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  • 1.
    Gu, Xiuquan
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - Ångström. China Univ Min & Technol, Sch Mat Sci & Engn, Xuzhou 221116, Peoples R China.
    Li, Cuiyan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - Ångström.
    Yuan, Shuai
    Shanghai Univ, Res Ctr Nanosci & Nanotechnol, Shanghai 200444, Peoples R China.
    Ma, Mingguo
    Beijing Forestry Univ, Coll Mat Sci & Technol, Beijing 100083, Peoples R China.
    Qiang, Yinghuai
    China Univ Min & Technol, Sch Mat Sci & Engn, Xuzhou 221116, Peoples R China.
    Zhu, Jie-Fang
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - Ångström, Strukturkemi.
    ZnO based heterojunctions and their application in environmental photocatalysis2016Ingår i: Nanotechnology, ISSN 0957-4484, E-ISSN 1361-6528, Vol. 27, nr 40, artikel-id 402001Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    As an alternative to TiO2 photocatalysts, ZnO exhibits a large potential for photocatalytic (PC) applications in environmental treatments, such as degradation of wastewater, sterilization of drinking water, and air cleaning. However, the efficiency achieved with ZnO to date is far from that expected for commercialization, due to rapid charge recombination, photo-corrosion as well as poor utilization of solar energy. Fortunately, in recent years, a great number of breakthroughs have been achieved in PC performance (including activity and stability) of micro-/ nano-structured ZnO by forming heterojunctions (HJs) with metal nanoparticles (NPs), carbon nanostructures and other semiconductors. In most cases, the improvement of PC performance was ascribed to the better charge separation at the interfaces between ZnO and the other components. Sometimes, the formation of hybrids is also in favor of visible light harvesting. This review summarizes recent advances in the fields of environmental photocatalysis by ZnO based HJs, and especially emphasizes their abilities in degradation of organic pollutants or harmful substances in water. We aim to reveal the mechanism underlying the enhanced PC performance by constructing HJs, and extend the potential of ZnO HJ photocatalysts for future trends, and practical, large-scale applications in environment-related fields.

  • 2.
    Yuan, Shuai
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Bäck, Magnus
    Karolinska Inst, Dept Med, Ctr Mol Med, SE-17176 Stockholm, Sweden;Karolinska Univ Hosp, Div Valvular & Coronary Dis, Heart & Vasc Theme, SE-17176 Stockholm, Sweden.
    Bruzelius, Maria
    Karolinska Univ Hosp, Dept Hematol, Coagulat Unit, SE-17176 Stockholm, Sweden;Karolinska Inst, Dept Med Solna, SE-17176 Stockholm, Sweden.
    Mason, Amy M.
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB1 8RN, England.
    Burgess, Stephen
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB1 8RN, England;Univ Cambridge, MRC Biostat Unit, Cambridge CB2 0SR, England.
    Larsson, Susanna C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Plasma Phospholipid Fatty Acids, FADS1 and Risk of 15 Cardiovascular Diseases: A Mendelian Randomisation Study2019Ingår i: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 11, nr 12, artikel-id 3001Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Whether circulating fatty acids (FAs) play a causal role in the development of cardiovascular disease (CVD) remains unclear. We conducted a Mendelian randomisation study to explore the associations between plasma phospholipid FA levels and 15 CVDs. Summary-level data from the CARDIoGRAMp1usC4D, MEGASTROKE, and Atrial Fibrillation consortia and UK Biobank were used. Sixteen single-nucleotide polymorphisms (SNPs) associated with ten plasma FAs were used as instrumental variables. SNPs in or close to the FADS1 gene were associated with most FAs. We performed a secondary analysis of the association between a functional variant (rs174547) in FADS1, which encodes Delta 5-desaturase (a key enzyme in the endogenous FA synthesis), and CVD. Genetic predisposition to higher plasma alpha-linolenic, linoleic, and oleic acid levels was associated with lower odds of large-artery stroke and venous thromboembolism, whereas higher arachidonic and stearic acid levels were associated with higher odds of these two CVDs. The associations were driven by SNPs in or close to FADS1. In the secondary analysis, the minor allele of rs174547 in FADS1 was associated with significantly lower odds of any ischemic stroke, large-artery stroke, and venous thromboembolism and showed suggestive evidence of inverse association with coronary artery disease, abdominal aortic aneurysm and aortic valve stenosis. Genetically higher plasma alpha-linolenic, linoleic, and oleic acid levels are inversely associated with large-artery stroke and venous thromboembolism, whereas arachidonic and stearic acid levels are positively associated with these CVDs. The associations were driven by FADS1, which was also associated with other CVDs.

