X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Phenotypic Refinement of Heart Failure in a National Biobank Facilitates Genetic Discovery
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Vol. 139, No. 4 ( 2019-01-22), p. 489-501
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 139, No. 4 ( 2019-01-22), p. 489-501
    Abstract: Heart failure (HF) is a morbid and heritable disorder for which the biological mechanisms are incompletely understood. We therefore examined genetic associations with HF in a large national biobank, and assessed whether refined phenotypic classification would facilitate genetic discovery. Methods: We defined all-cause HF among 488 010 participants from the UK Biobank and performed a genome-wide association analysis. We refined the HF phenotype by classifying individuals with left ventricular dysfunction and without coronary artery disease as having nonischemic cardiomyopathy (NICM), and repeated a genetic association analysis. We then pursued replication of lead HF and NICM variants in independent cohorts, and performed adjusted association analyses to assess whether identified genetic associations were mediated through clinical HF risk factors. In addition, we tested rare, loss-of-function mutations in 24 known dilated cardiomyopathy genes for association with HF and NICM. Finally, we examined associations between lead variants and left ventricular structure and function among individuals without HF using cardiac magnetic resonance imaging (n=4158) and echocardiographic data (n=30 201). Results: We identified 7382 participants with all-cause HF in the UK Biobank. Genome-wide association analysis of all-cause HF identified several suggestive loci ( P 〈 1×10 –6 ), the majority linked to upstream HF risk factors, ie, coronary artery disease ( CDKN2B-AS1 and MAP3K7CL ) and atrial fibrillation ( PITX2 ). Refining the HF phenotype yielded a subset of 2038 NICM cases. In contrast to all-cause HF, genetic analysis of NICM revealed suggestive loci that have been implicated in dilated cardiomyopathy ( BAG3 , CLCNKA-ZBTB17 ). Dilated cardiomyopathy signals arising from our NICM analysis replicated in independent cohorts, persisted after HF risk factor adjustment, and were associated with indices of left ventricular dysfunction in individuals without clinical HF. In addition, analyses of loss-of-function variants implicated BAG3 as a disease susceptibility gene for NICM (loss-of-function variant carrier frequency=0.01%; odds ratio,12.03; P =3.62×10 –5 ). Conclusions: We found several distinct genetic mechanisms of all-cause HF in a national biobank that reflect well-known HF risk factors. Phenotypic refinement to a NICM subtype appeared to facilitate the discovery of genetic signals that act independently of clinical HF risk factors and that are associated with subclinical left ventricular dysfunction.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.118.035774
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1466401-X
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 2
    Online Resource
    Online Resource
    DataSheet1.docx
    Frontiers Media SA ; 2023
    In:  Frontiers in Genetics Vol. 14 ( 2023-7-6)
    Details
    In: Frontiers in Genetics, Frontiers Media SA, Vol. 14 ( 2023-7-6)
    Abstract: Objective: Most methods to detect copy number variation (CNV) have high false positive rates, especially for small CNVs and in real-life samples from clinical studies. In this study, we explored a novel scatterplot-based method to detect CNVs in microarray samples. Methods: Illumina SNP microarray data from 13,254 individuals were analyzed with scatterplots and by PennCNV. The data were analyzed without the prior exclusion of low-quality samples. For CNV scatterplot visualization, the median signal intensity of all SNPs located within a CNV region was plotted against the median signal intensity of the flanking genomic region. Since CNV causes loss or gain of signal intensities, carriers of different CNV alleles pop up in clusters. Moreover, SNPs within a deletion are not heterozygous, whereas heterozygous SNPs within a duplication show typical 1:2 signal distribution between the alleles. Scatterplot-based CNV calls were compared with standard results of PennCNV analysis. All discordant calls as well as a random selection of 100 concordant calls were individually analyzed by visual inspection after noise-reduction. Results: An algorithm for the automated scatterplot visualization of CNVs was developed and used to analyze six known CNV regions. Use of scatterplots and PennCNV yielded 1019 concordant and 108 discordant CNV calls. All concordant calls were evaluated as true CNV-findings. Among the 108 discordant calls, 7 were false positive findings by the scatterplot method, 80 were PennCNV false positives, and 21 were true CNVs detected by the scatterplot method, but missed by PennCNV (i.e., false negative findings). Conclusion: CNV visualization by scatterplots allows for a reliable and rapid detection of CNVs in large studies. This novel method may thus be used both to confirm the results of genome-wide CNV detection software and to identify known CNVs in hitherto untyped samples.
