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34,778 results for “diseases”
Improving distribution models of sparsely-documented disease vectors by incorporating information on related species via joint modeling
<p>A necessary component of understanding vector-borne disease risk is the accurate characterization of the distributions of their vectors. Species distribution models have been successfully applied to data-rich species but may produce inaccurate results for sparsely-documented vectors. In light of global change, vectors that are currently not well-documented could become increasingly important, requiring tools to predict their distributions. One way to achieve this could be to leverage data on related species to inform the distribution of a<strong> </strong>sparsely-documented vector based on the assumption that the environmental niches of related species are not independent. Relatedly, there is a natural dependence of the spatial distribution of a disease on the spatial dependence of its vector. Here, we propose to exploit these correlations by fitting a hierarchical model jointly to data on multiple vector species and their associated human diseases to improve distribution models of sparsely-documented species. To demonstrate this approach, we evaluated the ability of twelve models—which differed in their pooling of data from multiple vector species and inclusion of disease data—to improve distribution estimates of sparsely-documented vectors. We assessed our models on two simulated data sets, which allowed us to generalize our results and examine their mechanisms. We found that when the focal species is sparsely documented, incorporating data on related vector species reduces uncertainty and improves accuracy by reducing overfitting. When data on vector species are already incorporated, disease data only marginally improve model performance. However, when data on other vectors are not available, disease data can improve model accuracy and reduce overfitting and uncertainty. We then assessed the approach on empirical data on ticks and tick-borne diseases in Florida and found that incorporating data on other vector species improved model performance. This study illustrates the value of exploiting correlated data via joint modeling to improve distribution models of data-limited species.</p>
Transcriptomic atlas reveals organ-specific disease tolerance in sickle cell mice. Dataset for bone marrow, HbSS Townes mice injected or not with heme
<p>The objective of this experiment was to explore the transcriptome of the HbSS Townes mouse model of sickle cell disease. Townes model mice carry several human hemoglobin knock-in genes replacing the endogenous mouse genes and may be useful in studying sickle cell disease. All mice were genotyped, age- and sex-matched littermates. All HbAA (control, normal human hemoglobin) vs HbSS (sickle cell disease, mutated human hemoglobin) mice were used for experimentations at 6-8 weeks of age, to limit intra-group heterogeneity. Hemin (Ferriprotoporphyrin IX) was purchased from Frontiers Scientific and injected intravenously (iv.) in a retroorbital sinus at a concentration of 24 µmol/kg. Control mice received PBS instead. Mice were anesthetized with isoflurane 2-3% for injections, blood collection and sacrifice. All mice were sacrificed by cervical dislocation, 4 hours after injection.</p> <p>Here the dataset for HbSS mice injected or not with heme is uploaded.</p> <p>The corresponding dataset for the HbAA mice injected or not with heme can be found at <strong>10.5281/zenodo.10961162</strong></p> <p>Bone marrow RNA was extracted by Macherey Nagel kit, according to the manufacturer’s instructions. The quality and quantity of mRNA were evaluated using a 2100<br>bioanalyzer with TNA 6000 NanoKits (all Agilent Technologies, Palo Alto, CA, USA). RNA Integrity Numbers superior to 7 were eligible for subsequent reverse transcription into cDNA. RNAseq was performed at the GenomIC plateform Cochin Institute INSERM U1016. After RNA extraction, RNA quality (RNA integrity number) was estimated. 