Imperial College London

DrDipenderGill

Faculty of MedicineSchool of Public Health

Clinical Research Fellow
 
 
 
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Contact

 

+44 (0)7904 843 810dipender.gill

 
 
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Location

 

School of a Public HealthMedical SchoolSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
to

243 results found

Gill D, Pan Y, Lash JP, Kelly TNet al., 2022, Revisiting the Effects of Blood Pressure on Kidney Function: New Insights From a Mendelian Randomization Analysis, HYPERTENSION, Vol: 79, Pages: 2682-2684, ISSN: 0194-911X

Journal article

Huang J, Su B, Karhunen V, Gill D, Zuber V, Ahola-Olli A, Palaniswamy S, Auvinen J, Herzig K-H, Keinänen-Kiukaanniemi S, Salmi M, Jalkanen S, Lehtimäki T, Salomaa V, Raitakari OT, Matthews PM, Elliott P, Tsilidis KK, Jarvelin M-R, Tzoulaki I, Dehghan Aet al., 2022, Inflammatory Diseases, Inflammatory Biomarkers, and Alzheimer Disease: An Observational Analysis and Mendelian Randomization., Neurology

OBJECTIVES: Whether chronic autoimmune inflammatory diseases causally affect the risk of AD is controversial. We characterised the relationship between inflammatory diseases and the risk of AD and explore the role of circulating inflammatory biomarkers in the relationships between inflammatory diseases and AD. METHODS: We performed observational analyses for chronic autoimmune inflammatory diseases and risk of AD using data from 2,047,513 participants identified in the UK Clinical Practice Research Datalink (CPRD). Using data of a total of more than 1,100,000 individuals from 15 large scale genome-wide association study (GWAS) datasets, we performed two-sample Mendelian randomisation (MR) to investigate the relationships between chronic autoimmune inflammatory diseases, circulating inflammatory biomarker levels, and risk of AD. RESULTS: Cox regression models using CPRD data showed that overall incidence of AD was higher among patients with inflammatory bowel disease (IBD) (hazard ratio (HR)=1.17; 95%CI 1.15 to 1.19; P-value=2.1×10-4), other inflammatory polyarthropathies & systematic connective tissue disorders (OID) (HR=1.13; 95%CI 1.12 to 1.14; P-value=8.6×10-5), psoriasis (HR=1.13; 95%CI 1.10 to 1.16; P-value=2.6×10-4), rheumatoid arthritis (RA) (HR=1.08; 95%CI 1.06 to 1.11; P-value=4.0×10-4), and multiple sclerosis (MS) (HR=1.06; 95%CI 1.04 to 1.07; P-value=2.8×10-4) compared to the age (± 5 years) and sex-matched comparison groups free from all inflammatory diseases under investigation. Bidirectional MR analysis identified relationships between chronic autoimmune inflammatory diseases and circulating inflammatory biomarkers. Particularly, circulating monokine induced by gamma interferon (MIG) level was suggestively associated with a higher risk of AD (odds ratio from inverse variance weighted (ORIVW)=1.23; 95%CI 1.06 to 1.42; PIVW=0.007), and lower risk of Crohn's disease (ORIVW=0.73; 95%CI -0.62, 0.86; PIVW=1.3×10

Journal article

Gill D, 2022, The effects of metabolic traits, lifestyle factors and pharmacological interventions on liver fat: a Mendelian randomization study, BMJ Medicine, ISSN: 2754-0413

Journal article

Chalitsios CV, Georgiou A, Bouras E, Evangelou E, Gill D, Tsilidis KK, Tzoulaki Iet al., 2022, Investigating modifiable pathways in psoriasis: a Mendelian randomization study., J Am Acad Dermatol