    Type of Medium: Online Resource
    ISSN: 1664-8021
    URL: Article
    URL: Article
    DOI: 10.3389/fgene.2023.1166972
    DOI: 10.3389/fgene.2023.1166972.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606823-0
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 3
    Online Resource
    Online Resource
    Abstract MIP-046: BLOOD TYPE, ABO GENETIC VARIANTS, AND OVARIAN CANCER SURVIVAL
    American Association for Cancer Research (AACR) ; 2017
    In:  Clinical Cancer Research Vol. 23, No. 11_Supplement ( 2017-06-01), p. MIP-046-MIP-046
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 23, No. 11_Supplement ( 2017-06-01), p. MIP-046-MIP-046
    Abstract: INTRODUCTION: In addition to a fundamental role in transfusion, blood type is also implicated in disease. Blood type antigens on red blood cells are determined by genetic variants in the ABO gene; both phenotype and genotype have been significantly associated with ovarian cancer risk. Meta–analysis of eight case–control studies indicated that women with genetic variants corresponding to blood type A had 9% greater ovarian cancer risk than women with variants corresponding to blood type O. Only one study to date has evaluated ovarian cancer prognosis; among 256 Chinese women, cases with blood type A had more than two–fold worse survival than cases with other blood types (B, AB, and O). AIMS: To evaluate blood type phenotype and genotype in relation to overall ovarian cancer survival in a predominantly Caucasian study population. APPROACH: Tumor registry confirmed ovarian or fallopian tube primary malignancies were identified from the Synthetic Derivative, a de–identified mirror of electronic medical records (EMR) from the Vanderbilt University Medical Center (VUMC). Blood type was ascertained from EMR linked laboratory reports. Ten common variants (minor allele frequency ≥0.05) in the ABO gene were ascertained using the Illumina Exome BeadChip. Subject vital status was determined from EMR and linkage to the National Death Index. Associations with overall survival were evaluated with proportional hazards regression in multivariable models that included adjustment for age, stage, grade, histologic subtype of disease, and year of diagnosis. RESULTS: Blood type phenotype and genotype were available for 556 and 154 tumor registry confirmed ovarian cancer cases, respectively. Among all women, cases with blood type A had significantly better overall survival compared to either blood type O (Hazard ratio (HR): 0.79, 95% confidence interval (CI): 0.63–0.99) or to cases with any blood type other than A (HR: 0.80, 95% CI: 0.65–0.98). A missense variant in exon 7 (rs1053878) with moderate linkage to a variant corresponding to the A phenotype was also associated with better overall survival in a dominant manner (HR: 0.50, 95% CI: 0.25–0.99). While our phenotype association differed by race (p–interaction=0.049) and was evident only among Caucasian cases (HR: 0.75, 95% CI: 0.60–0.93), our genotype association did not vary by race (p–interaction=0.279). CONCLUSIONS: Women with blood type A had better overall ovarian cancer survival, regardless of whether blood type was directly assayed, or inferred by genotype. These findings contradict the only existing ovarian cancer survival study to date, but include a larger, and predominantly Caucasian study population. Additional research is needed to either replicate or refute our ovarian cancer survival finding, and to determine if ABO variants and blood type are causally related to cancer development and progression. Citation Format: Hilary Toole, Rebecca T. Levinson, Gabriella D. Cozzi, Angie Deng, Jason T. Fromal, Malcolm–Robert Snyder, Dineo Khabele, Alicia Beeghly–Fadiel . BLOOD TYPE, ABO GENETIC VARIANTS, AND OVARIAN CANCER SURVIVAL [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr MIP-046.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1557-3265.OVCASYMP16-MIP-046
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 4
    Online Resource
    Online Resource
    Abstract 4229: Preliminary results from the Pharmacogenetics Ovarian Cancer Knowledge to Individualize Treatment (POCKIT) study
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 4229-4229
