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726 results for “prenatal”
Inter-Chemical Correlation results for the study: HHEARx2017-1740 (Mitochondrial DNA biomarkers of prenatal metal mixture exposure: intergenerational inheritance and infant growth)
Title: Mitochondrial DNA biomarkers of prenatal metal mixture exposure: intergenerational inheritance and infant growth <br>Species: Homo sapiens <br>Number of samples: 1423 <br>Number of named analytes: 20 <br>Datasource url: https://hheardatacenter.mssm.edu/PublicFile/ViewPublicFile?projectid=19 <br>
Inter-Chemical Correlation results for the study: HHEARx2016-1534 (A Nested Case-Control Study of Prenatal Exposure to Phthalates and Psychosocial Stress: Adverse Pregnancy Outcomes and the Mediating Role of Placental Function)
Title: A Nested Case-Control Study of Prenatal Exposure to Phthalates and Psychosocial Stress: Adverse Pregnancy Outcomes and the Mediating Role of Placental Function <br>Species: Homo sapiens <br>Number of samples: 5789 <br>Number of named analytes: 17 <br>Datasource url: https://hheardatacenter.mssm.edu/PublicFile/ViewPublicFile?projectid=14 <br>
Prenatal diet programs the transgenerational inheritance of brain macro and microstructure defects, coding for anxiety-like behavior in male rats.
<p>T1-w 3DFLASH Preprocessed MRI images used for wistar rat used for the deformation-based morphological (DBM) model are released.</p> <p>Nifti files are duplicated. DBM used only mnc format.</p> <p> </p> <p> </p> <p> </p> <p> </p> <p> </p>
Differential effects of early or late exposure to prenatal maternal immune activation on mouse embryonic neurodevelopment
<p>Exposure to maternal immune activation (MIA) in utero is a risk factor for neurodevelopmental and psychiatric disorders. MIA-induced deficits in adolescent and adult offspring have been well characterized, however, less is known about the effects of MIA-exposure on embryo development. To address this gap, we collected high-resolution ex vivo magnetic resonance imaging (MRI) of C57BL/6 mouse embryos (gestational day [GD]18) who were prenatally exposed to MIA either early (GD9) or late (GD17) in gestation. We further examined hippocampal neuroanatomy using electron microscopy and identified differential effects due to MIA-timing. </p> <p>The data published here was collected and analyzed for the following publication available as a preprint on BioRxiv (https://www.biorxiv.org/content/10.1101/2021.07.14.452084v2). Briefly, We identify striking neuroanatomical changes in the embryo brain, particularly in the late exposed offspring. An increase in apoptotic cell density was observed in the GD9 exposed offspring, while an increase in the density of dark neurons and glia, putative markers for increased neuroinflammation and oxidative stress, was observed in GD17 exposed offspring, particularly in females. Overall, our findings integrate imaging techniques across different scales to identify differential impact of MIA-timing on the earliest stages of neurodevelopment.</p> <p>In this dataset, you will find a total of <strong>187 preprocessed structural MRIs </strong>(in MINC format) of whole embryos at gestational day 18. These embryos were exposed to poly I:C or vehicle control (0.9% sterile saline) at GD9 or 17. A multi-channel 7.0-T MRI scanner with a 40 cm diameter bore (Varian Inc., Palo Alto, CA), with a custom-built 16-coil solenoid array was used to acquire T2-weighted, gadolinium enhanced structural images at 40 μm3 resolution images from 16 samples concurrently (3D fast spin echo sequence using a cylindrical k-space acquisition; TR/TE=350/12 ms, echo train length=6, two averages, field-of-view 20 mm x 20 mm x 25 mm, matrix size=504 x 504 x 630).