transvenous-embolization-carotid-cavernous-fistula-through-inferior

Transvenous Embolization of Carotid Cavernous Fistula through Inferior Petrosal Sinus with Detachable Coils and Ethylene Vinyl Alcohol Copolymer

Carotid cavernous fistula (CCF) is a rare disease caused by abnormal communications between the internal carotid artery (direct fistula) or meningeal ...

Zhejiang University School of Medicine

&#x5C3C;&#x53E4;&#x4E01;&#x548C;&#x9152;&#x7CBE;&#x6210;&#x763E;&#x662F;&#x5E38;&#x89C1;&#x7684;&#x6162;&#x6027;&#x8111;&#x969C;&#x788D;&#xFF0C;&#x662F;&#x5BF9;&#x4E2A;&#x4EBA;&#x548C;&#x793E;&#x4F1A;&#x7684;&#x6781;&#x5927;&#x5173;&#x6CE8;&#x3002;&#x867D;&#x7136;&#x9057;&#x4F20;&#x5B66;&#x5BF9;&#x8FD9;&#x4E9B;&#x969C;&#x788D;&#xFF0C;&#x6709;&#x5F88;&#x5927;&#x7684;&#x8D21;&#x732E;&#x7684;&#x6613;&#x611F;&#x57FA;&#x56E0;&#x548C;&#x5B83;&#x4EEC;&#x7684;&#x57FA;&#x672C;&#x7684;&#x53D8;&#x79CD;&#x4ECD;&#x7136;&#x5F88;&#x5927;&#x7A0B;&#x5EA6;&#x4E0A;&#x672A;&#x77E5;&#x3002;&#x8BB8;&#x591A;&#x5E74;&#x7684;&#x5168;&#x57FA;&#x56E0;&#x7EC4;&#x7684;&#x8054;&#x7CFB;&#x548C;&#x534F;&#x4F1A;&#x7814;&#x7A76;&#x6709;&#x7275;&#x8FDE;&#x5927;&#x91CF;&#x7684;&#x57FA;&#x56E0;&#x548C;&#x901A;&#x8DEF;&#x7684;&#x5C3C;&#x53E4;&#x4E01;&#x548C;&#x9152;&#x7CBE;&#x6210;&#x763E;&#x7684;&#x75C5;&#x56E0;&#x3002;&#x5728;&#x6B64;&#x4EA4;&#x6D41;&#x4E2D;&#xFF0C;&#x6211;&#x4EEC;&#x7740;&#x91CD;&#x73B0;&#x6709;&#x7684;&#x8BC1;&#x636E;&#xFF0C;&#x4E3B;&#x8981;&#x6765;&#x81EA;&#x4EBA;&#x7C7B;&#x7684;&#x9057;&#x4F20;&#x7814;&#x7A76;&#xFF0C;&#x5B89;&#x57FA;&#x4FE1;&#x53F7;&#x4F20;&#x8F93;&#x7CFB;&#x7EDF;&#x4E2D;&#x7684;&#x75C5;&#x56E0;&#x5C3C;&#x53E4;&#x4E01;&#x4F9D;&#x8D56;&#x548C;&#x9152;&#x7CBE;&#x4E2D;&#x6BD2;&#x8054;&#x52A8;&#x3001; &#x534F;&#x4F1A;&#x548C;&#x57FA;&#x56E0;&#x7684;&#x57FA;&#x56E0;&#x76F8;&#x4E92;&#x4F5C;&#x7528;&#x7814;&#x7A76;&#x57FA;&#x4E8E;&#x652F;&#x6301;&#x57FA;&#x56E0;&#x53CA;&#x5176;&#x53D8;&#x4F53;&#x7684;&#x53C2;&#x4E0E;&#x3002;&#x5F53;&#x524D;&#x52AA;&#x529B;&#x7684;&#x76EE;&#x7684;&#x4E0D;&#x4EC5;&#x8981;&#x590D;&#x5236;&#x8FD9;&#x4E9B;&#x5728;&#x72EC;&#x7ACB;&#x6837;&#x672C;&#x8C03;&#x67E5;&#x7684;&#x7ED3;&#x679C;&#x6765;&#x786E;&#x5B9A;&#x54EA;&#x4E9B;&#x53D8;&#x91CF;&#x6709;&#x52A9;&#x4E8E;&#x68C0;&#x6D4B;&#x5230;&#x7684;&#x534F;&#x4F1A;&#x548C;&#x901A;&#x8FC7;&#x54EA;&#x4E9B;&#x5206;&#x5B50;&#x673A;&#x5236;&#x3002;

