Admixture and Clinical Phenotypic Variation
All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources, including historical migrations, population isolation over time, genetic drift, and selection and adaptation. If differentiated populations remained...
Uložené v:
| Vydané v: | Human heredity Ročník 77; číslo 1/4; s. 73 - 86 |
|---|---|
| Hlavní autori: | , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
Basel, Switzerland
S. Karger AG
01.01.2014
|
| Predmet: | |
| ISBN: | 9783318027020, 3318027022 |
| ISSN: | 0001-5652, 1423-0062, 1423-0062 |
| On-line prístup: | Získať plný text |
| Tagy: |
Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
|
| Abstract | All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources, including historical migrations, population isolation over time, genetic drift, and selection and adaptation. If differentiated populations remained isolated from each other over a long period of time such that there is no mating of individuals between those populations, then some level of global consanguinity within those populations will lead to the formation of gene pools that will become more and more distinct over time. Global genetic differentiation of this sort can lead to overt phenotypic differences between populations if phenotypically relevant variants either arise uniquely within those populations or begin to exhibit frequency differences across the populations. This can occur at the single variant level for monogenic phenotypes or at the level of aggregate variant frequency differences across the many loci that contribute to a phenotype with a multifactorial or polygenic basis. However, if individuals begin to interbreed (or ‘admix’) from populations with different frequencies of phenotypically relevant genetic variants, then these admixed individuals will exhibit the phenotype to varying degrees. The level of phenotypic expression will depend on the degree to which the admixed individuals have inherited causative variants that have descended from the ancestral population in which those variants were present (or, more likely, simply more frequent). We review studies that consider the association between the degree of admixture (or ancestry) and phenotypes of clinical relevance. We find a great deal of literature-based evidence for associations between the degree of admixture and phenotypic variation for a number of admixed populations and phenotypes, although not all this evidence is confirmatory. We also consider the implications of such associations for gene-mapping initiatives as well as general clinical epidemiology studies and medical practice. We end with some thoughts on the future of studies exploring phenotypic differences among admixed individuals as well as individuals with different ancestral backgrounds. |
|---|---|
| AbstractList | All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources, including historical migrations, population isolation over time, genetic drift, and selection and adaptation. If differentiated populations remained isolated from each other over a long period of time such that there is no mating of individuals between those populations, then some level of global consanguinity within those populations will lead to the formation of gene pools that will become more and more distinct over time. Global genetic differentiation of this sort can lead to overt phenotypic differences between populations if phenotypically relevant variants either arise uniquely within those populations or begin to exhibit frequency differences across the populations. This can occur at the single variant level for monogenic phenotypes or at the level of aggregate variant frequency differences across the many loci that contribute to a phenotype with a multifactorial or polygenic basis. However, if individuals begin to interbreed (or 'admix') from populations with different frequencies of phenotypically relevant genetic variants, then these admixed individuals will exhibit the phenotype to varying degrees. The level of phenotypic expression will depend on the degree to which the admixed individuals have inherited causative variants that have descended from the ancestral population in which those variants were present (or, more likely, simply more frequent). We review studies that consider the