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 4229-4229
    Abstract: Introduction: With an overall five-year survival rate of only 46%, ovarian cancer is the most lethal gynecologic malignancy. Treatment includes surgical cytoreduction (debulking) followed by chemotherapy with platinum and taxane agents, and prognosis generally depends upon clinical characteristics, such as stage of disease at diagnosis, success of surgical debulking, and histologic subtype. However, even among women with comparable clinical characteristics, there can be variation in survival. Part of this variability may be due to inherited genetic variation in genes related to the absorption, distribution, metabolism, and excretion (ADME) of pharmacologic agents commonly used to treat ovarian cancer. Approach: To test the hypothesis that pharmacogenetic variants influence ovarian cancer prognosis, we assembled a clinical cohort of confirmed epithelial ovarian cancer cases from electronic medical records (EMR) at the Vanderbilt University Medical Center (VUMC) with banked DNA samples available. Clinical characteristics were abstracted from EMR using natural language processing (NLP)-assisted EMR review and a REDCap data collection instrument. Genotyping was conducted on the Sequenom iPLEX ADME PGx panel at the Vanderbilt Technologies for Advanced Genomics (VANTAGE) core facility. Associations with overall survival were evaluated using multivariable proportional hazards regression. Results: We identified a total of 391 epithelial ovarian cancer cases with banked DNA from VUMC EHR. Clinical characteristic abstracted by NLP followed expected distributions; the majority of cases were Caucasian (87%), with serous histology (63%), late-stage (62%), high-grade (60%) disease. Most common treatments included surgical cytoreduction (93%) and chemotherapy with a platinum (83%) and/or taxane agent (82%) agent. DNA was successfully pulled, plated, and genotyped for 327 cases (81.3%) for 73 common ADME variants in 30 genes. To prevent population stratification, genetic analyses were restricted to 287 Caucasians, where five nominally significant overall survival associations were identified: ABCB1 rs1045642, ABCC2 rs2273697, CYP2A6 rs1801272, CYP2E1 rs2070673, and SLCO2B1 rs2306168. Additional analyses, including for gene and drug scores, are currently under way. Conclusions: Individual variation in ADME genes may contribute to variation in ovarian cancer survival. Future steps include testing associations for replication, and evaluation of response to treatment. In addition, this research demonstrates that EMR-based study populations, in concert with linked biorepositories, can facilitate research on ovarian cancer. Citation Format: Ayush Giri, Rebecca T. Levinson, Spencer Keene, Gwendolyn Holman, Stacy D. Smith, Leshaun Clayton, Whitney Lovett, Samantha P. Stansel, Malcolm-Robert Bringhurst Snyder, Jason T. Fromal, Gabriella D. Cozzi, Dineo Khabele, Alicia Beeghly-Fadiel. Preliminary results from the Pharmacogenetics Ovarian Cancer Knowledge to Individualize Treatment (POCKIT) study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4229.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-4229
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 5
    Online Resource
    Online Resource
    Genetic Analysis of the Localization of APOBEC3F to Human Immunodeficiency Virus Type 1 Virion Cores
    American Society for Microbiology ; 2015
    In:  Journal of Virology Vol. 89, No. 4 ( 2015-02-15), p. 2415-2424
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 89, No. 4 ( 2015-02-15), p. 2415-2424