BACKGROUND: Potentially modifiable risk factors have previously been investigated only in conventional observational studies. OBJECTIVE: To assess whether genetically predicted exposures to modifiable factors are associated with the risk of psoriasis. METHODS: 2-sample Mendelian randomization (MR) analysis. RESULTS: An increased risk of psoriasis was noted for genetically predicted lifetime smoking index (ORMR-IVW = 2.11; 95% CI 1.28 to 3.51), childhood (OR MR-IVW = 1.40; 95% CI 1.14 to 1.71) and adult BMI (OR MR-IVW = 1.63; 95% CI 1.32 to 2), waist (ORIVW = 1.86; 95% CI 1.31 to 2.64), and hip circumference (OR MR-IVW = 1.55; 95% CI 1.15 to 2.07). Protective association was also reported between genetically predicted longer sleep duration (OR MR-IVW = 0.56; 95% CI 0.37 to 0.84) and increased years of education (OR MR-IVW = 0.78; 95% CI 0.62 to 0.98). This effect of education persisted in multivariable MR after adjusting for genetic predictors of smoking and adult BMI (ORMVMR-IVW = 0.72; 95%CI 0.56-0.92). LIMITATIONS: It was not possible to stratify for psoriasis severity. CONCLUSION: Smoking cessation and prevention of obesity are important strategies for decreasing the incidence of psoriasis. Similarly, targeting education inequality is expected to lead further to reductions in cases of psoriasis.

Journal article

Bakker MK, van Straten T, Chong M, Paré G, Gill D, Ruigrok YMet al., 2022, Anti-Epileptic Drug Target Perturbation and Intracranial Aneurysm Risk: Mendelian Randomization and Colocalization Study., Stroke

BACKGROUND: In a genome-wide association study of intracranial aneurysms (IA), enrichment was found between genes associated with IA and genes encoding targets of effective anti-epileptic drugs. Our aim was to assess if this pleiotropy is driven by shared disease mechanisms that could potentially highlight a treatment strategy for IA. METHODS: Using 2-sample inverse-variance weighted Mendelian randomization and genetic colocalization analyses we assessed: (1) if epilepsy liability in general affects IA risk, and (2) whether changes in gene- and protein-expression levels of anti-epileptic drug targets in blood and arterial tissue may causally affect IA risk. RESULTS: We found no overall effect of epilepsy liability on IA. Expression of 21 genes and 13 proteins corresponding to anti-epileptic drug targets supported a causal effect (P<0.05) on IA risk. Of those genes and proteins, genetic variants affecting CNNM2 levels showed strong evidence for colocalization with IA risk (posterior probability>70%). Higher CNNM2 levels in arterial tissue were associated with increased IA risk (odds ratio, 3.02; [95% CI, 2.32-3.94]; P=3.39×10-16). CNNM2 expression was best proxied by rs11191580. The magnitude of the effect of this variant was greater than would be expected if systemic blood pressure was the sole IA-causing mechanism in this locus. CONCLUSIONS: CNNM2 is a driver of the pleiotropy between IA and anti-epileptic drug targets. Administration of the anti-epileptic drugs phenytoin, valproic acid, or carbamazepine may be expected to decrease CNNM2 levels and therefore subsequently decrease IA risk. CNNM2 is therefore an important target to investigate further for its role in the pathogenesis of IA.

Journal article

Xie J, Prats-Uribe A, Maranon MG, Strauss VY, Gill D, Prieto-Alhambra Det al., 2022, Genetic risk and incident venous thromboembolism in middle-aged and older adults following COVID-19 vaccination, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, ISSN: 1538-7933

Journal article

Yuan S, Karhunen V, Larsson S, Gill Det al., 2022, Anthropometric Traits and Risk of Mitral Valve Prolapse: A Mendelian Randomization Study, CIRCULATION-GENOMIC AND PRECISION MEDICINE, Vol: 15, Pages: 473-475, ISSN: 2574-8300

Journal article

Zhao SS, Rajasundaram S, Karhunen V, Alam U, Gill Det al., 2022, Sodium-glucose cotransporter 1 inhibition and gout: Mendelian randomisation study, SEMINARS IN ARTHRITIS AND RHEUMATISM, Vol: 56, ISSN: 0049-0172

Journal article

Ryan DK, Karhunen V, Su B, Traylor M, Richardson TG, Burgess S, Tzoulaki I, Gill Det al., 2022, Genetic evidence for protective effects of angiotensin converting enzyme against Alzheimer's disease but not other neurodegenerative diseases in European populations, Neurology Genetics, Vol: 8, ISSN: 2376-7839

