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Numrering	Referens	Omslagsbild	Hitta
201.	Kurreeman, FAS, et al. (författare) A candidate gene approach identifies the TRAF1/C5 region as a risk factor for rheumatoid arthritis 2007 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 4:9, s. 1515-1524 Tidskriftsartikel (refereegranskat)
202.	Laugesen, K, et al. (författare) Overweight or obesity in children born after assisted reproductive technologies in Denmark: A population-based cohort study 2023 Ingår i: PLoS medicine. - 1549-1676. ; 20:12, s. e1004324- Tidskriftsartikel (refereegranskat)
203.	Lawlor, B., et al. (författare) Nilvadipine in mild to moderate Alzheimer disease: A randomised controlled trial 2018 Ingår i: Plos Medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 15:9 Tidskriftsartikel (refereegranskat)abstract Background This study reports the findings of the first large-scale Phase III investigator-driven clinical trial to slow the rate of cognitive decline in Alzheimer disease with a dihydropyridine (DHP) calcium channel blocker, nilvadipine. Nilvadipine, licensed to treat hypertension, reduces amyloid production, increases regional cerebral blood flow, and has demonstrated antiinflammatory and anti-tau activity in preclinical studies, properties that could have diseasemodifying effects for Alzheimer disease. We aimed to determine if nilvadipine was effective in slowing cognitive decline in subjects with mild to moderate Alzheimer disease. NILVAD was an 18-month, randomised, placebo-controlled, double-blind trial that randomised participants between 15 May 2013 and 13 April 2015. The study was conducted at 23 academic centres in nine European countries. Of 577 participants screened, 511 were eligible and were randomised (258 to placebo, 253 to nilvadipine). Participants took a trial treatment capsule once a day after breakfast for 78 weeks. Participants were aged > 50 years, meeting National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's disease Criteria (NINCDS-ADRDA) for diagnosis of probable Alzheimer disease, with a Standardised Mini-Mental State Examination (SMMSE) score of >= 12 and < 27. Participants were randomly assigned to 8 mg sustained-release nilvadipine or matched placebo. The a priori defined primary outcome was progression on the Alzheimer's Disease Assessment Scale Cognitive Subscale-12 (ADAS-Cog 12) in the modified intention-to-treat (mITT) population (n = 498), with the Clinical Dementia Rating Scale sum of boxes (CDR-sb) as a gated co-primary outcome, eligible to be promoted to primary end point conditional on a significant effect on the ADAS-Cog 12. The analysis set had a mean age of 73 years and was 62% female. Baseline demographic and Alzheimer disease +/- specific characteristics were similar between treatment groups, with reported mean of 1.7 years since diagnosis and mean SMMSE of 20.4. The prespecified primary analyses failed to show any treatment benefit for nilvadipine on the co-primary outcome (p = 0.465). Decline from baseline in ADASCog 12 on placebo was 0.79 (95% CI, -0.07 +/- 1.64) at 13 weeks, 6.41 (5.33 +/- 7.49) at 52 weeks, and 9.63 (8.33 +/- 10.93) at 78 weeks and on nilvadipine was 0.88 (0.02 +/- 1.74) at 13 weeks, 5.75 (4.66 +/- 6.85) at 52 weeks, and 9.41 (8.09 +/- 10.73) at 78 weeks. Exploratory analyses of the planned secondary outcomes showed no substantial effects, including on the CDR-sb or the Disability Assessment for Dementia. Nilvadipine appeared to be safe and well tolerated. Mortality was similar between groups (3 on nilvadipine, 4 on placebo); higher counts of adverse events (AEs) on nilvadipine (1,129 versus 1,030), and serious adverse events (SAEs; 146 versus 101), were observed. There were 14 withdrawals because of AEs. Major limitations of this study were that subjects had established dementia and the likelihood that non-Alzheimer subjects were included because of the lack of biomarker confirmation of the presence of brain amyloid. The results do not suggest benefit of nilvadipine as a treatment in a population spanning mild to moderate Alzheimer disease.
204.	Lawn, JE, et al. (författare) Setting research priorities to reduce almost one million deaths from birth asphyxia by 2015 2011 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 8:1, s. e1000389- Tidskriftsartikel (refereegranskat)
205.	Lees, CW, et al. (författare) Analysis of germline GLI1 variation implicates hedgehog signalling in the regulation of intestinal inflammatory pathways 2008 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 5:12, s. 1761-1775 Tidskriftsartikel (refereegranskat)
206.	Li, J, et al. (författare) Mortality after parental death in childhood: a nationwide cohort study from three Nordic countries 2014 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 11:7, s. e1001679- Tidskriftsartikel (refereegranskat)
207.	Lienhardt, C, et al. (författare) Translational Research for Tuberculosis Elimination: Priorities, Challenges, and Actions 2016 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 13:3, s. e1001965- Tidskriftsartikel (refereegranskat)
208.	Lindberg, L, et al. (författare) Association of childhood obesity with risk of early all-cause and cause-specific mortality: A Swedish prospective cohort study 2020 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 17:3, s. e1003078- Tidskriftsartikel (refereegranskat)
209.	Lisonkova, S, et al. (författare) Maternal age and severe maternal morbidity: A population-based retrospective cohort study 2017 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 14:5, s. e1002307- Tidskriftsartikel (refereegranskat)
210.	Lotta, LA, et al. (författare) Genetic Predisposition to an Impaired Metabolism of the Branched-Chain Amino Acids and Risk of Type 2 Diabetes: A Mendelian Randomisation Analysis 2016 Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 13:11, s. e1002179- Tidskriftsartikel (refereegranskat)

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