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  1. Article ; Online: Asthma and incident coronary heart disease: an observational and Mendelian randomisation study.

    Valencia-Hernández, Carlos A / Del Greco M, Fabiola / Sundaram, Varun / Portas, Laura / Minelli, Cosetta / Bloom, Chloe I

    The European respiratory journal

    2023  Volume 62, Issue 5

    Abstract: Background: Observational studies suggest asthma is a risk factor for coronary heart disease (CHD) and sex modifies the risk, but they may suffer from methodological limitations. To overcome these, we applied a "triangulation approach", where different ... ...

    Abstract Background: Observational studies suggest asthma is a risk factor for coronary heart disease (CHD) and sex modifies the risk, but they may suffer from methodological limitations. To overcome these, we applied a "triangulation approach", where different methodologies, with different potential biases, were leveraged to enhance confidence in findings.
    Methods: First, we conducted an observational study using UK medical records to match asthma patients 1:1, by age, sex and general practitioner (GP) practice, to the general population. We measured the association between asthma and incident CHD (myocardial infarction: hospitalisation/death) by applying minimal sufficient adjustment: model 1, smoking, body mass index, oral corticosteroids, atopy and deprivation; model 2, additionally adjusting for healthcare behaviour (GP consultation frequency). Second, we conducted a Mendelian randomisation (MR) study using data from the UK Biobank, Trans-National Asthma Genetic Consortium (TAGC) and Coronary Artery Disease Genome-wide Replication and Meta-analysis consortium (CARDIoGRAM). Using 64 asthma single nucleotide polymorphisms, the effect of asthma on CHD was estimated with inverse variance-weighted meta-analysis and methods that adjust for pleiotropy.
    Results: In our observational study (n=1 522 910), we found asthma was associated with 6% increased risk of CHD (model 1: HR 1.06, 95% CI 1.01-1.13); after accounting for healthcare behaviour, we found no association (model 2: HR 0.99, 95% CI 0.94-1.05). Asthma severity did not modify the association, but sex did (females: HR 1.11, 95% CI 1.01-1.21; males: HR 0.91, 95% CI 0.84-0.98). Our MR study (n=589 875) found no association between asthma and CHD (OR 1.01, 95% CI 0.98-1.04) and no modification by sex.
    Conclusions: Our findings suggest that asthma is not a risk factor for CHD. Previous studies may have suffered from detection bias or residual confounding.
    MeSH term(s) Female ; Humans ; Male ; Analysis of Variance ; Asthma/complications ; Asthma/epidemiology ; Asthma/genetics ; Coronary Artery Disease ; Genome-Wide Association Study ; Myocardial Infarction/epidemiology ; Polymorphism, Single Nucleotide ; Risk Factors ; Mendelian Randomization Analysis
    Language English
    Publishing date 2023-11-29
    Publishing country England
    Document type Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01788-2023
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  2. Article ; Online: A Mendelian randomization study investigating the causal role of inflammation on Parkinson's disease.

    Bottigliengo, Daniele / Foco, Luisa / Seibler, Philip / Klein, Christine / König, Inke R / Del Greco M, Fabiola

    Brain : a journal of neurology

    2022  Volume 145, Issue 10, Page(s) 3444–3453

    Abstract: There is increasing evidence for inflammation as a determinant in the pathogenesis of Parkinson's disease, but its role in parkinsonian neurodegeneration remains elusive. It is not clear whether inflammatory cascades are causes or consequences of ... ...

    Abstract There is increasing evidence for inflammation as a determinant in the pathogenesis of Parkinson's disease, but its role in parkinsonian neurodegeneration remains elusive. It is not clear whether inflammatory cascades are causes or consequences of dopamine neuron death. In the present study, we aim to perform an in-depth statistical investigation of the causal relationship between inflammation and Parkinson's disease using a two-sample Mendelian randomization design. Genetic instruments were selected using summary-level data from the largest genome-wide association studies to date (sample size ranging from 13 955 to 204 402 individuals) conducted on a European population for the following inflammation biomarkers: C-reactive protein, interleukin-6, interleukin 1 receptor antagonist and tumour necrosis factor α. Genetic association data on Parkinson's disease (56 306 cases and 1 417 791 controls) and age at onset of Parkinson's disease (28 568 cases) were obtained from the International Parkinson's Disease Genomics Consortium. On primary analysis, causal associations were estimated on sets of strong (P-value < 5 × 10-8; F-statistic > 10) and independent (linkage disequilibrium r2 < 0.001) genetic instruments using the inverse-variance weighted method. In sensitivity analysis, we estimated causal effects using robust Mendelian randomization methods and after removing pleiotropic genetic variants. Reverse causation was also explored. We repeated the analysis on different data sources for inflammatory biomarkers to check the consistency of the findings. In all the three data sources selected for interleukin-6, we found statistical evidence for an earlier age at onset of Parkinson's disease associated with increased interleukin-6 concentration [years difference per 1 log-unit increase = -2.364, 95% confidence interval (CI) = -4.789-0.060; years difference per 1 log-unit increase = -2.011, 95% CI = -3.706 to -0.317; years difference per 1 log-unit increase = -1.569, 95% CI = -2.891 to -0.247]. We did not observe any statistical evidence for causal effects of C-reactive protein, interleukin 1 receptor antagonist and tumour necrosis factor α on both Parkinson's disease and its age at onset. Results after excluding possible pleiotropic genetic variants were consistent with findings from primary analyses. When investigating reverse causation, we did not find evidence for a causal effect of Parkinson's disease or age at onset on any biomarkers of inflammation. We found evidence for a causal association between the onset of Parkinson's disease and interleukin-6. The findings of this study suggest that the pro-inflammatory activity of the interleukin-6 cytokine could be a determinant of prodromal Parkinson's disease.
    MeSH term(s) Humans ; Mendelian Randomization Analysis/methods ; Genome-Wide Association Study ; Parkinson Disease/genetics ; Tumor Necrosis Factor-alpha ; C-Reactive Protein/genetics ; Interleukin-6/genetics ; Inflammation/genetics ; Biomarkers ; Receptors, Interleukin-1/genetics ; Polymorphism, Single Nucleotide/genetics
    Chemical Substances Tumor Necrosis Factor-alpha ; C-Reactive Protein (9007-41-4) ; Interleukin-6 ; Biomarkers ; Receptors, Interleukin-1
    Language English
    Publishing date 2022-06-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awac193
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  3. Article: Molecular phenotypes of mitochondrial dysfunction in clinically non-manifesting heterozygous PRKN variant carriers.

    Castelo Rueda, Maria Paulina / Zanon, Alessandra / Gilmozzi, Valentina / Lavdas, Alexandros A / Raftopoulou, Athina / Delcambre, Sylvie / Del Greco M, Fabiola / Klein, Christine / Grünewald, Anne / Pramstaller, Peter P / Hicks, Andrew A / Pichler, Irene

    NPJ Parkinson's disease

    2023  Volume 9, Issue 1, Page(s) 65

    Abstract: Homozygous or compound heterozygous (biallelic) variants in PRKN are causal for PD with highly penetrant symptom expression, while the much more common heterozygous variants may predispose to PD with highly reduced penetrance, through altered ... ...

    Abstract Homozygous or compound heterozygous (biallelic) variants in PRKN are causal for PD with highly penetrant symptom expression, while the much more common heterozygous variants may predispose to PD with highly reduced penetrance, through altered mitochondrial function. In the presence of pathogenic heterozygous variants, it is therefore important to test for mitochondrial alteration in cells derived from variant carriers to establish potential presymptomatic molecular markers. We generated lymphoblasts (LCLs) and human induced pluripotent stem cell (hiPSC)-derived neurons from non-manifesting heterozygous PRKN variant carriers and tested them for mitochondrial functionality. In LCLs, we detected hyperactive mitochondrial respiration, and, although milder compared to a biallelic PRKN-PD patient, hiPSC-derived neurons of non-manifesting heterozygous variant carriers also displayed several phenotypes of altered mitochondrial function. Overall, we identified molecular phenotypes that might be used to monitor heterozygous PRKN variant carriers during the prodromal phase. Such markers might also be useful to identify individuals at greater risk of eventual disease development and for testing potential mitochondrial function-based neuroprotective therapies before neurodegeneration advances.
    Language English
    Publishing date 2023-04-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2819218-7
    ISSN 2373-8057
    ISSN 2373-8057
    DOI 10.1038/s41531-023-00499-9
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  4. Article ; Online: Evaluating the current state of Mendelian randomization studies: a protocol for a systematic review on methodological and clinical aspects using neurodegenerative disorders as outcome.

