about what and list ways you can help More about GNU Unix-like operating system That means collection many programs applications libraries developer tools even games The development GNU started January known the GNU Project Many the programs GNU are released under the auspices the GNU Project those call GNU packages The name und ldquo GNU und rdquo recursive acronym for und ldquo GNU Not Unix und rdquo und ldquo GNU und rdquo pronounced noo one syllable like saying und ldquo gre w und rdquo but replacing the with The program Unix-like system that allocates machine resources and talks the hardware called the und ldquo kernel und rdquo GNU typically used with kernel called Linux This combination the GNULinux operating system GNULinux used millions though many call und ldquo Linux und rdquo mistake GNU own kernel The Hurd was started before Linux was started Volunteers continue developing the Hurd because interesting technical project More information Try GNULinux! Planet GNU Scientific Library released Version the GNU Scientific Library GSL now available GSL provides large collection routines for numerical computing This more s many extensions over the standard utility doc Short for all GNU packages Take Action Support current FSF campaigns Defend privacy and support global reform with LQDN Support the efforts net neutrality Europe the USA and Canada Fight against software patents worldwide and Europe Watch and share this movie Patent Absurdity und mdash made possible FSF associate members like you Call WIPO change its name and mission Students! Claim refund your unused Microsoft licences Add the Free Software More action items Can you contribute any these High Priority Projects? Gnash coreboot free distributions GNULinux GNU Octave drivers for network routers reversible perating System Support GNU and the FSF buying manuals and gear joining the FSF associate member making donation either directly the FSF via Flattr BACK TOP The FSF also has sister organizations Europe Latin America and India meet the free software gang Please send general FSF und GNU inquiries GNU org There are also other ways contact the FSF Broken links and other corrections suggestions can sent webmasters gnu org Please see the Translations README for information coordinating and submitting translations this article Free Software Foundation Inc This page licensed under Creative Commons International License Infringement Notification Updated Date sible use computer without software that would trample your freedom recommend installable versions GNU more precisely GNULinux distributions which are entirely free software More about GNU below What the Free Software Movement? The free software movement campaigns win for the users computing the freedom that comes from free software puts its users control their own computing Non-free software puts its users under the power the software developer See the video explanation What Free Software? Free software means the users have the freedom run copy distribute study change and improve the software Free software matter liberty not price understand the co debugging GDB automatic PowerVR drivers and also free software replacements for Skype OpenDWG libraries and Oracle Forms Can you take over unmaintained GNU package? halifax metahtml orgadoc are all looking for maintainers Also these packages are looking for co-maintainers aspell gnuae metaexchange powerguru See the package web pages for more information FSF FREE SOFTWARE HARDWARE GNU ART GNU WHO? SITE MAP und ldquo Our mission preserve protect and promote the freedom use study copy modify and redistribute computer software and defend the rights Free Software users und rdquo The Free Software Foundation the principal organizational sponsor the GNU O The GNU Operating System and the Free Software Movement Common clauses for the Free Software Gang banner fs-gang img-container text-align left padding-top 5em margin auto fs-gang img-container font-size font-weight bold margin-left 5em color white text-decoration none fs-gang img-container img margin screen-specific fs-gang-definitions fs-gang clear both margin a50606 Fallback from gradient -moz-linear-gradient f71111 -webkit-gradient linear left top left bottom color-stop f71111 Safari Chrome -webkit-linear-gradient f71111 Safari Chrome -o-linear-gradient f71111 Opera filter progid Microsoft gradient startColorstr endColorstr f71111 IE6 und IE7 -ms -filter progid Microsoft gradient startColorstr endColorstr f71111 IE8 linear-gradient f71111 the standard Skip main text Set language English catal Deutsch espaol franais italiano lietuvi Nederlands polski EUR Shqip EUR GNU Health Conference Nov Las Palmas Spain GNUHealthCon2016 JOIN THE FSF Free Software Supporter GNU Operating System Sponsored the Free Software Foundation ABOUT GNU PHILOSOPHY LICENSES EDUCATION SOFTWARE HELP GNU the only operating system developed specifically give its users freedom What GNU and what freedom stake? What GNU? GNU operating system that free software und mdash that respects users freedom The development GNU made pos Free Software meeting recap for August Every week free software activists from around the world come fsf irc freenode org help improve the Free Softwar more FSF Job Opportunity and Licensing Associate This position reporting the executive director works part our licensing and compliance team protect and promote the use more For more news see Planet GNU and the list recent GNU releases Tar provides the ability create tar archives well the ability extract update list files existing archive useful for combining many files into one larger file while maintaining structure and file information such permissions and creationmodification dates GNU tar offer ncept you should think und ldquo free und rdquo und ldquo free speech und rdquo not und ldquo free beer und rdquo More precisely free software means users program have the four essential freedoms The freedom run the program you wish for any purpose freedom The freedom study how the program works and adapt your needs freedom Access the source code precondition for this The freedom redistribute copies you can help your neighbor freedom The freedom improve the program and release your improvements the public that the whole community benefits freedom Access the source code precondition for this Developments technology and network use have made these fre | Computer Software Notebooks Apple Hard Programme |
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element css cursor pointer click window location link href - ? EUR flexslider first slides li div cli exslider first slides li div clickable each index obj element obj link element find link ! undefined ckable each index obj element obj link element find link ! undefined element css cursor pointer click w Zealand Norge Russia Sverige Suisse Schweiz United Kingdom United States EUR ? EUR ReSound Verso fl ReSound EUR window NREUM info beacon bam nr-data net errorBeacon bam nr-data net licenseKey c5db4dfe window location link href gnEditMode false ReSound facebook ReSound EUR - EUR ? EUR ReSound - EUR Re exports call exports typeof require for Russia International Australia esterreich Brasil Canada Chin b2 applicationID 9328402 transactionName queueTime applicationTime ttGuid agent window NREUM require Sound EUR ? EUR ReSound - EUR ReSound EUR ? ? EUR ReSound eCademy EUR cookies EUR 2016 GN ReSound EUR a esk republika Danmark Espania Finland France Deutschland India Italia Japan EUR Korea Nederland Ne
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| gnome.org
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Sex xXx fick Erotik sexy hardcore | getImageData data fillText getImageData data case simple fillText getImageData data case unicode8 fillText getImageData data return!1 src type head appendChild for Array simple unicode8 diversity supports everything img wpstats display none page content main menu the field GNOME org GNOME Technologies Abo data When the went dead there were longer any Maps Thankfully didn und take long for und hellip July Call for GNOME Asia Summit Host Proposals The GNOME Asia Committee inviting interested parties submit proposals for hosting GNOME Asia Summit during the quarter GNOME Asia Summit the featured annual GNOME ut Get Involved Foundation GNOME Ease comfort and control GNOME easy and elegant way use your computer designed put you control and bring freedom everybody GNOME developed the GNOME community diverse international group contributors that supported independent non-profit foundation Discover GNOME Get GNOME ources Developer Center Wiki Mailing Lists IRC Channels Bug Development Code Build Tool News Press Releases Latest Release Planet GNOME Development News Identi Twitter The GNOME Project Free share and remix Creative Commons CC-BY Optimized for standards Hosted Canonical Powered WordPress paq push disableC ookies paq push location ? http webstats gnome org paq push setTrackerUrl piwik php paq push setSiteId g s getElementsByTagName type defer true async true src piwik parentNode insertBefore stq window stq push view v ext j 4 2 blog 72405960 post 547 tz srv www gnome org stq push clickTrackerInit 72405960 5 Day Cosimo Cecchi Jim Hall Meg Ford Nuritzi Sanchez Shaun McCance Congratulations! This year had registered voters which sent valid ballots Elections ran during the months May and und hellip News Archives The GNOME Project About Get Involved Teams Support GNOME Merchandise Contact The GNOME Foundation Res GNOME window wpemojiSettings baseUrl org images core emoji ext png source concatemoji www gnome org wp-includes wp-emoji-release min js?ver canvas getContext und getContext String fromCharCode !g!g fillText return!1 switch textBaseline top font Arial case fillText toDataURL length case diversity fillText Make donation and become Friend GNOME! Your donation will ensure that GNOME continues free and open source desktop providing resources developers software and education for end users and promotion for GNOME worldwide Get involved! The GNOME Project diverse international community which involves hundreds Conference Asia The focuses primarily the GNOME desktop but also covers applications and the development platform tools brings the GNOME community und hellip July GNOME Board Directors Announced ORINDA The GNOME Foundation welcomes its new Board Directors for the upcoming und term Alexandre Franke Allan contributors many whom are volunteers Anyone can contribute the GNOME! Latest news August Mapbox steps help GNOME und Maps application July GNOME und Maps application stopped working Like all mapping applications relies online provide data The had been using und MapQuest und discontinued free access their