    Abstract: Members of the APOBEC3 family of cytidine deaminases vary in their proportions of a virion-incorporated enzyme that is localized to mature retrovirus cores. We reported previously that APOBEC3F (A3F) was highly localized into mature human immunodeficiency virus type 1 (HIV-1) cores and identified that L306 in the C-terminal cytidine deaminase (CD) domain contributed to its core localization (C. Song, L. Sutton, M. Johnson, R. D'Aquila, J. Donahue, J Biol Chem 287: 16965–16974, 2012, http://dx.doi.org/10.1074/jbc.M111.310839 ). We have now determined an additional genetic determinant(s) for A3F localization to HIV-1 cores. We found that one pair of leucines in each of A3F's C-terminal and N-terminal CD domains jointly determined the degree of localization of A3F into HIV-1 virion cores. These are A3F L306/L368 (C-terminal domain) and A3F L122/L184 (N-terminal domain). Alterations to one of these specific leucine residues in either of the two A3F CD domains (A3F L368A, L122A, and L184A) decreased core localization and diminished HIV restriction without changing virion packaging. Furthermore, double mutants in these leucine residues in each of A3F's two CD domains (A3F L368A plus L184A or A3F L368A plus L122A) still were packaged into virions but completely lost core localization and anti-HIV activity. HIV virion core localization of A3F is genetically separable from its virion packaging, and anti-HIV activity requires some core localization. IMPORTANCE Specific leucine-leucine interactions are identified as necessary for A3F's core localization and anti-HIV activity but not for its packaging into virions. Understanding these signals may lead to novel strategies to enhance core localization that may augment effects of A3F against HIV and perhaps of other A3s against retroviruses, parvoviruses, and hepatitis B virus.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.01981-14
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2015
    detail.hit.zdb_id: 1495529-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 6
    Online Resource
    Online Resource
    Spatial multi-omic map of human myocardial infarction
    Springer Science and Business Media LLC ; 2022
    In:  Nature Vol. 608, No. 7924 ( 2022-08-25), p. 766-777
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 608, No. 7924 ( 2022-08-25), p. 766-777
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/s41586-022-05060-x
    RVK:
    TA 1000
    RVK:
    UA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
    SSG: 11
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 7
    Online Resource
    Online Resource
    Dyslipidemia, inflammation, calcification, and adiposity in aortic stenosis: a genome-wide study
    Oxford University Press (OUP) ; 2023
    In:  European Heart Journal Vol. 44, No. 21 ( 2023-06-01), p. 1927-1939
    Details
    In: European Heart Journal, Oxford University Press (OUP), Vol. 44, No. 21 ( 2023-06-01), p. 1927-1939
    Abstract: Although highly heritable, the genetic etiology of calcific aortic stenosis (AS) remains incompletely understood. The aim of this study was to discover novel genetic contributors to AS and to integrate functional, expression, and cross-phenotype data to identify mechanisms of AS. Methods and results A genome-wide meta-analysis of 11.6 million variants in 10 cohorts involving 653 867 European ancestry participants (13 765 cases) was performed. Seventeen loci were associated with AS at P ≤ 5 × 10−8, of which 15 replicated in an independent cohort of 90 828 participants (7111 cases), including CELSR2–SORT1, NLRP6, and SMC2. A genetic risk score comprised of the index variants was associated with AS [odds ratio (OR) per standard deviation, 1.31; 95% confidence interval (CI), 1.26–1.35; P = 2.7 × 10−51] and aortic valve calcium (OR per standard deviation, 1.22; 95% CI, 1.08–1.37; P = 1.4 × 10−3), after adjustment for known risk factors. A phenome-wide association study indicated multiple associations with coronary artery disease, apolipoprotein B, and triglycerides. Mendelian randomization supported a causal role for apolipoprotein B-containing lipoprotein particles in AS (OR per g/L of apolipoprotein B, 3.85; 95% CI, 2.90–5.12; P = 2.1 × 10−20) and replicated previous findings of causality for lipoprotein(a) (OR per natural logarithm, 1.20; 95% CI, 1.17–1.23; P = 4.8 × 10−73) and body mass index (OR per kg/m2, 1.07; 95% CI, 1.05–1.9; P = 1.9 × 10−12). Colocalization analyses using the GTEx database identified a role for differential expression of the genes LPA, SORT1, ACTR2, NOTCH4, IL6R, and FADS. Conclusion Dyslipidemia, inflammation, calcification, and adiposity play important roles in the etiology of AS, implicating novel treatments and prevention strategies.