</p> <p>An N4 correction for B1 bias field inhomogeneities and denoising using non-local means (minc_anlm) was applied to the T2-weighted images, and the background was set to zero using minc tools. The demographics information for each animal is included in the <strong>demographics.csv</strong> file. </p> <p>The dorsal hippocampus was selected as a region of interest in which the total number and density of total cells, dark neurons, dark glia, apoptotic cells were assessed (as presented in our manuscript). This is available in the <strong>EM_raw_data_per_slice.csv</strong> and <strong>EM_average_per_mouse.csv </strong>files. </p> <p>Included in this data set are the <strong>structural MRIs in MINC format</strong>, corresponding demographics information (<strong>demographics.csv</strong>), electron microscopy data from the dorsal hippocampus (<strong>EM_raw_data_per_slice.csv</strong> and <strong>EM_average_per_mouse.csv)</strong> data, and a <strong>readme.txt</strong> file providing further detail on the data structure and content, and on how to interpret the data column titles.The raw (not-preprocessed) MINC files, as well as MINC files cropped to the head of the embryos available upon request to the authors. </p> <p>Finally, the authors would like to acknowledge the funding bodies that supported the completion of this work including the Canadian Institute for Health Research, the Fonds de Recherche du Québec en Santé, and the Healthy Brains for Healthy Lives at McGill University.</p>
Longitudinal structural MRI, MRS, and behavioral data for mice prenatally exposed to maternal immune activation at gestational day 9
<p>Previous evidence from our lab (https://cobralab.ca/) and others suggest that prenatal exposure to maternal immune activation (MIA) can impact trajectories of neurodevelopment as measured through brain anatomy and behavior in mice. Yet, there are still open questions regarding the alterations to developmental trajectories, as well as the impact on brain chemistry, that this data set seeks to explore. The dataset presented here includes magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) data from two timepoints, adolescence (postnatal day [PND 35]) and young adulthood (PND 60) in C57BL/6J mice prenatally exposed either to poly I:C (POL) inducing maternal immune activation (MIA) or saline (SAL) at gestational day (GD) 9. The dataset also includes three behaviors acquired after each scanning session with 2 days of rest between the scans and each behavior: open field test, social novel object preference test, and prepule inhibition. Finally, the data also include cytokine assays acquired from a separate sample of pregnant mice and a test-retest of MRS acquired from a voxel in the anterior cingulate area. </p> <p>The data here published were collected and analyzed for a paper under review, available as a preprint where more details can be found here: https://www.preprints.org/manuscript/202203.0136/v1. In brief, using whole-brain, voxelwise analysis techniques (deformation-based morphometry) we found MIA subtly altered developmental trajectories, reducing volume relative to SAL offspring in the hippocampus and the anterior, right caudate putamen, and increasing volume in the posterior, left caudate putamen and cerebellum. Additionally, there was a trending decrease of myo-inositol and GABA in MIA offspring at PND 60 compared to SAL controls. Finally, there was a trending decrease in ratio of distance travelled in the anxiogenic center zone of an open field compared to the outer areas at PND 35 for MIA offspring. </p> <p>In this dataset you will find a total of <strong>80 preprocessed structural MRIs</strong> in minc format acquired at postnatal day ~35 and ~60 in mice exposed to 5mg/kg poly I:C or vehicle control (0.9% sterile saline) at GD9. The images are included in CUPO_MIA_mncs.zip. These are T1-weighted structural images with two averages; repetition time (TR)/echo time (TE) = 21.55 ms/5.13 ms, matrix size = 260 x 158 x 210, voxel dimensions =&thinsp;70 µm isotropic, flip angle =&thinsp;20°, 23 min total using 5% isoflurane for induction, 1.5% for maintenance of anesthesia during the scan on a cryogenically-cooled surface coil. T1-weighted scans were preprocessed by stripping native coordinates, flipping left-right to maintain fidelity, denoising, correcting inhomogeneities in the bias field using the N4 algorithm, and registering in LSQ6 alignment (i.e. 6 degrees of freedom are allowed for imagine alignment: translations and rotations along x, y, and z dimensions). The demographics information for each animal is included in the <strong>demographics.csv</strong> file. </p> <p>Behavioural tests were performed following the postnatal day 35 and 60 scans in all animals with a 2 day rest period. These include: open field test, three chambered social approach, and prepulse inhibition. The data for all of these tests is presented in individual .csv spreadsheet and includes data for both the timepoints evaluated. Additionally, cytokine panels were collected from an independent cohort of 7 dams. <strong>MRS </strong>data are included in two formats: 1) preprocessed quantifications from LCModel software in csvs, and 2) raw data with press and press_w (respectively water supressed and unsupressed acquisitions) for analysis. The raw data were released in upload version 1.1.0. MRS was acquired from a 1.2 x 2.6 x 2.5 mm3 voxel in the ACA with a Point Resolved Spectroscopy sequence (PRESS; TR/TE=3000/8.5 ms, 256 averages). Within the raw_data.zip,</p> <p>Included in this data set are the structural MRIs in MINC format, the behavioural .csv data, the MRS data (csvs and raw files), and a <strong>README</strong> file providing further detail on the data structure and content, and on how to interpret the data column titles. DICOMS are also available for the structural MRI data, as are the raw (not-preprocessed) MINC files, available upon request to the authors. </p>
Investigating the "two-hit hypothesis": effects of prenatal maternal immune activation and adolescent cannabis use on neurodevelopment in mice
<p>Prenatal exposure to maternal immune activation (MIA) and chronic adolescent cannabis use have both been identified as environmental risk factors for neuropsychiatric disorders. However, most individuals exposed to a single risk factor do not typically develop major mental illness, which suggests that multiple exposures may be required for illness onset. Here, we examine whether combined exposure to prenatal MIA and adolescent delta-9-tetrahydrocannabinol (THC), the main psychoactive component of cannabis, lead to enduring neuroanatomical and behavioural changes in adult offspring, potentially reflecting changes in humans indicative of mental illness. </p> <p>Mice were prenatally exposed to a viral mimetic, poly I:C (5mg/kg), or vehicle at gestational day (GD)9, and then postnatally exposed to chronic THC (5mg/kg) or vehicle by intraperitoneal injections during adolescent development (postnatal day [PND]28-45). Longitudinal in vivo whole-brain magnetic resonance imaging (MRI) was performed pre-treatment, PND25, post-treatment, PND50, and in adulthood, PND85, followed by a series of behavioural tests aimed at assessing anxiety-like and locomotor, social, and sensorimotor gating behaviour. Post-mortem assessment of cannabinoid (CB)1 and 2 receptor expressing cells was performed in developmentally altered regions identified by MRI (anterior cingulate and somatosensory cortices, striatum, and hippocampus). We hypothesized that there would be differential, but synergistic effects of each exposure.</p> <p>Briefly, we found subtle deviations in neurodevelopmental trajectory and subthreshold anxiety-like behaviours were observed in mice exposed to both risk factors. Sex-dependent effects were observed in patterns of shared brain-behaviour covariation, suggesting that exposure to MIA and THC may affect males and females in different ways. Density of CB1 and CB2 receptor positive cells was significantly decreased in all regions assessed for all mice exposed to either one or both risk factors, relative to controls.</p> <p>These findings suggest that there may be a cumulative effect of risk factor exposure on gross neuroanatomical and behavioural development, and that the endocannabinoid system may be sensitive to both prenatal MIA, adolescent THC, or the combination. For full details, see our publication: .</p> <p>In this dataset, you will find a total of 243 preprocessed structural MRIs (in MINC format) acquired at postnatal day ~25, ~50, and ~85 in mice exposed to poly I:C or vehicle control (0.9% sterile saline) at GD9, and then postnatally treated with vehicle or THC from PND 28-45. These are T1-weighted structural images at 100 micron isotropic resolution acquired on a 7 Tesla Bruker Biospec 70/30; matrix size of 180 x 160 x 90; 14.5 minutes, 20 degrees and TE/TR of 4.5/20 ms (2 averages, ~14 minutes). Anesthesia was induced with 3% isoflurane in oxygen and a (0.075 mg/kg bolus) dexmedetomidine injection. Anesthesia was maintained during the scan between 1.5-0.5% isoflurane, and a constant infusion of dexmedetomidine (0.05mg/kg/h continuous mg/kg during scan). T1-weighted scans were preprocessed by stripping native coordinates, flipping left-right to maintain fidelity, denoising, correcting inhomogeneities in the bias field using the N4 algorithm, and registering in LSQ6 alignment (i.e. 6 degrees of freedom are allowed for imagine alignment: translations and rotations along x, y, and z dimensions). The demographics information for each animal is included in the demographics.csv file. </p> <p>Behavioural tests were performed following the postnatal day 85 scans in all animals with a 2 day rest period. These include: open field test, three chambered social approach, and prepulse inhibition. The data for all of these tests is presented in its own individual .csv spreadsheet.</p> <p>Included in this data set are the structural MRIs in MINC format, the behavioural .csv data, and a readme.txt file providing further detail on the data structure and content, and on how to interpret the data column titles. DICOMS are also available for the structural MRI data, as are the raw (not-preprocessed) MINC files, available upon request to the authors. </p> <p>Finally, the authors would like to acknowledge the funding bodies that supported the completion of this work including the Canadian Institute for Health Research, the Fonds de Recherche du Québec en Santé, and the Healthy Brains for Healthy Lives at McGill University.</p>
Data from: The more you get, the more you give: Positive cascading effects shape the evolutionary potential of prenatal maternal investment
<p>Data from 'The more you get, the more you give: Positive cascading effects shape the evolutionary potential of prenatal maternal investment'</p> <p> </p> <p>Description of variables in CME_dat.csv</p> <p>egg.mass - mean offspring egg mass (grams)</p> <p>maternal.line - selection line of mother (H- high investment, L - low investment)</p> <p>paternal.line - selection lines of father (H- high investment, L - low investment)</p> <p>replicate - selection line replicate</p> <p>animal - animal id (links with data from Pick et al. 2016 on dryad)</p> <p>mother - mother id</p> <p>father - father id</p> <p>maternal.egg.mass - mean maternal egg mass (grams)</p>
Impact of prenatal THC exposure on mouse brain development; a lifespan approach with MRI
<p>Prenatal cannabis exposure has been demonstrated to impact neurodevelopment in offspring at different ages. To date, to our knowledge, no study has longitudinally examined the effects from embryos to adulthood. Here we collected and analyzed data to explore how prenatal exposure to delta-9-tetrahydrocannabinol (5 mg/kg subcutaneous injections, gestational dat [GD] 3-10) in mice impacts trajectories of brain development with structural magnetic resonance imaging. We supplement these findings with behavioural analyses and electron microscopy as described below.</p> <p>In the first cohort (embryos) embryos were extracted on GD 17 and scanned with MRI postnatally, as described in the methods of the accompanying paper. Electron microscopy was used to investigate dark neural and glial cells, apoptotic cells, and dividing cells in the hippocampus. In the second cohort (neonates) pups were born and scanned postnatally with manganese enhanced MRI on postnatal day (PND) 3, 5, 7, and 10. Separation-induced ultrasonic vocalizations were acquired on PND 12 and pups were perfused on PND 13. EM analyses were repeated in the neonatal hippocampi. In the third cohort (adults) pups were scanned on PND 25, 35, 60, and 90. Behavioral assessments for anxiety-like behavior with open-field test and sensorimotor gating with prepulse inhibition were performed on PND 35 and 37 respectively. </p> <p>Findings showed altered prenatal body volumes and weight-trajectories, altered brain volumes (especially sustained in females until adulthood), and indications of changes to behavior, including anxiety-like phenotypes in neonates and adolescents. Evidence from electron microscopy suggests increased cell division in the embryo hippocampus. Together these data suggest a profound and sustained impact of early gestation prenatal THC exposure on brain development. For further details on the methods, approach, and results, please see the forthcoming publication.