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sex | experience joy sadness disgust anger fear and surprise every known culture these emotions are indicated the same facial expressions und Complex adaptations like EURbeing little selfishEUR and EURnot being willing work without rewardEUR are human universals The strength might vary bit from person but everyoneEUR got the same machinery under the hood weEUR re just painted different colors Which means that trying raise perfect unselfish communists isnEUR like reading Childcraft books your kid itEUR like trying read Childcraft books your puppy The Soviets were not 50 right they were entirely wrong They werenEUR quantitatively wrong about the amount variance due the environment they were qualitatively wrong about what environmental manipulations could the face built-in universal human machinery Shermer und s argument was change from the line reasoning that have heard from him before which that the left understood that capitalism emergent system like evolution they would more accepting find that argument even less convincing understanding evolution provides one the strongest challenges libertarian leanings und evolution full wasteful competition for relative status and what good for the individual often not good for the group The weakness these arguments probably reflected the deeper rationale for Shermer und s libertarianism Yudkowsky questions human nature the real reason for Shermer und s libertarianism? Would Michael Shermer change his mind and become liberal these traits were shown hereditary? und Before you stake your argument point ask yourself advance what you would say that point were decisively refuted Would you relinquish your previous conclusion? Would you actually change your mind? not maybe that point isnEUR really the key issue Yudkowsky und s answer the question why he libertarian similar mine When ask myself this question think actual political views would change primarily with beliefs about how likely government interventions are practice more harm than good think libertarianism rests chiefly the empirical propositionEUR factual belief which either false true depending how the universe actually worksEUR that 90 the time you have bright idea like EURoffer government mortgage guarantees that more people can own houses EUR someone will somehow manage screw up thereEUR ll side effects you didnEUR think about and most the time youEUR ll end doing more harm than good and the next time wonEUR much different from the last time human nature thread could underlie some this explanation with the nature individuals government and bureaucracy shaping the outcomes from government intervention However understanding human nature itself does not settle the case for libertarianism may provide some support but provides just many challenges Posted Jason Collins September 17 2011 Questions for Charles C Mann comments Over Discover Blogs Mostly about 1493 Uncovering the New World Columbus Created Posted Razib Khan September 2011 Analysis Tutsi genotype Comment With this post Tutsi probably differ genetically from the Hutu hope tamp down all the talk about how the Belgians invented the Tutsi-Hutu division After putting the call out took months for get hands genotype and less than 24 hours post some results Posted Razib Khan August 2011 Thoughts the BGI study Comments und been following the development the BGI study pretty closely wanted note two main caveats people should aware with regard its methodology First with any case-control study volunteer bias will issue the cases are certain very smart people rather than representative sample then genes peculiar that smart people will show hits The BGI study choosing people who are more math than verbal-oriented will math-specific genes show general intelligence genes? Other confounds along these lines are possible und PhD genes Ashkenazi genes curiosity new study genes etc Second because the study doesn und completely control for family environments possible only comparing siblings each other gene-environment correlations and interactions can cause problems well For example suppose that high parents also confer better environments for their children Then the gene effects will get extra und 8220 boost und 8221 from that environment None this downgrade the awesomeness the BGI study should viewed important step resolving the nature vs nurture controversy Overeager journalists and bloggers are urged wait few more years before finally resolve the debate Posted ben August 26 2011 Looking for few good 145 Q individuals Comments Cross-posted from Discover friend Steve Hsu gave talk Google today Here are the details und ll giving talk Google tomorrow Thursday August 18 pm The slides are here The video will probably available Google und s TechTalk channel YouTube The Cognitive Genomics Lab BGI using this talk kick off the drive for US participants our intelligence GWAS More information www cog-genomics org including automatic qualifying standards for the study which are set just above SD Participants will receive free genotyping and help with interpreting the results The functional part the site should live after August 18 Title Genetics and Intelligence Abstract How genes affect cognitive ability? begin with brief review psychometric measurements intelligence introducing the idea und 8220 general factor und 8221 score The main results concern the stability validity predictive power and heritability adult Next discuss ongoing Genome Wide Association Studies which investigate the genetic basis intelligence Due mainly the rapidly decreasing cost sequencing likely that within the next 5-10 years will identify genes which account for significant fraction total variation are currently seeking volunteers for study high cognitive ability Participants will receive free genotyping From what recall discussion with Steve the aim here fish the extreme tail the distribution see that allows for easier catchment Q upward incrementing alleles standard deviations above the mean Q about out 750 individuals Posted Razib Khan August 19 2011 Older Entries amzn assoc placement adunit0 amzn assoc tracking id geneexpressio-20 amzn assoc mode manual amzn assoc type smart amzn assoc marketplace amazon amzn assoc region US amzn assoc linkid 2148257282b7a01f4bc1f083ccce92bc amzn assoc asins 0801880092 0763757373 0878933085 1605351539 Archives March September June May April February January December 2011 November 2011 October 2011 September 2011 August 2011 July 2011 June 2011 May 2011 April 2011 March 2011 February 2011 January 2011 December 2010 November 2010 October 2010 September 2010 August 2010 July 2010 June 2010 May 2010 April 2010 March 2010 February 2010 January 2010 December 2009 November 2009 October 2009 September 2009 August 2009 July 2009 June 2009 May 2009 April 2009 March 2009 February 2009 January 2009 December 2008 November 2008 October 2008 September 2008 August 2008 July 2008 June 2008 May 2008 April 2008 March 2008 February 2008 January 2008 December 2007 November 2007 October 2007 September 2007 August 2007 July 2007 June 2007 May 2007 April 2007 March 2007 February 2007 January 2007 December 2006 November 2006 October 2006 September 2006 August 2006 July 2006 June 2006 May 2006 April 2006 March 2006 February 2006 January 2006 December November October September August July June May April March February January December 2004 November 2004 October 2004 September 2004 August 2004 July 2004 June 2004 May 2004 April 2004 March 2004 February 2004 January 2004 December 2003 November 2003 October 2003 September 2003 August 2003 July 2003 June 2003 May 2003 April 2003 March 2003 February 2003 January 2003 December October September August Recent CommentsRambod Jump-starting regeneration injured nervesMackinder und s revenge and the rise the mongrels Gene Expression Who und s the barbarian now? Empires the Silk RoadIntelligence still heritable Biology News Biologged Small genetic effects not preclude drug developmentIntelligence still highly heritable Gene Expression Small genetic effects not preclude drug developmentPhilip Dick Preschool and Schrdinger und s Cat educationrealist und 8594 Academic Achievement Jason und s DeliciousTagsAdmin American History Books autism brain circuits CNVs common variants complex disorders complexity connectivity Culture demographics dopamine economics epigenetics epilepsy evolution fertility Genetics genius Genomics Geography HAP Harappa Ancestry Project History Books mental illness mind morality mutation mutations neurodevelopment oxytocin psychiatric rare variants Razib Khan Books savant schizophrenia social network synesthesia Tammett twins vasopressin wiring Categories Admin American History Books Genetics Genomics History Missing Neuroscience Personal Genomics Science Uncategorized Archives March September June May April February January December 2011 November 2011 October 2011 September 2011 August 2011 July 2011 June 2011 May 2011 April 2011 March 2011 February 2011 January 2011 December 2010 November 2010 October 2010 September 2010 August 2010 July 2010 June 2010 May 2010 April 2010 March 2010 February 2010 January 2010 December 2009 November 2009 October 2009 Se Gene Expression ssba img width !important padding box-shadow none !important display inline !important vertical-align middle ssba text-decoration none font-family Indie Flower font-size recentcomments display inline !important none Contact About GNXP status update comments This blog has been inactive for while und got the domain and perhaps one day there will regular contributors The internet has changed lot since started GNXP June don und know This domain has almost all the archives gnxp com including many comments going back specific content from this weblog ScienceBlogs and Discover can found Unz Review where und posting Posted Razib Khan March Sexual selection and economic growth Comments und not sure how much drive-by traffic gnxp continuing receive but figured worthwhile post note about latest working paper which explores whether male signalling may have role driving economic progress The abstract Sexual Selection Conspicuous Consumption and Economic Growth The evolution sexual selection the male propensity engage conspicuous consumption contributed the emergence modern rates economic growth develop model which males engage conspicuous consumption send honest signal their quality females Males who engage conspicuous consumption have higher reproductive success than those who not females respond the costly and honest signal increasing the prevalence signalling males the population over time males fund conspicuous consumption through participation the labour force the increase the prevalence signalling males who engage conspicuous consumption gives rise increase economic activity that leads economic growth und posted some the paper over Evolving Economics und also received some interesting feedback including this post The Conversation Rob Brooks Finally have posted SSRN update paper examining the Galor-Moav model which economic growth triggered the interplay between technological progress and inherited preference for quality quantity children posted about gnxp mid-last year The revision carries the same story the original paper but tighter and cuts out some the flotsam Posted Jason Collins September years Gene Expression Comments Just thought would mention that few days ago the weblog Gene Expression has been around for years won und say much more this point because time constraints But wanted enter into the record well admitting two minor points often used say the early days that foray into blogging was rather coincidence was playing around with the JSPServlet platform and wrote primitive blog software which decided test with own weblog und and somehow one thing led another But und sure now that some point would have started weblog and soon relation Second late notice that Gawker occasionally mentioned the media the locus for various politically correct outrages you had asked years ago that Gawker would such banal and conventional website would have been surprised The founding editor Gawker was occasional contributor the first incarnation GNXP People tend idealize the early blogosphere too much there was lot stupid Iraq warblogging going was part some extent but there definitely was some amalgamation heterodoxy Today the blogosphere reflects the mainstream media and large Posted Razib Khan June The genetic architecture economic and political preferences Comment This cross post from Evolving Economics Evidence from twin studies implies that economic and political traits have significant heritable component That some the variation between people genetic variation Despite this there has been failure demonstrate that the heritability can specific genes Candidate gene studies which single gene SNP examined for its potential influence trait have long failed identify effects beyond fraction one per cent Further many the candidate gene results fail replicated studies with new samples alternative approach genetic analysis now starting address this issue Genomic-relatedness-matrix restricted