    Type of Medium: Online Resource
    ISSN: 0195-668X , 1522-9645
    URL: Article
    DOI: 10.1093/eurheartj/ehad142
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2001908-7
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 8
    Online Resource
    Online Resource
    BMI Is Causally Associated With Pulmonary Artery Pressure But Not Hemodynamic Evidence of Pulmonary Vascular Remodeling
    Elsevier BV ; 2021
    In:  Chest Vol. 159, No. 1 ( 2021-01), p. 302-310
    Details
    In: Chest, Elsevier BV, Vol. 159, No. 1 ( 2021-01), p. 302-310
    Type of Medium: Online Resource
    ISSN: 0012-3692
    URL: Article
    DOI: 10.1016/j.chest.2020.07.038
    RVK:
    XA 36340
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2007244-2
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 9
    Online Resource
    Online Resource
    Consensus Transcriptional Landscape of Human End‐Stage Heart Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of the American Heart Association Vol. 10, No. 7 ( 2021-04-06)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 10, No. 7 ( 2021-04-06)
    Abstract: Transcriptomic studies have contributed to fundamental knowledge of myocardial remodeling in human heart failure (HF). However, the key HF genes reported are often inconsistent between studies, and systematic efforts to integrate evidence from multiple patient cohorts are lacking. Here, we aimed to provide a framework for comprehensive comparison and analysis of publicly available data sets resulting in an unbiased consensus transcriptional signature of human end‐stage HF. Methods and Results We curated and uniformly processed 16 public transcriptomic studies of left ventricular samples from 263 healthy and 653 failing human hearts. First, we evaluated the degree of consistency between studies by using linear classifiers and overrepresentation analysis. Then, we meta‐analyzed the deregulation of 14 041 genes to extract a consensus signature of HF. Finally, to functionally characterize this signature, we estimated the activities of 343 transcription factors, 14 signaling pathways, and 182 micro RNAs, as well as the enrichment of 5998 biological processes. Machine learning approaches revealed conserved disease patterns across all studies independent of technical differences. These consistent molecular changes were prioritized with a meta‐analysis, functionally characterized and validated on external data. We provide all results in a free public resource ( https://saezlab.shinyapps.io/reheat/ ) and exemplified usage by deciphering fetal gene reprogramming and tracing the potential myocardial origin of the plasma proteome markers in patients with HF. Conclusions Even though technical and sampling variability confound the identification of differentially expressed genes in individual studies, we demonstrated that coordinated molecular responses during end‐stage HF are conserved. The presented resource is crucial to complement findings in independent studies and decipher fundamental changes in failing myocardium.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.120.019667
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2653953-6
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 10
    Online Resource
    Online Resource
    Exploration of an alternative to body mass index to characterize the relationship between height and weight for prediction of metabolic phenotypes and cardiovascular outcomes
    Wiley ; 2022
    In:  Obesity Science & Practice Vol. 8, No. 1 ( 2022-02), p. 124-130
    Details
    In: Obesity Science & Practice, Wiley, Vol. 8, No. 1 ( 2022-02), p. 124-130
    Abstract: Body mass index (BMI) is the most commonly used predictor of weight‐related comorbidities and outcomes. However, the presumed relationship between height and weight intrinsic to BMI may introduce bias with respect to prediction of clinical outcomes. A series of analyses comparing the performance of models representing weight and height as separate interacting variables to models using BMI were performed using Vanderbilt University Medical Center's deidentified electronic health records and landmark methodology. Methods Use of BMI or height‐weight interaction in prediction models for established weight‐related cardiometabolic traits and metabolic syndrome was evaluated. Specifically, prediction models for hypertension, diabetes mellitus, low high‐density lipoprotein, and elevated triglycerides, atrial fibrillation, coronary artery disease, heart failure, and peripheral artery disease were developed. Model performance was evaluated using likelihood ratio, R 2 , and Somers' Dxy rank correlation. Differences in model predictions were visualized using heat maps. Results Compared to BMI, the maximally flexible height‐weight interaction model demonstrated improved prediction, higher likelihood ratio, R 2 , and Somers' Dxy rank correlation, for event‐free probability for all outcomes. The degree of improvement to the prediction model differed based on the outcome and across the height and weight range. Conclusions Because alternative measures of body composition such as waist‐to‐hip ratio are not routinely collected in the clinic clinical risk models quantifying risk based on height and weight measurements alone are essential to improve practice. Compared to BMI, modeling height and weight as independent, interacting variables results in less bias and improved predictive accuracy for all tested traits. Considering an individual's height and weight opposed to BMI is a better method for quantifying individual disease risk.
    Type of Medium: Online Resource
    ISSN: 2055-2238 , 2055-2238
    URL: Issue
    URL: Article
    DOI: 10.1002/osp4.v8.1
    DOI: 10.1002/osp4.543
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2836381-4
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
Nothing or not found what you are looking for? Please check your search query or use the Interlibrary Loan Search.
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages