Humaira Rasheed

• Moksnes, Marta R.; Hansen, Ailin F.; Wolford, Brooke N.; Thomas, Laurent F.; Rasheed, Humaira & Simic, Anica [Vis alle 24 forfattere av denne artikkelen] (2024). A genome-wide association study provides insights into the genetic etiology of 57 essential and non-essential trace elements in humans. Communications Biology. ISSN 2399-3642. 7(1), s. 1–14. doi: 10.1038/s42003-024-06101-z. Fulltekst i vitenarkiv
• Shah, Amil M.; Myhre, Peder Langeland; Arthur, Victoria; Dorbala, Pranav; Rasheed, Humaira & Buckley, Leo F. [Vis alle 22 forfattere av denne artikkelen] (2024). Large scale plasma proteomics identifies novel proteins and protein networks associated with heart failure development. Nature Communications. ISSN 2041-1723. 15(1). doi: 10.1038/s41467-023-44680-3.
• Scholz, Markus; Horn, Katrin; pott, janne; Wuttke, Matthias; Hallan, Stein Ivar & Schlosser, Pascal [Vis alle 12 forfattere av denne artikkelen] (2024). X-chromosome and kidney function: evidence from a multi-trait genetic analysis of 908,697 individuals reveals sex-specific and sex-differential findings in genes regulated by androgen response elements. Nature Communications. ISSN 2041-1723. 15:586(1), s. 1–17. doi: 10.1038/s41467-024-44709-1. Fulltekst i vitenarkiv
• Klevjer, Marie; Rasheed, Humaira; Romundstad, Pål Richard; Madssen, Erik; Brumpton, Ben Michael & Bye, Anja (2023). Insight into the relationship between resting heart rate and atrial fibrillation: a Mendelian randomization study. Europace. ISSN 1099-5129. 25(10). doi: 10.1093/europace/euad292. Fulltekst i vitenarkiv
• Howe, Laurence J; Rasheed, Humaira; Jones, Paul Remy; Boomsma, Dorret I; Evans, David M & Giannelis, Alexandros [Vis alle 46 forfattere av denne artikkelen] (2023). Educational attainment, health outcomes and mortality: a within-sibship Mendelian randomization study. International Journal of Epidemiology. ISSN 0300-5771. 52(5), s. 1579–1591. doi: 10.1093/ije/dyad079. Fulltekst i vitenarkiv
• Zheng, Jie; Wheeler, Eleanor; Pietzner, Maik; Andlauer, Till F.M.; Yau, Michelle S. & Hartley, April E. [Vis alle 37 forfattere av denne artikkelen] (2023). Lowering of Circulating Sclerostin May Increase Risk of Atherosclerosis and its Risk Factors: Evidence From a Genome-Wide Association Meta-Analysis Followed by Mendelian Randomization. Arthritis & Rheumatology. ISSN 2326-5191. 75(10), s. 1781–1792. doi: 10.1002/art.42538. Fulltekst i vitenarkiv
• Hosier, Hillary; Lipkind, Heather S.; Rasheed, Humaira; DeWan, Andrew & Rogne, Tormod (2023). Dyslipidemia and Risk of Preeclampsia: A Multiancestry Mendelian Randomization Study. Hypertension. ISSN 0194-911X. 80(5), s. 1067–1076. doi: 10.1161/HYPERTENSIONAHA.122.20426. Vis sammendrag