Background and Objectives: Angiotensin-converting enzyme (ACE) inhibitors are a commonly prescribed class of medication used to treat heart failure, hypertension, and chronic kidney disease. However, previous observational studies have shown conflicting directions of associations between ACE inhibitors and risk of Alzheimer disease. Genetic evidence has supported a protective effect of cerebral ACE against Alzheimer disease (AD). However, it is unclear whether this effect is mediated through blood pressure and extends to other neurodegenerative diseases.Methods: We performed genetic colocalization investigating an effect of cortical ACE expression on AD risk in people of European ancestry. We further investigated whether any effect of ACE expression on AD risk is mediated through changes in blood pressure and whether effects extend to Parkinson disease, small-vessel disease, or cognitive function in a Mendelian randomization paradigm.Results: There was genetic evidence supporting a protective effect of cortical ACE expression on AD risk in people of European ancestry. Although higher cortical ACE expression was associated with higher blood pressure, there was no strong evidence to support that its association with AD was mediated through blood pressure nor that ACE expression affected risk of other neurodegenerative traits.Discussion: Genetic evidence supports protective effects of cerebral ACE expression on AD, but not other neurodegenerative outcomes in people of European ancestry. Further work is required to investigate whether therapeutic inhibition of ACE increases risk of Alzheimer disease.

Journal article

Zhang Z, Wang M, Gill D, Liu Xet al., 2022, Genetically Predicted Smoking and Alcohol Consumption and Functional Outcome After Ischemic Stroke., Neurology

OBJECTIVE: Smoking and alcohol consumption have been adversely associated with post-stroke outcome in traditional epidemiological studies. The present study explored the association of genetically predicted smoking and alcohol consumption on post-stroke outcomes using the Mendelian randomization (MR) framework. METHODS: Instrumental variables for smoking initiation and alcohol consumption were selected from a genome-wide association study (GWAS) data of European ancestry individuals. Summary-level data for functional outcome after ischemic stroke was obtained from the Genetics of Ischemic Stroke Functional Outcome network study of European ancestry patients. The univariable and multivariable inverse-variance weighted MR methods were performed to obtain the causal estimates. The weighted median, MR-Robust Adjusted Profile Score and MR-Egger regression approaches were adopted as sensitivity analyses. Q and I 2 statistics were used to evaluate heterogeneity in MR estimates across variants. RESULTS: Genetic predisposition to smoking initiation was associated with worse functional outcome after ischemic stroke in univariable IVW MR analysis (OR = 1.48; 95% CI: 1.08-2.01, P = 0.013). This association remained significant when adjusting for genetically predicted alcohol consumption in multivariable MR analyses (OR = 1.56; 95% CI: 1.05-2.32, P = 0.027). Genetically predicted alcohol consumption was not associated with functional outcome after ischemic stroke (P > 0.05). Sensitivity analyses with other approaches and in analyses restricted to models without adjustment for baseline stroke severity produced similar results, and no evidence of heterogeneity in MR estimates between variants was detected (P > 0.05). CONCLUSION: Our results provide genetic support for a causal association of smoking with worse functional outcome after ischemic stroke, and have important implications for post stroke recovery. Smoking cessation and avoidance should be promoted in ischemic stro

Journal article

Ardissino M, Rajasundaram S, Reddy R, Ng F, Gill Det al., 2022, Safety of beta-blocker and calcium channel blocker antihypertensive drugs in pregnancy: a Mendelian randomization study, BMC Medicine, Vol: 20, ISSN: 1741-7015

Background: Beta-blocker (BB) and calcium channel blocker (CCB)antihypertensive drugs are commonly used in pregnancy. However, data on theirrelative impact on maternal and fetal outcomes are limited. We leveraged geneticvariants mimicking BB and CCB antihypertensive drugs to investigate their effects onrisk of pre-eclampsia, gestational diabetes and birthweight using the Mendelianrandomization paradigm.Methods: Genetic association estimates for systolic blood pressure (SBP) wereextracted from summary data of a genome-wide association study (GWAS) on757,601 participants. Uncorrelated single-nucleotide polymorphisms (SNPs)associated with SBP (p<5x10-8) in BB and CCB drug target gene regions wereselected as proxies for drug target perturbation. Genetic association estimates forthe outcomes were extracted from GWASs on 4,743 cases and 136,325 controls(women without a hypertensive disorder in pregnancy) for pre-eclampsia oreclampsia, 7,676 cases and 130,424 controls (women without any pregnancy-relatedmorbidity) for gestational diabetes, and 155,202 women (who have given birth atleast once) for birthweight of the first child. All studies were in European ancestrypopulations. Mendelian randomization estimates were generated using the twosample inverse-variance weighted model.Results: Although not reaching the conventional threshold for statistical significance,genetically-proxied BB was associated with reduced risk of pre-eclampsia (OR per10mmHg SBP reduction 0.27, 95%CI 0.06-1.19, p=0.08) and increased risk ofgestational diabetes (OR per 10mmHg SBP reduction 2.01, 95%CI 0.91-4.42,p=0.08), and significantly associated with lower birthweight of first child (beta per 10mmHg SBP reduction -0.27, 95%CI -0.39 to -0.15, p=1.90x10-5). Geneticallyproxied CCB was associated with reduced risk of pre-eclampsia and eclampsia (OR0.62, 95%CI 0.43-0.89, p=9.33x10-3), and was not associated with gestationaldiabetes (OR 1.05, 95% CI 0.76-1.45, p=0.76) or changes in birthweight of first