&#x9057;&#x4F20;&#x5B66;&#x7814;&#x7A76;&#x5B89;&#x57FA;&#x4FE1;&#x53F7;&#x4E2D;&#x5C3C;&#x53E4;&#x4E01;&#x548C;&#x9152;&#x7CBE;&#x4F9D;&#x8D56;&#x3002;

Both nicotine and alcohol addictions are common chronic brain disorders that are of great concern to individuals and society. Although genetics contributes significantly to these disorders, the susceptibility genes and variants underlying them remain largely unknown. Many years of genome-wide linkage and association studies have implicated a number of genes and pathways in the etiology of nicotine and alcohol addictions. In this communication, we focus on current evidence, primarily from human genetic studies, supporting the involvement of genes and variants in the GABAergic signaling system in the etiology of nicotine dependence and alcoholism based on linkage, association, and gene-by-gene interaction studies. Current efforts aim not only to replicate these findings in independent samples, but also to identify which variant contributes to the detected associations and through what molecular mechanisms.

Genetics of GABAergic signaling in nicotine and alcohol dependence.

D&eacute;pendance de la nicotine et d&#39;alcool est communs troubles du cerveau chroniques qui sont de grande importance pour les individus et la soci&eacute;t&eacute;. Bien que la g&eacute;n&eacute;tique contribue de mani&egrave;re significative &agrave; ces troubles, les g&egrave;nes de susceptibilit&eacute; et les variantes qui les sous-tendent demeurent largement inconnus. Plusieurs ann&eacute;es d&#39;&eacute;tudes de lien et d&#39;association pang&eacute;nomique ont mis en cause un certain nombre de g&egrave;nes et les voies dans l&#39;&eacute;tiologie de la d&eacute;pendance de la nicotine et d&#39;alcool. Dans cette communication, nous nous concentrons sur les donn&eacute;es probantes actuelles, principalement des &eacute;tudes de g&eacute;n&eacute;tique humaines, soutenir l&#39;implication des g&egrave;nes et des variantes dans le syst&egrave;me de signalisation GABAergique dans l&#39;&eacute;tiologie de d&eacute;pendance &agrave; la nicotine et l&#39;alcoolisme, bas&eacute; sur le lien, association et &eacute;tudes sur les interactions de g&egrave;ne par g&egrave;ne. Les efforts actuels visent non seulement &agrave; reproduire ces r&eacute;sultats dans les &eacute;chantillons ind&eacute;pendants, mais aussi d&#39;identifier quelle variante contribue aux associations d&eacute;tect&eacute;es et par quels m&eacute;canismes mol&eacute;culaires.

G&eacute;n&eacute;tique de la signalisation GABAergique dans la d&eacute;pendance de la nicotine et d&#39;alcool.