    Grover, Sandeep / Del Greco M, Fabiola / König, Inke R

    Systematic reviews

    2018  Volume 7, Issue 1, Page(s) 145

    Abstract: Background: Mendelian randomization (MR) is fast becoming a popular method to judge causality from routinely conducted observational studies. However, stringent underlying statistical assumptions, missing biological information, and high sample size ... ...

    Abstract Background: Mendelian randomization (MR) is fast becoming a popular method to judge causality from routinely conducted observational studies. However, stringent underlying statistical assumptions, missing biological information, and high sample size requirement might make it prone to misuse. Furthermore, rapidly updating methodologies and increasingly available datasets to researchers are making the interpretations of heterogeneous results even more complicated. In this protocol, we provide our design for a multifaceted systematic review on MR studies using neurodegenerative disease as an example outcome. The planned systematic review which has already passed the pilot stage will help to develop an in-depth understanding of how various MR methods have been applied, what has been achieved, and what can be done in future for to arrive at true causal risk factors.
    Methods: During the pilot phase of this systematic review, several versions of questionnaires and frequent consultations between reviewers helped us to finalize a comprehensive list of questions. This will be used to extract information on systematically searched MR articles investigating causality underlying neurodegenerative diseases. A literature search of the electronic databases (Embase, MEDLINE, Web of Science, Scopus, and databases listed in the Cochrane library) will be conducted. The search strategy will include terms related to MR and the spectrum of neurodegenerative diseases. Two independent reviewers will screen the studies, and three will extract the data. The included studies will be further judged by two reviewers for accuracy and completeness of available information. We will perform descriptive and quantitative synthesis using sensitivity analyses of causal association by study design, selection of genetic instrument, validity of MR assumptions, MR method, and sensitivity analysis based on exclusion of potential pleiotropic variants. The quality of conduct as well as quality of reporting in the included studies will be assessed and reported. A meta-analysis will be conducted, if effect estimates on identical genetic instruments are available for both exposure and outcome in the studies using data from participants from ethnically similar populations.
    Discussion: This systematic review protocol utilizes a unique comprehensive data abstraction tool based on recent methodological advancements in the field of MR. The planned systematic review will further integrate information on methodological details with clinical findings in latest available large-scale genome-wide association study datasets. Our findings aim to help raising awareness and promoting transparent reporting of MR studies.
    Systematic review registration: PROSPERO CRD42018091434 .
    MeSH term(s) Causality ; Genome-Wide Association Study/methods ; Humans ; Mendelian Randomization Analysis/methods ; Neurodegenerative Diseases/diagnosis ; Research Design/standards ; Risk Factors ; Systematic Reviews as Topic
    Language English
    Publishing date 2018-09-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2662257-9
    ISSN 2046-4053 ; 2046-4053
    ISSN (online) 2046-4053
    ISSN 2046-4053
    DOI 10.1186/s13643-018-0809-3
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  5. Article ; Online: The use of two-sample methods for Mendelian randomization analyses on single large datasets.

    Minelli, Cosetta / Del Greco M, Fabiola / van der Plaat, Diana A / Bowden, Jack / Sheehan, Nuala A / Thompson, John

    International journal of epidemiology

    2021  Volume 50, Issue 5, Page(s) 1651–1659

    Abstract: Background: With genome-wide association data for many exposures and outcomes now available from large biobanks, one-sample Mendelian randomization (MR) is increasingly used to investigate causal relationships. Many robust MR methods are available to ... ...