Journal article

Giontella A, Lotta LA, Baras A, Minuz P, Gill D, Melander O, Fava Cet al., 2022, Calcium, Its Regulatory Hormones, and Their Causal Role on Blood Pressure: A Two-Sample Mendelian Randomization study, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, ISSN: 0021-972X

Journal article

Cohen JB, Mitchell GF, Gill D, Burgess S, Rahman M, Hanff T, Ramachandran VS, Mutalik K, Townsend RR, Chirinos JAet al., 2022, Arterial Stiffness and Diabetes Risk in Framingham Heart Study and UK Biobank, CIRCULATION RESEARCH, Vol: 131, Pages: 545-554, ISSN: 0009-7330

Journal article

Xie J, Strauss VY, Prats-Uribe A, Gill D, Paredes R, Prieto-Alhambra Det al., 2022, Genetic risk and incident venous thromboembolism in middle-aged and older adults following COVID-19 vaccination, PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Vol: 31, Pages: 118-118, ISSN: 1053-8569

Journal article

Xie J, Prats-Uribe A, Feng Q, Wang Y, Gill D, Paredes R, Prieto-Alhambra Det al., 2022, Clinical and genetic risk factors for acute incident venous Thromboembolism in ambulatory patients with COVID-19., JAMA Internal Medicine, Vol: 182, Pages: 1063-1070, ISSN: 2168-6106

Importance: The risk of venous thromboembolism (VTE) in ambulatory COVID-19 is controversial. In addition, the association of vaccination with COVID-19-related VTE and relevant clinical and genetic risk factors remain to be elucidated. Objective: To quantify the association between ambulatory COVID-19 and short-term risk of VTE, study the potential protective role of vaccination, and investigate clinical and genetic risk factors for post-COVID-19 VTE. Design, Setting, and Participants: This population-based cohort study of patients with COVID-19 from UK Biobank included participants with SARS-CoV-2 infection that was confirmed by a positive polymerase chain test reaction result between March 1, 2020, and September 3, 2021, who were then propensity score matched to COVID-19-naive people during the same period. Participants with a history of VTE who used antithrombotic drugs (1 year before index dates) or tested positive in hospital were excluded. Exposures: First infection with SARS-CoV-2, age, sex, ethnicity, socioeconomic status, obesity, vaccination status, and inherited thrombophilia. Main Outcomes and Measures: The primary outcome was a composite VTE, including deep vein thrombosis or pulmonary embolism, which occurred 30 days after the infection. Hazard ratios (HRs) with 95% CIs were calculated using cause-specific Cox models. Results: In 18 818 outpatients with COVID-19 (10 580 women [56.2%]; mean [SD] age, 64.3 [8.0] years) and 93 179 matched uninfected participants (52 177 women [56.0%]; mean [SD] age, 64.3 [7.9] years), the infection was associated with an increased risk of VTE in 30 days (incidence rate of 50.99 and 2.37 per 1000 person-years for infected and uninfected people, respectively; HR, 21.42; 95% CI, 12.63-36.31). However, risk was substantially attenuated among the fully vaccinated (HR, 5.95; 95% CI, 1.82-19.5; interaction P = .02). In patients with COVID-19, older age, male sex, and obesity were independently associated with highe

Journal article

Gill D, Vujkovic M, 2022, The Potential of Genetic Data for Prioritizing Drug Repurposing Efforts, NEUROLOGY, Vol: 99, Pages: 267-268, ISSN: 0028-3878

Journal article

Georgakis MK, Malik R, Richardson TG, Howson JMM, Anderson CD, Burgess S, Hovingh GK, Dichgans M, Gill Det al., 2022, Associations of genetically predicted IL-6 signaling with cardiovascular disease risk across population subgroups, BMC MEDICINE, Vol: 20, ISSN: 1741-7015