maximum likelihood GREML und the term used the authors the paper discussed below technique that looks examine how the variance traits can explained all the SNPs simultaneously This approach has been used examine intelligence personality and several diseases and has generally shown that half the heritability estimated twin studies can the sampled SNPs new paper released PNAS seeks apply this approach economic and political phenotypes The paper Benjamin and colleagues shows that around half the heritability economic and political behaviour observed behavioural studies could explained the array SNPs The authors used the results recent surveys subjects from the Swedish Twin Registry who had their educational attainment four economic preferences risk patience fairness and trust and five political preferences immigrationcrime foreign policy environmentalism feminism and equality and economic policy measured The GREML analysis found that for one economic preference trust the variance explained the SNPs was statistically significant with estimate narrow heritability over Two the political preferences economic policy and foreign policy had narrow heritability that was statistically significant with heritability estimates above for each these The authors noted that the estimates are noisy and GREML provides lower bound the results are consistent with low moderate heritability for these traits Educational attainment was also found have statistically significant result although the more precise measurement educational attainment and the availability this data across all subjects made that result more likely This result corroboration the evidence from twin studies and provides basis for believing that molecular genetic data could used predict phenotypic traits However one interesting feature the GREML method analysis that after conducting this analysis with one sample the data obtained does not assist predicting the traits for someone out the sample This technique shows the potential molecular genetic data without directly realising those results comparison the authors examined whether any individual SNPs might predict economic political preferences but found none that met the significance test standard Such high significance required reflect the huge number SNPs that are being tested The authors also conducted the standard comparison between monozygotic identical and dizygotic fraternal twins which resulted heritability estimates consistent with the existing literature although with much larger sample than typically used Looking through the supplementary materials the major surprise was that the twin analysis suggests that patience has low heritability with very low correlation between twins and almost difference between monozygotic and dizygotic twins fact for males dizygotic twins were more similar The authors draw few conclusions from their work many which reflect the argument Journal Economic Perspectives article from late last year The first and most obvious that should treat all candidate gene studies with caution Hopefully some journals that insist publishing low sample size candidate gene studies will pay attention this Where they are going conducted you need very large samples and significantly larger than are being used most studies being published Meanwhile they are still hopeful that there can contribution from genetic particularly the biological pathways between the gene and trait can determined This might include using genes instrumental variables control variables non-genetic empirical work The use instrumental variables does require however some understanding the pathways through which the gene acts may have multiple roles that pleiotropic They also suggest that the focus turned SNPs for which there are known large effects and the results have been replicated element analyses political and economic preferences that makes slightly uncomfortable the loose nature these preferences For one the manner which they are elicited from subjects can vary substantially can the nature the measurement Take the paper Alford and colleagues political preferences which canvassed political preferences Many the views are likely change over time and highly correlated with each other And why stop 28? result may preferable take step back and ensure that data higher traits are collected generally consider that and the big five personality traits openness conscientiousness agreeableness extraversion and stability are good starting point and are likely capture much the variation political and economic preferences For example preferences such patience are likely reflected while openness captures much the liberal-conservative spectrum political leaning Starting from basis such this may also give greater scope for working back the biological pathways The Social Science Genetics Association Consortium doing some work harmonising phenotypes across large samples Hopefully their work will lead this direction Posted Jason Collins May Robustness and fragility neural development Comments many things can wrong the development the human brain amazing that ever goes right The fact that usually does EUR that the majority people not suffer from neurodevelopmental disord such common outcomes? These are the questions that will get us the underlying biology Mitchell K What complex about complex disorders? Genome Biology 13 DOI 1186gb-2012-13-1-237 Manolio Collins F Cox N Goldstein D Hindorff L Hunter D McCarthy Ramos Cardon L Chakravarti Cho J Guttmacher Kong Kruglyak L Mardis Rotimi C Slatkin Valle D Whittemore Boehnke Clark Eichler Gibson Haines J Mackay McCarroll und Visscher P 2009 Finding the missing heritability complex diseases Nature 461 7265 747-753 DOI 1038nature08494 Zuk O Hechter Sunyaev und Lander The mystery missing heritability Genetic interactions create phantom heritability Proceedings the National Academy Sciences 109 1193-1198 DOI 1073pnas 1119675109 Posted kjmtchl February From miswired brain psychopathology EUR modelling neurodevelopmental disorders mice comments takes lot genes wire the human brain Billions cells myriad different types have specified directed migrate the right position organised clusters layers and finally connected their appropriate targets When the genes that specify these neurodevelopmental processes are mutated the result can severe impairment which can manifest neurological psychiatric disease How those kinds neurodevelopmental defects actually lead the emergence particular pathological states EUR like psychosis seizures social withdrawal EUR mystery however Many researchers are trying tackle this problem using mouse models EUR animals carrying mutations known cause autism schizophrenia humans for example recent study from own lab open access PLoS One adds this effort examining the consequences mutation important neurodevelopmental gene and providing evidence that the mice end state resembling psychosis this case start with discovery mice entry point the underlying neurodevelopmental processes just the past few years over hundred different mutations have been discovered that are believed cause disorders like autism schizophrenia many cases particular mutations can actually predispose many different disorders having been linked different patients ADHD epilepsy mental retardation intellectual disability TouretteEUR syndrome depression bipolar disorder and others These clinical categories may thus represent more less distinct endpoints that can arise from common neurodevelopmental origins For condition like schizophrenia the genetic overlap with other conditions does not invalidate the clinical category There still something distinctive about the symptoms this disorder that needs explained have argued that schizophrenia can clearly caused single mutations any very large number different genes many with roles neurodevelopment that model correct then the big question how these presumably diverse neurodevelopmental insults ultimately converge that specific phenotype? after all highly unusual condition The positive symptoms psychosis EUR hallucinations and delusions for example EUR especially require explanation view the brain from engineering perspective then can say that the system not just not working well EUR failing particular and peculiar manner try address how this kind state can arise have been investigating particular mouse EUR one with mutation gene called Semaphorin-6A This gene encodes protein that spans the membranes nerve cells acting some contexts signal other cells and other contexts receptor information has been implicated controlling cell migration the guidance growing axons the specification synaptic connectivity and other processes deployed many parts the developing brain and required for proper development the cerebral cortex hippocampus thalamus cerebellum retina spinal cord and probably other areas donEUR yet know about Despite widespread cellular disorganisation and miswiring their brains Sema6A mutant mice seem overtly pretty normal They are quite healthy and fertile and casual inspection would not pick them out different from their littermates However more detailed investigation revealed electrophysiological and behavioural differences that piqued our interest Because these animals have subtly malformed hippocampus which looks superficially like the kind neuropathology observed many cases temporal lobe epilepsy wanted test they had seizures this attached electrodes their scalp and recorded their electroencephalogram EEG This technique measures patterned electrical activity the underlying parts the brain and showed quite clearly that these animals not have seizures But did show something EUR generally elevated amount activity these animals all the time What was particularly interesting about this that the pattern change specific increase alpha frequency oscillations was very similar that reported animals that are sensitised amphetamine EUR well-used model psychosis rodents High doses amphetamine can acutely induce psychosis humans and suite behavioural responses rodents addition regimen repeated low doses amphetamine over extended time period can induce sensitisation the effects this drug rodents characterised behavioural differences like hyperlocomotion well the EEG differences mentioned above Amphetamine believed cause these effects inducing increases dopaminergic signaling either chronically acute stimuli This was particular interest us that kind hyperdopaminergic state thought final common pathway underlying psychosis humans Alterations dopamine signaling are observed schizophrenia patients using PET imaging and also all relevant animal models far studied explore possible further parallels these effects Sema6A mutants examined their behaviour and found very similar profile many known animal models psychosis namely hyperlocomotion and hyper-exploratory phenotype addition various other phenotypes like defect working memory The positive symptoms psychosis can ameliorated humans with number different antipsychotic drugs which have common blocking action dopamine receptors Administering such drugs the Sema6A mutants normalised both their activity and the EEG dose that had effect wild-type animals These data are least consistent with though they means prove the hypothesis that Sema6A mutants end hyperdopaminergic state But how they end that state? There does not seem direct effect the development the dopaminergic system EUR Sema6A at least not required direct these axons their normal targets Our working hypothesis that the changes the dopaminergic system emerge over time secondary response the primary neurodevelopmental defects seen these animals well documented that early alterations for example the hippocampus can have cascading effects over subsequent activity-dependent development and maturation brain circuits particular can alter the excitatory drive the part the midbrain where dopamine neurons are located turn altering