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Objective: The radiopharmaceuticals radium-223 and the pharmacy preparation 177Lu-PSMA-I&T are reimbursed in the Netherlands for metastatic castration-resistant prostate cancer (mCRPC) treatment. Although shown to be life-prolonging in patients with mCRPC, the treatment procedures associated with these radiopharmaceuticals can be challenging for both patients and hospitals. This study investigates the costs of mCRPC treatment in Dutch hospitals for currently reimbursed radiopharmaceuticals with a demonstrated overall survival benefit.Methods: A cost model that calculated the direct medical per-patient costs of radium-223 and 177Lu-PSMA-I&T was developed, following clinical trial regimens. The model considered six 4-weekly administrations (i.e. ALSYMPCA regimen) of radium-223. Regarding 177Lu-PSMA-I&T, the model used both the VISION regimen (i.e. five 6-weekly administrations) and the SPLASH regimen (i.e. four 8-weekly administrations). Based on health insurance claims, we also estimated the coverage a hospital would receive for providing treatment. No fitting health insurance claim for 177Lu-PSMA-I&T is currently available; therefore, we calculated a break-even value for a potential health insurance claim that would exactly counterbalance the per-patient costs and coverage.Results: Radium-223 administration is associated with per-patient costs of €30,905, and these costs are fully covered by the coverage a hospital receives. The per-patient costs of 177Lu-PSMA-I&T range between €35,866 and €47,546 per administration period, depending on the regimen. Current healthcare insurance claims do not fully cover the costs of providing 177Lu-PSMA-I&T: hospitals must pay €4,414–€4,922 for each patient out of their own budget. The break-even value for the potential insurance claim covering 177Lu-PSMA-I&T administration with a VISION (SPLASH) regimen is €1,073 (€1,215).Conclusion: This study shows that, without consideration of the treatment effect, radium-223 treatment for mCRPC leads to lower per-patient costs than treatment with 177Lu-PSMA-I&T. The detailed overview of the costs associated with radiopharmaceutical treatment provided by this study is relevant for both hospitals and healthcare insurers.

Background Disparities in influenza vaccination exist between Hispanic and non-Hispanic White US nursing home (NH) residents, but the geographic areas with the largest disparities remain unknown. We examined how these racial/ethnic disparities differ across states and hospital referral regions (HRRs). Methods This retrospective cohort study included >14 million short-stay and long-stay US NH resident-seasons over 7 influenza seasons from October 1, 2011, to March 31, 2018, where residents could contribute to 1 or more seasons. Residents were aged ≥65 years and enrolled in Medicare fee-for-service. We used the Medicare Beneficiary Summary File to ascertain race/ethnicity and Minimum Data Set assessments for influenza vaccination. We calculated age- and sex-standardized percentage point (pp) differences in the proportions vaccinated between non-Hispanic White and Hispanic (any race) resident-seasons. Positive pp differences were considered disparities, where the proportion of non-Hispanic White residents vaccinated was greater than the proportion of Hispanic residents vaccinated. States and HRRs with ≥100 resident-seasons per age–sex stratum per racial/ethnic group were included in analyses. Results Among 7 442 241 short-stay resident-seasons (94.1% non-Hispanic White, 5.9% Hispanic), the median standardized disparities in influenza vaccination were 4.3 pp (minimum, maximum: 0.3, 19.2; n = 22 states) and 2.8 pp (minimum, maximum: −3.6, 10.3; n = 49 HRRs). Among 6 758 616 long-stay resident-seasons (93.7% non-Hispanic White, 6.5% Hispanic), the median standardized differences were −0.1 pp (minimum, maximum: −4.1, 11.4; n = 18 states) and −1.8 pp (minimum, maximum: −6.5, 7.6; n = 34 HRRs). Conclusions Wide geographic variation in influenza vaccination disparities existed across US states and HRRs. Localized interventions targeted toward areas with high disparities may be a more effective strategy to promote health equity than one-size-fits-all national interventions.

Background Limited health literacy (LHL) is associated with multiple adverse health outcomes in chronic kidney disease (CKD). Interventions are needed to improve this situation, but evidence on intervention targets and strategies is lacking. This systematic review aims to identify potential targets and strategies by summarizing the evidence on: (i) patient- and system-level factors potentially mediating the relation between LHL and health outcomes; and (ii) the effectiveness of health literacy interventions customized to CKD patients. Methods We performed a systematic review of peer-reviewed research articles in Medline, Embase and Web of Science, 2009–19. We assessed the quality of the studies and conducted a best-evidence synthesis. Results We identified 860 publications and included 48 studies. Most studies were of low quality (n = 26) and focused on dialysis and transplantation (n = 38). We found strong evidence for an association of LHL with smoking and having a suboptimal transplantation process. Evidence was weak for associations between LHL and a variety of factors related to self-care management (n = 25), utilization of care (n = 23), patient–provider interaction (n = 8) and social context (n = 5). Six interventions were aimed at improving knowledge, decision-making and health behaviours, but evidence for their effectiveness was weak. Conclusions Study heterogeneity, low quality and focus on kidney failure largely impede the identification of intervention targets and strategies for LHL. More and higher quality studies in earlier CKD stages are needed to unravel how LHL leads to worse health outcomes, and to identify targets and strategies to prevent disease deterioration. Healthcare organizations need to develop and evaluate efforts to support LHL patients.

Objective: This study aimed to evaluate the impacts of deep surgical site infections (dSSIs) regarding hospital readmissions, prolonged length of stay (LoS), and estimated costs. Patients and Methods: We designed and applied a matched case–control observational study using the electronic health records at the University Medical Center Groningen in the Netherlands. We compared patients with dSSI and non-SSI, matched on the basis of having similar procedures. A prevailing topology of surgeries categorized as clean, clean-contami-nated, contaminated, and dirty was applied. Results: Out of a total of 12,285 patients, 393 dSSI were identified as cases, and 2864 patients without SSIs were selected as controls. A total of 343 dSSI patients (87%) and 2307 (81%) controls required hospital readmissions. The median LoS was 7 days (P25-P75: 2.5–14.5) for dSSI patients and 5 days (P25-P75: 1–9) for controls (p-value

Background INTEVAL_Spain was a complex workplace intervention to prevent and manage musculoskeletal pain among nursing staff. Process evaluations can be especially useful for complex and multifaceted interventions through identifying the success or failure factors of an intervention to improve the intervention implementation. Objectives This study performed a process evaluation of INTEVAL_Spain and aimed to examine whether the intervention was conducted according to the protocol, to investigate the fulfilment of expectations and the satisfaction of workers. Methods The intervention was a two-armed cluster randomized controlled trial and lasted 1 year. The process evaluation included quantitative and qualitative methods. Quantitative methods were used to address the indicators of Steckler and Linnan’s framework. Data on recruitment was collected through a baseline questionnaire for the intervention and the control group. Reach and dose received were collected through participation sheets, dose delivered and fidelity through internal registries, and fulfilment of expectations and satisfaction were collected with two questions at 12-months follow-up. Qualitative methods were used for a content analysis of discussion groups at the end of the intervention led by an external moderator to explore satisfaction and recommendations. The general communication and activities were discussed, and final recommendations were agreed on. Data were synthesized and results were reported thematically. Results The study was performed in two Spanish hospitals during 2016-2017 and 257 workers participated. Recruitment was 62 and 51% for the intervention and the control group, respectively. The reach of the activities ranged from 96% for participatory ergonomics to 5% for healthy diet. The number of sessions offered ranged from 60 sessions for Nordic walking to one session for healthy diet. Fidelity of workers ranged from 100% for healthy diet and 79% for participatory ergonomics, to 42 and 39% for Nordic walking and case management, respectively. Lowest fidelity of providers was 75% for case management and 82% for Nordic walking. Fulfilment of expectations and satisfaction ranged from 6.6/10 and 7.6/10, respectively, for case management to 10/10 together for the healthy diet session. Discussion groups revealed several limitations for most of the activities, mainly focused on a lack of communication between the Champion (coordinator) and the workers. Conclusions This process evaluation showed that the implementation of INTEVAL_Spain was predominantly carried out as intended. Process indicators differed depending on the activity. Several recommendations to improve the intervention implementation process are proposed. Trial registration ISRCTN15780649.