</p> <p>In this dataset you will find the following data:</p> <p>Pregnancy/dam-level outcomes can be found in maternal_outcomes.zip</p> <ul> <li><a href="../api/records/13820978/draft/files/zenodo_pregnancy_README.txt/content" target="_blank" rel="noopener noreferrer">zenodo_pregnancy_README.txt</a>: includes description of the data and fields available in each csv.</li> <li>dam_weights.csv: A spreadsheet including the information related to each dam pooled across the studies</li> <li>nest_quality.csv: A spreadsheet including the manually-rated nest quality from a pilot and the full experiment</li> <li>master_maternal_observations_old_thc.csv: A spreadsheet including data for time spent on and off nest extracted automatically and manually from Ethovision</li> </ul> <p>Embryo outcomes:</p> <ul> <li>zenodo_embryos_README.txt: includes description of the data and fields available in each csv.</li> <li>demographics_for_analysis.csv: A spreadsheet with relevant information for each embryo sample.</li> <li>raw_embryo_mincs.zip: includes 84 embryo scans, full body</li> <li>embryo_heads.zip: includes 57 embryo scans that all passed qc, head only niftis </li> <li>squish_qc.csv: QC of whether the embryos were squished or not</li> <li>em_embryo_hc_mm2csv.csv: cells per mm^2 from electron microscopy</li> </ul> <p>Neonate outcomes:</p> <ul> <li>zenodo_neonates_README.txt: includes description of data and fields available in each csv</li> <li>demographics.csv: A spreadsheet with the demographic information for each pup and timepoint in the study</li> <li>raw_neonate_niftis.zip: 172 scans from neonates in nifti format</li> <li>agreement_qc.csv: quality control file with assessments of raw images</li> <li>milestones_999_as_NA.csv: Record of which milestones were tested and whether they were obtained</li> <li>master_usv.csv: Spreadsheet including data for ultrasonic vocalizations from all tested pups</li> <li>neo_cell_counts_mm2.csv: cells per mm^2 from electron microscopy for the neonates</li> </ul> <p>Adult outcomes: </p> <ul> <li>zenodo_adult_README.txt: includes description of the data and fields available in each csv.</li> <li>demographics.csv: A spreadsheet with the demographic information for each mouse and timepoint in the study</li> <li>adult_raw_niftis.zip: The raw data (before preprocessing) in nifti format</li> <li>master_qc.csv: Quality control assessment of the raw images</li> <li>master_oft.csv: Values for open field test extracted from Ethovision</li> <li>avg_trials_ppi.csv: Data from prepulse inhibition trials, average startle of 100 ms following pulse</li> <li>max_trials_ppi.csv Dat afrom prepulse inhibition trials, maximum startle of 100 ms following pulse</li> </ul>
Longitudinal structural MRI and behavioural data for mice prenatally exposed to maternal immune activation either early or late in gestation
<p>Prenatal maternal immune activation (MIA) is a risk factor for neurodevelopmental disorders. How the gestational timing of MIA-exposure differentially impacts downstream development remains unclear. The data presented here includes longitudinal structural magnetic resonance imaging (MRI) data from weaning to adulthood, and behavioural testing in adolescence and adulthood on C57BL/6 mice exposed to MIA induced by the viral mimetic, polyinosinic:polycytidylic acid (poly I:C) either early (gestational day [GD]9) or late (GD17) in gestation. </p> <p>The data published here was collected and analyzed for the following publication, where more details can be found (Guma et al., 2021 https://doi.org/10.1016/j.biopsych.2021.03.017). Briefly, we found that early MIA-exposure was associated with accelerated brain volume increases in adolescence/early-adulthood that normalized in later adulthood, in regions including the striatum, hippocampus, and cingulate cortex. Similarly, alterations in anxiety-like, stereotypic, and sensorimotor gating behaviours observed in adolescence normalized in adulthood. In contrast, MIA-exposure in late gestation had less impact on anatomical and behavioural profiles. </p> <p>In addition to the univariate analyses described above, we also undertook a multivariate analysis (partial least squares) to relate imaging and behavioural variables for the time