dopaminergic tone the forebrain This can induce compensatory changes that ultimately this context may prove maladaptive pushing the system into pathological state which may self-reinforcing For now this just hypothesis and one that and many other researchers working other models are working test The important thing that provides possible explanation for why many different mutations can result this strange phenotype which manifests humans psychosis this emerges secondary response range primary insults then that reactive process provides common pathway convergence final phenotype Importantly also provides possible point early intervention EUR may not possible EURcorrectEUR early differences brain wiring but may possible prevent them causing transition state florid psychopathology Rnker AE O und Tuathaigh C Dunleavy Morris DW Little GE Corvin AP Gill Henshall DC Waddington JL und Mitchell KJ 2011 Mutation Semaphorin-6A disrupts limbic and cortical connectivity and models neurodevelopmental psychopathology PloS one 6 PMID 22132072 Mitchell K Huang Z Moghaddam B und Sawa 2011 Following the genes framework for animal modeling psychiatric disorders BMC Biology DOI 11861741-7007-9-76 Mitchell K 2011 The genetics neurodevelopmental disease Current Opinion Neurobiology 21 197-203 DOI 1016j conb 2010 08 009 Howes O und Kapur 2009 The Dopamine Hypothesis Schizophrenia Version III und The Final Common Pathway Schizophrenia Bulletin 35 549-562 DOI 1093schbulsbp006 Posted kjmtchl January 25 Jump-starting regeneration injured nerves Comments Unlike many other animals injured nerve fibres the mammalian central nervous system not regenerate EUR least not spontaneously lot research has gone finding ways coax them unfortunately with only modest success The main problem that there are many reasons why central nerve fibres donEUR regenerate after injury EUR tackling them singly not sufficient new study takes combined approach hit two distinct molecular pathways injured nerves and achieves substantial regrowth animal model Many lower vertebrates like frogs and salamanders for example can regrow damaged nerves quite readily And even mammals nerves the periphery will regenerate and reconnect given enough time But nerve fibres the brain and spinal cord not regenerate after injury Researchers trying solve this problem focused initially figuring out what different about the environment the central versus the peripheral nervous sys ptember 2009 August 2009 July 2009 June 2009 May 2009 April 2009 March 2009 February 2009 January 2009 December 2008 November 2008 October 2008 September 2008 August 2008 July 2008 June 2008 May 2008 April 2008 March 2008 February 2008 January 2008 December 2007 November 2007 October 2007 September 2007 August 2007 July 2007 June 2007 May 2007 April 2007 March 2007 February 2007 January 2007 December 2006 November 2006 October 2006 September 2006 August 2006 July 2006 June 2006 May 2006 April 2006 March 2006 February 2006 January 2006 December November October September August July June May April March February January December 2004 November 2004 October 2004 September 2004 August 2004 July 2004 June 2004 May 2004 April 2004 March 2004 February 2004 January 2004 December 2003 November 2003 October 2003 September 2003 August 2003 July 2003 June 2003 May 2003 April 2003 March 2003 February 2003 January 2003 December October September August July 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Jon Entine Joseph LeDoux Judith Rich Harris Justin L Barrett Ken Miller Matthew Stewart Parag Khanna Peter Turchin Warren Treadgold Tags Browse Admin American History Books amphetamine antidepressants autism brain circuits cadherin Charles C Mann CNVs common variants complex disorders complexity connectivity consciousness corpus callosum Culture demographics novo development dopamine dyscalculia dyslexia economics EEG environment epigenetics epilepsy evolution fertility Gene Expression Genetics genius genome-wide association studies Genomics Geography GWAS hallucinations HAP hapmap Harappa Ancestry Project hearing voices heritability hippocampus History Books homosexuality innateness materialism mental illness mind missing heritability morality mouse model mutation mutations natural selection neural networks neurodevelopment noise oxytocin Peer-review Personal Genomics personality plasticity pruning psychiatric psychosis rare mutations rare variants Razib Khan Books regeneration retina robustness savant schizophrenia self social network soul synesthesia Tammett target selection twins vasopressin whole-genome sequencing wiring Theme Designed Rajveer Singh Rathore Powered WordPress uacct UA-232670-1 urchinTracker http www gnxp EUR screen these proteins revealed several expressed distinct regions the brain receiving inputs from subtypes RGCs One particular Cadherin-6 expressed non-image-forming brain regions that receive retinal inputs EUR those controlling eye movements and pupillary reflexes for example The protein also expressed very discrete subset RGCs EUR specifically those that project the Cadherin-6-expressing targets the brain The obvious hypothesis was that this matching protein expression allowed those RGCs recognise their correct targets literally sticking them test this they analysed these projections mice lacking the Cadherin-6 molecule Sure enough the projections those targets were severely affected EUR the axons spread out over the general area the brain but failed zero the specific subregions that they normally targeted These results illustrate general principle likely repeated using different Cadherins different RGC subsets and also other parts the brain Indeed paper published the same time shows that Cadherin-9 may play similar the developing hippocampus addition other families molecules such Leucine-Rich Repeat proteins may play similar role synaptic matchmakers promoting homophilic adhesion between neurons and their targets Both Cadherins and LRR proteins also have important EURheterophilicEUR interactions with other proteins The expansion these families vertebrates could conceivably linked the greater complexity the nervous system which presumably requires more such labels specify But these molecules may more than just academic interest understanding the molecular logic and evolution the genetic program that specifies brain wiring Mutations various members the Cadherin and related protocadherin and LRR gene families have also been implicated neurodevelopmental disorders including autism schizophrenia TouretteEUR syndrome and others Defining the molecules and mechanisms involved normal development may thus crucial understanding the roots neurodevelopmental disease Osterhout J Josten N Yamada J Pan F Wu Nguyen P Panagiotakos Inoue Y Egusa Volgyi B Inoue Bloomfield Barres B Berson D Feldheim D und Huberman 2011 Cadherin-6 Mediates Axon-Target Matching Non-Image-Forming Visual Circuit Neuron 71 632-639 DOI 1016j neuron 2011 07 006 Williams Wilke Daggett Davis Otto Ravi D Ripley B Bushong Ellisman Klein und Ghosh 2011 Cadherin-9 Regulates Synapse-Specific Differentiation the Developing Hippocampus Neuron 71 640-655 DOI 1016j neuron 2011 06 019 Posted kjmtchl February und got your missing heritability right here und Comments debate raging human genetics these days why the massive genome-wide association studies GWAS that have been carried out for every trait and disorder imaginable over the last several years have not explained more the underlying heritability This especially true for many the so-called complex disorders that have been investigated where results have been far less than hoped for good deal effort has gone into quantifying exactly how much the genetic variance has been EURexplainedEUR and how much remains EURmissingEUR The problem with this question that limits the search space for the solution forces our thinking further and further along certain path when what really need draw back and question the assumptions which the whole approach founded Rather than asking what the right answer this question should asking what the right question? The idea performing genome-wide association studies for complex disorders rests number very fundamental and very big assumptions These are explored recent article wrote for Genome Biology referenced below reprints available request They are That what call complex disorders are unitary conditions That clinical categories like schizophrenia diabetes asthma are each single disease and appropriate investigate them lumping everyone the population who has such diagnosis EUR allowing us calculate things like heritability and relative risks Such population-based figures are only informative all patients with these symptoms really have common etiology That the underlying genetic architecture polygenic EUR e the disease arises each individual due toxic combinations many genetic variants that are individually segregating high frequency the population e EURcommon variantsEUR That despite the observed dramatic discontinuities actual risk for the disease across the population there some underlying quantitative trait called EURliabilityEUR that normally distributed the population personEUR load risk variants exceeds some threshold liability then disease arises All these assumptions typically unquestioned EUR often unmentioned fact EUR yet there evidence that any them valid fact the more you step back and look them with objective eye the more outlandish they seem even from first principles First what reason there think that there only one route the symptoms observed any particular complex disorder? know there are lots ways genetically speaking cause mental retardation blindness deafness EUR why should this not also the case for psychosis seizures poor blood sugar regulation? the clinical diagnosis specific disorder based superficial criteria especially the case for psychiatric disorders then this assumption unlikely hold Second the idea that common variants could contribute significantly disease runs against the effects natural selection pretty quickly EUR variants that cause disease get selected against and are therefore rare You can propose models balancing selection where specific variant beneficial some genomic contexts and harmful others but there evidence that this mechanism widespread general the more arcane your model has become accommodate contradictory evidence the more inclined you should question the initial premise Third the idea that common disorders where people either are not affected really can treated quantitative traits with smooth distribution the population with really truly bizarre The history this idea can traced back early geneticists but was popularised Douglas Falconer the godfather quantitative genetics he literally wrote the book attempt demonstrate the relevance quantitative genetics the study human disease Falconer came with nifty solution Even though disease states are typically all-or-nothing and even though the actual risk disease clearly very discontinuously distributed the population dramatically higher relatives affecteds for example he claimed that was reasonable assume that there was something called the underlying liability the disorder that was actually continuously distributed This could converted discontinuous distribution further assuming that only individuals whose burden genetic variants passed imagined threshold actually got the disease transform discontinuous incidence data mean rates disease various groups such people with different genetic relatedness affected individuals into mean liability continuous scale was necessary further assume that this liability was normally distributed the population The corollary that liability affected many genetic variants each small effect Q D This model EUR simply declared fiat EUR forms the mathematical basis for most GWAS analyses and for simulations regarding proportions heritability explained combinations genetic variants the