association between the degree of admixture (or ancestry) and phenotypes of clinical relevance. We find a great deal of literature-based evidence for associations between the degree of admixture and phenotypic variation for a number of admixed populations and phenotypes, although not all this evidence is confirmatory. We also consider the implications of such associations for gene-mapping initiatives as well as general clinical epidemiology studies and medical practice. We end with some thoughts on the future of studies exploring phenotypic differences among admixed individuals as well as individuals with different ancestral backgrounds. All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources, including historical migrations, population isolation over time, genetic drift, and selection and adaptation. If differentiated populations remained isolated from each other over a long period of time such that there is no mating of individuals between those populations, then some level of global consanguinity within those populations will lead to the formation of gene pools that will become more and more distinct over time. Global genetic differentiation of this sort can lead to overt phenotypic differences between populations if phenotypically relevant variants either arise uniquely within those populations or begin to exhibit frequency differences across the populations. This can occur at the single variant level for monogenic phenotypes or at the level of aggregate variant frequency differences across the many loci that contribute to a phenotype with a multifactorial or polygenic basis. However, if individuals begin to interbreed (or 'admix') from populations with different frequencies of phenotypically relevant genetic variants, then these admixed individuals will exhibit the phenotype to varying degrees. The level of phenotypic expression will depend on the degree to which the admixed individuals have inherited causative variants that have descended from the ancestral population in which those variants were present (or, more likely, simply more frequent). We review studies that consider the association between the degree of admixture (or ancestry) and phenotypes of clinical relevance. We find a great deal of literature-based evidence for associations between the degree of admixture and phenotypic variation for a number of admixed populations and phenotypes, although not all this evidence is confirmatory. We also consider the implications of such associations for gene-mapping initiatives as well as general clinical epidemiology studies and medical practice. We end with some thoughts on the future of studies exploring phenotypic differences among admixed individuals as well as individuals with different ancestral backgrounds. © 2014 S. Karger AG, Basel [PUBLICATION ABSTRACT] All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources, including historical migrations, population isolation over time, genetic drift, and selection and adaptation. If differentiated populations remained isolated from each other over a long period of time such that there is no mating of individuals between those populations, then some level of global consanguinity within those populations will lead to the formation of gene pools that will become more and more distinct over time. Global genetic differentiation of this sort can lead to overt phenotypic differences between populations if phenotypically relevant variants either arise uniquely within those populations or begin to exhibit frequency differences across the populations. This can occur at the single variant level for monogenic phenotypes or at the level of aggregate variant frequency differences across the many loci that contribute to a phenotype with a multifactorial or polygenic basis. However, if individuals begin to interbreed (or 'admix') from populations with different frequencies of phenotypically relevant genetic variants, then these admixed individuals will exhibit the phenotype to varying degrees. The level of phenotypic expression will depend on the degree to which the admixed individuals have inherited causative variants that have descended from the ancestral population in which those variants were present (or, more likely, simply more frequent). We review studies that consider the association