Nikotin und Alkohol-sucht sind h&auml;ufige chronische Gehirn-Erkrankungen, die von gro&szlig;er Bedeutung f&uuml;r den einzelnen und die Gesellschaft sind. Obwohl die Genetik dieser Erkrankungen erheblichen Beitrag leistet, bleiben die ver&auml;nderten Gene und Varianten, die ihnen zugrunde liegenden weitgehend unbekannt. Langj&auml;hrige genomweiten Linkage und Verband Studien haben eine Reihe von Genen und Wege in der &Auml;tiologie von Nikotin und Alkohol sucht verwickelt. In dieser Mitteilung konzentrieren wir uns auf aktuelle Hinweise, vor allem aus genetischen Studien an Menschen, unterst&uuml;tzt die Beteiligung der Gene und Varianten im GABAergic Signalling System in der &Auml;tiologie der Nikotin-Abh&auml;ngigkeit und Alkoholismus basiert auf Bindung, Zuordnung und gen-durch-Gen-Interaktion Studien. Aktuelle Bem&uuml;hungen zielen nicht nur auf diese Erkenntnisse in unabh&auml;ngige Stichproben replizieren, sondern auch zu identifizieren, welche Variante den erkannten Vereinigungen und durch welche molekularen Mechanismen tr&auml;gt.

Genetik der GABAergic signalisieren in Abh&auml;ngigkeit von Nikotin und Alkohol.

Dipendenze di nicotina e l&#39;alcool sono comuni disturbi cerebrali croniche che sono di grande interesse per gli individui e la societ&agrave;. Anche se la genetica contribuisce significativamente a questi disturbi, i geni di suscettibilit&agrave; e varianti sottostanti li rimangono in gran parte sconosciuti. Molti anni di studi di linkage e associazione genome-wide hanno coinvolto un numero di geni e percorsi nell&#39;eziologia della nicotina e alcool dipendenze. In questa comunicazione, ci concentriamo sull&#39;evidenza corrente, principalmente da studi di genetici umani, sostenendo il coinvolgimento dei geni e le varianti nel sistema di segnalazione GABAergico nell&#39;eziologia della dipendenza da nicotina e alcolismo basato sul sollevatore, associazione e studi di interazione gene-gene-da. Gli sforzi attuali lo scopo non solo di replicare questi risultati in campioni indipendenti, ma anche per identificare quale variante contribuisce alle associazioni riconosciute e attraverso quali meccanismi molecolari.

Genetica di GABAergic segnalazione nella dipendenza da nicotina e alcol.