recent paper from Eric LanderEUR group is extraordinary claim which you would think would require extraordinary evidence accepted Despite the fact that has evidence support and fundamentally makes biological sense see Genome Biology article for more that goes largely unquestioned and unchallenged the cold light day the most fundamental assumptions underlying population-based approaches investigate the genetics EURcomplex disordersEUR can seen flawed unsupported and opinion clearly invalid More importantly there now lots direct evidence that complex disorders like schizophrenia autism epilepsy are really umbrella terms reflecting common symptoms associated with large numbers distinct genetic conditions More and more mutations causing such conditions are being identified all the time thanks genomic array and next generation sequencing approaches Different individuals and families will have very rare sometimes even unique mutations some cases will possible identify specific single mutations clearly causal others may require combination two three There clear evidence for very wide range genetic etiologies leading the same symptoms time for the field assimilate this paradigm shift and stop analysing the data population-based terms Rather than asking how much the genetic variance across the population can currently explained question that nonsensical the disorder not unitary condition should asking about causes disease individuals - How many cases can currently explained the mutations far identified ? - Why are the mutations not completely penetrant? - What factors contribute the variable phenotypic expression different individuals carrying the same mutation? - What are the biological functions the genes involved and what are the consequences their disruption? - Why many different mutations give rise the same phenotypes? - Why are specific symptoms like psychosis seizures social withdrawal tion which appears important point attracting Manski this use Noting the wealth data being created and the possibility observing changes the effect genes the environment changes Manski considers that these regression exercises may assist examining how genes and environment interact don und disagree with Manski but present genome association studies have plenty issues First there the missing heritability problem date the magnitude the identified effect genes most traits accounts for miniscule proportion the trait und s heritability This points the important role played heritability provide direction research genes covariates also indicates that until these genes are found heritability estimates will more informative for social policy second issue that with 000 odd genes and the ability test many them for correlation with traits many are found have statistically significant relationship through chance blogged about recently Razib this shown when people seek replicate earlier results und such when was found that most reported genetic associations with general intelligence are probably false positives pdf Finally genome based now feeding back into estimates heritability From recent paper conducted genome-wide analysis 3511 unrelated adults with data 549EUR 692 single nucleotide polymorphisms SNPs and detailed phenotypes cognitive traits estimate that 40 the variation crystallized-type intelligence and 51 the variation fluid-type intelligence between individuals accounted for linkage disequilibrium between genotyped common SNP markers and unknown causal variants These estimates provide lower bounds for the narrow-sense heritability the traits Despite all the critiques about methodology most new studies confirm that the old und 8220 methodologically poor und 8221 heritability estimates were the right ballpark The problem not that the estimates are not useful but rather that they are not used Manski C 2011 Genes Eyeglasses and Social Policy Journal Economic Perspectives 25 83-94 DOI 1257jep 25 83 Posted Jason Collins December 13 2011 Why Eurasians aren und very pale Comment few years ago wondered offhand why Eurasians weren und very pale since East Asians and Europeans developed light skin different loci over the past few tens thousands years hindsight the answer seems pretty obvious realized the solution when looking the skin pigmentation loci parents und genotypes They und re both homozygous for the derived und 8220 light und 8221 variant SLC24A5 but interestingly father has more und 8220 light und 8221 alleles than mother This peculiar because mother notably lighter complected than father Then realized that there was likelihood that mother carried East Asian allele which conferred light complexion since she und s East Asian course the reason that East Asian-European hybrids aren und exceedingly pale that pigmentation predominantly additive trait value effect and they und d heterozygotes many loci where their parental populations would homozygotes the other hand the F2 generation might potentially very light indeed dark und Posted Razib Khan November 14 2011 What gene und 8220 for und 8221 ? Comments EURScientists discover gene for autismEUR ovarian cancer depression cocaine addiction obesity happiness schizophreniaEUR and whatever youEUR re having yourself These are typical newspaper headlines all from the last year and all use the popular shorthand EURa gene forEUR something view this phrase both lazy and deeply misleading and has caused widespread confusion about what genes are and about their influences human traits and disease The problem with this phrase stems from the ambiguity what mean EURgeneEUR and what mean EURforEUR These can mean different things different and unfortunately these meanings are easily conflated First gene can defined several different ways From molecular perspective segment DNA that codes for protein along with the instructions for when and where and what amounts this protein should made Some genes encode RNA molecules rather than proteins but the general point the same the gene cellular thus store the information that allows this protein made and its production regulated you have gene for haemoglobin and gene for insulin and gene for rhodopsin etc around 25 such genes the human genome The question what the gene for then becomes biochemical question EUR what does the encoded protein do? But that not the only way probably even the main way that people think about what genes EUR certainly not how geneticists think about The gene commonly defined indeed often discovered looking what happens when mutated EUR when the sequence DNA bases that make the gene altered some way which affects the production activity the encoded protein The visible manifestation the effect such mutation the phenotype usually defined the organismal EUR altered anatomy physiology behaviour often the presence disease From this perspective the gene defined separable unit heredity EUR something that can passed from generation that affects particular trait This much closer the popular concept gene such gene for blue eyes gene for breast cancer What this really means mutation for blue eyes mutation for breast cancer The challenge relating the gene cellular the effects variation that gene which are most commonly observed the organismal The at cellular can defined pretty directly make protein X but the effect the organismal much more indirect and context-dependent involving interaction with many other genes that also contribute the phenotype question often highly complex and dynamic systems you are talking about simple trait like blue eyes then the gene molecular can actually related the mutant phenotype fairly easily EUR the gene encodes enzyme that makes brown pigment When that enzyme not made does not work properly the pigment not made and the eyes are blue Easy-peasy But what the phenotype some complex physiological trait even worse psychological behavioural trait? These traits are often defined very superficial far removed from the possible molecular origins individual differences The neural systems underlying such traits may incredibly complex EUR they may break down due very indirect consequences mutations any large number genes For example mutations the genes encoding two related proteins neuroligin-3 and neuroligin-4 have been found patients with autism and there good evidence that these mutations are responsible for the condition those patients Does this make them EURgenes for autismEUR ? That phrase really makes sense EUR these genes certainly not cause autism nor prevent autism The real link between these genes and autism extremely indirect The neuroligin proteins are involved the formation synaptic connections between neurons the developing brain they are mutated then the connections that form between specific types neurons are altered This changes the local circuits the brain affecting their information-processing parameters and changing how different regions the brain communicate Ultimately this impacts neural systems controlling things like social behaviour communication and behavioural flexibility leading the symptoms that define autism the behavioural mutations these genes can cause autism but these are not genes for autism They are not even usefully accurately thought genes for social behaviour for cognitive flexibility EUR they are required along with the products thousands other genes for those faculties develop But perhaps there are other genetic variants the population that affect the various traits underlying these faculties EUR not such severe way result clinical disorder but enough cause the observed variation across the general population certainly true that traits like extraversion are moderately heritable EUR e fair proportion the differences between people this trait are genetic differences When someone asks EURare there genes for extraversion?EUR the answer yes they mean EURare differences extraversion partly due genetic differences?EUR they mean the some genetic variant make people more less extroverted then they have suddenly often unknowingly gone from talking about the activity gene the effect mutation that gene considering the utility specific variant This suggests deeper meaning EUR not just that the gene has but that has purpose EUR biological terms this means that particular version the gene was selected for the basis its effect some trait This can applied the specific sequence gene humans distinct from other animals variants within humans which may specific sub-populations polymorphic within populations While geneticists may know what they mean the shorthand EURgenes forEUR various traits too easily taken different unintended ways particular there are genes EURforEUR something then many people infer that the something question also EURforEUR something For example there are EURgenes for homosexualityEUR the inference that homosexuality must somehow have been selected for either currently under some ancestral conditions Even sophisticated thinkers like Richard Dawkins fall foul this confusion EUR the apparent need explain why condition like homosexual orientation persists Similar arguments ar genome any affected individual for mutated genes The problem each carry hundreds such mutations making difficult recognise the ones that are really causing disease The solution sequence the DNA large numbers people with the same condition and see the same genes pop multiple times That what these studies aimed with samples couple hundred patients each They also concentrated families where autism was present only one child and looked specifically for mutations that child that were not carried either parent EUR so-called novo mutations that arise the generation sperm eggs These are the easiest detect because they are likely the most severe Mutations with very severe effects are unlikely passed because the people who carry them are far less likely have children There already strong evidence that novo mutations play important role the etiology autism EUR first