  Abstract Background: Preeclampsia is a leading cause of maternal morbidity, and dyslipidemia has been associated with preeclampsia in observational studies. We use Mendelian randomization analyses to estimate the association between lipid levels, their pharmacological targets, and the risk of preeclampsia in 4 ancestry groups. Methods: We extracted uncorrelated (R2<0.001) single-nucleotide polymorphisms strongly associated (P<5×10-8) with LDL-C (low-density lipoprotein cholesterol), HDL-C (high-density lipoprotein cholesterol), and triglycerides from genome-wide association studies of European, admixed African, Latino, and East Asian ancestry participants. Genetic associations with risk of preeclampsia were extracted from studies of the same ancestry groups. Inverse-variance weighted analyses were performed separately for each ancestry group before they were meta-analyzed. Sensitivity analyses were conducted to evaluate bias due to genetic pleiotropy, demography, and indirect genetic effects. Results: The meta-analysis across 4 ancestry groups included 1.5 million subjects with lipid measurements, 7425 subjects with preeclampsia, and 239 290 without preeclampsia. Increasing HDL-C was associated with reduced risk of preeclampsia (odds ratio, 0.84 [95% CI, 0.74–0.94]; P=0.004; per SD increase in HDL-C), which was consistent across sensitivity analyses. We also observed cholesteryl ester transfer protein inhibition—a drug target that increases HDL-C—may have a protective effect. We observed no consistent effect of LDL-C or triglycerides on the risk of preeclampsia. Conclusions: We observed a protective effect of elevated HDL-C on risk of preeclampsia. Our findings align with the lack of effect in trials of LDL-C modifying drugs but suggest that HDL-C may be a new target for screening and intervention.

• Wang, Ying; Namba, Shinichi; Lopera, Esteban; Kerminen, Sini; Tsuo, Kristin & Läll, Kristi [Vis alle 47 forfattere av denne artikkelen] (2023). Global Biobank analyses provide lessons for developing polygenic risk scores across diverse cohorts. Cell Genomics. 3(1). doi: 10.1016/j.xgen.2022.100241. Fulltekst i vitenarkiv
• Zhao, Huiling; Rasheed, Humaira; Nøst, Therese Haugdahl; Cho, Yoonsu; Liu, Yi & Bhatta, Laxmi [Vis alle 14 forfattere av denne artikkelen] (2022). Proteome-wide Mendelian randomization in global biobank meta-analysis reveals multi-ancestry drug targets for common diseases. Cell Genomics. 2(11). doi: 10.1016/j.xgen.2022.100195. Fulltekst i vitenarkiv
• Brumpton, Ben Michael; Graham, Sarah; Surakka, Ida; Skogholt, Anne Heidi; Løset, Mari & Fritsche, Lars G. [Vis alle 30 forfattere av denne artikkelen] (2022). The HUNT study: A population-based cohort for genetic research. Cell Genomics. 2(10). doi: 10.1016/j.xgen.2022.100193. Fulltekst i vitenarkiv
• Howe, Laurence J.; Brumpton, Ben Michael; Rasheed, Humaira; Åsvold, Bjørn Olav; Davey Smith, George & Davies, Neil Martin (2022). Taller height and risk of coronary heart disease and cancer: A within-sibship Mendelian randomization study. eLIFE. ISSN 2050-084X. 11. doi: 10.7554/eLife.72984. Fulltekst i vitenarkiv
• Zheng, Jie; Zhang, Yuemiao; Rasheed, Humaira; Walker, Venexia M.; Sugawara, Yuka & Li, Jiachen [Vis alle 43 forfattere av denne artikkelen] (2021). Trans-ethnic Mendelian-randomization study reveals causal relationships between cardiometabolic factors and chronic kidney disease. International Journal of Epidemiology. ISSN 0300-5771. 50(6), s. 1995–2010. doi: 10.1093/ije/dyab203. Fulltekst i vitenarkiv Vis sammendrag

  Background: This study was to systematically test whether previously reported risk factors for chronic kidney disease (CKD) are causally related to CKD in European and East Asian ancestries using Mendelian randomization. Methods: A total of 45 risk factors with genetic data in European ancestry and 17 risk factors in East Asian participants were identified as exposures from PubMed. We defined the CKD by clinical diagnosis or by estimated glomerular filtration rate of <60 ml/min/1.73 m2. Ultimately, 51 672 CKD cases and 958 102 controls of European ancestry from CKDGen, UK Biobank and HUNT, and 13 093 CKD cases and 238 118 controls of East Asian ancestry from Biobank Japan, China Kadoorie Biobank and Japan-Kidney-Biobank/ToMMo were included. Results: Eight risk factors showed reliable evidence of causal effects on CKD in Europeans, including genetically predicted body mass index (BMI), hypertension, systolic blood pressure, high-density lipoprotein cholesterol, apolipoprotein A-I, lipoprotein(a), type 2 diabetes (T2D) and nephrolithiasis. In East Asians, BMI, T2D and nephrolithiasis showed evidence of causality on CKD. In two independent replication analyses, we observed that increased hypertension risk showed reliable evidence of a causal effect on increasing CKD risk in Europeans but in contrast showed a null effect in East Asians. Although liability to T2D showed consistent effects on CKD, the effects of glycaemic phenotypes on CKD were weak. Non-linear Mendelian randomization indicated a threshold relationship between genetically predicted BMI and CKD, with increased risk at BMI of >25 kg/m2. Conclusions: Eight cardiometabolic risk factors showed causal effects on CKD in Europeans and three of them showed causality in East Asians, providing insights into the design of future interventions to reduce the burden of CKD.