    Abstract Background: With genome-wide association data for many exposures and outcomes now available from large biobanks, one-sample Mendelian randomization (MR) is increasingly used to investigate causal relationships. Many robust MR methods are available to address pleiotropy, but these assume independence between the gene-exposure and gene-outcome association estimates. Unlike in two-sample MR, in one-sample MR the two estimates are obtained from the same individuals, and the assumption of independence does not hold in the presence of confounding.
    Methods: With simulations mimicking a typical study in UK Biobank, we assessed the performance, in terms of bias and precision of the MR estimate, of the fixed-effect and (multiplicative) random-effects meta-analysis method, weighted median estimator, weighted mode estimator and MR-Egger regression, used in both one-sample and two-sample data. We considered scenarios differing by the: presence/absence of a true causal effect; amount of confounding; and presence and type of pleiotropy (none, balanced or directional).
    Results: Even in the presence of substantial correlation due to confounding, all two-sample methods used in one-sample MR performed similarly to when used in two-sample MR, except for MR-Egger which resulted in bias reflecting direction and magnitude of the confounding. Such bias was much reduced in the presence of very high variability in instrument strength across variants (IGX2 of 97%).
    Conclusions: Two-sample MR methods can be safely used for one-sample MR performed within large biobanks, expect for MR-Egger. MR-Egger is not recommended for one-sample MR unless the correlation between the gene-exposure and gene-outcome estimates due to confounding can be kept low, or the variability in instrument strength is very high.
    MeSH term(s) Bias ; Causality ; Genome-Wide Association Study ; Humans ; Mendelian Randomization Analysis ; Polymorphism, Single Nucleotide ; Research Design
    Language English
    Publishing date 2021-04-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 187909-1
    ISSN 1464-3685 ; 0300-5771
    ISSN (online) 1464-3685
    ISSN 0300-5771
    DOI 10.1093/ije/dyab084
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  6. Article ; Online: The causal relationship between gastro-oesophageal reflux disease and idiopathic pulmonary fibrosis: a bidirectional two-sample Mendelian randomisation study.

    Reynolds, Carl J / Del Greco M, Fabiola / Allen, Richard J / Flores, Carlos / Jenkins, R Gisli / Maher, Toby M / Molyneaux, Philip L / Noth, Imre / Oldham, Justin M / Wain, Louise V / An, Jiyuan / Ong, Jue-Sheng / MacGregor, Stuart / Yates, Tom A / Cullinan, Paul / Minelli, Cosetta

    The European respiratory journal

    2023  Volume 61, Issue 5

    Abstract: Background: Gastro-oesophageal reflux disease (GORD) is associated with idiopathic pulmonary fibrosis (IPF) in observational studies. It is not known if this association arises because GORD causes IPF or because IPF causes GORD, or because of ... ...

    Abstract Background: Gastro-oesophageal reflux disease (GORD) is associated with idiopathic pulmonary fibrosis (IPF) in observational studies. It is not known if this association arises because GORD causes IPF or because IPF causes GORD, or because of confounding by factors, such as smoking, associated with both GORD and IPF. We used bidirectional Mendelian randomisation (MR), where genetic variants are used as instrumental variables to address issues of confounding and reverse causation, to examine how, if at all, GORD and IPF are causally related.
    Methods: A bidirectional two-sample MR was performed to estimate the causal effect of GORD on IPF risk and of IPF on GORD risk, using genetic data from the largest GORD (78 707 cases and 288 734 controls) and IPF (4125 cases and 20 464 controls) genome-wide association meta-analyses currently available.
    Results: GORD increased the risk of IPF, with an OR of 1.6 (95% CI 1.04-2.49; p=0.032). There was no evidence of a causal effect of IPF on the risk of GORD, with an OR of 0.999 (95% CI 0.997-1.000; p=0.245).
    Conclusions: We found that GORD increases the risk of IPF, but found no evidence that IPF increases the risk of GORD. GORD should be considered in future studies of IPF risk and interest in it as a potential therapeutic target should be renewed. The mechanisms underlying the effect of GORD on IPF should also be investigated.
    MeSH term(s) Humans ; Gastroesophageal Reflux/complications ; Gastroesophageal Reflux/genetics ; Gastroesophageal Reflux/drug therapy ; Genome-Wide Association Study ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/complications
    Language English
    Publishing date 2023-05-25
    Publishing country England
    Document type Journal Article ; Meta-Analysis
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01585-2022
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  7. Article: Whole Exome Sequencing Enhanced Imputation Identifies 85 Metabolite Associations in the Alpine CHRIS Cohort.