1μg of high-quality total RNA sample (RIN &gt;7) was processed to build up the libraries, using TruSeq Stranded mRNA kit (Illumina) according to manufacturer instructions. Briefly, purified poly-A containing mRNA molecules were fragmented and reverse-transcribed using random primers. Replacement of dTTP by dUTP during second strand synthesis allowed us to achieve strand specificity. Addition of a single A base to the cDNA was followed by ligation of Illumina adapters.<br>Libraries were quantified by qPCR using KAPA Library Quantification Kits for Illumina Libraries (KapaBiosystems, Wilmington, MA). Library profiles were assessed using DNA High Sensitivity LabChip kits on an Agilent Bioanalyzer. Libraries were sequenced on an Illumina Nextseq 500 instrument using 75 base-lengths read V2 chemistry in a paired-end mode. After sequencing, primary analysis based on AOZAN software (ENS, Paris), was applied to demultiplex and control the quality of the raw data (based of FastQC modules / version 0.11.5).</p> <p>The dataset here represents 4 groups of mice, 4 mice per group as follows: HbAA PBS, HbAA heme, HbSS PBS, HbSS heme. </p> <p> </p>
Work-related burden of diseases and disorders
<p><span>The burden of the work-related diseases is a major global health challenge. This data provides the global, regional and country level estimates on the work-related burden of occupational diseases and accidents for the year 2019 in terms of deaths, disability adjusted life years (DALYs) and economic loss as a percentage of total gross domestic product (GDP). </span></p> <p><span>The data contains calculated estimates based on the employment figures, mortality rates, occupational injuries, accidents, self-reported occupational illnesses and injuries from electronic data sources of international organizations, institutions, and public websites. Risk ratios (RR) and population attributable fractions (PAF) for the risk factors outcome pairs were derived from literature. Estimated mortality and DALYs for a group of seven major diseases covering 120 risk-outcome pairs attributable to work are calculated at global, WHO regions and at country level. The details of the methodology of the data have been published already (<a href="https://www.sjweh.fi/article/4132"><span>https://www.sjweh.fi/article/4132</span></a>).</span></p> <p><span>In general, the method is based on the number of problems identified at work: injuries, illnesses, and disorders including fatal or no-fatal cases. This was implemented by calculating the deaths, Years of Life Lost (YLL), Years Lived with Disability (YLD) and their combination Disability Adjusted Life Years (DALY) based on primarily ILO numbers as adjusted by the Institute of Health Metrics and Evaluation (IHME) Global Burden of Disease and Injury (GBD) process outcomes. While there are existing estimates updated annually by the GBD process, latest for the year 2019, these do cover only a selected group of occupational risks. Therefore, the GBD 2019 outcomes would not be comparable to ILO Estimates and – if directly used – would end up in clear underestimates of the size of the problem. The differences between ILO and GBD2015 outcomes are reported elsewhere. </span></p> <div> <div> <p><span> </span></p> </div> </div>
Summary statistics from "Genetic Association Study of Eight Steroid Hormones and Implications for Sexual Dimorphism of Coronary Artery Disease"
<p>GWAMA summary statistics of four steroid hormone levels using fixed-effect model and GWAS summary statistics of four other steroid hormones.</p> <p>When using this data, please cite: Pott J, Bae YJ, Horn K, et al.. Genetic Association Study of Eight Steroid Hormones and Implications for Sexual Dimorphism of Coronary Artery Disease. <em>J Clin Endocrinol Metab</em> <strong>2019</strong> Nov 1;104(11):5008-5023. doi: 10.1210/jc.2019-00757</p> <p>All txt files contain the following columns:</p> <ul> <li>markername</li> <li>chr</li> <li>bp_hg19 (base position according to hg19)</li> <li>effect_allele</li> <li>other_allele</li> <li>effect_allele_freq</li> <li>min_info (minimal info score across all used studies)</li> <li>n (sample size per SNP)</li> <li>beta (effect estimate)</li> <li>se (standard error)</li> <li>p (p-value)</li> <li>CochransQ (only in GWAMA; SNP heterogeneity across studies)</li> <li>pCochransQ (only in GWAMA; p-value of Cochrans Q value)</li> </ul>
Outdoor air pollution impacts chronic obstructive pulmonary disease deaths in South Asia and China: a systematic review and meta-analysis
<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is among leading causes of death globally. Exposure to outdoor pollution is an important cause for increased mortality and morbidity. This study presents a systemic review regarding the impact of outdoor pollution on COPD mortality in South Asia and China.</p> <p><strong>Methods: </strong>A systematic search was conducted from 1990 to June 30<sup>th</sup> 2020 in English electronic databases: PubMed, Google Scholar and CDSR (Cochrane Database of Systematic Reviews) following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The following terms were used: Chronic Obstructive Pulmonary disease OR COPD OR Chronic Bronchitis OR Emphysema OR COPD Deaths OR Chronic Obstructive Lung Disease OR Airflow Obstruction OR Chronic Airflow Obstruction OR Airflow Obstruction, Chronic OR Bronchitis, Chronic AND Mortality OR Death OR Deceased AND Outdoor pollution, ambient pollution was conducted.</p> <p><strong>Results:</strong> Out of 1899 papers screened only 17 were found eligible to be included. Subjects with COPD exposed to higher levels of outdoor air pollution had a 49% higher risk of death as compared to COPD subjects exposed to lower levels of outdoor air pollution. When taking common air pollutants individually into consideration, PM10 had an odds ratio (OR) of 1.99 respectively at CI 95%, whereas SO2 had OR of 1.8 at 95% CI, and NO2 had an OR of 1.23 OR at 95% CI. These values suggest that there is an effect of outdoor pollution on COPD but not to a significant level.</p> <p><strong>Conclusion: </strong>Despite heterogeneity across selected studies, individuals exposed to outdoor pollutants were found to be at risk of COPD mortality. Though it appears to have risk, COPD mortality was not significantly associated with outdoor pollutants. Controlling air pollution can substantially decrease the risk of COPD in South Asia and China. Further researches including more prospective and longitudinal studies are urgently needed in COPD sub-groups.</p>
Classification of blood cells dynamics with convolutional and recurrent neural networks: a sickle cell disease case study
<p>The fraction of red blood cells (RBC) adopting a specific motion under low shear flow is a promising inexpensive marker for monitoring the clinical status of patients with sickle cell disease (SCD). Its high-throughput measurement relies on the video analysis of thousands of cell motions for each blood sample to eliminate a large majority of unreliable samples(out of focus or overlapping cells) and discriminate between tank-treading and flipping motion, characterizing highly and poorly deformable cells respectively. These videos are of different durations (from 6 to more than 100 frames).</p> <p>This dataset contains four adult patients with SCD. They were enrolled in the study Drepaforme (approved by the institutional review board CPP Ouest 6 under the reference n°2018A00679-46) and were sampled weekly for several months. The movies were processed using in-house routines in Matlab (Matlab, R2016a) and RBC were detected individually and tracked over time. The database provided in this repository are already pre-processed sequences of tracked and centered RBC over time, each time step image being normalized to 31x31 pixels. Within the 32 experiments, the total number of sequences (or samples) is nearly 150 000. All sequences were semi-automatically labelled into 3 classes, depending on the dynamic of the cell: tank-treading, flipping and unreliable (140 000 are unreliable). The percentage of tank-treading cells with respect to all reliable cells (tank-treading+flipping) in every experiment is the final goal of this study.</p> <p>This dataset is very interesting to the community as it is a large database for cell dynamics classification: the class depends on the movement of the cell.