of greatest alteration, i.e. adolescence/early adulthood. We further explored the molecular underpinnings of region-specific alterations in early MIA-exposed mice in adolescence using RNA sequencing (data for differentially expressed genes in the anterior cingulate cortex, dorsal hippocampus, and ventral hippocampus are available via the original publication https://doi.org/10.1016/j.biopsych.2021.03.017 for a separate cohort of adolescent mice prenatally exposed to MIA or vehicle at GD9). </p> <p>In this dataset, you will find a total of <strong>376 preprocessed structural MRIs</strong> (in MINC format) acquired at postnatal day ~21, ~38, ~60, and ~90 in mice exposed to poly I:C or vehicle control (0.9% sterile saline) at GD9 or 17. These are T1-weighted, manganese enhanced (50mg/kg 24 hours pre-scan), structural images at 100 micron isotropic resolution acquired on a 7 Tesla Bruker Biospec 70/30; matrix size of 180 x 160 x 90; 14.5 minutes, 2 averages, using 5% isoflurane for induction, 1.5% for maintenance of anesthesia during the scan. T1-weighted scans were preprocessed by stripping native coordinates, flipping left-right to maintain fidelity, denoising, correcting inhomogeneities in the bias field using the N4 algorithm, and registering in LSQ6 alignment (i.e. 6 degrees of freedom are allowed for imagine alignment: translations and rotations along x, y, and z dimensions). The demographics information for each animal is included in the <strong>demographics.csv</strong> file. </p> <p>Behavioural tests were performed following the postnatal day 38 and 90 scans in all animals with a 2 day rest period. These include: open field test, marble burying test, three chambered social approach, and prepulse inhibition. The attentional set shifting task was also performed following the final behavioural test in the postnatal day 90 wave of behaviours. The data for all of these tests is presented in its own individual .csv spreadsheet and includes data for both the timepoints evaluated.</p> <p>Included in this data set are the structural MRIs in MINC format, the behavioural .csv data, and a <strong>readme.txt</strong> file providing further detail on the data structure and content, and on how to interpret the data column titles. DICOMS are also available for the structural MRI data, as are the raw (not-preprocessed) MINC files, available upon request to the authors. </p> <p>Finally, the authors would like to acknowledge the funding bodies that supported the completion of this work including the Canadian Institute for Health Research, the Fonds de Recherche du Québec en Santé, and the Healthy Brains for Healthy Lives at McGill University.</p>
Data files for manuscript "Prenatal phenotype of PNKP-related primary microcephaly associated with variants in the FHA and Phosphatase domain"
<p>#2021-08-26<br> #Summary<br> This ZIP-file contains the Excel files used for the clinical and variant analyses of the PNKP protein/gene for the manuscript "Prenatal phenotype of PNKP-related primary microcephaly associated with variants in the FHA and Phosphatase domain".</p> <p>#Folder structure<br> ./ (parent directory containing this README file and all subfolders)<br> ./Clinical/ (contains an Excel sheet with complete clinical data of 4 affected individuals)<br> ./Variants/ (contains an Excel sheet with all variant annotation and domain information used in 6 sheets)</p> <p>#Files and checksums<br> 4B5BE914E77EB6511DF3DB94C6918E45 ./Clinical/FileS2_PNKP_Clinical.xlsx<br> 0228C6EF543D597C1C800B8D78E3097D ./Variants/FileS3_PNKP_Variants.xlsx</p>
Prenatal skeletogenesis partially recovers from absent skeletal muscle as development progresses
<p>Raw data (measurements made) for paper entitled "Prenatal skeletogenesis partially recovers from absent skeletal muscle as development progresses"</p>
Happy Mother-Healthy Baby: An Anxiety-focused Early Prenatal Intervention
ClinicalTrials.gov study NCT03880032. IPD Sharing: YES. Countries: 1. Publications: 17.
PRenatal Video-Based Education and PostPARtum Effects
ClinicalTrials.gov study NCT04258709. IPD Sharing: YES. Countries: 1. Publications: 1.
Prenatal treatment with the antidepressant fluoxetine on maternal and neonatal behavior in sheep
Open the record for dataset details and reuse information.