&#x30CB;&#x30B3;&#x30C1;&#x30F3;&#x3068;&#x30A2;&#x30EB;&#x30B3;&#x30FC;&#x30EB;&#x4E2D;&#x6BD2;&#x306F;&#x3001;&#x500B;&#x4EBA;&#x3084;&#x793E;&#x4F1A;&#x306B;&#x5927;&#x304D;&#x306A;&#x61F8;&#x5FF5;&#x306E;&#x3042;&#x308B;&#x5171;&#x901A;&#x306E;&#x6162;&#x6027;&#x8133;&#x75BE;&#x60A3;&#x3067;&#x3059;&#x3002;&#x907A;&#x4F1D;&#x5B66;&#x304C;&#x3053;&#x308C;&#x3089;&#x306E;&#x75BE;&#x60A3;&#x306B;&#x5927;&#x304D;&#x304F;&#x8CA2;&#x732E;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x304C;&#x3001;&#x611F;&#x53D7;&#x6027;&#x907A;&#x4F1D;&#x5B50;&#x304A;&#x3088;&#x3073;&#x305D;&#x308C;&#x3089;&#x306E;&#x57FA;&#x306B;&#x306A;&#x308B;&#x4E9C;&#x7A2E;&#x5927;&#x304D;&#x304F;&#x4E0D;&#x660E;&#x306E;&#x307E;&#x307E;&#x3002;&#x5168;&#x30B2;&#x30CE;&#x30E0;&#x9023;&#x9396;&#x89E3;&#x6790;&#x304A;&#x3088;&#x3073;&#x95A2;&#x9023;&#x7814;&#x7A76;&#x306E;&#x591A;&#x304F;&#x306E;&#x5E74;&#x306E;&#x907A;&#x4F1D;&#x5B50;&#x3068;&#x30CB;&#x30B3;&#x30C1;&#x30F3;&#x3068;&#x30A2;&#x30EB;&#x30B3;&#x30FC;&#x30EB;&#x4E2D;&#x6BD2;&#x306E;&#x75C5;&#x56E0;&#x306B;&#x304A;&#x3051;&#x308B;&#x7D4C;&#x8DEF;&#x306E;&#x6570;&#x95A2;&#x4E0E;&#x3057;&#x3066;&#x304F;&#x3060;&#x3055;&#x3044;&#x3002;&#x3053;&#x306E;&#x901A;&#x4FE1;&#x3067;&#x306F;&#x3001;&#x6211;&#x3005; &#x4EBA;&#x9593;&#x306E;&#x907A;&#x4F1D;&#x5B66;&#x7684;&#x7814;&#x7A76;&#x304B;&#x3089;&#x4E3B;&#x306B;&#x3001;&#x73FE;&#x5728;&#x306E;&#x8A3C;&#x62E0;&#x306B;&#x3001;&#x30CB;&#x30B3;&#x30C1;&#x30F3;&#x4F9D;&#x5B58;&#x3068;&#x30EA;&#x30F3;&#x30B1;&#x30FC;&#x30B8;&#x3001;&#x5354;&#x4F1A;&#x3001;&#x304A;&#x3088;&#x3073;&#x907A;&#x4F1D;&#x5B50;&#x306B;&#x3088;&#x308B;&#x907A;&#x4F1D;&#x5B50;&#x76F8;&#x4E92;&#x4F5C;&#x7528;&#x306E;&#x7814;&#x7A76;&#x306B;&#x57FA;&#x3065;&#x3044;&#x3066;&#x30A2;&#x30EB;&#x30B3;&#x30FC;&#x30EB;&#x4F9D;&#x5B58;&#x75C7;&#x306E; gaba &#x4F5C;&#x52D5;&#x6027;&#x30B7;&#x30B0;&#x30CA;&#x30EB;&#x4F1D;&#x9054;&#x30B7;&#x30B9;&#x30C6;&#x30E0;&#x306E;&#x75C5;&#x56E0;&#x907A;&#x4F1D;&#x5B50;&#x3068;&#x4E9C;&#x7A2E;&#x306E;&#x95A2;&#x4E0E;&#x3092;&#x652F;&#x63F4;&#x7126;&#x70B9;&#x3057;&#x307E;&#x3059;&#x3002;&#x73FE;&#x5728;&#x306E;&#x52AA;&#x529B;&#x306F;&#x3001;&#x3053;&#x308C;&#x3089;&#x306E;&#x8ABF;&#x67FB;&#x7D50;&#x679C;&#x306E;&#x72EC;&#x7ACB;&#x3057;&#x305F;&#x30B5;&#x30F3;&#x30D7;&#x30EB;&#x3092;&#x8907;&#x88FD;&#x3059;&#x308B;&#x3060;&#x3051;&#x3067;&#x3082;&#x3069;&#x306E;&#x5909;&#x7A2E;&#x304C;&#x691C;&#x51FA;&#x3055;&#x308C;&#x305F;&#x56E3;&#x4F53;&#x3068;&#x3069;&#x306E;&#x3088;&#x3046;&#x306A;&#x5206;&#x5B50;&#x30E1;&#x30AB;&#x30CB;&#x30BA;&#x30E0;&#x3092;&#x4ECB;&#x3057;&#x3066;&#x8CA2;&#x732E;&#x3092;&#x8B58;&#x5225;&#x3059;&#x308B;&#x76EE;&#x6307;&#x3057;&#x3066;&#x3044;&#x307E;&#x3059;&#x3002;

&#x30CB;&#x30B3;&#x30C1;&#x30F3;&#x3068;&#x30A2;&#x30EB;&#x30B3;&#x30FC;&#x30EB;&#x4F9D;&#x5B58;&#x306E; gaba &#x4F5C;&#x52D5;&#x6027;&#x30B7;&#x30B0;&#x30CA;&#x30EB;&#x4F1D;&#x9054;&#x306E;&#x907A;&#x4F1D;&#x3002;