L-M.C. and P.d.V. acknowledge support from the European Research Council (ERC) (Grant 678140-FluctEvol). The Montpellier tit group acknowledges the long-term support of the Observatoire des Sciences de l’Univers – Obser-vatoire de REcherche Montpelliérain de l’Environnement (OSU-OREME). The bighorn, mountain goat, and eastern gray kangaroo studies were supported by Natural Sciences and Engineering Research Council (NSERC) of Canada. Recent data collection for Wytham has been provided by grants from Biotechnology and Biological Sciences Research Council (BB/L006081/1), ERC (AdG250164), and the UK Natural Environment Research Council (NERC) (NE/K006274/1, NE/S010335/1). The Columbian ground squirrel study was supported by the National Science Foundation (Grant DEB-0089473). Trait and fitness data for hihi were collected/managed by John Ewen under New Zealand Department of Conservation hihi management contracts and research permits AK/15073/RES, AK-24128-FAU, 36186-FAU, and 44300-FAU and with additional financial support via NERC UK, The Leverhulme Trust UK, Marsden Fund New Zealand, and the Hihi Conservation Charitable Trust. The data on reindeer were made available through the Reindeer husbandry in a Globalizing North Nordic Center of Excellence, and the crew at Kutuharju Experimental Reindeer Research Station in the Reindeer Herder’s Association are thanked for their valuable assistance and logistic support in data collection. The red deer, Silwood blue tit, and Soay sheep datasets were supported by UK NERC. Lundy sparrow data were supported by NERC, a Marie Skłodowska-Curie Action, and Volkswagenstiftung. The red squirrel project was funded by NSERC of Canada and the National Science Foundation. J.C.S. was supported by a grant from the Ministry of Economy and Competitivity, Spanish Research Council (CGL-2016-79568-C3-3-P). J.T., T.K., and M.G. were supported by the Research Council of Norway through its Centers for Excellence funding scheme, Project 223257. Research on fairy wrens has been supported by the Australian Research Council. The Northern wheatear and the flycatcher studies were supported by grants from the Swedish Research Council VR. Temporal variation in natural selection is predicted to strongly impact the evolution and demography of natural populations, with consequences for the rate of adaptation, evolution of plasticity, and extinction risk. Most of the theory underlying these predictions assumes a moving optimum phenotype, with predictions expressed in terms of the temporal variance and autocorrelation of this optimum. However, empirical studies seldom estimate patterns of fluctuations of an optimum phenotype, precluding further progress in connecting theory with observations. To bridge this gap, we assess the evidence for temporal variation in selection on breeding date by modeling a fitness function with a fluctuating optimum, across 39 populations of 21 wild animals, one of the largest compilations of long-term datasets with individual measurements of trait and fitness components. We find compelling evidence for fluctuations in the fitness function, causing temporal variation in the magnitude, but not the direction of selection. However, fluctuations of the optimum phenotype need not directly translate into variation in selection gradients, because their impact can be buffered by partial tracking of the optimum by the mean phenotype. Analyzing individuals that reproduce in consecutive years, we find that plastic changes track movements of the optimum phenotype across years, especially in bird species, reducing temporal variation in directional selection. This suggests that phenological plasticity has evolved to cope with fluctuations in the optimum, despite their currently modest contribution to variation in selection. Postprint

Gut microbiota has been implicated in major diseases affecting the human population and has also been linked to triglycerides and high-density lipoprotein levels in the circulation. Recent development in metabolomics allows classifying the lipoprotein particles into more details. Here, we examine the impact of gut microbiota on circulating metabolites measured by Nuclear Magnetic Resonance technology in 2309 individuals from the Rotterdam Study and the LifeLines-DEEP cohort. We assess the relationship between gut microbiota and metabolites by linear regression analysis while adjusting for age, sex, body-mass index, technical covariates, medication use, and multiple testing. We report an association of 32 microbial families and genera with very-low-density and high-density subfractions, serum lipid measures, glycolysis-related metabolites, ketone bodies, amino acids, and acute-phase reaction markers. These observations provide insights into the role of microbiota in host metabolism and support the potential of gut microbiota as a target for therapeutic and preventive interventions., Here, the authors provide an in-depth study of the metabolome in two large population-based prospective cohorts and identify 32 microbial traits associated with various metabolic biomarkers and specific lipoprotein subfractions, providing insights into the role of microbiota in influencing host lipid levels.

The respective effects of tissue alarmins interleukin (IL)-15 and interferon beta (IFNβ), and IL-21 produced by T cells on the reprogramming of cytotoxic T lymphocytes (CTLs) that cause tissue destruction in celiac disease is poorly understood. Transcriptomic and epigenetic profiling of primary intestinal CTLs showed massive and distinct temporal transcriptional changes in response to tissue alarmins, while the impact of IL-21 was limited. Only anti-viral pathways were induced in response to all the three stimuli, albeit with differences in dynamics and strength. Moreover, changes in gene expression were primarily independent of changes in H3K27ac, suggesting that other regulatory mechanisms drive the robust transcriptional response. Finally, we found that IL-15/IFNβ/IL-21 transcriptional signatures could be linked to transcriptional alterations in risk loci for complex immune diseases. Together these results provide new insights into molecular mechanisms that fuel the activation of CTLs under conditions that emulate the inflammatory environment in patients with autoimmune diseases., Highlights • We report the epigenetic and transcriptomic response of IE-CTLs to tissue-derived alarmins and adaptive cytokine. • IL-15 and IFNβ induce massive and distinct transcriptional changes in IE-CTLs, while the impact of IL-21 was limited. • Genes associated with immune-mediated intestinal diseases are enriched in genes responding to IL-15, IFNβ and IL-21 in IE-CTLs.

