Search bioRxivSearch

SEARCH · Search bioRxiv

Search Search bioRxiv

Search indexed bioRxiv preprints in genomics, neuroscience, cell biology and bioinformatics. Read source abstracts and check manuscript versions; preprints are not peer reviewed.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,657 records · Page 92Linked to original sources

The role of climate change education on individual lifetime carbon emissions

Strategies to mitigate climate change often center on clean technologies such as electric vehicles and solar panels, while the mitigation potential of a quality educational experience is rarely discussed. In this paper, we investigate the long-term impact that an intensive one-year university course had on individual carbon emissions by surveying students at least five years after having taken the course. A majority of course graduates reported pro-environmental decisions (i.e., type of car to buy, food choices) that can be attributed to experiences gained in the course. Furthermore, our carbon footprint analysis demonstrates that for the average course graduate, these decisions reduced their individual carbon emissions by 2.86 tons of CO2 per year. Focus group interviews identify that course graduates have developed a strong personal connection to climate change solutions, and this is realized in their daily behaviors and through their professional careers. The paper discusses in more detail the specific components of the course that are believed to be most impactful, and it shares preliminary outcomes from similar curriculum designs that are being used with K-12 students. Our analysis also demonstrates that if similar education programs were applied at scale, the potential reductions in carbon emissions would be of similar magnitude to other large-scale mitigation strategies such as rooftop solar or electric vehicles.

scientific communication and education

Thymic Stromal Lymphopoietin Promotes Proliferation and Contractility of Human Pulmonary Artery Smooth Muscle

Hypoxia is a well-recognized risk factor in several pulmonary vascular diseases including pulmonary hypertension (PH). Furthermore, hypoxia-associated inflammatory changes enhance the structural and functional changes in the pulmonary artery (PA) of PH patients. Understanding the mechanisms that link hypoxia and inflammation, particularly early in disease, is key to development of novel therapeutic avenues for PH. Thymic stromal lymphopoietin (TSLP) is an \"early\" inflammatory mediator thought to be critical in diseases such as asthma, chronic obstructive pulmonary disease and atopic dermatitis. TSLP has canonical effects on the immune system, but can also have non-canonical effects on resident lung cells, e.g. airway smooth muscle. Currently, the expression and role of TSLP in the PA is unknown. We hypothesized that locally-produced TSLP potentiates the effects of hypoxia in PA remodeling and contractility relevant to PH. Experiments in human PA endothelial cells (PAECs) and smooth muscle cells (PASMCs) found PAECs to be a larger source of TSLP which targets PASMCs to enhance intracellular Ca2+ responses to vasoconstrictor agonist as well as cell proliferation, acting via a number of signaling cascades including Stat3 and PI3/Akt. Hypoxia, acting via HIF1, enhanced PAEC production of TSLP, and promoted TSLP effects on PASMCs. Interestingly, TSLP per se enhance HIF1a. Overall, these novel data highlight a role for TSLP in hypoxia effects on the PA, and thus relevance for inflammation in PH.

physiology

Prevalence and correlates of anemia among children aged 6-23 months in Wolaita Zone, Southern Ethiopia

BackgroundAnemia, the worlds most common micro-nutrient deficiency disorder, can affect a person at any time and at all stages of life, although children aged 6 -23 months are particularly at higher risk. If left untreated, it adversely affects the health, cognitive development, school achievement, and work performance. However, littlewas investigated among young children in Sub-Saharan countries including Ethiopia. This research aimed to investigate its magnitude and correlates to address the gap and guide design of evidence based intervention.\n\nMethodsA community-based cross-sectional study was conducted from May -June 2016 in rural districts of Wolaita Zone. Multi-stage sampling technique was applied to select 990 mother-child pairs. Socio-demography, health and nutritional characteristics were collected by administering interview type questionnaire to mothers/care-givers. Blood samples were taken to diagnose anemia by using HemoCue device, and status was determined using cut-offs used for children aged 6-59 months. Hemoglobin concentration below 11.0 g/dl was considered anemic. Data were analyzed with Statav 14. Bivariate and multivariable logistic regressions were applied to identify candidate and predictor variables respectively. Statistical significance was determined at p-value < 0.05 at 95% confidence interval.\n\nResultsThe mean hemoglobin level of children was 10.44{+/-}1.3g/dl, and 65.7% of them were anemic. Among anemic children, 0.4% were severely anemic (<7.0g/dl), while 28.1% and 37.2% were mildly (10.0-10.9g/dl) and moderately (7.0-9.9g/dl) anemic, respectively. In the multivariable analysis, having maternal age of 35 years and above (AOR=1.96), being government employee (AOR=0.29),being merchant (AOR= 0.43) and other occupation (AOR=3.17) were correlated with anemia in children in rural Wolaita. Similarly, receiving antihelminthic drugs (AOR= 0.39), being female child (AOR= 1.76), consuming poor dietary diversity (AOR=1.40), and having moderate household food insecurity (AOR=1.72) were associated with anemia in rural Wolaita.\n\nConclusionA large majority of children in the rural Wolaita were anemic and the need for proven public health interventions such as food diversification, provision of anti-helminthic drugs and ensuring household food security is crucial. In addition, educating women on nutrition and diet diversification, as well as helping them with alternative sources of income might be interventions in the study area.

epidemiology

Deficient skeletal muscle regeneration after injury induced by a Clostridium perfringens strain associated with gas gangrene

Very little is known about the muscle regeneration process that follows myonecrosis induced by C. perfringens, the main agent of gas gangrene. This study revealed that, in a murine model of the infection with a sublethal inoculum of C. perfringens, muscle necrosis occurs concomitantly with significant vascular damage, which limits the migration of inflammatory cells. A significant increase in cytokines that promote inflammation explains the presence of inflammatory infiltrate; however, an impaired IFN{gamma} expression, a reduced number of Ml macrophages, a deficient phagocytic activity, and the prolongation of the permanence of inflammatory cells, lead to deficient muscle regeneration. The expression of TGF{beta}1 and the consequent accumulation of collagen in the muscle, likely contribute to the fibrosis observed 30 days after infection. These results provide new information on the pathogenesis of gas gangrene caused by C. perfringens, shed light on the basis of the poor muscle regenerative activity, and may open new perspectives for the development of novel therapies for patients suffering this disease.

microbiology

Bodily sensations in social scenarios: Where in the body?

Bodily states are fundamental to emotions emergence and are believed to constitute the first step in the chain of events that culminate in emotional awareness. Recent works have given fresh support to this view by showing that distinct topographical maps can be derived to describe how basic and more complex emotions are represented in the body. However, it is still unclear whether these bodily maps can also extend to emotions experienced specifically within social interactions and how these representations relate to basic emotions. To address this issue, we used the emBODY tool to obtain high-resolution bodily maps that represent the body activation and deactivation experienced by healthy participants in social scenarios depicting establishment or loss of social bonds. We show that clear patterns of activation/deactivation across the body emerge depending on the valence and on the characteristics of the single social scenarios, but also a common activation of head, chest and limbs across scenarios. Furthermore, we showed that maps related to complex social scenarios are strongly correlated with bodily states experienced in basic emotions, suggesting that the patterns of body activation/deactivation found for social scenarios might represent a combination of different basic emotions these experiences elicit. Our data tackle conscious emotional experiences and show for the first time how painful social events are felt on the body, providing findings that complement verbal reports and neuroimaging data on social rejection. Furthermore, they show that bodily feelings related to complex social scenarios, despite referring to unified independent emotional states, are also related to bodily correlates of basic emotions.

neuroscience

Conditioned place avoidance using encapsulated calcium propionate as an appetite suppressant for broiler breeders

Broiler breeders, the parent stock of meat chicks, are feed-restricte throughout rearing to avoid obesity-related problems in their health and reproductive performance. Broiler breeders often show signs of chronic hunger, lack of satiety and feeding frustration, and the development of alternative feeding strategies has investigated the inclusion of calcium propionate (CaP) as an appetite suppressant. However, the mechanisms involved in the reduction of voluntary feed intake are unknown, but are thought to be due to low palatability, gastrointestinal discomfort, or both. The objective of this experiment was to examine the effect of CaP as an appetite suppressant on the experience of a negative affective state, using a conditioned place preference test. Twenty four broiler breeders were trained to associate the consumption of CaP or a placebo pill with a red or blue place, depending on inherent colour preference. Pullets consumed two pills followed by 20 g feed allotment. The CaP pill contained 160 mg of CaP and the placebo pill had 160 mg of feed. Conditioning lasted for 90 min/pullet/day over 8 consecutive days at 7 and 9 weeks of age, and pullets choice was tested in a T-maze twice on two consecutive days at both 8 and 10 weeks of age. Data were analysed using a linear mixed regression model, with pen nested in the model and age as a repeated measure. Pullets were less likely to choose the place conditioned with the consumption of CaP (P<0.05) and the preference of the placebo linearly increased with training sessions (P<0.05). These results suggest that calcium propionate as an appetite suppressant can induce a negative affective state, with the lower feed intake resulting from a conditioned response to the negative effect of calcium propionate rather than to satiety.

animal behavior and cognition

Empirically-Derived Synthetic Populations to Overcome Small Sample Sizes

Limited sample sizes can hinder biomedical research and lead to spurious findings. The objective of this work is to present a new method to generate synthetic populations (SPs) from sparse data samples to aid in modeling developments. Matched case-control data (n=180 pairs) defined the limited samples. Cases and controls were considered as two separate limited samples. Synthetic populations were generated for these observed samples using multivariate unconstrained bandwidth kernel density estimations. We included four continuous variables and one categorical variable for each individual. Bandwidth matrices were determined with Differential Evolution (DE) optimization driven by covariance comparisons. Four synthetic samples (n=180) were constructed from their respective SP for comparison purposes. Similarity between the observed samples with equally sized synthetic-samples was compared under the hypothesis that their sample distributions were the same. Distributions were compared with the maximum mean discrepancy (MMD) test statistic based on a Kernel Two-Sample Test. To evaluate similarity within a modeling context, Principal Component Analysis (PCA) score distributions and residuals were summarized with the distance to the model in X-space (DModX) as additional comparisons.\n\nFour SPs were generated with the optimization procedure. The probability of selecting a replicate when randomly constructing synthetic samples with n=180 was infinitesimally small. The MMD tests indicated that the observed sample distributions were similar to the respective synthetic distributions. For both case and control samples, PCA scores and residuals did not deviate significantly when compared with their respective synthetic samples.\n\nThe reasonableness of this SP generation approach was demonstrated. This approach produced synthetic data at the patient level statistically similar to the observed samples, and thus could be used to generate larger-sized simulated data. The methodology coupled kernel density estimation with DE optimization and deployed novel similarity metrics derived from PCA. The use of large-sized synthetic samples may be a way to overcome sparse datasets. To further develop this approach into a research tool for model building purposes, additional evaluation with increased dimensionality is required; moreover, comparisons with other techniques such as bootstrapping and cross-validation will be required for a complete evaluation.

bioinformatics

Dosage Matters: A Randomized Controlled Trial of Rehabilitation Dose in the Chronic Phase after Stroke

Background and PurposeFor stroke rehabilitation, task-specific training in animal models and human rehabilitation trials is considered important to trigger inherent neuroplasticity, promote motor learning, and functional recovery. Little is known, however, about what constitutes an effective dosage of therapy.\n\nMethodsThis is a parallel group, four arm, single blind, phase I, randomized control trial of four dosages of upper extremity therapy delivered in an outpatient setting during the chronic phase after stroke. Participants were randomized into groups that varied in total dosage of therapy (i.e., 0, 15, 30, or 60 hours). Seven hundred and four participants were assessed for eligibility, 50 were eligible to enroll, 45 were randomized, 44 participated and 41 completed the study. Planned primary analyses used linear mixed effects regression to model baseline to post-intervention changes in the Motor Activity Log-Quality of Movement rating (MALQ) and the Wolf Motor Function Test (WMFT) time score as a function of therapy dosage. A series of hierarchical models were constructed using the MALQ and WMFT.\n\nResultsWe observed a significant dose response curve: the greater the dosage of training, the greater the change in MALQ, with the dose by week slope parameter of 0.0045 ({Delta}MAL/hour/week; p = 0.0011; 95% CI = [0.0019; 0.0071]). Over the 3 weeks of therapy, this corresponds to a gain of 0.81 in MALQ for the 60 hour dose.\n\nConclusionsFor mild-to-moderately impaired stroke survivors, the dosage of a patient-centered, task specific motor therapy was shown to systematically influence the gain in quality of arm use in the natural environment, but not functional capacity as measured in the laboratory. We highlight the importance of recovery outcomes that capture arm use vs. functional capacity.\n\nClinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT 01749358

clinical trials

Hidden ‘risk’ in polygenic scores: clinical use today could exacerbate health disparities

Polygenic risk scores (PRS) are poised to improve biomedical outcomes via precision medicine. However, the major ethical and scientific challenge surrounding clinical implementation is that they are many-fold more accurate in European ancestry individuals than others. This disparity is an inescapable consequence of Eurocentric genome-wide association study biases. This highlights that--unlike clinical biomarkers and prescription drugs, which may individually work better in some populations but do not ubiquitously perform far better in European populations--clinical uses of PRS today would systematically afford greater improvement to European descent populations. Early diversifying efforts show promise in levelling this vast imbalance, even when non-European sample sizes are considerably smaller than the largest studies to date. To realize the full and equitable potential of PRS, we must prioritize greater diversity in genetic studies and public dissemination of summary statistics to ensure that health disparities are not increased for those already most underserved.

genetics

The mouse HP1 proteins are not required for cell viability but are essential for preventing liver tumorigenesis

Chromatin organization plays essential roles in cell identity and functions. Here, we demonstrated by hepatocyte-specific inactivation of the genes encoding the three Heterochromatin Protein 1 (HP1, {beta} and {gamma}) in mice (HP1-TKO) that these proteins are dispensable for hepatocyte activity and survival. Conversely, the chronic absence of these proteins led to a drastic increased incidence of liver tumor development. Molecular characterization of HP1-TKO hepatocytes revealed that HP1 proteins are required for maintenance of histone marks associated with heterochromatin, and for the appropriate expression of large number of genes involved in liver-specific functions as well as in genes encoding for transcriptional repressors of the KRAB-ZFP family. Moreover, several specific endogenous retrovirus families were upregulated in HP1-TKO hepatocytes, leading to the deregulated expression of genes in their vicinity. Our findings indicate that HP1 proteins act as guardians of liver homeostasis to prevent tumor development through the modulation of multiple chromatin-associated events.

cancer biology

Synthetic essentiality of metabolic regulator PDHK1 in PTEN-deficient cells and cancers

PTEN is a tumor suppressor that is often inactivated in cancer and possesses both lipid and protein phosphatase activities. We report the metabolic regulator PDHK1 (pyruvate dehydrogenase kinase1) is a synthetic-essential gene in PTEN-deficient cancer and normal cells. The predominant mechanism of PDHK1 regulation and dependency is the PTEN protein phosphatase dephosphorylates NF{kappa};B activating protein (NKAP) and limits NF{kappa}B activation to suppress expression of PDHK1, a NF{kappa}B target gene. Loss of the PTEN protein phosphatase upregulates PDHK1 to drive aerobic glycolysis and induce PDHK1 cellular dependence. PTEN-deficient human tumors harbor increased PDHK1, which is a biomarker of decreased patient survival, establishing clinical relevance. This study uncovers a PTEN-regulated signaling pathway and reveals PDHK1 as a potential target in PTEN-deficient cancers.\n\nSIGNIFICANCEThe tumor suppressor PTEN is widely inactivated in cancers and tumor syndromes. PTEN antagonizes PI3K/AKT signaling via its lipid phosphatase activity. The modest success of PI3K/AKT inhibition in PTEN-deficient cancer patients provides rationale for identifying other vulnerabilities in PTEN-deficient cancers to improve clinical outcomes. We show that PTEN-deficient cells are uniquely sensitive to PDHK1 inhibition. PTEN and PDHK1 co-suppression reduced colony formation and induced cell death in vitro and tumor regression in vivo. PDHK1 levels were high in PTEN-deficient patient tumors and associated with inferior patient survival, establishing clinical relevance. Our study identifies a PTEN-regulated signaling pathway linking the PTEN protein phosphatase to the metabolic regulator PDHK1 and provides a mechanistic basis for PDHK1 targeting in PTEN-deficient cancers.

cancer biology

Elevated de novo fatty acid biosynthesis gene expression promotes melanoma cell survival and drug resistance

