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Folder 1. Raw 13C NMR data for the liver glycogen samples. Folder names with CTL refer to mice fed standard chow, folder names with HS1 refer to mice given sugar supplements with U-13C-glucose and folder names with HS2 refer to mice given sugar enriched with U-13C-fructose. These data can be opened and processed by widely available NMR processing software such as ACD labs, Mestre Nova and NUTS. Folder 2. Spreadsheets for the NMR signal areas measured from the 13C NMR spectra and estimation of PPP fluxes from these signal areas Hepatic PPP fluxes from both [U-13C] glucose and [U-13C]fructose precursors were assessed by 13C NMR analysis of glycogen 13C isotopomers Glucose-6-phosphate generated via glucokinase and the direct pathwayis preferentially utilized by PPP. European Commission ITN Treatment H2020-MSCA-ITN-721236 Peer reviewed

Direct effects of SGAs on macrophage-adipocyte communication. The xls file shows the raw data obtained from the measurement of gene expression from the isolated human mature adipocytes co-cultured with THP-1 derived macrophages pre-treated with ARI, OLA, and dehydroaripiprazole (dARI) and gene expression in macrophages treated with ARI, OLA and dARI during and after their polarisation. Macrophages induce expression of pro-inflammatory genes in human subcutaneous adipocytes without affecting the expression of adipokines or genes involved in energy regulation SGAs and dexamethasone had a mild effect on macrophage-adipocyte communication in M1 macrophage phenotype European Comission ITN Treatment H2020-MSCA-ITN-721236 Peer reviewed

This dataset contains approximately 60 hours of recordings from a prototype chewing detection system. The sensor signals include photoplethysmography (PPG) and processed audio from the ear-worn chewing sensor, and signals from a belt-mounted 3D accelerometer. The recording sessions include 14 participants and were conducted in the context of the EU funded SPLENDID project, at Wageningen University, The Netherlands, during the summer of 2015. The purpose of the dataset is to help develop effective algorithms for chewing detection based PPG, audio and accelerometer signals. -x-x-x-x-x-x-x-x- If you use this dataset, please cite the following papers: [1] V. Papapanagiotou, C. Diou, L. Zhou, J. van den Boer, M. Mars and A. Delopoulos, “The SPLENDID chewing detection challenge,” 2017 39th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC), Jeju Island, South Korea, 2017, pp. 817-820. doi: 10.1109/EMBC.2017.8036949 URL: http://ieeexplore.ieee.org/document/8036949/ [2] V. Papapanagiotou, C. Diou, L. Zhou, J. van den Boer, M. Mars and A. Delopoulos, “A Novel Chewing Detection System Based on PPG, Audio, and Accelerometry,” in IEEE Journal of Biomedical and Health Informatics, vol. 21, no. 3, pp. 607-618, May 2017. doi: 10.1109/JBHI.2016.2625271 URL: http://ieeexplore.ieee.org/document/7736096/ ****ATTENTION: This publication is replaced by a new version of the data. For the new version please look at the reference list****

[Adverse Drug Reactions and CT] The xls file shows relevant information about the treatment with aripiprazole and olanzapine, as well as about their possible adverse effects and the frequency with which they occur. [Genotypes] This is a doc files where It is showm the genotype and phenotype frequencies of the analysed polymorphisms [Objective] To assess adverse events (AEs) and safety of aripiprazole (ARI) and olanzapine (OLA) treatment. [Conclusions] OLA induced more cardiovascular changes; however, more ADRs were registered to ARI. In addition, some polymorphisms may explain the difference in the incidence of these effects among subjects. European Comission ITN Treatment H2020-MSCA-ITN-721236 Peer reviewed

A simple and sensitive liquid chromatography-tandem mass spectrometry method was developed and validated in human plasma for the simultaneous determination of aripiprazole (ARI) and its metabolite dehydro-aripiprazole (DARI); olanzapine (OLA), risperidone (RIS), paliperidone (PAL), quetiapine (QUE), clozapine (CLO) and caffeine (CAF). CAF is included to the method because it can have an influence on drug metabolism due to competitive inhibition. The above mentioned compounds and their isotope-labeled internal standards were extracted from 200 µL human plasma samples by both, effective phospholipids-eliminating three-step microelution-solid-phase extraction (µ-SPE) and protein precipitation (PPT) for comparison. A combination of formic acid (0.2%)-acetonitrile (pH 3.0; 65:35, v/v) was used as mobile phase and the chromatogram was run under gradient conditions at a flow rate of 0.6 mL/min. Run time lasted 6 min, followed by a re-equilibration time of 3 min. All analytes were monitored by mass spectrometric detection operating in multiple reaction monitoring mode and the method was validated covering the corresponding therapeutic ranges: 0.18-120 ng/mL for ARI, 0.25-80 ng/mL for DARI, 1.00-100 ng/mL for OLA, 0.70-60 ng/mL for RIS, 0.20-30 ng/mL for PAL, 0.50-160 ng/mL for QUE, 0.50-1000 ng/mL for CLO, and finally 1200-3700 ng/mL for CAF. The method was validated based on the recommendations of regulatory agencies through tests of precision, accuracy, extraction recovery, identity confirmation, trueness, matrix effect, process efficiency, stability, selectivity, linearity and carry-over effect fulfilling the guideline requirements. Our µ-SPE method results in the elimination of more than 99% of early eluting and more than 92% of late-eluting phospholipids compared to PPT. Additionally, the method was successfully applied for quantifying ARI and OLA plasma concentrations from healthy volunteers. File 1. This xls files shows the data related to the main charateristics used for the development and validation of the new method as long as the measures for letting assure the repeatability and intermediate precision and accuracy values. The results obtained for the pharmacokinetic parameters are also included in the file File 2 This jpg file shows the product ion spectra and chemical structures of the antipsychotics and their metabolites obtained by collision-induced dissociation (CID) of the indicated precursor ions [M+H]+. The fragmentation patterns of all analytes are indicated by an arrow on their chemical structure of each analyte. The results are presented as the percentage of counts versus Mass-to-Charge (m/z). All mass peaks have been normalized to the most abundant European Comission ITN Treatment H2020-MSCA-ITN-721236 Peer reviewed