• Stanzick, Kira J.; Li, Yong; Schlosser, Pascal; Gorski, Mathias; Wuttke, Matthias & Thomas, Laurent [Vis alle 24 forfattere av denne artikkelen] (2021). Discovery and prioritization of variants and genes for kidney function in >1.2 million individuals. Nature Communications. ISSN 2041-1723. 12(1). doi: 10.1038/s41467-021-24491-0. Fulltekst i vitenarkiv Vis sammendrag

  Genes underneath signals from genome-wide association studies (GWAS) for kidney function are promising targets for functional studies, but prioritizing variants and genes is challenging. By GWAS meta-analysis for creatinine-based estimated glomerular filtration rate (eGFR) from the Chronic Kidney Disease Genetics Consortium and UK Biobank (n = 1,201,909), we expand the number of eGFRcrea loci (424 loci, 201 novel; 9.8% eGFRcrea variance explained by 634 independent signal variants). Our increased sample size in fine-mapping (n = 1,004,040, European) more than doubles the number of signals with resolved fine-mapping (99% credible sets down to 1 variant for 44 signals, ≤5 variants for 138 signals). Cystatin-based eGFR and/or blood urea nitrogen association support 348 loci (n = 460,826 and 852,678, respectively). Our customizable tool for Gene PrioritiSation reveals 23 compelling genes including mechanistic insights and enables navigation through genes and variants likely relevant for kidney function in human to help select targets for experimental follow-up.

• Rogne, Tormod; Liyanarachi, Kristin Vardheim; Rasheed, Humaira; Thomas, Laurent; Flatby, Helene Marie & Stenvik, Jørgen [Vis alle 16 forfattere av denne artikkelen] (2021). GWAS Identifies LINC01184/SLC12A2 as a Risk Locus for Skin and Soft Tissue Infections. Journal of Investigative Dermatology. ISSN 0022-202X. 141(8), s. 2083–2086.e8. doi: 10.1016/j.jid.2021.01.020.
• Rasheed, Humaira; Zheng, Jie; Rees, Jessica; Sanderson, Eleanor; Thomas, Laurent & Richardson, Tom G. [Vis alle 20 forfattere av denne artikkelen] (2021). The causal effects of serum lipids and apolipoproteins on kidney function: Multivariable and bidirectional Mendelian-randomization analyses. International Journal of Epidemiology. ISSN 0300-5771. 50(5), s. 1569–1579. doi: 10.1093/ije/dyab014. Vis sammendrag