Data from: Single cell RNA-seq analysis reveals that prenatal arsenic exposure results in long-term, adverse effects on immune gene expression in response to Influenza A infection
<p>Arsenic exposure via drinking water is a serious environmental health concern. Epidemiological studies suggest a strong association between prenatal<i> </i>arsenic exposure and subsequent childhood respiratory infections, as well as morbidity from respiratory diseases in adulthood, long after systemic clearance of arsenic.<i> </i>We investigated the impact of exclusive prenatal arsenic exposure on the inflammatory immune response and respiratory health after an adult influenza A (IAV) lung infection. C57BL/6J mice were exposed to 100 ppb sodium arsenite<i> in utero,</i> and subsequently infected with IAV (H1N1) after maturation to adulthood. Assessment of lung tissue and bronchoalveolar lavage fluid (BALF) at various time points post IAV infection reveals greater lung damage and inflammation in arsenic exposed mice versus control mice. Single-cell RNA sequencing analysis of immune cells harvested from IAV infected lungs suggests that the enhanced inflammatory response is mediated by dysregulation of innate immune function of monocyte derived macrophages, neutrophils, NK cells, and alveolar macrophages. Our results suggest that prenatal arsenic exposure results in lasting effects on the adult host innate immune response to IAV infection, long after exposure to arsenic, leading to greater immunopathology. This study provides the first direct evidence that exclusive prenatal exposure to arsenic in drinking water causes predisposition to a hyperinflammatory response to IAV infection in adult mice, which is associated with significant lung damage.</p>
Targeted Disruption of Mouse Dip2B Leads to Abnormal Lung Development and Prenatal Lethality
<p>Supplementary Figures</p> <p><strong>Figure S1</strong>. Picro-sirius red stained sections of lung at E18.5.</p> <p><strong>Figure S2</strong>. Cell apoptosis assay by TUNEL staining. A. Immunofluorescent TUNEL staining of E18.5 lungs. Scale bar: 66.2μm. B. Quantitative analysis by counting of multiple sections from 3 independent samples per group. NS= not significant by student’s t- test.</p> <p><strong>Table S1</strong>. Summary of RNA-Seq mapping results. The raw reads were mapped to the Mus Musculus genome (GRCm38) using TopHat2.</p> <p><strong>Table S2</strong>. List of DEG (Differentially Expressed Gene) from RNA-Seq analysis results. Differentail expression analysis was carried out using DESeq2.</p> <p><strong>Table S3</strong>. List of DEGs annotated under Gene Ontology (GO) terms cell cycle and immune system process.</p> <p><strong>Table S4</strong>. List of DEGs annotated under KEGG Pathway oxidative phosphorylation and hematopoietic cell lineage pathways. </p>
Data from: Avian offspring prenatal DNA methylation response to maternal corticosterone dosing during reproduction
<p>Avian embryos develop in an egg composition which reflects both maternal condition and the recent environment of their mother. In birds, yolk corticosterone (CORT) influences development by impacting pre- and postnatal growth, as well as nestling stress responses and development. One possible mechanism through which maternal CORT may affect offspring development is via changes to offspring DNA methylation. We sought to investigate this, for the first time in birds, by quantifying the impact of manipulations to maternal CORT on offspring DNA methylation. We non-invasively manipulated plasma CORT concentrations of egg-laying female zebra finches (<em>Taeniopygia </em><em>castanotis</em>) with an acute dose of CORT administered around the time of ovulation and collected their eggs. We then assessed DNA methylation in the resulting embryonic tissue and in their associated vitelline membrane blood vessels, during early development (5 days after lay), using two established methods - liquid chromatography–mass spectrometry (LC-MS) and methylation-sensitive amplification fragment length polymorphism (MS-AFLP). LC-MS analysis showed that global DNA methylation was lower in embryos from CORT-treated mothers, compared to control embryos. In contrast, blood vessel DNA from eggs from CORT-treated mothers showed global methylation increases, compared to control samples. There was a higher proportion of global DNA methylation in the embryonic DNA of second clutches, compared to first clutches. Locus-specific analyses using MS-AFLP did not reveal a treatment effect. Our results indicate that an acute elevation of maternal CORT around ovulation impacts DNA methylation patterns in their offspring. This could provide a mechanistic understanding of how a mother's experience can affect her offspring's phenotype.</p>
Supplemental Files for manuscript "Prenatal Transmission of Bacteriophage DNA in Humans"