&#xB2C8;&#xCF54;&#xD2F4;&#xACFC; &#xC54C;&#xCF54;&#xC62C; &#xC911;&#xB3C5;&#xC740; &#xAC1C;&#xC778;&#xACFC; &#xC0AC;&#xD68C;&#xC5D0; &#xD070; &#xAD00;&#xC2EC;&#xC0AC;&#xB294; &#xC77C;&#xBC18;&#xC801;&#xC778; &#xB9CC;&#xC131; &#xB1CC; &#xC9C8;&#xD658;&#xC785;&#xB2C8;&#xB2E4;. &#xC720;&#xC804;&#xD559;&#xC774;&#xC774; &#xC9C8;&#xD658;&#xC5D0; &#xD06C;&#xAC8C; &#xAE30;&#xC5EC; &#xD558; &#xACE0;, &#xBE44;&#xB85D; &#xBBFC;&#xAC10;&#xC131; &#xC720;&#xC804;&#xC790;&#xC640; &#xBCC0;&#xC885; &#xB4E4;&#xC744; &#xAE30;&#xBCF8; &#xD06C;&#xAC8C; &#xC54C;&#xB824;&#xC9C0;&#xC9C0; &#xC54A;&#xC740; &#xB0A8;&#xC544; &#xC788;&#xC2B5;&#xB2C8;&#xB2E4;. &#xB2E4;&#xB144;&#xAC04;&#xC758; &#xAC8C;&#xB188; &#xB113;&#xC740; &#xD611;&#xD68C; &#xC5F0;&#xAD6C; &#xC5F0;&#xACC4; &#xC720;&#xC804;&#xC790; &#xBC0F; &#xB2C8;&#xCF54;&#xD2F4;&#xACFC; &#xC54C;&#xCF54;&#xC62C; &#xC911;&#xB3C5;&#xC758; &#xBCD1; &#xC778;&#xC5D0; &#xC788;&#xB294; &#xD1B5;&#xB85C; &#xC218;&#xB97C; &#xC5F0;&#xB8E8; &#xC788;&#xB2E4;. &#xC774; &#xD1B5;&#xC2E0;&#xC5D0; &#xB2C8;&#xCF54;&#xD2F4; &#xC758;&#xC874; &#xBC0F; &#xC5F0;&#xACC4;, &#xD611;&#xD68C;, &#xADF8;&#xB9AC;&#xACE0; &#xC720;&#xC804;&#xC790;&#xC5D0; &#xC758;&#xD574; &#xC720;&#xC804;&#xC790;&#xC758; &#xC0C1;&#xD638; &#xC791;&#xC6A9; &#xC5F0;&#xAD6C;&#xC5D0; &#xB530;&#xB77C; &#xC54C;&#xCF54;&#xC62C; &#xC911;&#xB3C5;&#xC758; &#xBCD1; &#xC778;&#xC5D0;&#xC11C; GABAergic &#xC2E0;&#xD638; &#xC2DC;&#xC2A4;&#xD15C;&#xC5D0;&#xC11C; &#xC720;&#xC804;&#xC790; &#xBCC0;&#xD615;&#xC5D0;&#xC758; &#xCC38;&#xC5EC;&#xB97C; &#xC9C0; &#xC6D0;&#xD558;&#xB294; &#xC778;&#xAC04; &#xC720;&#xC804;&#xC790; &#xC5F0;&#xAD6C;&#xC5D0;&#xC11C; &#xC8FC;&#xB85C; &#xD604;&#xC7AC; &#xC99D;&#xAC70;&#xC5D0; &#xCD08;&#xC810;&#xC744; &#xC6B0;&#xB9AC;. &#xD604;&#xC7AC; &#xB178;&#xB825; &#xBFD0;&#xB9CC; &#xC544;&#xB2C8;&#xB77C; &#xB3C5;&#xB9BD;&#xC801;&#xC778; &#xC0D8;&#xD50C;&#xC5D0;&#xC11C; &#xC774;&#xB7EC;&#xD55C; &#xACB0;&#xACFC; &#xBCF5;&#xC81C; &#xBFD0;&#xB9CC; &#xC544;&#xB2C8;&#xB77C; &#xC5B4;&#xB5A4; &#xBCC0;&#xC885; &#xAE30;&#xC5EC; &#xC5B4;&#xB5A4; &#xBD84;&#xC790; &#xBA54;&#xCEE4;&#xB2C8;&#xC998;&#xC744; &#xD1B5;&#xD574; &#xAC80;&#xC0C9; &#xB41C; &#xC5F0;&#xACB0;&#xC744; &#xC2DD;&#xBCC4; &#xD558;&#xB294; &#xAC83;&#xC744; &#xBAA9;&#xD45C;&#xB85C;.