</p> <p>An automatic processing of the database using a 2-stage deep learning model is available here https://github.com/icannos/redbloodcells_disease_classification</p> <p>For opening the data in python:</p> <p> from scipy.io import loadmat<br> x=loadmat('BG20191003shear10s01_Export.mat')</p> <p> * x['Norm_Tab'] is of size nb_samples x max_len_sequences x 31 x 31, where max_len_sequences is the length of the longest sequence of the series, typically ~150 to 180. The other sequences are padded with 31x31 zero matrices at the end in order to fill this maximal length.</p> <p> * x['Labels_Num'] is the corresponding label of each sequence, of size nb_samples. Label can be:<br> - 0 : "tank-treading" (or healthy)<br> - 1 : "flipping" (or tumbling, i.e. related to a SCD)<br> - 2 : "unreliable"</p>
Data from: The impact of long-term azithromycin on antibiotic resistance in HIV-associated chronic lung disease
<p><b>Background</b>: Selection for resistance to azithromycin (AZM) and other antibiotics such as tetracyclines and lincosamides remains a concern with long-term AZM use for treatment of chronic lung diseases (CLD). We investigated the impact of 48 weeks of AZM on the carriage and antibiotic resistance of common respiratory bacteria among children with HIV-associated CLD.</p> <p><b>Methods</b>: Nasopharyngeal (NP) swabs and sputa were collected at baseline, 48 and 72 weeks from participants with HIV-associated CLD randomised to receive weekly AZM or placebo for 48 weeks and followed post-intervention until 72 weeks. The primary outcomes were prevalence and antibiotic resistance of <i>Streptococcus pneumoniae</i> (SP), <i>Staphylococcus aureus </i>(SA), <i>Haemophilus influenzae </i>(HI), and <i>Moraxella catarrhalis </i>(MC) at these timepoints. Mixed-effects logistic regression and Fisher's exact test were used to compare carriage and resistance respectively.</p> <p><b>Results</b>: Of 347 (174 AZM, 173 placebo) participants (median age 15 years [IQR =13–18], females 49%),NP carriage was significantly lower in the AZM (n=159) compared to placebo (n=153) arm for SP (18% vs 41%, <i>p</i><0.001)<i>, </i>HI (7% vs 16%, p=0.01)<i>, </i>and MC (4% vs 11%, <i>p</i>=0.02); SP resistance to AZM (62% [18/29] vs 13%[8/63], <i>p</i><0.0001) or tetracycline (60%[18/29] vs 21%[13/63], <i>p</i><0.0001) were higher in the AZM arm. Carriage of SA resistant to AZM (91% [31/34] vs 3% [1/31],<i> p</i><0.0001), tetracycline (35% [12/34] vs 13% [4/31],<i> p</i>= 0.05) and clindamycin (79% [27/34] vs 3% [1/31],<i> p</i><0.0001) was also significantly higher in the AZM arm and persisted at 72 weeks. Similar findings were observed for sputa.</p> <p><b>Conclusions</b>: The persistence of antibiotic resistance and its clinical relevance for future infectious episodes requiring treatment needs further investigation.</p>
OpenData for the Independent morphological variables correlate to aging, Mild Cognitive Impairment, and Alzheimer's Disease manuscript
<p>Results from processed structural MRI images from the <a href="https://www.sciencedirect.com/science/article/pii/S1053811920306868">AHEAD</a> and <a href="https://www.nature.com/articles/s41597-021-00870-6">AOMIC</a> dataset included in the Supplementary Information at the Independent morphological variables correlate to aging, Mild Cognitive Impairment, and Alzheimer's Disease manuscript from de Moraes et al. submitted to PNAS.</p> <p>For this data, we processed the datasets with <a href="https://surfer.nmr.mgh.harvard.edu/">FreeSurfer</a> v6.0.0 standard processing pipeline (<em>recon-all</em>) and the estimation of the <a href="https://surfer.nmr.mgh.harvard.edu/fswiki/LGI">local Gyrification Index</a> from <a href="http://ltswww.epfl.ch/~schaer/Schaer_TMI.pdf">Schaer, M. et al. 2008</a>. We further extracted the morphological measurements from the generated surfaces using the Cortical Folding Analysis Tools from <a href="https://zenodo.org/record/3608675">Wang et al. 2019</a>. Here, we included the raw morphological datasets joined with the demographics and subjects' information.</p>
Animal disease data complementing the European Union One Health 2020 Zoonoses Report