Journal article

Nhu NL, Tran TQB, Lip S, McCallum L, McClure J, Dominiczak AF, Gill D, Padmanabhan Set al., 2022, Unravelling the Distinct Effects of Systolic and Diastolic Blood Pressure Using Mendelian Randomisation, GENES, Vol: 13

Journal article

Woolf B, Gill D, 2022, TwoStepCisMR: A novel method and R package for attenuating bias in <i>cis</i>-MR

<jats:title>Abstract</jats:title><jats:p>Mendelian randomisation (MR) is an increasingly popular method for strengthening causal inference in epidemiological studies. cis-MR in particular uses genetic variants in the gene region for a genetic proxy of a drug target to provide quasi-experimental evidence for drug efficacy. A major problem for this framework is when the causal variant is correlated to another variant which effects the outcome of interest (confounding through linkage disequilibrium). Methods for correcting bias such as multivariable MR struggle in a cis setting because of the high correlation among genetic variants. Here, we therefore present an alternative method for attenuating bias which does not suffer from this problem. We have additionally developed a simple R package to facilitate the implementation of the method.</jats:p>

Journal article

Karageorgiou V, Gill D, Bowden J, Zuber Vet al., 2022, Sparse Dimensionality Reduction Approaches in Mendelian Randomization with highly correlated exposures

<jats:title>ABSTRACT</jats:title><jats:p>Multivariable Mendelian randomization (MVMR) is an instrumental variable technique that generalizes the MR framework for multiple exposures. Framed as a linear regression problem, it is subject to the pitfall of multi-collinearity. The bias and efficiency of MVMR estimates thus depends on the correlation of exposures. Dimensionality reduction techniques such as principal component analysis (PCA) provide transformations of all the included variables that are effectively uncorrelated. We propose the use of sparse PCA (sPCA) algorithms that create principal components of subsets of the exposures and may provide more interpretable and reliable MR estimates. The approach consists of three steps. We first apply a sparse dimension reduction method and transform the variant-exposure summary statistics to principal components. We then choose a subset of the principal components based on data-driven cutoffs, and estimate their strength as instruments with an adjusted <jats:italic>F</jats:italic>-statistic. Finally, we perform MR with these transformed exposures. This pipeline is demonstrated in a simulation study of highly correlated exposures and an applied example using summary data from a genome-wide association study of 118 highly correlated lipid metabolites. As a positive control, we tested the causal associations of the transformed exposures on CHD. Compared to the conventional inverse-variance weighted MVMR method and a weak-instrument robust MVMR method (MR GRAPPLE), sparse component analysis achieved a superior balance of sparsity and biologically insightful grouping of the lipid traits.</jats:p><jats:sec><jats:title>Key Messages</jats:title><jats:list list-type="bullet"><jats:list-item><jats:p>In multivariable MR, investigation of multiple highly correlated exposures can hinder the efficiency of the estimators and mask true associations.</ja

Journal article

Moksnes MR, Graham SE, Wu K-H, Hansen AF, Gagliano Taliun SA, Zhou W, Thorstensen K, Fritsche LG, Gill D, Mason A, Cucca F, Schlessinger D, Abecasis GR, Burgess S, Asvold BO, Nielsen JB, Hveem K, Willer CJ, Brumpton BMet al., 2022, Genome-wide meta-analysis of iron status biomarkers and the effect of iron on all-cause mortality in HUNT, COMMUNICATIONS BIOLOGY, Vol: 5

Journal article

Zhao SS, Gill D, 2022, Genetically proxied IL-6 receptor inhibition and risk of polymyalgia rheumatica, ANNALS OF THE RHEUMATIC DISEASES, Vol: 81, Pages: 1480-1482, ISSN: 0003-4967

Journal article

Carter AR, Harrison S, Gill D, Davey Smith G, Taylor AE, Howe LD, Davies NMet al., 2022, Educational attainment as a modifier for the effect of polygenic scores for cardiovascular risk factors: cross-sectional and prospective analysis of UK Biobank., Int J Epidemiol, Vol: 51, Pages: 885-897