between the degree of admixture (or ancestry) and phenotypes of clinical relevance. We find a great deal of literature-based evidence for associations between the degree of admixture and phenotypic variation for a number of admixed populations and phenotypes, although not all this evidence is confirmatory. We also consider the implications of such associations for gene-mapping initiatives as well as general clinical epidemiology studies and medical practice. We end with some thoughts on the future of studies exploring phenotypic differences among admixed individuals as well as individuals with different ancestral backgrounds.All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources, including historical migrations, population isolation over time, genetic drift, and selection and adaptation. If differentiated populations remained isolated from each other over a long period of time such that there is no mating of individuals between those populations, then some level of global consanguinity within those populations will lead to the formation of gene pools that will become more and more distinct over time. Global genetic differentiation of this sort can lead to overt phenotypic differences between populations if phenotypically relevant variants either arise uniquely within those populations or begin to exhibit frequency differences across the populations. This can occur at the single variant level for monogenic phenotypes or at the level of aggregate variant frequency differences across the many loci that contribute to a phenotype with a multifactorial or polygenic basis. However, if individuals begin to interbreed (or 'admix') from populations with different frequencies of phenotypically relevant genetic variants, then these admixed individuals will exhibit the phenotype to varying degrees. The level of phenotypic expression will depend on the degree to which the admixed individuals have inherited causative variants that have descended from the ancestral population in which those variants were present (or, more likely, simply more frequent). We review studies that consider the association between the degree of admixture (or ancestry) and phenotypes of clinical relevance. We find a great deal of literature-based evidence for associations between the degree of admixture and phenotypic variation for a number of admixed populations and phenotypes, although not all this evidence is confirmatory. We also consider the implications of such associations for gene-mapping initiatives as well as general clinical epidemiology studies and medical practice. We end with some thoughts on the future of studies exploring phenotypic differences among admixed individuals as well as individuals with different ancestral backgrounds. All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources, including historical migrations, population isolation over time, genetic drift, and selection and adaptation. If differentiated populations remained isolated from each other over a long period of time such that there is no mating of individuals between those populations, then some level of global consanguinity within those populations will lead to the formation of gene pools that will become more and more distinct over time. Global genetic differentiation of this sort can lead to overt phenotypic differences between populations if phenotypically relevant variants either arise uniquely within those populations or begin to exhibit frequency differences across the populations. This can occur at the single variant level for monogenic phenotypes or at the level of aggregate variant frequency differences across the many loci that contribute to a phenotype with a multifactorial or polygenic basis. However, if individuals begin to interbreed (or admix') from populations with different frequencies of phenotypically relevant genetic variants, then these admixed individuals will exhibit the phenotype to varying degrees. The level of phenotypic expression will depend on the degree to which the admixed individuals have inherited causative variants that have descended from the ancestral population in which those variants were present (or, more likely, simply more frequent). We review studies that consider the association between the degree of admixture (or ancestry) and phenotypes of clinical relevance. We find a great deal of literature-based evidence for associations between the degree of admixture and phenotypic variation for a number of admixed populations and phenotypes, although not all this evidence is confirmatory. We also consider the implications of such associations for gene-mapping initiatives as well as general clinical epidemiology studies and medical practice. We end with some thoughts on the future of studies exploring phenotypic differences among admixed individuals as well as individuals with different ancestral backgrounds. copyright 2014 S. Karger AG, Basel |