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  • 3.
    Yuan, Shuai
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, Stockholm, Sweden.
    Jiang, Xia
    Karolinska Inst, Inst Environm Med, Unit Translat Epidemiol, Stockholm, Sweden;Harvard Univ, TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Larsson, Susanna C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, Stockholm, Sweden.
    Genetic Prediction of Serum 25-Hydroxyvitamin D, Calcium, and Parathyroid Hormone Levels in Relation to Development of Type 2 Diabetes: A Mendelian Randomization Study2019Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 42, nr 12, s. 2197-2203Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE We conducted a Mendelian randomization study to investigate the associations of genetically predicted serum 25-hydroxyvitamin D (S-25OHD), calcium (S-Ca), and parathyroid hormone (S-PTH) levels with type 2 diabetes (T2DM). RESEARCH DESIGN AND METHODS Seven, six, and five single nucleotide polymorphisms (SNPs) associated with S-25OHD, S-Ca, and S-PTH levels, respectively, were used as instrumental variables. Data on T2DM were available for 74,124 case subjects with T2DM and 824,006 control subjects. The inverse variance-weighted method was used for the primary analyses, and the weighted median and Mendelian randomization (MR)-Egger methods were used for supplementary analyses. RESULTS Genetically predicted S-25OHD but not S-Ca and S-PTH levels were associated with T2DM in the primary analyses. For 1 SD increment of S-25OHD levels, the odds ratio (OR) of T2DM was 0.94 (95% CI 0.88-0.99; P = 0.029) in an analysis based on all seven SNPs and 0.90 (95% CI 0.83-0.98; P = 0.011) in an analysis based on three SNPs within or near genes involved in vitamin D synthesis. Only the association based on the SNPs involved in vitamin D synthesis remained in the weighted median analysis, and no pleiotropy was detected (P = 0.153). Pleiotropy was detected in the analysis of S-Ca (P = 0.013). After correcting for this bias using MR-Egger regression, the OR of T2DM per 1 SD increment of S-Ca levels was 1.41 (95% CI 1.12-1.77; P = 0.003). CONCLUSIONS Modest lifelong higher S-25OHD levels were associated with reduced odds of T2DM, but the association was only robust for SNPs in the vitamin D synthesis pathway. The possible role of S-Ca levels for T2DM development requires further research.

  • 4.
    Yuan, Shuai
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, Stockholm, Sweden.
    Larsson, Susanna C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, Stockholm, Sweden.
    A causal relationship between cigarette smoking and type 2 diabetes mellitus: A Mendelian randomization study2019Ingår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 9, artikel-id 19342Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The causality between smoking and type 2 diabetes is unclear. We conducted a two-sample Mendelian randomization study to explore the causal relationship between smoking initiation and type 2 diabetes. Summary-level data for type 2 diabetes were obtained from a meta-analysis of 32 genome-wide association studies (DIAbetes Genetics Replication And Meta-analysis consortium), which included 898 130 individuals of European ancestry. Totally, 377 single-nucleotide polymorphisms associated with smoking initiation at genome wide significance threshold (p < 5 x 10(-8)) were identified from the hitherto largest genome-wide association study on smoking. The inverse-variance weighted, weighted median, MR-Egger regression, and MR-PRESSO approaches were used to analyze the data. Genetically predicted smoking initiation was associated with type 2 diabetes with an odds ratio of 1.28 (95% confidence interval, 1.20, 1.37; p = 2.35 x 10(-12)). Results were consistent across sensitivity analyses and there was no evidence of horizontal pleiotropy. This study provides genetic evidence supporting a causal association between the smoking initiation and type 2 diabetes. Reducing cigarette smoking initiation can now be even more strongly recommended for type 2 diabetes prevention.

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  • 5.
    Yuan, Shuai
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, Nobelsvag 13, S-17177 Stockholm, Sweden.
    Larsson, Susanna C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, Nobelsvag 13, S-17177 Stockholm, Sweden.
    No association between coffee consumption and risk of atrial fibrillation: A Mendelian randomization study2019Ingår i: NMCD. Nutrition Metabolism and Cardiovascular Diseases, ISSN 0939-4753, E-ISSN 1590-3729, Vol. 29, nr 11, s. 1185-1188Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background and aims: Some observational studies have found that habitual coffee and caffeine consumption might reduce the risk of atrial fibrillation (AF). We conducted a two-sample Mendelian randomization study to explore the potential association between coffee consumption and AF.