  Background The causal nature of the observed associations between serum lipids and apolipoproteins and kidney function are unclear. Methods Using two-sample and multivariable Mendelian randomization (MR), we examined the causal effects of serum lipids and apolipoproteins on kidney function, indicated by the glomerular-filtration rate estimated using creatinine (eGFRcrea) or cystatin C (eGFRcys) and the urinary albumin-to-creatinine ratio (UACR). We obtained lipid- and apolipoprotein-associated genetic variants from the Global Lipids Genetics Consortium (n = 331 368) and UK Biobank (n = 441 016), respectively, and kidney-function markers from the Trøndelag Health Study (HUNT; n = 69 736) and UK Biobank (n = 464 207). The reverse causal direction was examined using variants associated with kidney-function markers selected from recent genome-wide association studies. Results There were no strong associations between genetically predicted lipid and apolipoprotein levels with kidney-function markers. Some, but inconsistent, evidence suggested a weak association of higher genetically predicted atherogenic lipid levels [indicated by low-density lipoprotein cholesterol (LDL-C), triglycerides and apolipoprotein B] with increased eGFR and UACR. For high-density lipoprotein cholesterol (HDL-C), results differed between eGFRcrea and eGFRcys, but neither analysis suggested substantial effects. We found no clear evidence of a reverse causal effect of eGFR on lipid or apolipoprotein traits, but higher UACR was associated with higher LDL-C, triglyceride and apolipoprotein B levels. Conclusion Our MR estimates suggest that serum lipid and apolipoprotein levels do not cause substantial changes in kidney function. A possible weak effect of higher atherogenic lipids on increased eGFR and UACR warrants further investigation. Processes leading to higher UACR may lead to more atherogenic lipid levels.

• Moksnes, Marta Riise; Røsjø, Helge; Richmond, Anne; Lyngbakken, Magnus N; Graham, Sarah E & Hansen, Ailin Falkmo [Vis alle 30 forfattere av denne artikkelen] (2021). Genome-wide association study of cardiac troponin i in the general population. Human Molecular Genetics. ISSN 0964-6906. 30(21), s. 2027–2039. doi: 10.1093/hmg/ddab124. Fulltekst i vitenarkiv Vis sammendrag

  Circulating cardiac troponin proteins are associated with structural heart disease and predict incident cardiovascular disease in the general population. However, the genetic contribution to cardiac troponin I (cTnI) concentrations and its causal effect on cardiovascular phenotypes are unclear. We combine data from two large population-based studies, the Trøndelag Health Study and the Generation Scotland Scottish Family Health Study, and perform a genome-wide association study of high-sensitivity cTnI concentrations with 48 115 individuals. We further use two-sample Mendelian randomization to investigate the causal effects of circulating cTnI on acute myocardial infarction (AMI) and heart failure (HF). We identified 12 genetic loci (8 novel) associated with cTnI concentrations. Associated protein-altering variants highlighted putative functional genes: CAND2, HABP2, ANO5, APOH, FHOD3, TNFAIP2, KLKB1 and LMAN1. Phenome-wide association tests in 1688 phecodes and 83 continuous traits in UK Biobank showed associations between a genetic risk score for cTnI and cardiac arrhythmias, metabolic and anthropometric measures. Using two-sample Mendelian randomization, we confirmed the non-causal role of cTnI in AMI (5948 cases, 355 246 controls). We found indications for a causal role of cTnI in HF (47 309 cases and 930 014 controls), but this was not supported by secondary analyses using left ventricular mass as outcome (18 257 individuals). Our findings clarify the biology underlying the heritable contribution to circulating cTnI and support cTnI as a non-causal biomarker for AMI in the general population. Using genetically informed methods for causal inference helps inform the role and value of measuring cTnI in the general population.

• Flatby, Helene Marie; Rasheed, Humaira; Ravi, Anuradha; Thomas, Laurent; Liyanarachi, Kristin Vardheim & Afset, Jan Egil [Vis alle 15 forfattere av denne artikkelen] (2021). Risk of lower respiratory tract infections: a genome-wide association study with Mendelian randomization analysis in three independent European populations. Clinical Microbiology and Infection (CMI). ISSN 1198-743X. 28(5), s. 732.e1–732.e7. doi: 10.1016/j.cmi.2021.11.004. Fulltekst i vitenarkiv Vis sammendrag