Due to limited sepsis patient cohort size and extreme heterogeneity, only one significant locus and suggestive associations at several independent loci were implicated by three genome-wide association studies. However, genes from such suggestive loci may also provide crucial information to unravel genetic mechanisms that determine sepsis heterogeneity. Therefore, in this study, we made use of integrative approaches to prioritize genes and pathways affected by sepsis associated genetic variants. By integrating expression quantitative trait loci (eQTL) results from the largest whole-blood eQTL database, cytokine QTLs from pathogen-stimulated peripheral blood mononuclear cells (PBMCs), publicly available blood transcriptome data from pneumoniae-derived sepsis patients, and transcriptome data from pathogen-stimulated PBMCs, we identified 55 potential genes affected by 39 independent loci. By performing pathway enrichment analysis at these loci we found enrichment of genes for adherences-junction pathway. Finally, we investigated the functional role of the only one GWAS significant SNP rs4957796 on sepsis survival in altering transcription factor binding affinity in monocytes and endothelial cells. We also found that transient deficiency of FER and MAN2A1 affect endothelial response to stimulation, indicating that both FER and MAN2A1 could be the causal genes at this locus. Taken together, our study suggests that in addition to immune pathways, genetic variants may also affect non-immune related pathways.

Germline pathogenic variants in the BRCA1-associated protein-1 (BAP1) gene cause the BAP1-tumor predisposition syndrome (BAP1-TPDS, OMIM 614327). BAP1-TPDS is associated with an increased risk of developing uveal melanoma (UM), cutaneous melanoma (CM), malignant mesothelioma (MMe), renal cell carcinoma (RCC), meningioma, cholangiocarcinoma, multiple non-melanoma skin cancers, and BAP1-inactivated nevi. Because of this increased risk, it is important to identify patients with BAP1-TPDS. The associated tumors are treated by different medical disciplines, emphasizing the need for generally applicable guidelines for initiating genetic analysis. In this study, we describe the path to identification of BAP1-TPDS in 21 probands found in the Netherlands and the family history at the time of presentation. We report two cases of de novo BAP1 germline mutations (2/21, 9.5%). Findings of this study combined with previously published literature, led to a proposal of guidelines for genetic referral. We recommend genetic analysis in patients with &ge, 2 BAP1-TPDS-associated tumors in their medical history and/or family history. We also propose to test germline BAP1 in patients diagnosed with UM &lt, 40 years, CM &lt, 18 years, MMe &lt, 50 years, or RCC &lt, 46 years. Furthermore, other candidate susceptibility genes for tumor types associated with BAP1-TPDS are discussed, which can be included in gene panels when testing patients.

Contains fulltext : 209008.pdf (Publisher’s version ) (Open Access) BACKGROUND: Previous studies have reported associations between attention-deficit/hyperactivity disorder symptoms and DNA methylation in children. We report the first epigenome-wide association study meta-analysis of adult attention-deficit/hyperactivity disorder symptoms, based on peripheral blood DNA methylation (Infinium HumanMethylation450K array) in three population-based adult cohorts. METHODS: An epigenome-wide association study was performed in the Netherlands Twin Register (N = 2258, mean age 37 years), Dunedin Multidisciplinary Health and Development Study (N = 800, age 38 years), and Environmental Risk Longitudinal Twin Study (N = 1631, age 18 years), and results were combined through meta-analysis (total sample size N = 4689). Region-based analyses accounting for the correlation between nearby methylation sites were also performed. RESULTS: One epigenome-wide significant differentially methylated position was detected in the Dunedin study, but meta-analysis did not detect differentially methylated positions that were robustly associated across cohorts. In region-based analyses, six significant differentially methylation regions (DMRs) were identified in the Netherlands Twin Register, 19 in the Dunedin study, and none in the Environmental Risk Longitudinal Twin Study. Of these DMRs, 92% were associated with methylation quantitative trait loci, and 68% showed moderate to large blood-brain correlations for DNA methylation levels. DMRs included six nonoverlapping DMRs (three in the Netherlands Twin Register, three in the Dunedin study) in the major histocompatibility complex, which were associated with expression of genes in the major histocompatibility complex, including C4A and C4B, previously implicated in schizophrenia. CONCLUSIONS: Our findings point at new candidate loci involved in immune and neuronal functions that await further replication. Our work also illustrates the need for further research to examine to what extent epigenetic associations with psychiatric traits depend on characteristics such as age, comorbidities, exposures, and genetic background.