    König, Eva / Rainer, Johannes / Hernandes, Vinicius Verri / Paglia, Giuseppe / Del Greco M, Fabiola / Bottigliengo, Daniele / Yin, Xianyong / Chan, Lap Sum / Teumer, Alexander / Pramstaller, Peter P / Locke, Adam E / Fuchsberger, Christian

    Metabolites

    2022  Volume 12, Issue 7

    Abstract: Metabolites are intermediates or end products of biochemical processes involved in both health and disease. Here, we take advantage of the well-characterized Cooperative Health Research in South Tyrol (CHRIS) study to perform an exome-wide association ... ...

    Abstract Metabolites are intermediates or end products of biochemical processes involved in both health and disease. Here, we take advantage of the well-characterized Cooperative Health Research in South Tyrol (CHRIS) study to perform an exome-wide association study (ExWAS) on absolute concentrations of 175 metabolites in 3294 individuals. To increase power, we imputed the identified variants into an additional 2211 genotyped individuals of CHRIS. In the resulting dataset of 5505 individuals, we identified 85 single-variant genetic associations, of which 39 have not been reported previously. Fifteen associations emerged at ten variants with >5-fold enrichment in CHRIS compared to non-Finnish Europeans reported in the gnomAD database. For example, the CHRIS-enriched ETFDH stop gain variant p.Trp286Ter (rs1235904433-hexanoylcarnitine) and the MCCC2 stop lost variant p.Ter564GlnextTer3 (rs751970792-carnitine) have been found in patients with glutaric acidemia type II and 3-methylcrotonylglycinuria, respectively, but the loci have not been associated with the respective metabolites in a genome-wide association study (GWAS) previously. We further identified three gene-trait associations, where multiple rare variants contribute to the signal. These results not only provide further evidence for previously described associations, but also describe novel genes and mechanisms for diseases and disease-related traits.
    Language English
    Publishing date 2022-06-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662251-8
    ISSN 2218-1989
    ISSN 2218-1989
    DOI 10.3390/metabo12070604
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  8. Article ; Online: Thyroid Function Affects the Risk of Stroke via Atrial Fibrillation: A Mendelian Randomization Study.

    Marouli, Eirini / Kus, Aleksander / Del Greco M, Fabiola / Chaker, Layal / Peeters, Robin / Teumer, Alexander / Deloukas, Panos / Medici, Marco

    The Journal of clinical endocrinology and metabolism

    2020  Volume 105, Issue 8

    Abstract: Context: Observational studies suggest that variations in normal range thyroid function are associated with cardiovascular diseases. However, it remains to be determined whether these associations are causal or not.: Objective: To test whether ... ...

    Abstract Context: Observational studies suggest that variations in normal range thyroid function are associated with cardiovascular diseases. However, it remains to be determined whether these associations are causal or not.
    Objective: To test whether genetically determined variation in normal range thyroid function is causally associated with the risk of stroke and coronary artery disease (CAD) and investigate via which pathways these relations may be mediated.
    Design, setting, and participants: Mendelian randomization analyses for stroke and CAD using genetic instruments associated with normal range thyrotropin (TSH) and free thyroxine levels or Hashimoto's thyroiditis and Graves' disease. The potential mediating role of known stroke and CAD risk factors was examined. Publicly available summary statistics data were used.
    Main outcome measures: Stroke or CAD risk per genetically predicted increase in TSH or FT4 levels.
    Results: A 1 standard deviation increase in TSH was associated with a 5% decrease in the risk of stroke (odds ratio [OR], 0.95; 95% confidence interval [CI], 0.91-0.99; P = 0.008). Multivariable MR analyses indicated that this effect is mainly mediated via atrial fibrillation. MR analyses did not show a causal association between normal range thyroid function and CAD. Secondary analyses showed a causal relationship between Hashimoto's thyroiditis and a 7% increased risk of CAD (OR, 1.07; 95% CI, 1.01-1.13; P = 0.026), which was mainly mediated via body mass index.
    Conclusion: These results provide important new insights into the causal relationships and mediating pathways between thyroid function, stroke, and CAD. We identify variation in normal range thyroid function and Hashimoto's thyroiditis as risk factors for stroke and CAD, respectively.
    MeSH term(s) Adult ; Atrial Fibrillation/epidemiology ; Atrial Fibrillation/genetics ; Body Mass Index ; Coronary Artery Disease/epidemiology ; Coronary Artery Disease/genetics ; Datasets as Topic ; Female ; Graves Disease/blood ; Graves Disease/complications ; Graves Disease/diagnosis ; Graves Disease/genetics ; Hashimoto Disease/blood ; Hashimoto Disease/complications ; Hashimoto Disease/diagnosis ; Hashimoto Disease/genetics ; Humans ; Male ; Mendelian Randomization Analysis ; Middle Aged ; Polymorphism, Single Nucleotide ; Reference Values ; Risk Factors ; Stroke/epidemiology ; Stroke/genetics ; Thyroid Function Tests ; Thyroid Gland/physiopathology ; Thyrotropin/blood ; Thyroxine/blood
    Chemical Substances Thyrotropin (9002-71-5) ; Thyroxine (Q51BO43MG4)
    Language English
    Publishing date 2020-05-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/clinem/dgaa239
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  9. Article ; Online: Mendelian Randomization using Public Data from Genetic Consortia.