novo copy number variants deletions duplications chunks chromosomes appear significantly higher rate autism patients compared controls patients compared controls Second has been known for while that the risk autism increases with paternal age EUR that older fathers are more likely have child with autism Initial studies suggested the risk was five-fold greater fathers over forty EUR these figures have been revised downwards with increasing sample sizes but the effect remains very significant with risk increasing monotonically with paternal age This also true schizophrenia and fact dominant Mendelian disorders general those caused single mutations The reason that the germ cells generating sperm men continue divide throughout their lifetime leading increased chance mutation having happened time goes The three studies Nature were looking for different mutation EUR point mutations changes single DNA bases They each provide list genes with novo mutations found specific patients Several these showed mutation more than one unrelated patient providing strong evidence that these mutations are likely causing autism those patients The genes with multiple hits include CHD8 SCN2A KATNAL2 and NTNG1 Mutations the last these NTNG1 were only found two patients but have been previously implicated rare cause Rett syndrome This gene encodes the protein Netrin-G1 which involved the guidance growing nerves and the specification neuronal connections CHD8 chromatin-remodeling factor and involved Wnt signaling major neurodevelopmental pathway well interacting with p53 which controls cell growth and division SCN2A encodes sodium channel subunit mutations this gene are involved variety epilepsies Not much known about KATNAL2 except homology EUR related proteins katanin and spastin which sever microtubules EUR mutations spastin are associated with hereditary spastic paraplegia How the specific mutations observed these genes cause the symptoms autism these patients contribute them not clear EUR these discoveries are just starting point but they will greatly aid the quest understand the biological basis this disorder The fact that these studies only got few repeat hits also means that there are probably many hundreds even thousands genes that can cause autism when mutated there were only small number would see more repeat hits Some these will among the other genes the lists provided these studies and will doubt recognisable more patients are sequenced Interestingly many the genes the lists are involved aspects nervous system development and encode proteins that interact closely with each other EUR this makes more likely that they are really involved These studies reinforce the fact that autism not one disorder und not clinically and not genetically either Like intellectual disability epilepsy many other conditions can caused mutations any very large number genes The ones know about far make around cases EUR these new studies add that list and also show how far have complete should recognise too that the picture will also get more complex EUR many cases there may more than one mutation involved causing the disease novo mutations are likely the most severe and thus most likely cause disease with high penetrance themselves But many inherited mutations may cause autism only combination with one few other mutations These complexities will emerge over time but for now can aim recognise the simpler cases where mutation particular gene clearly implicated Each new gene discovered means that the fraction cases can assign specific cause increases learn more about the biology each case those genetic diagnoses will have important implications for prognosis treatment and reproductive decisions can aim diagnose and treat the underlying cause each patient and not just the symptoms Posted kjmtchl April economics and evolutionary biology reading list comments have added new page over Evolving Economics with suggested reading list for those interested the intersection economics and evolutionary biology The list here The list work progress and plan update new sources emerge are suggested when realise what oversights have made also intend constrain the best sources rather than being complete list every thought the topic interested suggestions from gnxp readers please let know you have any thoughts Comments can also made the bottom the reading list page Posted Jason Collins April Nerves feather wire comments Finding your soulmate for neuron daunting task With many opportunities for casual hook-ups how you know when you find EURthe oneEUR ? the early 1960EUR Roger Sperry proposed his famous EURchemoaffinity theoryEUR explain how neural connectivity arises This was based observations remarkable specificity the projections nerves regenerating from the eye frogs their targets the brain His first version this theory proposed that each neuron found its target expression matching labels their respective surfaces He quickly realised however that with 200 neurons the retina the genome was not large enough encode separate connectivity molecules for each one This led him the insight that regular array connections one field neurons like the retina across target field the optic tectum this case could readily achieved gradients only one few molecules The molecules question Ephrins and Eph receptors were discovered thirty-some years later They are now known control topographic projections sets neurons other sets neurons across many areas the brain such that nearest-neighbour relationships are maintained neurons next each other the retina connect neurons next each other the tectum this way the map the visual world that generated the retina transmitted intact its targets Actually maintenance nearest-neighbour topography seems general property projections between any two areas even ones that not obviously map some external property across them But the idea matching labels was not wrong EUR they exist and they play very important part earlier step wiring EUR finding the correct target region the first place This nicely illustrated beautiful paper studying projections retinal neurons the mouse which implicates proteins the Cadherin family this process the retina photoreceptor cells sense light and transmit this information through couple relays retinal ganglion cells RGCs These are the cells that send their projections out the retina through the optic nerve the brain But the tectum not the only target these neurons There are fact least 20 different types RGCs with distinct functions that project from the retina various parts the brain mammals EURseeingEUR mediated projections the visual centre the thalamus which projects turn the primary visual cortex But conscious vision only one thing use our eyes for The equivalent the tectum called the superior colliculus mammals also target for RGCs and mediates reflexive eye movements head turns and shifts attention might even responsible for blindsight EUR subconscious visual responsiveness consciously blind patients Other RGCs send messages regions controlling circadian rhythms the suprachiasmatic nuclei pupillary reflexes areas the midbrain called the olivary pretectal nuclei These RGCs express photoresponsive pigment melanopsin and respond light directly This likely reflects the fact that early eyes contained both ciliated photoreceptors like current rods and cones and rhabdomeric photoreceptors possibly the ancestors RGCs and other retinal cells how these various RGCs know which part the brain project to? This was the question investigated Andrew Huberman and colleagues who looked for inspiration the fly eye had previously been shown that member the Cadherin family proteins was involved fly photoreceptor axons choosing the right layer project the optic lobe Cadherins are EURhomophilicEUR adhesion molecules EUR they are expressed the surface cells and like bind themselves Two cells expressing the same Cadherin protein will therefore stick each other This stickiness may used signal make synaptic connection between neuron and its target The protein implicated flies N-Cadherin widely expressed mammals and thus unlikely specify connections different targets the retina But Cadherins comprise large family proteins suggesting that other members might play more specific roles This turns out the case er EUR due the property engineers call robustness This property has important implications for understanding the genetic architecture neurodevelopmental disorders EUR what kinds insults will the system able tolerate and what kind will vulnerable to? The development the brain involves many thousands different gene products acting hundreds distinct molecular and cellular processes all tightly coordinated space and time EUR from patterning and proliferation cell migration axon guidance synapse formation and many others Large numbers proteins are involved the biochemical pathways and networks underlying each cell biological process Each these systems has evolved not just particular job but robustly EUR make sure this process happens even the face diverse challenges Robustness emergent and highly adaptive property complex systems that can selected for response particular pressures These include extrinsic factors such variability temperature supply nutrients etc but also intrinsic factors major source intrinsic variation noise gene expression EUR random fluctuations the all proteins all cells These fluctuations arise due the probabilistic nature gene EUR whether messenger RNA actively being made from gene any particular moment The system must able deal with these fluctuations and can argued that the noise the system actually acts buffer the system only worked within narrow operating range for each component then would very vulnerable failure any single part Natural selection will therefore favour system architectures that are more robust environmental and intrinsic variation the process such systems also indirectly become robust the other major source variation EUR mutations Many individual components can deleted entirely with discernible effect the system which why looking exhaustively for phenotype mouse mutants can frustrating EUR many gene knockouts are irritatingly normal You could say that the knockout gene does not affect particular process that means the gene product not actually involved that process but that not always the case One can often show that protein involved biochemically and even that the system sensitive changes the that protein EUR increased expression can often cause phenotype even when manipulations not Direct evidence for robustness neurodevelopmental systems comes from examples genetic effects phenotypes caused specific mutations While many components the system can deleted without effect others cause clear phenotype when mutated However such phenotypes are often modified the genetic This commonly seen mouse experiments for example where the effect mutation may vary widely when crossed into various inbred strains The implication that there are some genetic differences between strains that themselves have effect the phenotype but that are clearly involved the system process they strongly modify the effect another mutation How this relevant understanding so-called complex disorders? There are two schools thought the genetic architecture these conditions One considers the symptoms say autism schizophrenia epilepsy the consequence mutation any one very large number distinct genes This the scenario for intellectual disability for example and also for many other conditions like inherited blindness deafness There are hundreds distinct mutations that can result these symptoms The mutations these cases are almost always ones that have dramatic effect the encoded protein The other model that complex disorders arise many cases due the combined effects very large number common polymorphisms EUR these are bases the genome where the sequence variable the population there might