In sepsis, dysregulated immune responses to infections cause damage to the host. Previous studies have attempted to capture pathogen-induced leukocyte responses. However, the impact of mediators released after pathogen-leukocyte interaction on endothelial cells, and how endothelial cell responses vary depending on the pathogen-type is lacking. Here, we comprehensively characterized the transcriptomic responses of human leukocytes and endothelial cells to Gram negative-bacteria, Gram positive-bacteria, and fungi. We showed that whole pathogen lysates induced strong activation of leukocytes but not endothelial cells. Interestingly, the common response of leukocytes to various pathogens converges on endothelial activation. By exposing endothelial cells to leukocyte-released mediators, we observed a strong activation of endothelial cells at both transcription and protein levels. By adding IL-1RA and TNF-alpha antibody in leukocyte-released mediators before exposing to endothelial cells, we identified specific roles for IL-1 and TNF-alpha in driving the most, but not all, endothelial activation. We also showed for the first time, activation of interferon response by endothelial cells in response to leukocyte-released mediators, independently from IL-1 and TNF-alpha pathways. Our study therefore, not only provides pathogen-dependent transcriptional changes in leukocytes and endothelial cells during infections, but also reveals a role for IFN, together with IL1 and TNF alpha signaling, in mediating leukocyte-endothelial interaction in infections.

Our aim was to develop a prediction model for infants from the general population, with easily obtainable predictors, that accurately predicts risk of future developmental delay at age 4 and then assess its performance. Longitudinal cohort data were used (N = 1983), including full-term and preterm children. Development at age 4 was assessed using the Ages and Stages Questionnaire. Candidate predictors included perinatal and parental factors as well as growth and developmental milestones during the first two years. We applied multiple logistic regression with backwards selection and internal validation, and we assessed calibration and discriminative performance (i.e., area under the curve (AUC)). The model was evaluated in terms of sensitivity and specificity at several cut-off values. The final model included sex, maternal educational level, pre-existing maternal obesity, several milestones (smiling, speaking 2&ndash, 3 word sentences, standing) and weight for height z score at age 1. The fit was good, and the discriminative performance was high (AUC: 0.837). Sensitivity and specificity were 73% and 80% at a cut-off probability of 10%. Our model is promising for use as a prediction tool in community-based settings. It could aid to identify infants in early life (age 2) with increased risk of future developmental problems at age 4 that may benefit from early interventions.

Contains fulltext : 195595.pdf (Publisher’s version ) (Open Access) Here we conducted a large-scale genetic association analysis of educational attainment in a sample of approximately 1.1 million individuals and identify 1,271 independent genome-wide-significant SNPs. For the SNPs taken together, we found evidence of heterogeneous effects across environments. The SNPs implicate genes involved in brain-development processes and neuron-to-neuron communication. In a separate analysis of the X chromosome, we identify 10 independent genome-wide-significant SNPs and estimate a SNP heritability of around 0.3% in both men and women, consistent with partial dosage compensation. A joint (multi-phenotype) analysis of educational attainment and three related cognitive phenotypes generates polygenic scores that explain 11-13% of the variance in educational attainment and 7-10% of the variance in cognitive performance. This prediction accuracy substantially increases the utility of polygenic scores as tools in research.

Item does not contain fulltext The autosomal dominant cerebellar ataxias, referred to as spinocerebellar ataxias in genetic nomenclature, are a rare group of progressive neurodegenerative disorders characterized by loss of balance and coordination. Despite the identification of numerous disease genes, a substantial number of cases still remain without a genetic diagnosis. Here, we report five novel spinocerebellar ataxia genes, FAT2, PLD3, KIF26B, EP300, and FAT1, identified through a combination of exome sequencing in genetically undiagnosed families and targeted resequencing of exome candidates in a cohort of singletons. We validated almost all genes genetically, assessed damaging effects of the gene variants in cell models and further consolidated a role for several of these genes in the aetiology of spinocerebellar ataxia through network analysis. Our work links spinocerebellar ataxia to alterations in synaptic transmission and transcription regulation, and identifies these as the main shared mechanisms underlying the genetically diverse spinocerebellar ataxia types.