<p>This repository includes the following files:</p> <p>1) Maternal_UCB_Phage_Analysis.RMD<br>This is an R markdown file to reproduce the analysis in the manuscript “Prenatal Transmission of Bacteriophage DNA in Humans”. It depends on the following files:</p> <p>2) BLAST_Processing.R<br>R script used for the processing of BLAST outputs. The outputs of this analysis for our two cohorts and negative controls with each phage database are provided as R objects. <br> a. POPE_AllPhage_Stats.RDS<br> b. POPE_GPD_Stats.RDS<br> c. Witt_AllPhage_Stats.RDS<br> d. Witt_GPD_Stats.RDS<br> e. Neg_AllPhage_Stats.RDS<br> f. Neg_GPD_Stats.RDS</p> <p>3) Clean_Data_Structures.R<br>This script includes 3 sections to generate the data structures used in subsequent analyses. </p> <p>4) Phage_Plots_Tables.R<br>This script includes 3 sections to reproduce the figures and tables from the manuscript “Prenatal Transmission of Bacteriophage DNA in Humans”. </p> <p>5) POPE_index.csv<br>This CSV file contains the metadata for the POPE cohort.</p> <p>6) SummaryMetaData.csv<br>This CSV file contains the metadata for the Witt cohort as relayed by the study authors from the original publication of this dataset.</p> <p>7) README.txt which summarizes the above as well as provides links to other relevant data.</p> <p>These scripts can be used to re-process our sequencing data or to process and interpret additional datasets.</p>
Association between prenatal provision of lipid‐based nutrient supplements and cesarean delivery: Findings from a randomized controlled trial in Malawi
<p>Data set for a published manuscript on Maternal & Child Nutrition.</p> <p><strong>ABSTRACT:</strong> In populations with a high prevalence of childhood and adolescent undernutrition, supplementation during pregnancy aiming at improving maternal nutritional status and preventing fetal growth restriction might theoretically lead to cephalopelvic disproportion and delivery complications. We investigated whether the prenatal provision of small-quantity lipid-based nutrient supplements (SQ-LNS) was associated with an increased risk of caesarean section (CS) or other delivery complications. Pregnant Malawian women were randomised to receive daily i) iron–folic acid (IFA) capsule (control), ii) multiple micronutrient (MMN) capsule of 18 micronutrients (second control), or iii) SQ-LNS with similar micronutrients as MMN, plus four minerals and macronutrients contributing 118 kcal. We analysed the associations of SQ-LNS, CS, and other delivery complications using log-binomial regressions. Among 1391 women enrolled, 1255 had delivery information available. The incidence of CS and delivery complications was 6.3% and 8.2%, respectively. The incidence of CS was 4.0%, 6.0%, and 8.9% (p = 0.017) in the IFA, MMN, and LNS groups, respectively. Compared to the IFA group, the relative risk (95% confidence interval) of CS was 2.2 (1.3–3.8) (p = 0.006) in the LNS group and 1.5 (0.8–2.7) (p = 0.200) in the MMN group. We found no significant differences for other delivery complications. Provision of SQ-LNS to pregnant women may have increased the incidence of CS. The baseline rate was, however, lower than recommended. It is unclear if the higher CS incidence in the SQ-LNS group resulted from increased obstetric needs or more active health seeking and a better supply of services. Trial registered at clinicaltrials.gov, NCT01239693.</p>
When ancestors transmit their stress: Prenatal maternal stress transmission across generations in a precocial bird
<p>Prenatal maternal stress (PMS) induces life-long effects in offspring. Accumulating evidence suggests that these effects can be transmitted across generations. Although multigenerational effects (F0 mother to F2 grand-offspring) of PMS have been demonstrated in different species, transgenerational transmission (F0 mother to F3 great-grand-offspring) has been less explored. We showed previously in the Japanese quail that PMS increased F1 offspring's emotional reactivity related to epigenetic marks levels in their brain and to modulation of testosterone concentrations in eggs from which they hatched. Here, we evaluated the multi- and transgenerational effects of PMS by analysing the emotional reactivity of the F2 and the F3 offspring. We also investigated the mechanisms potentially involved in the transmission of PMS across generations by analysing the hormonal composition of F1 and F2 eggs and by studying histone post-translational modifications in F3 brains. We showed that PMS increased the neophobia of F2 offspring and F3 females' offspring. We also observed modulations of androgens levels in F1 and F2 eggs but no modifications of the level of histone post-translational modification in F3 brains. Although the mechanisms involved in PMS transmission still need to be explored, our results demonstrate a multi- and transgenerational behavioural effect of PMS in birds.</p>
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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.