<p>This dataset contains the mandatory annual data reported for bovine tuberculosis and for bovine and ovine and caprine brucellosis based on Directive 2003/99 that cites in Recital 7 the Council Directives 64/432/EEC and 91/68/EEC. The relevant Commission Decisions relating to the officially free (OF) MS and MS' regions and related reporting are: Decision 2003/467/EC for bovine tuberculosis and bovine brucellosis, and Decision 93/52/EC for sheep and goat brucellosis (B. melitensis). REPORTING AUTHORITIES CONTRIBUTING TO EACH DATA COLLECTION: Disease_status_data_2020_20211109: >></p>
Novel disease state model finds most juvenile green turtles develop and recover from fibropapillomatosis
<p>Fibropapillomatosis (FP) is a sea turtle disease characterized by benign tumor development on skin, eyes, and/or internal organs. It primarily affects juvenile green turtles (Chelonia mydas) in coastal foraging sites. The Indian River Lagoon (IRL), Florida, USA, is a coastal green turtle foraging site where the observed FP annual rate averaged 49% between 1983 and 2018. FP is not a major cause of sea turtle mortality and most individuals fully recover; however, the overall dynamics of this disease are poorly understood because prior disease history is unknown for individuals without FP at capture time, and future disease outcome is unknown for individuals with FP at capture time. To better evaluate FP dynamics for green turtles in the IRL, we developed a hierarchical model for predicting disease state change. We used data from 4,149 captures of 3,700 individual green turtles captured in the IRL. The hierarchical disease state model contained two levels: level one modeled whether an individual would develop FP, and level two modeled disease state progression, including states for pre-FP affliction, active FP affliction, and full recovery from FP. From the hierarchical model, we estimated 99.8% (95% credibility intervals 99.1-100%) of juvenile green turtles in the IRL developed FP, indicating that nearly every individual in the IRL is affected by this disease. The model also suggested that turtles quickly developed FP upon recruitment to the IRL and then recovered at different rates, with most completely recovering before emigrating from the IRL as they mature. This is the first analysis of long-term sea turtle data suggesting nearly every turtle in an aggregation both develops and recovers from FP.</p>
Machine Learning Dataset for Poultry Diseases Diagnostics - PCR annotated
<p>The dataset of poultry disease diagnostics was annotated using Polymerase Chain Reaction (PCR). Polymerase Chain Reaction (PCR) is a molecular biology technique for rapid diagnostics. We gathered both the fecal images and fecal samples from layers, cross and indigenous breeds of chicken from poultry farms in Arusha and Kilimanjaro regions in Tanzania between September 2020 and February 2021. Each fecal sample collected was coded to its corresponding image during data collection. PCR method is used for detection and identification of pathogens through amplification of DNA sequences unique to the pathogen. We used existing primers from literature to amplify the target DNA/RNA on the poultry fecal samples for PCR. The targets were Coccidiosis, Newcastle disease and Salmonella. We used the primers for PCR diagnostics at the molecular laboratory of the Nelson Mandela African Institution of Science and Technology (NM-AIST). The fecal samples were stored at -80 degrees celsius. The PCR diagnostics were conducted using reagents and kits from Zymo Research and the protocol is summarized in these five stages: 1. DNA sample loading 2. DNA extraction 3. Amplification; 4. Quantification and 5. Detection.</p> <p>All the PCR annotated fecal images are in the <strong><strong>.zip files</strong></strong>; “pcrcocci.zip” has 373 images, “pcrhealthy.zip” has 347 images, “pcrsalmo.zip” has 349 images, "pcrncd.zip" has 186 images. A total of 1,255 image files are labeled.</p> <p>The research project is funded by the Organization for Women in Science for the Developing World (OWSD) with Grant Award Number: 4500406715.</p>