    Thompson, John R / Minelli, Cosetta / Del Greco M, Fabiola

    The international journal of biostatistics

    2016  Volume 12, Issue 2

    Abstract: Mendelian randomization (MR) is a technique that seeks to establish causation between an exposure and an outcome using observational data. It is an instrumental variable analysis in which genetic variants are used as the instruments. Many consortia have ... ...

    Abstract Mendelian randomization (MR) is a technique that seeks to establish causation between an exposure and an outcome using observational data. It is an instrumental variable analysis in which genetic variants are used as the instruments. Many consortia have meta-analysed genome-wide associations between variants and specific traits and made their results publicly available. Using such data, it is possible to derive genetic risk scores for one trait and to deduce the association of that same risk score with a second trait. The properties of this approach are investigated by simulation and by evaluating the potentially causal effect of birth weight on adult glucose level. In such analyses, it is important to decide whether one is interested in the risk score based on a set of estimated regression coefficients or the score based on the true underlying coefficients. MR is primarily concerned with the latter. Methods designed for the former question will under-estimate the variance if used for MR. This variance can be corrected but it needs to be done with care to avoid introducing bias. MR based on public data sources is useful and easy to perform, but care must be taken to avoid false precision or bias.
    Language English
    Publishing date 2016-11-01
    Publishing country Germany
    Document type Journal Article
    ISSN 1557-4679
    ISSN (online) 1557-4679
    DOI 10.1515/ijb-2015-0074
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  10. Article ; Online: Mendelian Randomization as an Approach to Assess Causality Using Observational Data.

    Sekula, Peggy / Del Greco M, Fabiola / Pattaro, Cristian / Köttgen, Anna

    Journal of the American Society of Nephrology : JASN

    2016  Volume 27, Issue 11, Page(s) 3253–3265

    Abstract: Mendelian randomization refers to an analytic approach to assess the causality of an observed association between a modifiable exposure or risk factor and a clinically relevant outcome. It presents a valuable tool, especially when randomized controlled ... ...

    Abstract Mendelian randomization refers to an analytic approach to assess the causality of an observed association between a modifiable exposure or risk factor and a clinically relevant outcome. It presents a valuable tool, especially when randomized controlled trials to examine causality are not feasible and observational studies provide biased associations because of confounding or reverse causality. These issues are addressed by using genetic variants as instrumental variables for the tested exposure: the alleles of this exposure-associated genetic variant are randomly allocated and not subject to reverse causation. This, together with the wide availability of published genetic associations to screen for suitable genetic instrumental variables make Mendelian randomization a time- and cost-efficient approach and contribute to its increasing popularity for assessing and screening for potentially causal associations. An observed association between the genetic instrumental variable and the outcome supports the hypothesis that the exposure in question is causally related to the outcome. This review provides an overview of the Mendelian randomization method, addresses assumptions and implications, and includes illustrative examples. We also discuss special issues in nephrology, such as inverse risk factor associations in advanced disease, and outline opportunities to design Mendelian randomization studies around kidney function and disease.
    MeSH term(s) Cardiovascular Diseases/genetics ; Causality ; Humans ; Mendelian Randomization Analysis ; Observational Studies as Topic ; Renal Insufficiency, Chronic/genetics
    Language English
    Publishing date 2016-08-02
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2016010098
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