The incidence of Type 2 Diabetes Mellitus (T2DM) is reaching epidemic proportions. Recent investigations have demonstrated that long-term treatment with Second Generation Antipsychotics (SGAs), the main-line treatment for schizophrenia, can induce T2DM. Beta cell dysfunction is proposed as a plausible mechanism by which SGAs cause T2DM, but the process remains largely unknown. In this Thesis, we have investigated whether two unrelated SGAs, olanzapine, a common prescribed SGA with diabetogenic properties, and aripiprazole, a more recently developed SGA with less explored metabolic-side effects, can impact on beta cells. We analyzed beta cell functionality and pancreatic islet plasticity in two in vivo studies: female mice treated with olanzapine for 6 weeks via intraperitoneal and female mice fed an olanzapine- or aripiprazole-supplemented diet for 6 months. Additionally, we conducted gene expression analysis in islets of mice receiving the medicated diet and in vitro studies to evaluate beta cell functionality and the molecular mechanisms associated to the treatments. Our results evidenced that long-term treatment with olanzapine or aripiprazole induced weight gain, glucose intolerance and beta cell dysfunction, but the mechanisms behind these alterations are specific for each SGA. Whereas olanzapine effects in the pancreas in female mice seem to be dependent on an obesogenic-like phenotype, it activated endoplasmic reticulum (ER) stress in both INS-1 cells and pancreatic islets. Alleviation of olanzapine-induced ER stress with Tauroursodeoxycholic acid (TUDCA) recovered insulin secretion, suggesting that inhibition of insulin secretion by olanzapine is dependent on ER stress activation. On the other hand, aripiprazole treatment during 6 months induced serotonin production through tryptophan hydroxylase 1 (TPH1) activation in pancreatic islets. Moreover, beta cell hypertrophy and higher beta cell mass were found in aripiprazole-treated mice concomitantly to the activation of mTORC1/S6. Additionally, ex vivo experiments using pancreatic islets revealed that aripiprazole inhibition of insulin secretion was due to a reduction in calcium entry into the beta cell. Until now, regulation of the serotonergic system in islets has been associated to beta cell compensation in pregnancy and postnatal growth. Thus, in this Thesis, we have described for the first time the modulation of the serotonergic system in pancreatic islets by pharmacological treatment with aripiprazole, showing that serotonin production induced by this SGA plays a critical role in intra-islet functionality and beta cell mass and it might also explain other metabolic disturbances associated with aripiprazole treatment Folder 1. Analysis of in vivo chronic dietary treatment with both olanzapine and aripiprazole (5.5-6 mg/kg/d) for 6 months in WT females to assess disturbances in glucose metabolism as well as beta-cell dysfunction. Metabolic tests have been done before sacrifice: glucose tolerance test (GTT), insulin tolerance test (ITT), and glucose-stimulated insulin secretion (GSIS). The xls file shows the statistics analysis and raw data analysis of the parameters measured. The immunofluorescence and immunohistochemistry analysis are also included in xls file. The pzfx files can be opened with GraphPad Prism 8 XML Project show the relationships between some of the parameters showed in xls files. Folder 2. In vitro data in INS-1 cells. The xls files showed the quantification of the short-term impact of olanzapine (1-6 µM) and the long-term impact of both olanzapine and aripiprazole (1-6 µM) in glucose-stimulated insulin secretion (GSIS) and the western blot quantification of the molecular machinery associated with ER stress activation (mainly PERK/eIF2a and IRE1-alpha) in INS-1 cells after olanzapine/aripiprazole treatment with different concentrations (1-6 µM) for 4h. The pzfx files can be opened with GraphPad Prism 8 XML Project and show the relationships between some of the parameters showed in xls files. European Comission ITN Treatment H2020-MSCA-ITN-721236 Peer reviewed

, NL4-3Balor ATP and NL4-3Bal. Next, cells were extensively washed and either stained immediately or cultured for 48 h in complete medium before staining. Cells were stained with antibodies specific for CD83, DC-SIGN, or MR and analyzed by flow cytometry. Results from one representative experiment and flow data acquired after 48 h are presented. %, Percentage of cells expressing the studied cell surface marker as defined by flow cytometry. Statistical analyses were performed on the results of three independent experiments (, P < 0.01 ; , P < 0.05).Copyright information:Taken from "Extracellular ATP reduces HIV-1 transfer from immature dendritic cells to CD4T lymphocytes"http://www.retrovirology.com/content/5/1/30Retrovirology 2008;5():30-30.Published online 28 Mar 2008PMCID:PMC2346478.

For conspecific parasites sharing the same host, kin recognition can be advantageous when the fitness of one individual depends on what another does; yet, evidence of kin recognition among parasites remains limited. Some trematodes, like Coitocaecum parvum, have plastic life cycles including two alternative life-history strategies. The parasite can wait for its intermediate host to be eaten by a fish definitive host, thus completing the classical three-host life cycle, or mature precociously and produce eggs while still inside its intermediate host as a facultative shortcut. Two different amphipod species are used as intermediate hosts by C. parvum, one small and highly mobile and the other larger, sedentary, and burrow dwelling. Amphipods often harbour two or more C. parvum individuals, all capable of using one or the other developmental strategy, thus creating potential conflicts or cooperation opportunities over transmission routes. This model was used to test the kin recognition hypothesis according to which cooperation between two conspecific individuals relies on the individuals' ability to evaluate their degree of genetic similarity. First, data showed that levels of intrahost genetic similarity between co-infecting C. parvum individuals differed between host species. Second, genetic similarity between parasites sharing the same host was strongly linked to their likelihood of adopting identical developmental strategies. Two nonexclusive hypotheses that could explain this pattern are discussed: kin recognition and cooperation between genetically similar parasites and/or matching genotypes involving parasite genotype–host compatibility filters. P. excavatum Pair-wise Rousset's distance between individual parasitesP. fluviatilis_Pair-wise Rousset's distance between individual parasites

Supplementary data from the second Critical Assessment of protein Function Annotation (CAFA2). See preprint here: http://arxiv.org/abs/1601.00891

Excessive sugar intake including high-fructose corn syrup (HFCS) is implicated in the rise of obesity, insulin resistance and non-alcoholic fatty liver disease. Liver glycogen synthesis is influenced by both fructose and insulin signaling. Therefore, the effect of HFCS on hepatic glycogenesis was evaluated in mice feeding ad-libitum. Using deuterated water: the fraction of glycogen derived from triose-P sources, Krebs cycle substrates, and direct pathway + cycling, was measured in 9 normal-chow fed mice (NC) and 12 mice fed normal chow plus a 55% fructose/45% glucose mix in the drinking water at 30% w/v (HFCS-55). This was enriched with [U-13C]fructose or [U-13C]glucose to determine the contribution of each to glycogenesis. For NC, direct pathway + cycling, Krebs cycle, and triose-P sources accounted for 66 ± 0.7%, 23 ± 0.8% and 11 ± 0.4% of glycogen synthesis, respectively. HFCS-55 mice had similar direct pathway + cycling (64 ± 1%) but lower Krebs cycle (12 ± 1%, p < 0.001) and higher triose-P contributions (24 ± 1%, p < 0.001). HFCS-55-fructose contributed 17 ± 1% via triose-P and 2 ± 0% via Krebs cycle. HFCS-55-glucose contributed 16 ± 3% via direct pathway and 1 ± 0% via Krebs cycle. In conclusion, HFCS-55 supplementation resulted in similar hepatic glycogen deposition rates. Indirect pathway contributions shifted from Krebs cycle to Triose-P sources reflecting HFCS-55-fructose utilization, while HFCS-55-glucose was incorporated almost exclusively by the direct pathway. Folder 1. Raw 1H and 2H NMR data for the liver glycogen samples. Folder names with CTL refer to mice fed standard chow, folder names with HS1 refer to mice given sugar supplements with U-13C-glucose and folder names with HS2 refer to mice given sugar enriched with U-13C-fructose. These data can be opened and processed by widely available NMR processing software such as ACD labs, Mestre Nova and NUTS. Folder 2. Raw 1H and 13C NMR data for the liver glycogen samples. Folder names with CTL refer to mice fed standard chow, folder names with HS1 refer to mice given sugar supplements with U-13C-glucose and folder names with HS2 refer to mice given sugar enriched with U-13C-fructose. These data can be opened and processed by widely available NMR processing software such as ACD labs, Mestre Nova and NUTS. Folder 3. Spreadsheets for the NMR signal areas measured from the 2H NMR spectra and estimation of glycogen synthesis sources from direct and indirect pathways based on these data (Excel 1) and the NMR signals measured from the 13C NMR spectra and estimation of the contributions of [U-13C]glucose and [U-13C]fructose to glycogen synthesis (Excel 2). European Commission ITN Treatment H2020-MSCA-ITN-721236 Peer reviewed