BACKGROUND: Understanding the interplay between educational attainment and genetic predictors of cardiovascular risk may improve our understanding of the aetiology of educational inequalities in cardiovascular disease. METHODS: In up to 320 120 UK Biobank participants of White British ancestry (mean age = 57 years, female 54%), we created polygenic scores for nine cardiovascular risk factors or diseases: alcohol consumption, body mass index, low-density lipoprotein cholesterol, lifetime smoking behaviour, systolic blood pressure, atrial fibrillation, coronary heart disease, type 2 diabetes and stroke. We estimated whether educational attainment modified genetic susceptibility to these risk factors and diseases. RESULTS: On the additive scale, higher educational attainment reduced genetic susceptibility to higher body mass index, smoking, atrial fibrillation and type 2 diabetes, but increased genetic susceptibility to higher LDL-C and higher systolic blood pressure. On the multiplicative scale, there was evidence that higher educational attainment increased genetic susceptibility to atrial fibrillation and coronary heart disease, but little evidence of effect modification was found for all other traits considered. CONCLUSIONS: Educational attainment modifies the genetic susceptibility to some cardiovascular risk factors and diseases. The direction of this effect was mixed across traits considered and differences in associations between the effect of the polygenic score across strata of educational attainment was uniformly small. Therefore, any effect modification by education of genetic susceptibility to cardiovascular risk factors or diseases is unlikely to substantially explain the development of inequalities in cardiovascular risk.

Journal article

Kamiza AB, Toure SM, Vujkovic M, Machipisa T, Soremekun OS, Kintu C, Corpas M, Pirie F, Young E, Gill D, Sandhu MS, Kaleebu P, Nyirenda M, Motala AA, Chikowore T, Fatumo Set al., 2022, Transferability of genetic risk scores in African populations, NATURE MEDICINE, Vol: 28, Pages: 1163-+, ISSN: 1078-8956

Journal article

Vujkovic M, Ramdas S, Lorenz KM, Guo X, Darlay R, Cordell HJ, He J, Gindin Y, Chung C, Myers RP, Schneider CV, Park J, Lee KM, Serper M, Carr RM, Kaplan DE, Haas ME, MacLean MT, Witschey WR, Zhu X, Tcheandjieu C, Kember RL, Kranzler HR, Verma A, Giri A, Klarin DM, Sun YV, Huang J, Huffman JE, Townsend Creasy K, Hand NJ, Liu C-T, Long MT, Yao J, Budoff M, Tan J, Li X, Lin HJ, Chen Y-DI, Taylor KD, Chang R-K, Krauss RM, Vilarinho S, Brancale J, Nielsen JB, Locke AE, Jones MB, Verweij N, Baras A, Reddy KR, Neuschwander-Tetri BA, Schwimmer JB, Sanyal AJ, Chalasani N, Ryan KA, Mitchell BD, Gill D, Wells AD, Manduchi E, Saiman Y, Mahmud N, Miller DR, Reaven PD, Phillips LS, Muralidhar S, DuVall SL, Lee JS, Assimes TL, Pyarajan S, Cho K, Edwards TL, Damrauer SM, Wilson PW, Gaziano JM, O'Donnell CJ, Khera AV, Grant SFA, Brown CD, Tsao PS, Saleheen D, Lotta LA, Bastarache L, Anstee QM, Daly AK, Meigs JB, Rotter JI, Lynch JA, Rader DJ, Voight BF, Chang K-Met al., 2022, A multiancestry genome-wide association study of unexplained chronic ALT elevation as a proxy for nonalcoholic fatty liver disease with histological and radiological validation, NATURE GENETICS, Vol: 54, Pages: 761-+, ISSN: 1061-4036

Journal article

Page C, Smith D, Rajasundaram S, Gill D, Kumar Vet al., 2022, Translating pharmacological developments into clinical practice: case study of Ronapreve for COVID-19, Publisher: SPRINGER HEIDELBERG, Pages: S68-S69, ISSN: 0031-6970

Conference paper

Burgess S, Chirinos JA, Damrauer SM, Gill Det al., 2022, Genetically Predicted Pulse Pressure and Risk of Abdominal Aortic Aneurysm: A Mendelian Randomization Analysis, CIRCULATION-GENOMIC AND PRECISION MEDICINE, Vol: 15, ISSN: 2574-8300

Journal article

Coscia C, Gill D, Benitez R, Perez T, Malats N, Burgess Set al., 2022, Avoiding collider bias in Mendelian randomization when performing stratified analyses, EUROPEAN JOURNAL OF EPIDEMIOLOGY, Vol: 37, Pages: 671-682, ISSN: 0393-2990

Journal article

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