Elevated de novo fatty acid biosynthesis (DNFA) is a hallmark adaptation in many cancers that supports survival, proliferation, and metastasis. Here we elucidate previously unexplored aspects of transcription regulation and clinical relevance of DNFA in melanomas. We show that elevated expression of DNFA genes is characteristic of many tumor types and correlates with poor prognosis. Elevated DNFA gene expression depends on transcription factor SREBP1 in multiple melanoma cell lines. SREBP1 predominantly binds to the transcription start sites of DNFA genes, directly regulating transcription via RNA polymerase II recruitment and productive elongation. We find that SREBP1-regulated DNFA represents an intrinsic survival mechanism in melanoma cells, regardless of proliferative state and oncogenic mutation status. Indeed, malignant melanoma cells exhibit elevated DNFA gene expression after pro-survival signaling pathways are blocked (e.g. by the BRAF inhibitor vemurafenib). Altogether, these results implicate SREBP1 and DNFA enzymes as enticing therapeutic targets in melanomas.

cancer biology

Flux-Balance Based Modeling of Biofilm Communities

Models of microbial community dynamics generally rely on a sub-scale model for microbial metabolisms. In systems such as distributed multispecies communities like biofilms, where it is not reasonable to simplify to a small number of limiting substrates, tracking the large number of active metabolites likely requires measurement or estimation of large numbers of kinetic and regulatory parameters. Alternatively, a largely kinetics-free methodology is proposed combining cellular level constrained, steady state metabolic flux analysis with macro scale microbial community models. The methodology easily allows coupling of macroscale information, including measurement data, with cell-scale metabolism. Illustrative examples are included.

microbiology

Phenotypic and genotypic resistance to commonly used insecticides in Aedes aegypti among four cities in southern Ecuador

Insecticide resistance (IR) can undermine efforts to control vector species of public health importance. Aedes aegypti is the main vector of resurging diseases in the Americas such as yellow fever and dengue, as well as recently emerging chikungunya and Zika viruses, which have caused unprecedented epidemics in the region. Vector control remains the primary public health intervention to prevent outbreaks of Aedes transmitted diseases. In many high-risk regions, like southern Ecuador, we have limited information on IR in Ae. aegypti. In this study, IR status in Ae. aegypti was measured across four cities in El Oro Province in Ecuador using phenotypic assays and genetic screening for alleles associated with resistance to pyrethroid insecticides. Bottle bioassays showed significant inter-seasonal variation in resistance to deltamethrin, a pyrethroid insecticide commonly used by the Ministry of Health, and alpha cypermethrin, as well as differences in deltamethrin resistance between cities. There was also a significant difference in phenotypic response to the organophosphate, Malathion, between two of the cities during the second sampling season. Genotyping showed moderate to high frequencies of the V1016I and F1534C resistance alleles in all four cites. Frequency of resistance genotypes varied significantly between cities in the first sampling season, and not in the later seasons, suggesting a possible selective response to vector control activity. Overall, resistance levels were highest in Machala, a city where dengue is hyperendemic and where insecticide use has historically been more intense than in the other cities included in the study. Despite statistically significant evidence that resistance alleles conferred phenotypic resistance, there was not precise correspondence between these indicators. We found that 17.6% of F1534C and 45.6% of V1016I mutant mosquitoes were susceptible in the bottle bioassays. This study shows there is spatiotemporal variability in IR in southern Ecuador, and serves as an initial examination of the genotypic and phenotypic indicators of IR in this region, providing important information to guide the vector control interventions by the public health sector.

epidemiology

A comparison of automated lesion segmentation approaches for chronic stroke T1-weighted MRI data

Accurate stroke lesion segmentation is a critical step in the neuroimaging processing pipeline to assess the relationship between post-stroke brain structure, function, and behavior. While many multimodal segmentation algorithms have been developed for acute stroke neuroimaging, few are effective with only a single T1-weighted (T1w) anatomical MRI. This is a critical gap because most stroke rehabilitation research relies on a single T1w MRI for defining the lesion. Although several attempts to automate the segmentation of chronic lesions on single-channel T1w MRI have been made, these approaches have not been systematically evaluated on a large dataset. Here, we performed an exhaustive review of the literature and identified one semi- and three fully automated approaches for segmentation of chronic stroke lesions using T1w MRI within the last ten years: Clusterize, Automated Lesion Identification, Gaussian naive Bayes lesion detection, and LINDA. We evaluated each method on a large T1w stroke dataset (N=181) using visual and quantitative methods. LINDA was the most computationally expensive approach, but performed best across the three main evaluation metrics (median values: Dice Coefficient=0.50, Hausdorffs Distance=36.34 mm, and Average Symmetric Surface Distance = 4.97 mm), whereas the Gaussian Bayes method had the highest recall/least false negatives (median=0.80). Segmentation accuracy in all automated methods were influenced by size (small: worst) and stroke territory (brainstem, cerebellum: worst) of the lesion. To facilitate reproducible science, we have made our analysis files publicly available online at https://github.com/npnl/elsa. We hope these findings are informative to future development of T1w lesion segmentation algorithms.