# Single-cell network biology characterizes cell type gene regulation for drug repurposing and phenotype prediction in Alzheimer's disease
<p>Dysregulation of gene expression in Alzheimer’s disease (AD) remains elusive, especially at the cell type level. Gene regulatory network, a key molecular mechanism linking transcription factors (TFs) and regulatory elements to govern target gene expression, can change across cell types in the human brain and thus serve as a model for studying gene dysregulation in AD. However, it is still challenging to understand how cell type networks work abnormally under AD. To address this, we integrated single-cell multi-omics data and predicted the gene regulatory networks in AD and control for four major cell types, excitatory and inhibitory neurons, microglia and oligodendrocytes. Importantly, we applied network biology approaches to analyze the changes of network characteristics across these cell types, and between AD and control. For instance, many hub TFs target different genes between AD and control (rewiring). Also, these networks show strong hierarchical structures in which top TFs (master regulators) are largely common across cell types, whereas different TFs operate at the middle levels in some cell types (e.g., microglia). The regulatory logics of enriched network motifs (e.g., feed-forward loops) further uncover cell type-specific TF-TF cooperativities in gene regulation. The cell type networks are highly modular and several network modules with cell-type-specific expression changes in AD pathology are enriched with AD-risk genes and putative targets of approved and pending AD drugs, suggesting possible cell-type genomic medicine in AD. Finally, using the cell type gene regulatory networks, we developed machine learning models to classify and prioritize additional AD genes. We found that top prioritized genes predict clinical phenotypes (e.g., cognitive impairment) with reasonable accuracy. Overall, this single-cell network biology analysis provides a comprehensive map linking genes, regulatory networks, cell types and drug targets and reveals dysregulated cell type gene dysregulatory mechanisms in AD.</p>
Immuno-proteomic profiling reveals aberrant immune cell regulation in the airways of individuals with ongoing post-COVID-19 respiratory disease
<p><span><span><span><span><span><span><span><span><span><span><span>Some patients hospitalized with acute COVID-19 suffer respiratory symptoms that persist for many months. We delineated the immune-proteomic landscape in the airway and peripheral blood of healthy controls and post-COVID-19 patients 3 to 6 months after hospital discharge. Post-COVID-19 patients showed abnormal airway (but not plasma) proteomes, with elevated concentration of proteins associated with apoptosis, tissue repair and epithelial injury versus healthy individuals. Increased numbers of cytotoxic lymphocytes were observed in individuals with greater airway dysfunction, while increased B cell numbers and altered monocyte subsets were associated with more widespread lung abnormalities. 1 year follow-up of some post-COVID-19 patients indicated that these abnormalities resolved over time. In summary, COVID-19 causes a prolonged change to the airway immune landscape in those with persistent lung disease, with evidence of cell death and tissue repair linked to ongoing activation of cytotoxic T cells. </span></span></span></span></span></span></span></span></span></span></span></p>
Immune disease variants modulate gene expression in regulatory CD4+ T cells
<p>We mapped genetic regulation (QTL) of gene expression and chromatin activity in Tregs and we identified 133 colocalizing loci with immune disease variants.<br> For the time being, the preprint DOI: <a href="https://doi.org/10.1101/654632">10.1101/654632</a></p>
Investigating the role of miRNA in neural crest development and diseases
<p>This is a recording of the poster presentation of Mr Marco Antonaci (UEA) at the Swiss RNA Workshop 2022, January 21st</p>
An epidemiological Study to Assess Household Transmission & Associated Risk Factors for COVID-19 Disease amongst Residents of Delhi, India.