  Objective: Lower respiratory tract infections (LRTIs) are a leading cause of morbidity and mortality worldwide. Few studies have previously investigated the genetic susceptibility and potential risk factors for LRTI. Methods: We used data from UK Biobank, HUNT, and FinnGen, to conduct a genome-wide association study (GWAS). Cases were subjects hospitalized with LRTI, and controls were subjects with no such hospitalization. We conducted stratification and interaction analyses to evaluate if the genetic effect of LRTI differed by sex or smoking. Mendelian randomization [MR] analyses were conducted to identify the unconfounded relationship between cardiometabolic risk factors and LRTI. Results: A total of 25,320 cases and 575,294 controls were included. The 15q25.1 locus reached genome-wide significance in the meta-analysis (rs10519203: OR = 0.94, P = 3.87e-11). The protective effect of effect allele of rs10519203 was present among smokers (OR = 0.90 [95% CI = 0.87 - 0.92, P = 1.38e-15]) but not among never-smokers (OR = 1.01 [95% CI = 0.97 - 1.06, P = 5.20e-01]). In MR analyses, we found that increasing body mass index (OR = 1.31 [95% CI = 1.24 - 1.40, P = 3.78e-18]), lifetime smoking (OR = 2.83 [95% CI = 2.34 - 3.42, P = 6.56e-27]), and systolic blood pressure robustly increased the risk of LRTIs (OR = 1.11 [95% CI = 1.02 - 1.22, P = 1.48e-02]). Conclusion: A region in 15q25.1 was strongly associated with LRTI susceptibility. Reduction of the prevalence of smoking, overweight, obesity, and hypertension may reduce the disease burden of LRTIs. Keywords: body mass index, genome-wide association study, lowerrespiratory tract infection, mendelianrandomization, pneumonia, respiratory infection, smoking