| Author | Quarless, Danjuma Libiger, Ondrej Goetz, Laura H. Schork, Nicholas J. Uribe-Bruce, Liliana |
| Author_xml | – sequence: 1 givenname: Laura H. surname: Goetz fullname: Goetz, Laura H. – sequence: 2 givenname: Liliana surname: Uribe-Bruce fullname: Uribe-Bruce, Liliana – sequence: 3 givenname: Danjuma surname: Quarless fullname: Quarless, Danjuma – sequence: 4 givenname: Ondrej surname: Libiger fullname: Libiger, Ondrej – sequence: 5 givenname: Nicholas J. surname: Schork fullname: Schork, Nicholas J. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25060271$$D View this record in MEDLINE/PubMed |
| BookMark | eNqF0ktLxDAQAOD4QnfVg3eVBS-KVCfPpkdZ1BUEPajXkDapZu22a9KC_nuj-xBE8BTCfDNMZtJH63VTW4T2MJxhzLNzAKCCEEpXUJ9SLIGkQGEV9TAjNAEQZA3tZqlcxAiso15MwgkXnGyhfgjjeJWQ0k20RTiIqHAPnV6YiXtvO28HujaDYeVqV-hqcP9i66b9mLpi8KS9061r6h20Ueoq2N35uY0ery4fhqPk9u76ZnhxmxSMkzaxlGQ2NYIzXUCqieWl4SbLscxzQ4UWTNPYGOOZNXleSmFoaiUwDCUUWQxuo-NZ3alv3jobWjVxobBVpWvbdEHhVEgu4yzE_5QzKajA3_ToFx03na_jQ6ISlHIB4ksdzlWXT6xRU-8m2n-oxcQiOJ-BwjcheFuqwrXf42m9dpXCoL4WppYLixknvzIWRf-y8yZftX-2filHo8uZUFNTRrX_p1oWOZiFx6FtfqJM8vhZBKOfEvKqTg |
| CitedBy_id | crossref_primary_10_1016_j_jtho_2018_05_032 crossref_primary_10_1016_j_ajhg_2024_12_005 crossref_primary_10_1186_s40246_014_0023_x crossref_primary_10_3390_jcm9010216 crossref_primary_10_1038_s41598_019_50362_2 crossref_primary_10_3389_fgene_2023_1091269 crossref_primary_10_1007_s10549_021_06264_x crossref_primary_10_1177_1076029620962225 crossref_primary_10_1038_jhg_2015_8 crossref_primary_10_1016_j_smrv_2016_05_004 crossref_primary_10_1038_s41598_021_91530_7 crossref_primary_10_1002_ajpa_70124 crossref_primary_10_1016_j_neuroimage_2015_04_057 crossref_primary_10_1016_j_heliyon_2024_e37504 crossref_primary_10_1371_journal_pone_0169315 crossref_primary_10_3389_fgene_2021_636542 crossref_primary_10_1093_bib_bby112 crossref_primary_10_3389_fgene_2025_1559496 crossref_primary_10_1093_bib_bby044 crossref_primary_10_1016_j_gde_2016_09_003 |
| ContentType | Journal Article |
| Copyright | 2014 S. Karger AG 2014 S. Karger AG, Basel Copyright (c) 2014 S. Karger AG, Basel |
| Copyright_xml | – notice: 2014 S. Karger AG – notice: 2014 S. Karger AG, Basel – notice: Copyright (c) 2014 S. Karger AG, Basel |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7X7 7XB 88A 88E 88I 8AO 8FD 8FE 8FH 8FI 8FJ 8FK 8G5 ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FR3 FYUFA GHDGH GNUQQ GUQSH HCIFZ K9. LK8 M0S M1P M2O M2P M7P MBDVC P64 PHGZM PHGZT PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS Q9U RC3 7X8 |
| DOI | 10.1159/000362233 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Health & Medical Collection ProQuest Central (purchase pre-March 2016) Biology Database (Alumni Edition) Medical Database (Alumni Edition) Science Database (Alumni Edition) ProQuest Pharma Collection Technology Research Database ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) Research Library (Alumni Edition) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection (subscription) ProQuest Central Natural Science Collection ProQuest One Community College ProQuest Central Engineering Research Database Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student Research Library Prep SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) ProQuest Biological Science Collection Health & Medical Collection (Alumni Edition) PML(ProQuest Medical Library) Research Library Science Database Biological Science Database Research Library (Corporate) Biotechnology and BioEngineering Abstracts ProQuest Central Premium ProQuest One Academic (New) ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic (retired) ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic Genetics Abstracts MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Research Library Prep ProQuest Central Student Technology Research Database ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing Research Library (Alumni Edition) ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Central China ProQuest Biology Journals (Alumni Edition) ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Genetics Abstracts Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Health & Medical Research Collection Biological Science Collection ProQuest Research Library ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest Central Basic ProQuest Science Journals ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition Engineering Research Database ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE Research Library Prep MEDLINE - Academic Genetics Abstracts |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Biology |
| EISBN | 3318027030 9783318027037 |
| EISSN | 1423-0062 |
| EndPage | 86 |
| ExternalDocumentID | 3436797821 25060271 10_1159_000362233 362233 48514264 |
| Genre | Journal Article Review |
| GroupedDBID | --- 0~5 0~B 29I 30W 326 36B 3O. 4.4 5GY 5RE 7X7 88E 88I 8AO 8FE 8FH 8FI 8FJ 8FW 8G5 8UI AAYIC AAZDW ABBHK ABBTS ABJNI ABPAZ ABUWG ABWCG ABXSQ ACGFS ACGOD ACPRK ACPSR ADBBV ADULT AENEX AEUPB AEYAO AFJJK AFKRA AHFRZ AHMBA AILCM ALDHI ALIPV ALMA_UNASSIGNED_HOLDINGS AZPMC AZQEC BBNVY BENPR BHPHI BPHCQ BVXVI CCPQU CS3 CYUIP DU5 DWQXO E0A EBS EJD EMB EMOBN F5P FB. FYUFA GNUQQ GUQSH HCIFZ HMCUK HZ~ IY7 JAAYA JENOY JKPJF JPL JPM JST JVCUD KUZGX L7B LK8 M-- M1P M2O M2P M7P N9A O1H O9- OK1 PHGZM PHGZT PQQKQ PROAC PSQYO RKO SA0 SV3 UJ6 UKHRP 3V. 88A ADACV AEJYH JSODD M0L .GJ 34G 39C 53G AAYXX ACQXL ADAGL AFFHD AFFNX AFSIO AI. AIOBO CAG CITATION COF IAO IGS IHR INH ITC PJZUB PPXIY PQGLB RXVBD VH1 ZGI ZXP CGR CUY CVF ECM EIF NPM RIG 7XB 8FD 8FK FR3 K9. MBDVC P64 PKEHL PQEST PQUKI PRINS Q9U RC3 7X8 PUEGO |
| ID | FETCH-LOGICAL-c452t-e329e7d654ac07a2e5fd5d9b18bbd36a64a3001459edbbf86d37e80410f0c94a3 |
| IEDL.DBID | M2P |
| ISBN | 9783318027020 3318027022 |
| ISICitedReferencesCount | 21 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000339321800009&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 0001-5652 1423-0062 |
| IngestDate | Fri Sep 05 14:32:23 EDT 2025 Sun Nov 09 09:18:42 EST 2025 Mon Oct 06 17:54:32 EDT 2025 Mon Jul 21 05:49:46 EDT 2025 Tue Nov 18 21:57:12 EST 2025 Sat Nov 29 07:59:45 EST 2025 Thu Aug 29 12:04:39 EDT 2024 Thu Sep 05 17:58:01 EDT 2024 Thu Jun 19 22:45:41 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1/4 |
| Keywords | Metabolic disease Principal components analysis Admixture Genetic ancestry Cancer |
| Language | English |
| License | Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. 2014 S. Karger AG, Basel |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c452t-e329e7d654ac07a2e5fd5d9b18bbd36a64a3001459edbbf86d37e80410f0c94a3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 |
| OpenAccessLink | https://karger.com/hhe/article-pdf/77/1-4/73/2909685/000362233.pdf |
| PMID | 25060271 |
| PQID | 1563356066 |
| PQPubID | 40827 |
| PageCount | 14 |
| ParticipantIDs | jstor_primary_48514264 crossref_citationtrail_10_1159_000362233 crossref_primary_10_1159_000362233 proquest_miscellaneous_1768582336 proquest_miscellaneous_1548636136 proquest_journals_1563356066 karger_primary_362233 pubmed_primary_25060271 |
| PublicationCentury | 2000 |
| PublicationDate | 2014-01-01 |
| PublicationDateYYYYMMDD | 2014-01-01 |
| PublicationDate_xml | – month: 01 year: 2014 text: 2014-01-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | Basel, Switzerland |
| PublicationPlace_xml | – name: Basel, Switzerland – name: Switzerland – name: Basel |
| PublicationTitle | Human heredity |
| PublicationTitleAlternate | Hum Hered |
| PublicationYear | 2014 |
| Publisher | S. Karger AG |
| Publisher_xml | – name: S. Karger AG |
| SSID | ssj0008073 |
| Score | 2.119872 |
| SecondaryResourceType | review_article |
| Snippet | All human populations exhibit some level of genetic differentiation. This differentiation, or population stratification, has many interacting sources,... |
| SourceID | proquest pubmed crossref karger jstor |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 73 |