Idiopathic achalasia is a severe motility disorder of the esophagus and is characterized by a failure of the lower esophageal sphincter to relax due to a loss of neurons in the myenteric plexus. Most recently, we identified an eight-amino-acid insertion in the cytoplasmic tail of HLA-DQβ1 as strong achalasia risk factor in a sample set from Central Europe, Italy and Spain. Here, we tested whether the HLA-DQβ1 insertion also confers achalasia risk in the Polish and Swedish population. We could replicate the initial findings and the insertion shows strong achalasia association in both samples (Poland P=1.84 × 10(-04), Sweden P=7.44 × 10(-05)). Combining all five European data sets - Central Europe, Italy, Spain, Poland and Sweden - the insertion is achalasia associated with Pcombined=1.67 × 10(-35). In addition, we observe that the frequency of the insertion shows a geospatial north-south gradient. The insertion is less common in northern (around 6-7% in patients and 2% in controls from Sweden and Poland) compared with southern Europeans (~16% in patients and 8% in controls from Italy) and shows a stronger attributable risk in the southern European population. Our study provides evidence that the prevalence of achalasia may differ between populations.European Journal of Human Genetics advance online publication, 6 January 2016; doi:10.1038/ejhg.2015.262. ispartof: European Journal of Human Genetics vol:24 issue:8 pages:1228-1231 ispartof: location:England status: published

Background— Abdominal aortic aneurysm (AAA) is a common cardiovascular disease among older people and demonstrates significant heritability. In contrast to similar complex diseases, relatively few genetic associations with AAA have been confirmed. We reanalyzed our genome-wide study and carried through to replication suggestive discovery associations at a lower level of significance. Methods and Results— A genome-wide association study was conducted using 1830 cases from the United Kingdom, New Zealand, and Australia with infrarenal aorta diameter ≥30 mm or ruptured AAA and 5435 unscreened controls from the 1958 Birth Cohort and National Blood Service cohort from the Wellcome Trust Case Control Consortium. Eight suggestive associations with P −4 were carried through to in silico replication in 1292 AAA cases and 30 503 controls. One single-nucleotide polymorphism associated with P LDLR ) rs6511720 A was significantly associated overall and in 3 of 5 individual replication studies. The full study showed an association that reached genome-wide significance (odds ratio, 0.76; 95% confidence interval, 0.70–0.83; P =2.08×10 −10 ). Conclusions— LDLR rs6511720 is associated with AAA. This finding is consistent with established effects of this variant on coronary artery disease. Shared causal pathways with other cardiovascular diseases may present novel opportunities for preventative and therapeutic strategies for AAA.

There is an urgent need to standardize the semantics of biomedical data values, such as phenotypes, to enable comparative and integrative analyses. However, it is unlikely that all studies will use the same data collection protocols. As a result, retrospective standardization is often required, which involves matching of original (unstructured or locally coded) data to widely used coding or ontology systems such as SNOMED CT (clinical terms), ICD-10 (International Classification of Disease) and HPO (Human Phenotype Ontology). This data curation process is usually a time-consuming process performed by a human expert. To help mechanize this process, we have developed SORTA, a computer-aided system for rapidly encoding free text or locally coded values to a formal coding system or ontology. SORTA matches original data values (uploaded in semicolon delimited format) to a target coding system (uploaded in Excel spreadsheet, OWL ontology web language or OBO open biomedical ontologies format). It then semi- automatically shortlists candidate codes for each data value using Lucene and n-gram based matching algorithms, and can also learn from matches chosen by human experts. We evaluated SORTA's applicability in two use cases. For the LifeLines biobank, we used SORTA to recode 90 000 free text values (including 5211 unique values) about physical exercise to MET (Metabolic Equivalent of Task) codes. For the CINEAS clinical symptom coding system, we used SORTA to map to HPO, enriching HPO when necessary (315 terms matched so far). Out of the shortlists at rank 1, we found a precision/recall of 0.97/0.98 in LifeLines and of 0.58/0.45 in CINEAS. More importantly, users found the tool both a major time saver and a quality improvement because SORTA reduced the chances of human mistakes. Thus, SORTA can dramatically ease data (re)coding tasks and we believe it will prove useful for many more projects. Database URL: http://molgenis.org/sorta or as an open source download from http://www.molgenis.org/wiki/SORTA.