    Methods and results: This study was based on summary-level data from the Atrial Fibrillation Consortium, including 588 190 individuals (65 446 cases and 522 744 non-cases). Nine single-nucleotide polymorphisms associated with coffee consumption at significance level of P < 5 x 10(-8) were used as instrumental variables and were obtained from a genome-wide association study that included up to 375 833 individuals. The odds ratio of AF per genetically-predicted 50% increase of coffee consumption was 0.98 (95% confidence interval, 0.88, 1.10; P = 0.80) in the standard inverse-variance weighted analysis. Results were consistent in sensitivity analyses using the weighted median and MR-Egger methods, and no directional pleiotropy (P = 0.37) was observed. Moreover, complementary analyses that separated the coffee-related single-nucleotide polymorphisms based on their association with blood levels of caffeine metabolites (lower, higher, unrelated or unknown association) revealed no association with AF.

    Conclusions: This study does not support a causal association between habitual coffee consumption and risk of AF. 

  • 6.
    Yuan, Shuai
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Larsson, Susanna C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Plasma Phospholipid Fatty Acids and Risk of Atrial Fibrillation: A Mendelian Randomization Study2019Ingår i: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 11, nr 7, artikel-id 1651Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Available evidence on the associations of dietary and circulating levels of long-chain n-3 fatty acids, which have potential antiarrhythmic properties, and other fatty acids with atrial fibrillation is conflicting and limited. We conducted a Mendelian randomization study to assess the associations between plasma phospholipid fatty acid levels and atrial fibrillation. Summary-level data of atrial fibrillation were available from 65,446 cases and 522,744 non-cases included in the Atrial Fibrillation Consortium. Sixteen single-nucleotide polymorphisms associated with ten fatty acids at significance level of p < 5 x 10(-8) were identified as instrumental variables from the hitherto largest genome-wide association studies for plasma fatty acids. The fixed-effects inverse-variance weighted method was used to assess the association of individual plasma fatty acids and atrial fibrillation risk. The random-effects inverse-variance weighted method, weighted median method, and Mendelian randomization (MR)-Egger method were employed as the sensitivity analyses. Genetic predisposition to higher levels of any of the ten individual fatty acids was not associated with atrial fibrillation risk.

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  • 7.
    Yuan, Shuai
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Wan, Zihao
    Chinese Univ Hong Kong, Fac Med, Dept Orthopaed & Traumatol, Shatin, Hong Kong, Peoples R China.
    Larsson, Susanna C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Associations of Smoking and Alcohol and Coffee Intake with Fracture and Bone Mineral Density: A Mendelian Randomization Study2019Ingår i: Calcified Tissue International, ISSN 0171-967X, E-ISSN 1432-0827, Vol. 105, nr 6, s. 582-588Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The causal associations of smoking and alcohol and coffee intake with fracture and bone mineral density are unknown. We investigated the associations using Mendelian randomization (MR). Summary-level data from UK Biobank for bone fractures (main outcome) (53,184 cases; 373,611 non-cases) and estimated bone mineral density (eBMD) (n = 426,824 individuals) were used. Single-nucleotide polymorphisms associated with smoking initiation (n = 378) and alcohol (n = 99) and coffee (n = 15) intake at the genome-wide significance threshold (P = 5 x 10(-8)) were identified from published genome-wide association studies. Univariable and multivariable inverse-variance weighted, weighted median, MR-Egger, and MR-PRESSO methods were used for statistical analyses. Genetic predisposition to smoking initiation was associated with fracture but not eBMD. The odds ratio of fracture per one-unit increase in log odds of smoking was 1.09 (95% confidence interval 1.04, 1.15; P = 8.58 x 10(-4)) after adjustment for alcohol intake in the multivariable MR analysis. The association remained in complementary analyses. Genetically predicted alcohol and coffee intake was not associated with fracture or eBMD. Nevertheless, genetic liability to alcohol dependence, based on variants in the ALD1B gene, was associated with fracture and lower eBMD. The odds ratio was 1.06 (95% confidence interval 1.01, 1.12; P = 0.018) per genetically predicted one-unit higher log odds of liability to alcohol dependence. This MR study strengthens the causal inference on an association between smoking and higher fracture risk but found no linear association of modestly higher alcohol and coffee intake with fracture or BMD. However, alcohol dependence may increase fracture risk.

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