| SubjectTerms | Clinical trials Genetic Diseases, Inborn - epidemiology Genetic Diseases, Inborn - genetics Genetic Variation Genetics, Population - methods Genotype & phenotype Humans Phenotype Population Aspects of Consanguinity Reproductive Isolation |
| Title | Admixture and Clinical Phenotypic Variation |
| URI | https://www.jstor.org/stable/48514264 https://karger.com/doi/10.1159/000362233 https://www.ncbi.nlm.nih.gov/pubmed/25060271 https://www.proquest.com/docview/1563356066 https://www.proquest.com/docview/1548636136 https://www.proquest.com/docview/1768582336 |
| Volume | 77 |
| WOSCitedRecordID | wos000339321800009&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVPQU databaseName: Biological Science Database isbn: 9783318027020 customDbUrl: eissn: 1423-0062 dateEnd: 20150930 omitProxy: false ssIdentifier: ssj0008073 issn: 0001-5652 databaseCode: M7P dateStart: 19980101 isFulltext: true eisbn: 3318027030 titleUrlDefault: http://search.proquest.com/biologicalscijournals providerName: ProQuest – providerCode: PRVPQU databaseName: Health & Medical Collection isbn: 9783318027020 customDbUrl: eissn: 1423-0062 dateEnd: 20241212 omitProxy: false ssIdentifier: ssj0008073 issn: 0001-5652 databaseCode: 7X7 dateStart: 19980101 isFulltext: true eisbn: 3318027030 titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central isbn: 9783318027020 customDbUrl: eissn: 1423-0062 dateEnd: 20241212 omitProxy: false ssIdentifier: ssj0008073 issn: 0001-5652 databaseCode: BENPR dateStart: 19980101 isFulltext: true eisbn: 3318027030 titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: Research Library isbn: 9783318027020 customDbUrl: eissn: 1423-0062 dateEnd: 20241212 omitProxy: false ssIdentifier: ssj0008073 issn: 0001-5652 databaseCode: M2O dateStart: 19980101 isFulltext: true eisbn: 3318027030 titleUrlDefault: https://search.proquest.com/pqrl providerName: ProQuest – providerCode: PRVPQU databaseName: Science Database isbn: 9783318027020 customDbUrl: eissn: 1423-0062 dateEnd: 20241212 omitProxy: false ssIdentifier: ssj0008073 issn: 0001-5652 databaseCode: M2P dateStart: 19980101 isFulltext: true eisbn: 3318027030 titleUrlDefault: https://search.proquest.com/sciencejournals providerName: ProQuest |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB71AYgLhdLCQrsKiAOXqElsx8kJQbXVHug2qgDtLYofUSuq7LK7RfTfM2N7g0C0l1582JlNrMzY_sYz-gbgXaEU11yKOLEGA5RCiFg1qYq5xPWnjFbcOHb9z3IyKabTsgoXbstQVrneE91GbWaa7siPMM5gTBDc_jD_EVPXKMquhhYam7CNyCalkq7TrOp34iIJGWYMmRG4ZIFZCE_wI0_EkjH213nkSxLxMPpOZdiL21GnO31Odu4776fwJODO6KN3lGewYbtdeOg7Ud7swqPTkGN_Do5P9xclFqKmM1EgDr2KqgvbzVY380sdfcMA21l0D76ejL4cj-PQUiHWXGSr2LKstNLkgjc6kU1mRWuEKVWKNjMsb3LeMIqaRGmNUm2RGyYtURQlbaJLFO7DVjfr7EuIdGpzqSTDB2hOFDUI_DjhJUQwSdLKAbxff9haB75xantxVbu4Q5R1b4MBvO1V555k439K-846vQY6Vkp4bgB73ly9ZP2Hg39-H49HXlTPTYvitcHqsG6X9R9rDeBNL8YVR2mUprOza9LhRc4QBt2lI4nXH9-EOi-84_SzyIjTMZPpq7sn8BoeIzjj_rrnALZWi2t7CA_0z9XlcjGETTmVbiyGsP1pNKnOh-T8Z26saJTVb7-iBNw |
| linkProvider | ProQuest |
| linkToHtml | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V3dT9RAEJ8gfsALKgIeoFajiS8N7X502wdjjEKOcFzuAQ1vtfvRSCS98-5Q75_ib2Sm29ZolDcefO1M2013dvY3O9PfALxMtRZGKBlGzmKAkkoZ6iLWoVC4_rQ1WtiaXX-ghsP09DQbLcFl-y8MlVW2PrF21HZs6Ix8D-MMziXB7beTbyF1jaLsattCw5vFkVv8wJBt9ubwA87vK8YO9k_e98Omq0BohGTz0HGWOWUTKQoTqYI5WVppMx3jsC1PikQUnAIHmTmrdZkmlitHLD1RGZkMhfjcW3BbELMYlQqyUef506jJaGOIjkCJNUxGiBj2PPEL4_y3_c-XQOLm95XKvqf_Rrn1bndw_3_7Tg9grcHVwTu_EB7CkqvW4a7vtLlYh3vHTQ3BI6j5gn9S4iQoKhs0xKjnweiLq8bzxeTMBJ-KqbfYDfh4I4PehOVqXLnHEJjYJUorjg8wgih4ENgKwoOI0KKoVD143U5kbho-dWrrcZ7XcZXM8m7Oe_CiU514EpG_KW3W1tBp4MKJCa_2YMObRydpb9j943q_v-9F-cSWKG4NJG_80iz_ZR09eN6J0aNQmqio3PiCdESacIR51-ko6luAb0KdLW-o3SgYcVYyFW9fP4BnsNI_OR7kg8Ph0Q6sIhAV_mhrF5bn0wv3BO6Y7_Oz2fRpvcgC-HzT1noFyMZdKw |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Admixture+and+Clinical+Phenotypic+Variation&rft.jtitle=Human+heredity&rft.au=Goetz%2C+Laura+H&rft.au=Uribe-bruce%2C+Liliana&rft.au=Quarless%2C+Danjuma&rft.au=Libiger%2C+Ondrej&rft.date=2014-01-01&rft.pub=S.+Karger+AG&rft.issn=0001-5652&rft.eissn=1423-0062&rft.volume=77&rft.issue=1-4&rft.spage=73&rft_id=info:doi/10.1159%2F000362233&rft.externalDocID=3436797821 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0001-5652&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0001-5652&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0001-5652&client=summon |