EURAEUR some people but EURGEUR others The human genome contains millions such sites and many consider the specific combination variants that each person inherits these sites the most important determinant their phenotype disagree especially when comes disease The idea for disorders such schizophrenia that many these sites perhaps thousands them one the variants may predispose slightly the illness Each one has almost negligible effect alone but you are unlucky enough inherit lot them then the system might pushed over the burden that can tolerate into pathogenic state These are the two most extreme positions EUR there are also many models that incorporate effects both rare mutations and common polymorphisms Models incorporating common variants modifiers the effects rare mutations make lot biological sense What want consider here the model that the disease caused some individuals purely the combined effects hundreds thousands common variants without what call EURproper mutationEUR Ironically robustness has been invoked both proponents and opponents this idea have argued that neurodevelopmental systems should robust the combined effects many variants that have only very tiny effects protein expression which the case for most common variants This precisely because the system has evolved buffer fluctuations many components all the time addition being intrinsic passive property the architecture developmental networks robustness also actively promoted through homeostatic feedback loops which can maintain optimal performance the face variations regulating the other components compensate The effects such variants should therefore NOT cumulative EUR they should absorbed the system fact you could argue that certain noise the system EURdesign featureEUR because enables this buffering Others have argued precisely the opposite EUR that robustness permits cryptic genetic variation accumulate populations Cryptic genetic variation has effect the context which arises allowing escape selection but another context EUR say different environment different genetic EUR can have large effect This exactly what robustness allows happen EUR indeed the fact that cryptic genetic variation exists provides some the best evidence that have that the systems are robust shows directly that mutations some components are tolerated most contexts But there any evidence that such cryptic variation comprises hundreds thousands common variants? fair proving that the case would very difficult You could argue from animal breeding experiments that the continuing response selection many traits means that there must vast pool genetic variation that can affect them which can cumulatively enriched selective breeding almost infinitum However new mutations are known make least some contribution this continued response selection addition most cases where the genetics such continuously distributed traits have been unpicked identifying the specific factors contributing strain differences for example they come down perhaps tens loci showing very strong and complex epistatic interactions Thus just because variation trait multigenic does not mean affected mutations small individual effect EUR effectively continuous distribution can emerge due very complex epistatic interactions between fairly small number mutations which have surprisingly large effects isolation would keen hear any examples showing real polygenicity the hundreds thousands variants the case genetic modifiers specific mutations EUR say where mutation causes very different phenotype different mouse strains EUR most the effects that have been identified have been mapped one small number mutations which have effect themselves but which strongly modify the phenotype caused another mutation These and other findings suggest that cryptic genetic variation relevant disease certainly likely exist and have important effects phenotype but that such genetic effects can most likely ascribed one several perhaps tens mutations opposed hundreds thousands common polymorphisms This already too long but begs the question neurodevelopmental systems are robust then why ever get neurodevelopmental disease? The paradox systems that are generally robust that they may quite vulnerable large variation specific subset components Why specific types genes are this set while others can completely deleted without effect the big question More that subsequent postEUR Posted kjmtchl April novo mutations autism Comments trio papers this weekEUR Nature identifies mutations causing autism four new genes demonstrate the importance novo mutations the etiology this disorder and suggest that there may more genes which high-risk autism-causing mutations can occur These studies provide explanation for what seems like paradox the one hand twin studies show that autism very strongly genetic identical twins are much more likely share diagnosis than fraternal twins EUR the other many cases are sporadic with one the family affected How can the condition EURgeneticEUR but not always run the family? The explanation that many cases are caused new mutations EUR ones that arise the germline the parents This similar conditions like Down syndrome The studies reported Nature are trying find those mutations and see which genes are affected They are only possible because the tremendous advances our ability sequence DNA The first genome cost three billion dollars sequence and took ten years EUR can one now for couple thousand dollars few days That means you can scan through the entire tem mammals was discovered early that the myelin EUR the fatty sheath insulation surrounding nerve fibres EUR the central nervous system different from that the periphery particular inhibits nerve growth number groups have tried figure out what components central myelin are responsible for this activity Myelin composed large number proteins well lipid membranes One these subsequently named Nogo was discovered block nerve growth This discovery prompted understandable excitement especially because antibody that binds that protein was found promote regrowth injured spinal nerves the rat even prompted film Extreme Measures with Gene Hackman and Hugh Grant EUR under-rated thriller with some surprisingly accurate science and some very serious medical malfeasance Unfortunately the regrowth rats that promoted blocking the Nogo protein very limited Similarly mice that are mutant for this protein its receptor show very minor regeneration What observed some cases extra sprouting uninjured axons downstream the spinal injury site This can lead some minor recovery but itEUR really remodelling rather than regeneration But does suggest answer the question why would have evolved system that seems actively harmful that prevents regeneration after injury? Well first the selective pressure mammals able regenerate damaged nerves probably not very great simply because injured animals would not typically get the chance regenerate the wild And second suggests that the proteins like Nogo may not prevent regeneration but prevent sprouting nerve fibres after they have already made their appropriate connections lot effort goes wiring the nervous system with exquisite specificity EUR once that wiring pattern established probably pays actively keep that way There are number reasons why blocking the Nogo protein does not allow nerves fully regenerate First not the only protein myelin that blocks growth EUR there are many others Second the injury itself can give rise scarring and inflammation that generates secondary barrier And third neurons the mature nervous system may simply not inclined grow Not only that EUR the distances they may have travel the fully grown adult may orders magnitude longer than those required wire the nervous system during development There are nerves adult human that are almost metre long but these connections were first formed the embryo when the distance was measured millimetres This last problem has been addressed more recently researchers asking there something the neurons themselves that changes over time EUR after all neurons the developing nervous system grow like crazy That propensity for growth seems dampened down the adult nervous system EUR again once the nervous system wired important restrict further growth Researchers have therefore looked for biochemical differences between young developing neurons and mature neurons that have already formed connections The hope that understand the molecular pathways that differ might able target them EURrejuvenateEUR damaged neurons restoring their internal urge grow The lab Zhigang He Harvard Medical School has been one the leaders this area and has previously found that targeting either two biochemical pathways allowed some modest regeneration injured neurons They study the optic nerve more accessible model central nerve regrowth than the spinal cord new study recently published Nature they show that simultaneously blocking both these proteins leads remarkably impressive regrowth EUR far greater than simply additive effect blocking the two proteins alone The two proteins are called PTEN and SOCS3 EUR they are both intracellular regulators cell growth including the ability respond extracellular growth factors The authors used genetic approach delete these genes two weeks prior injury and found that regrowth was hugely promoted That obviously not very medically useful approach however EUR more important show that deleting them after the injury can permit regeneration and indeed this what they found Presumably neurons this EURgrow grow grow!EUR state are either insensitive the inhibitory factors myelin the instructions for growth can override these factors They went characterise the changes that occur the neurons when these genes are deleted and observed that many other proteins associated with active growth states are upregulated including ones that get repressed response the injury itself The hope now that drugs may developed target the PTEN and SOCS3 pathways human patients especially those with devastating spinal cord injuries encourage damaged nerves regrow with all such discoveries translation the clinic will difficult and lengthy process likely take years and there guarantee success But compared previous benchmarks regeneration animal models this study shows what looks like real progress Sun F Park KK Belin Wang D Lu Chen Zhang K Yeung C Feng Yankner BA und He Z 2011 Sustained axon regeneration induced co-deletion PTEN and SOCS3 Nature 480 7377 372-5 PMID 22056987 Posted kjmtchl January The use heritability policy development Comments cross post from Evolving Economics The heritability straw man has copped another bashing this time the Journal Economic Perspectives Charles Manski picks old line argument Goldberger from 1979 and argues that heritability uninformative for the analysis policy Manski starts arguing that heritability estimates are based the assumption that there gene-environment correlation Manski writes The assumption that and are uncorrelated at odds with the reasonable conjecture that persons who inherit relatively strong genetic endowments tend grow families with more favorable environments for child development Any review discussions heritability whether the peer-reviewed literature the blogosphere will show that his claim generally false The proviso that the heritability estimate only relevant the existing environment usually threaded through any discussion heritability true that gene-environment covariance can affect estimates heritability Yet this does not mean that existing estimates have value nor that there are not methods that seek account for the covariance For example the use comparisons between misdiagnosed identical twins and actual identical twins allows for bounded estimates heritability developed pdf Manski und s broader claim adopted directly from Goldberger that even you knew the heritability trait tells you nothing about social policy