neuroscience

An E2-ubiquitin thioester-driven approach to identify substrates modified with ubiquitin and ubiquitin-like molecules

Covalent modifications of proteins with ubiquitin and ubiquitin-like molecules are instrumental to many biological processes. However, identifying the E3 ligase responsible for these modifications remains a major bottleneck in ubiquitin research. Here, we present an E2-thioester-driven identification (E2~dID) method for the targeted identification of substrates of specific E2 and E3 enzyme pairs. E2~dID exploits the central position of E2-conjugating enzymes in the ubiquitination cascade and provides in vitro generated biotinylated E2~ubiquitin thioester conjugates as the sole source for ubiquitination in extracto. This enables purification and mass spectrometry-based identification of modified proteins under stringent conditions independently of the biological source of the extract. We demonstrate the sensitivity and specificity of E2-dID by identifying and validating substrates of APC/C in human cells. Finally, we perform E2~dID with SUMO in S. cerevisiae, showing that this approach can be easily adapted to other ubiquitin-like modifiers and experimental models.

biochemistry

PCF11 connects alternative polyadenylation to formation and spontaneous regression of neuroblastoma

Diversification at the transcriptome 3end is an important and evolutionarily conserved layer of gene regulation associated with differentiation and dedifferentiation processes. However the underlying mechanisms and functional consequences are poorly defined. Here, we identify extensive transcriptome-3end-alterations in neuroblastoma, a tumour entity with a paucity of recurrent somatic mutations and an unusually high frequency of spontaneous regression. Utilising extensive RNAi-screening we reveal the landscape and drivers of transcriptome-3end-diversification, discovering PCF11 as critical regulator, directing alternative polyadenylation (APA) of hundreds of transcripts including a differentiation RNA-operon. PCF11 shapes inputs converging on WNT-signalling, and governs cell cycle, proliferation, apoptosis and neurodifferentiation. Postnatal PCF11 down-regulation induces a neurodifferentiation program, and low-level PCF11 in neuroblastoma associates with favourable outcome and spontaneous tumour regression. Our findings document a critical role for APA in tumourigenesis and describe a novel mechanism for cell fate reprogramming in neuroblastoma with important clinical implications. An interactive data repository of transcriptome-wide APA covering >170 RNAis, and an APA-network map with regulatory hubs is provided.

developmental biology

C/VDdb: a multi-omics expression profiling database for a knowledge-driven approach in cardiovascular disease (CVD)

The cardiovascular disease (C/VD) database is an integrated and clustered information resource that covers multi-omic studies (microRNA, genomics, proteomics and metabolomics) of cardiovascular-related traits with special emphasis on coronary artery disease (CAD). This resource was built by mining existing literature and public databases and thereafter manual biocuration was performed. To enable integration of omic data from distinct platforms and species, a specific ontology was applied to tie together and harmonise multi-level omic studies based on gene and protein clusters (CluSO) and mapping of orthologous genes (OMAP) across species.\n\nCAD continues to be a leading cause of death in the population worldwide, and it is generally thought to be an age-related disease. However, CAD incidence rates are now known to be highly influenced by environmental factors and interactions, in addition to genetic determinants. With the complexity of CAD aetiology, there is a difficulty in research studies to elucidate general elements compared to other cardiovascular diseases.\n\nData from 92 studies, covering 13945 molecular entries (4353 unique molecules) is described, including data descriptors for experimental setup, study design, discovery-validation sample size and associated fold-changes of the differentially expressed molecular features (p-value<0.05). A dedicated interactive web interface, equipped with a multi-parametric search engine, data export and indexing menus are provided for a user-accessible browsing experience.\n\nThe main aim of this work was the development of a data repository linking clinical information and molecular differential expression in several CVD-related traits from multi-omics studies (genomics, transcriptomics, proteomics and metabolomics). As an example case of how to query and identify data sets within the database framework and concomitantly demonstrate the database utility, we queried CAD-associated studies and performed a systems-level integrative analysis.\n\nURL: www.padb.org/cvd

systems biology