&#xB2C8;&#xCF54;&#xD2F4;&#xACFC; &#xC54C;&#xCF54;&#xC62C; &#xC758;&#xC874;&#xC5D0;&#xC11C; GABAergic &#xC2E0;&#xD638;&#xC758; &#xC720;&#xC804;&#xD559;.

Las adicciones de la nicotina y el alcohol son trastornos comunes de la cr&oacute;nica del cerebro que son de gran preocupaci&oacute;n para los individuos y la sociedad. Aunque la gen&eacute;tica contribuye significativamente a estos trastornos, los genes de susceptibilidad y variantes les que siguen siendo en gran parte desconocidas. Muchos a&ntilde;os de estudios de ligamiento y Asociaci&oacute;n de genoma han implicado a una serie de genes y v&iacute;as en la etiolog&iacute;a de la adicci&oacute;n de la nicotina y alcohol. En esta comunicaci&oacute;n, nos centramos en las pruebas actuales, sobre todo de los estudios gen&eacute;ticas humanas, apoyando la participaci&oacute;n de los genes y variantes en el sistema de se&ntilde;alizaci&oacute;n de GABA&eacute;rgico en la etiolog&iacute;a de la dependencia de la nicotina y el alcoholismo, basada en estudios de interacci&oacute;n del gen por gen, vinculaci&oacute;n y asociaci&oacute;n. Los esfuerzos actuales tienen como objetivo no s&oacute;lo para replicar estos resultados en muestras independientes, sino tambi&eacute;n para identificar qu&eacute; variante contribuye a las asociaciones detectadas y a trav&eacute;s de qu&eacute; mecanismos moleculares.

Gen&eacute;tica de se&ntilde;alizaci&oacute;n GABA&eacute;rgico en dependencia de la nicotina y alcohol.

To further our understanding of the effects of nicotine on the molecular responses of macrophages during virus or virus-like infections, poly(I:C)-stimulated macrophage-like RAW264.2 cells or mouse primary peritoneal macrophages were challenged with nicotine; and their molecular responses were evaluated using a qRT-PCR array, antibody array, ELISA, Western blotting, and Ca(2+) imaging. Of 51 genes expressed in the Toll-like receptor (TLR) and RIG-I-like receptor (RLR) pathways, mRNA expression of 15 genes in RAW264.7 cells was attenuated by nicotine, of which mRNA expression of IL-6, TNF-α, and IL-1β was confirmed to be attenuated in peritoneal macrophages. Concurrently, nicotine treatment attenuated the release of IL-6 and TNF-α from poly(I:C)-stimulated macrophages. However, when poly(I:C)-stimulated macrophages were challenged with nicotine plus α-bungarotoxin (α-BTX), secretion of IL-6 and TNF-α was found to be in a level seen with poly(I:C) stimulation only, indicating that α7-nAChR, a highly Ca(2+) permeable ion channel sensitive to blockade by α-BTX, is involved in this process. Furthermore, results from an antibody array indicated that nicotine treatment attenuated the phosphorylation of 82 sites, including Thr286 on CaMKIIα, from poly(I:C)-stimulated RAW264.7 cells, of which 28 are expressed in the downstream cascade of Ca(2+) signaling. Coincidentally, poly(I:C)-stimulated macrophages showed attenuated expression of phosphorylated CaMKIIα when pretreated with nicotine. In addition, nicotine attenuated intracellular Ca(2+) signal from poly(I:C)-stimulated RAW264.7 cells. Collectively, these results indicate that poly(I:C)-induced molecular responses of macrophages could be significantly attenuated by nicotine.