Manski uses Goldberger und s eyeglasses example illustration Consider GoldbergerEUR use distribution eyeglasses the intervention For simplicity suppose that nearsightedness derives entirely from the presence particular allele specific gene Suppose that this gene observable taking the value 0 person has the allele for nearsightedness and he has the one that yields normal sight Let the outcome interest effective quality sight where EUReffectiveEUR means sight when augmented eyeglasses should they available person has effective normal sight either he has the allele for normal sight if eyeglasses are available person effectively nearsighted that person has the allele for nearsightedness and eyeglasses are unavailable Now suppose that the entire population lacks eyeglasses Then the heritability effective quality sight one What does this imply about the usefulness distributing eyeglasses treatment for nearsightedness? Nothing course The policy question interest concerns effective quality sight conjectured environment where eyeglasses are available However the available data only reveal what happens when eyeglasses are unavailable Manski and Goldberger may correct that the heritability estimate uninformative the efficacy distributing eyeglasses but useful assessing other policy responses the problem and the trade-offs between them possible prevent the eyesight loss the first place? that policy cheaper and more effective than eyeglasses? the heritability estimate was zero you would look the environmental causes and ask whether the eyesight problem more appropriately dealt with addressing the cause rather than distribution eyeglasses There shortage other areas where heritability estimates might add value Heritability estimates can inform whether effective use resources make sure that everyone has university degree over six-foot tall everyone putty the hands the policy maker are there some constraints? personal Bryan Caplan und s use heritability Selfish Reasons Have More Kids useful input his parenting strategy For the most salient example the usefulness heritability comes from examination the heritability among children Among high socioeconomic status families the heritability tends high Among low socioeconomic status families significantly lower This suggests that there significant room improve the outcomes the children the bottom the socioeconomic ladder the early years their life assuming those changes have effects that persist into adulthood Increasing heritability might evidence that environmental disadvantages are being ameliorated and opportunity equalised The latter part Manski und s paper turns the use genes covariates statistical regressions Regression identifies statistical association and not causa e often advanced for depression schizophrenia autism EUR that maybe ancestral environments these conditions conferred some kind selective advantage That one supposed explanation for why EURgenes for schizophrenia autismEUR persist the population Natural selection powerful force but that does not mean every genetic variation see humans was selected for nor does mean every condition affecting human psychology confers some selective advantage fact mutations like those the neuroligin genes are rapidly selected against the population due the much lower average number offspring people carrying them The problem that new ones keep arising EUR those genes and thousands other required build the brain analogy not beneficial for car break down EUR this fact does not require some teleological explanation Breaking down occasionally various ways not design feature EUR just that highly complex systems bring associated higher risk due possible failure many components just because the conditions persist some does not mean that the individual variants causing them Most the mutations causing disease are probably very recent and will rapidly selected against EUR they are not EURforEUR anything Jamain Quach H Betancur C Rstam Colineaux C Gillberg IC Soderstrom H Giros B Leboyer Gillberg C Bourgeron und Paris Autism International Sibpair Study 2003 Mutations the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism Nature genetics 34 27-9 PMID 12669065 Posted kjmtchl November 2011 Does brain plasticity trump innateness? 19 Comments The fact that the adult brain very plastic often held evidence against the idea that many psychological cognitive behavioural traits are innately determined first glance there does indeed appear paradox the one hand behavioural genetic studies show that many human psychological traits are strongly heritable and thus likely determined least part innate biological differences the other very clear that even the adult brain highly plastic and changes itself response experience The evidence both sides very strong general for traits like intelligence and personality characteristics such extraversion neuroticism conscientiousness among many others the findings from genetic studies are remarkably consistent Just for physical traits people who are more closely related resemble each other for psychological traits more than people with more distant relationship Twin study designs get around the obvious objection that such similarities might due having been raised Identical twins tend far more like each other for these traits than fraternal twins though the family environment shared both cases Even more telling identical twins who are raised apart tend pretty much similar each other pairs who are raised Clearly come fairly strongly pre-wired and the family environment has little effect these kinds traits Yet know the brain can EURchange itselfEUR You could say that one its main jobs fact EUR altering itself response experience better adapt the conditions which finds itself For example children learn language their auditory system specialises recognise the typical sounds that language Their brains become highly expert distinguishing those sounds and the process lose the ability distinguish sounds they hear less often This why many Japanese people cannot distinguish between the sounds the letters EURlEUR and EURrEUR for example and why many Westerners have difficulty hearing the crucial tonal variations languages like Cantonese Learning motor skills similarly improves performance and induces structural changes the relevant brain circuits fact most circuits the brain develop experience-dependent fashion summed by two adages EURcells that fire wire togetherEUR and EURuse lose itEUR Given the clear evidence for brain plasticity the implication would seem that even our brains come pre-wired with some particular tendencies that experience especially early experience should able override them would argue that the effect experience-dependent development typically exactly the opposite EUR that while the right kind experience can principle act overcome innate tendencies practice the effect reversed The reason that our innate tendencies shape the experiences have leading us select ones that tend instead reinforce even amplify these tendencies Our environment does not just shape us EUR shape child who naturally shy EUR due innate differences the brain circuits mediating social behaviour general anxiety risk-aversion and other parameters EUR will tend have less varied and less intense social experience result they will not develop the social skills that might make social interaction more enjoyable for them vicious circle emerges EUR perhaps intense practice social situations would alter the preconfigured settings shy childEUR social brain circuits but they tend not get that experience precisely because those settings contrast their extroverted classmates may constantly seeking out social interactions continue develop this innate faculty This circle may most vicious children with autism most whom have reduced innate interest other people They tend for example not find faces intrinsically fascinating other infants This may contribute delay language acquisition they miss out interpersonal cues that strongly facilitate learning speak similar situation may hold for children who have difficulties reading with mathematics Dyslexia seems caused innate difficulty associating the sounds and shapes letters This can traced genetic effects during early development the brain which may cause interruptions long-range connections between brain areas This innate disadvantage cruelly amplified the typical experience many dyslexics Learning read hard enough and requires years practice and active instruction For children who have basic difficulties recognising letters and words reading remains effortful for far longer and they will therefore tend read less missing out the intensive practice that would help their brain circuitry specialise for reading Though less widely known dyscalculia selective difficulty mathematics equally common and shares many characteristics with dyslexia The initial problem innate number sense EUR the ability estimate and compare small numbers objects This faculty present very young infants and even shared with many other animal species notably crows Formal mathematical instruction required build this innate number sense but also crucially relies with reading mathematics requires hard work learn and numbers are inherently mysterious then this will change the nature the childEUR experience lessen interest and reduce practice the other end the spectrum those with strong mathematical talent may gravitate towards the subject further amplifying the differences between these two groups Thus while certain type experience can alter the innate tendency the innate tendency makes getting that experience far less likely Brain plasticity tends instead amplify initial differences That sounds rather fatalistic but the good news that this vicious circle can broken innate difficulties are recognised early enough EUR actively changing the nature early experience There good evidence that intense early intervention children with autism such Applied Behaviour Analysis allows them compensate for innate deficits and lead improvements cognitive communication and adaptive skills Similarly intense intervention children with dyslexia has also proven effective Thus even not possible reverse whatever neurodevelopmental differences lead these kinds deficits should least possible prevent their being amplified subsequent experience Duff FJ und Clarke PJ 2011 Practitioner Review Reading disorders what are the effective interventions and how should they implemented and evaluated? Journal child psychology and psychiatry and allied disciplines 52 3-12 PMID 21039483 Vismara L und Rogers 2010 Behavioral Treatments Autism Spectrum Disorder What Know? Annual Review Clinical Psychology 6 447-468 DOI 1146annurev clinpsy 121208 131151 Posted kjmtchl October 2011 Human nature and libertarianism 20 Comments cross-post from Evolving Economics There another interesting topic this month und s Cato Unbound with Michael Shermer arguing the lead essay that human nature best represented the libertarian political philosophy Shermer rightly spends most the essay shooting down the blank slate vision humans that underpins many policies the left and suggests that moderates both the left and right should accept und 8220 Realistic vision und 8221 human nature He then simply states that the libertarian philosophy best represents this vision Unfortunately Shermer provides explanation about why that might the case and particular does not detail why libertarianism might better reflect human nature than conservatism the first response Shermer und s essay Eliezer Yudkowsky puts Shermer und s argument such B ecause variance seems around 50 genetic and 50 environmental the Soviets were half right And that this turn makes libertarianism the wise mature compromise path between liberalism and conservatism Yudkowsky und s response this argument spot every known culture humans
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