<p><strong><em>Executive summary</em></strong>: Studying the spread and epidemiological characteristics of COVID-19 virus specially in household settings are needed to prepare our self-better in preventing and controlling this epidemic. In this study we proposed a conceptual framework of four level of determinates and tried to understand the transmission dynamics of COVID-19 among household contacts along with clinical, epidemiological and virologic characteristics of the infection. </p> <p><strong>Aims & Objectives:</strong></p> <ol> <li>the proportion of asymptomatic cases and symptomatic cases;</li> <li>the incubation period of COVID-19 and the duration of infectiousness and of detectable shedding;</li> <li>the serial interval of COVID-19 infection; </li> <li>clinical risk factors for COVID-19, and the clinical course and severity of disease; </li> <li>high-risk population subgroups;</li> <li>the secondary infection rate and secondary clinical attack rate of COVID-19 infection among household contacts; and</li> <li>the associations of various factors across four dimensions interaction associated with risk of transmission</li> </ol> <p><strong>Methodology:</strong> This was a case-ascertained study where all susceptible contacts of a laboratory confirmed COVID-19 case were studied prospective for four weeks after their enrolment. It was done in New Delhi, during the end of first wave as well as whole second wave from December 2020 to July 2021. The study team collected the key information by questionnaire along with blood and oro-nasal swab during the household visits. Follow-up was done on day 7, 14 and 28 for observing the disease characteristic and symptomatology along with confirmation by serum and oro-nasal swab testing. Daily characteristics of the infection were noted by the participants on symptoms diary.</p> <p><strong>Results: </strong>We enrolled 99 households, each having one laboratory-confirmed COVID-19 index case along with their 318 susceptible contacts. By the end of the follow-up, secondary infection rate was seen at 55.5%, while seroconversion in 46.6%. Hospitalization and case fatality rate was 3.83% and 1.7% respectively. Among epidemiological characteristics we observed serial interval of 8.0 ± 6.7 days, generation time 3.8 ± 6.4, while secondary attack rate was 54.9%. The predictors of secondary infection among individual contact level were being female (OR:2.13, 95% CI:1.27 - 3.57), age of the household contact (1.01;1.00 - 1.03), symptoms at baseline (3.39; 1.61- 7.12) and during follow-up (3.18; 1.64 - 6.19), while only symptoms during follow-up (3.81: 1.43 - 10.14) and being RT-PCR positive (8.32; 3.22 -21.54) was significantly and independently associated with seroconversion among household contacts. Among index case-level age of the primary case (1.03; 1.01 -1.04) and any symptoms during follow-up (6.29; 1.83-21.63) significantly and independently associated with secondary infection while any symptoms during follow-up was associated with seroconversion among household contacts. Among household-level characteristics having more rooms (4.44; 2.16 - 9.13) independently associated with secondary infection, while more rooms (3.98; 1.23 -12.90) along with overcrowding (0.37; 0.16 - 0.82) associated with seroconversion. Among contact pattern only taking care of the index case (2.02;1.21- 3.38) was significantly and independently associated with secondary infection, while none was associated with seroconversion.</p> <p><strong>Conclusion: </strong>A high secondary cases and secondary attack rate was seen in our study. This highlights the need to adopts strict measure and advocate COVID appropriate behaviours in order to break the transmission chain at household level. The targeted approach at household contacts with higher risk would be efficient in limiting the development of infection among susceptible contacts. </p>
Pretrained network for segmentation of kidneys and exophytic cysts in subjects with autosomal dominant polycystic kidney disease (ADPKD)
<p>This pretrained network based on the 3D U-Net is for segmentation of kidneys and exophytic cysts in subjects with autosomal dominant polycystic kidney disease (ADPKD). The network was trained with 157 (including 53 cases with exophytic cysts) subjects with ADPKD. The details of trained dataset and the performance of the network will be updated after our manuscript is accepted for publication.</p>
Data analysis pipeline for investigating drug-host-microbiome relationships in cardiometabolic disease (MetaCardis cohort).