Identification and characterization of poly(I:C)-induced molecular responses attenuated by nicotine in mouse macrophages.

Individuals with gallbladder carcinoma (GBC), the most aggressive malignancy of the biliary tract, have a poor prognosis. Here we report the identification of somatic mutations for GBC in 57 tumor-normal pairs through a combination of exome sequencing and ultra-deep sequencing of cancer-related genes. The mutation pattern is defined by a dominant prevalence of C>T mutations at TCN sites. Genes with a significant frequency (false discovery rate (FDR)<0.05) of non-silent mutations include TP53 (47.1%), KRAS (7.8%) and ERBB3 (11.8%). Moreover, ErbB signaling (including EGFR, ERBB2, ERBB3, ERBB4 and their downstream genes) is the most extensively mutated pathway, affecting 36.8% (21/57) of the GBC samples. Multivariate analyses further show that cases with ErbB pathway mutations have a worse outcome (P=0.001). These findings provide insight into the somatic mutational landscape in GBC and highlight the key role of the ErbB signaling pathway in GBC pathogenesis.

Whole-exome and targeted gene sequencing of gallbladder carcinoma identifies recurrent mutations in the ErbB pathway.

On the basis of the genotypic/phenotypic data from Chinese Longitudinal Healthy Longevity Survey (CLHLS) and Cox proportional hazard model, the present study demonstrates that interactions between carrying FOXO1A-209 genotypes and tea drinking are significantly associated with lower risk of mortality at advanced ages. Such a significant association is replicated in two independent Han Chinese CLHLS cohorts (p = 0.028-0.048 in the discovery and replication cohorts, and p = 0.003-0.016 in the combined dataset). We found the associations between tea drinking and reduced mortality are much stronger among carriers of the FOXO1A-209 genotype compared to non-carriers, and drinking tea is associated with a reversal of the negative effects of carrying FOXO1A-209 minor alleles, that is, from a substantially increased mortality risk to substantially reduced mortality risk at advanced ages. The impacts are considerably stronger among those who carry two copies of the FOXO1A minor allele than those who carry one copy. On the basis of previously reported experiments on human cell models concerning FOXO1A-by-tea-compounds interactions, we speculate that results in the present study indicate that tea drinking may inhibit FOXO1A-209 gene expression and its biological functions, which reduces the negative impacts of FOXO1A-209 gene on longevity (as reported in the literature) and offers protection against mortality risk at oldest-old ages. Our empirical findings imply that the health outcomes of particular nutritional interventions, including tea drinking, may, in part, depend upon individual genetic profiles, and the research on the effects of nutrigenomics interactions could potentially be useful for rejuvenation therapies in the clinic or associated healthy aging intervention programs. 

Article	Year
Genetics of GABAergic signaling in nicotine and alcohol dependence. Human genetics\| PubMed ID: 22048727	2011
Identification and characterization of poly(I:C)-induced molecular responses attenuated by nicotine in mouse macrophages. Molecular pharmacology\| PubMed ID: 23028093	2013
Whole-exome and targeted gene sequencing of gallbladder carcinoma identifies recurrent mutations in the ErbB pathway. Nature genetics\| PubMed ID: 24997986	2014
Interaction Between the FOXO1A-209 Genotype and Tea Drinking Is Significantly Associated with Reduced Mortality at Advanced Ages. Rejuvenation research\| PubMed ID: 26414954	2016

Jun Gu

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