• Zheng, Jie; Brion, Marie-Jo; Kemp, John P.; Warrington, Nicole M.; Borges, Maria C. & Hemani, Gibran [Vis alle 14 forfattere av denne artikkelen] (2020). The effect of plasma lipids and lipid-lowering interventions on bone mineral density: A Mendelian randomization study. Journal of Bone and Mineral Research. ISSN 0884-0431. 35(7), s. 1224–1235. doi: 10.1002/jbmr.3989.
• Zhou, Wei; Brumpton, Ben Michael; Kabil, Omer; Gudmundsson, Julius; Thorleifsson, Gudmar & Weinstock, Joshua [Vis alle 56 forfattere av denne artikkelen] (2020). GWAS of thyroid stimulating hormone highlights pleiotropic effects and inverse association with thyroid cancer. Nature Communications. ISSN 2041-1723. 11:3981, s. 1–13. doi: 10.1038/s41467-020-17718-z. Fulltekst i vitenarkiv
• Ponsford, Mark J; Gkatzionis, Apostolos; Walker, Venexia M; Grant, Andrew J; Wootton, Robyn E & Moore, Luke [Vis alle 21 forfattere av denne artikkelen] (2020). Cardiometabolic traits, sepsis and severe covid-19: a Mendelian randomization investigation. Circulation. ISSN 0009-7322. 142(18), s. 1791–1793. doi: 10.1161/CIRCULATIONAHA.120.050753.
• Nayor, Matthew; Short, Meghan I.; Rasheed, Humaira; Lin, Honghuang; Jonasson, Christian & Yang, Qiong [Vis alle 23 forfattere av denne artikkelen] (2020). Aptamer-Based Proteomic Platform Identifies Novel Protein Predictors of Incident Heart Failure and Echocardiographic Traits. Circulation: Heart Failure. ISSN 1941-3289. 13(5). doi: 10.1161/CIRCHEARTFAILURE.119.006749.
• Brumpton, Ben Michael; Fritsche, Lars; Zheng, Jie; Nielsen, Jonas Bille; Mannila, Maria Nastase & Surakka, Ida [Vis alle 23 forfattere av denne artikkelen] (2019). Variation in serum PCSK9 (proprotein convertase subtilisin/kexin type 9), cardiovascular disease risk, and an investigation of potential unanticipated effects of PCSK9 inhibition. Circulation: Genomic and precision medicine. ISSN 2574-8300. 12(1). doi: 10.1161/CIRCGEN.118.002335. Fulltekst i vitenarkiv
• Rasheed, Humaira; Stamp, Lisa K.; Dalbeth, Nicola & Merriman, Tony R. (2017). Interaction of the GCKR and A1CF loci with alcohol consumption to influence the risk of gout. Arthritis Research & Therapy. ISSN 1478-6354. 19.
• Rasheed, Humaira; Phipps-Green, Amanda; Topless, Ruth K; Smith, Malcolm D.; Hill, Catherine & Lester, Susan [Vis alle 22 forfattere av denne artikkelen] (2016). Replication of association of the apolipoprotein A1-C3-A4 gene cluster with the risk of gout. Rheumatology. ISSN 1462-0324. 55, s. 1421–1430.
• Rasheed, Humaira; McKinney, Cushla; Stamp, Lisa K.; Dalbeth, Nicola; Topless, Ruth K & Day, Richard [Vis alle 21 forfattere av denne artikkelen] (2016). The Toll-like receptor 4 (TLR4) variant rs2149356 and risk of gout in European and Polynesian sample sets. PLOS ONE. ISSN 1932-6203. 11.
• Rasheed, Humaira; Hsu, Angela; Dalbeth, Nicola; Stamp, Lisa K.; McCormick, Sally P & Merriman, Tony (2014). The relationship of apolipoprotein B and very low-density lipoprotein triglyceride with hyperuricemia and gout. Arthritis Research & Therapy. ISSN 1478-6354. 16.
• Rasheed, Humaira; Hughes, Kim; Flynn, Tanya J & Merriman, Tony (2014). Mendelian randomization provides no evidence for a causal role of serum urate in increasing serum triglyceride levels. Circulation: Cardiovascular Genetics. ISSN 1942-325X. 7, s. 830–837.
• Rasheed, Humaira; Phipps-Green, Amanda; Topless, Ruth K; Hollis-Moffatt, Jade E.; Harré-Hindmarsh, Jennie & Franklin, Christopher S. [Vis alle 11 forfattere av denne artikkelen] (2013). Association of the lipoprotein receptor-related protein 2 gene with gout and non-additive interaction with alcohol consumption. Arthritis Research & Therapy. ISSN 1478-6354. 15.
• Rasheed, Humaira; Elahi, Shan & Ajaz, Humayun (2012). Serum magnesium and atherogenic lipid fractions in type II diabetic patients of Lahore, Pakistan. Biological Trace Element Research. ISSN 0163-4984. 148, s. 165–169.
• Elahi, Shan; Rasheed, Humaira; Syed, Zara; Aman, Zainab & Yasmeen, Riffat (2010). Serum concentration of thyroid hormone in children suspected of thyroid dysfunction. Journal of Scientific Research. ISSN 0555-7674. 40(2), s. 31–36.
• Rasheed, Humaira; Elahi, Shan; Syed, Zulqurnain & Rizvi, Nayab Batool (2009). Trend of thyroid dysfunction associated with visible goiter. Journal of Scientific Research. ISSN 0555-7674. 39(2), s. 41–47.
• Rasheed, Humaira; Elahi, Shan; Naeem, Muhammad; Shahid, Mariam & Rizvi, Nayab Batool (2008). Concentration of thyroid related hormone in non-goitrous patients. Journal of Scientific Research. ISSN 0555-7674. 38(1), s. 29–34.

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• Ravi, Anuradha; Liyanarachi, Kristin Vardheim; Afset, Jan Egil; Rasheed, Humaira; Brumpton, Ben Michael & Hveem, Kristian [Vis alle 11 forfattere av denne artikkelen] (2024). A genome-wide association study of susceptibility to upper urinary tract infections.
• Zhang, Yue-Miao; Wang, Yong-Fei; Rasheed, Humaira & Ott, Jurg (2021). Multi-Omics Study in Revealing Underlying Pathogenesis of Complex Diseases: A Translational Perspective. Frontiers in Genetics. ISSN 1664-8021. 12.
• Zhou, Wei; Brumpton, Ben Michael; Kabil, Omer; Gudmundsson, Julius; Thorleifsson, Gudmar & Weinstock, Joshua [Vis alle 56 forfattere av denne artikkelen] (2021). Author Correction: GWAS of thyroid stimulating hormone highlights the pleiotropic effects and inverse association with thyroid cancer (Nature Communications, (2020), 11, 1, (3981), 10.1038/s41467-020-17718-z). Nature Communications. ISSN 2041-1723. 12(1). doi: 10.1038/s41467-021-27675-w.

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