<p>*******************************************************************<br> MetaDrugs workflow<br> *******************************************************************</p> <p>Data analysis pipeline for investigating drug-host-microbiome relationships in cardiometabolic disease (MetaCardis cohort).</p> <p>For questions and requests, please contact:<br> Sofia K. Forslund (sofia.forslund@mdc-berlin.de)<br> and Till Birkner (till.birkner@mdc-berlin.de)</p> <p>*******************************************************************<br> Contents:<br> -------------------------------------------------------------------<br> Data files:<br> metadata.tar.gz - archived cohort metadata files*<br> input_features.tar.gz - archived preprocessed serum and urine metabolome and gut microbiome features<br> output_complete.tar.gz - archived example analysis output files for each of the input feature file<br> output_rerun.tar.gz - archived empty directory for generating test output files as described in this document<br> <br> *Please note: Due to conflicts with Danish Data Protection laws, metadata from the Danish subset of the cohort were removed in this repository. Please reach out for a potential case-by-case access request for access to the complete set of metadata.<br> -------------------------------------------------------------------<br> Text files:<br> archived in feature_names.tar.gz:<br> atcs_names - full names for atcs drug compounds<br> contrast_names - full names for disease comparison groups<br> file_names - brief description of the files in input_features folder<br> gmm_names - full names of GMM modules<br> kegg_names - full names of KEGG modules<br> ko_names - full names of KO modules<br> metadata_names - full names of metadata features<br> mOTU_names - species names for metagenomics data<br> taxon_names - taxon names for metagenomics data<br> -------------------------------------------------------------------<br> Scripts:<br> -------------------------------------------------------------------<br> runFrame.r - main wrapper script envoking the analysis pipeline<br> -------------------------------------------------------------------<br> runFrame_rel_comb.r - script calculating drug combination effects<br> runFrame_rel.r - script calculating dosage effects<br> testCombPresenceSeparate.r - testing of significant drug combination effects beyond single drug effects<br> testDosagePresenceSeparate.pl - testing of significant drug dosage effects beyond single drug effects<br> testDosagePresenceSeparateNegative.pl - testing of unique drug dosage effects beyond single drug effects<br> -------------------------------------------------------------------<br> prettifyResults_uncollapsed.pl - wrapper scripts to create and format a single analysis output file<br> makeTables.r - wrapper script to make excel tables with analysis results<br> -------------------------------------------------------------------<br> Example output file:<br> -------------------------------------------------------------------<br> output_all_formatted_noc_uncollapsed_complete.tsv - contains all disease-drug-host-microbiome feature analysis results in one place.<br> *******************************************************************</p>
Microchromosomes and their association with human diseases
<p>Supply table-S1: Commonly used patient derived cell lines, number of average microchromosomes, citation to original article.</p> <p>Supply table-S2: List of PubMed abstracts and annotation of disease identified by artificial intelligence-based technique related to incidence of microchromosomes in human</p> <p>Machine Learning_NER_code_output_20220120.zip: File containing the PubMed abstracts, machine learning analysis output and disease interpretation output.</p> <p>Cell lines karyotype.zip: File containing the raw karyotype data of all head & neck cancer cell lines.</p> <p> </p> <p>Brief description of methodology:</p> <p>To investigate the incidence of microchromosomes in human genome, we mine the PubMed literature for studies related to keywords “((microchromosome) OR ("marker chromosome") OR ("small chromosome"))” and applying the filter “human”. A total of 1,365 abstracts are obtained from PubMed as per date 08-Jan-2022. We analyze the PubMed abstracts using the Named Entity Recognition (NER) technique of Machine Learning (ML) implemented in Spacy (3.0) – scispaCy (0.4.0) – Python (3.7) running on Windows 11 system. The scispaCy package NER model “en_ner_bc5cdr_md” which is pretrained on BC5CDR corpus was used for disease entity recognition (<a href="https://allenai.github.io/scispacy/">https://allenai.github.io/scispacy/</a>). Approximately 2000 disease entities are recognized by the model from the abstract text of the 1365 articles. The disease entities present in the abstract texts are extracted and then grouped together for most common broad disease classes as shown in excel file Supply_Table-S1.xlsx. The Python code, PubMed input and output files are available in "Machine Learning_NER_code_output_20220120.zip". Overall, inherited or somatically acquired microchromosomes in human individuals are frequently reported with diseases and disorders like Cancer, Trisomy, Turner’s syndrome, Epilepsy, Infertility, and Autism.</p>
Beyond depression and anxiety; a systematic review about the role of corticotropin-releasing hormone antagonists in diseases of the pelvic and abdominal organs-Worksheets
<p>This file has several worksheets corresponding to the data used for the review with the same table as indicated in the file</p>
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.