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1,875 results for “homeostasis”
Patient-specific induced pluripotent stem cell properties implicate Ca2+-homeostasis in clinical arrhythmia associated with combined heterozygous RYR2 and SCN10A variants
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Data from: Dynamic changes in chloride homeostasis coordinate midbrain inhibitory network activity during reward learning
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Data and code from: Distinct transmission sites within a synapse for strengthening and homeostasis
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Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction
<p>The raw data of the manuscript” Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction”</p>
Data sets for Shiburah et al., "The absence of the Leishmania major telomerase TERT component links telomeres and cell homeostasis with infectivity"
<p>These files correspond to the figures and information contained in Shiburah et al., "The absence of the <em>Leishmania major</em> telomerase TERT component links telomeres and cell homeostasis with infectivity"</p>
Multi-omics reveals the attenuation of metabolic cardiomyopathy in mice by extracts from Clausena0 lansium (Lour.) by transiting gastrointestinal microbiota to an alternative homeostasis
<p>The raw data for MS "<strong>Multi-omics reveals the attenuation of metabolic cardiomyopathy in mice by extracts from </strong><i><strong>Clausena0 lansium</strong></i><strong> (Lour.) by transiting gastrointestinal microbiota to an alternative homeostasis".</strong></p>
Hypoxia-inducible factor induces cysteine dioxygenase and promotes cysteine homeostasis in Caenorhabditis elegans
<p>Dedicated genetic pathways regulate cysteine homeostasis. For example, high levels of cysteine activate cysteine dioxygenase, a key enzyme in cysteine catabolism in most animal and many fungal species. The mechanism by which cysteine dioxygenase is regulated is largely unknown. In an unbiased genetic screen for mutations that activate cysteine dioxygenase (<em>cdo-1</em>) in the nematode <em>C. elegans, </em>we isolated loss-of-function mutations in <em>rhy-1 </em>and <em>egl-9, </em>which encode proteins that negatively regulate the stability or activity of the oxygen-sensing hypoxia-inducible transcription factor (<em>hif-1</em>). EGL-9 and HIF-1 are core members of the conserved eukaryotic hypoxia response. However, we demonstrate that the mechanism of HIF-1-mediated induction of <em>cdo-1 </em>is largely independent of EGL-9 prolyl hydroxylase activity and the von Hippel-Lindau E3 ubiquitin ligase, the classical hypoxia signaling pathway components. We demonstrate that <em>C. elegans cdo-1 </em>is transcriptionally activated by high levels of cysteine and <em>hif-1</em>. <em>hif-1-</em>dependent activation of <em>cdo-1</em> occurs downstream of an H<sub>2</sub>S-sensing pathway that includes <em>rhy-1, cysl-1, </em>and <em>egl-9.</em> <em>cdo-1 </em>transcription is primarily activated in the hypodermis where it is also sufficient to drive sulfur amino acid metabolism. Thus, the regulation of <em>cdo-1 </em>by <em>hif-1 </em>reveals a negative feedback loop that maintains cysteine homeostasis. High levels of cysteine stimulate the production of an H<sub>2</sub>S signal. H<sub>2</sub>S then acts through the <em>rhy-1/cysl-1/egl-9 </em>signaling pathway to increase HIF-1-mediated transcription of <em>cdo-1, </em>promoting the degradation of cysteine via CDO-1.</p>
The intestinal circadian clock drives microbial rhythmicity to maintain gastrointestinal homeostasis
<p><strong>Diurnal (<em>i.e.</em>, 24-hour) oscillations of the gut microbiome have been described in various species including mice and humans. However, the driving force behind these rhythms remains less clear. In this study, we differentiate between endogenous and exogenous time cues driving microbial rhythms.</strong> <strong>Our results demonstrate that fecal microbial oscillations are maintained in mice kept in the absence of light, supporting a role of the host’s circadian system rather than representing a diurnal response to environmental changes. Intestinal epithelial cell-specific ablation of the core clock gene <em>Bmal1</em> disrupts rhythmicity of microbiota. Targeted metabolomics functionally link intestinal clock-controlled bacteria to microbial-derived products, in particular branched-chain fatty acids and secondary bile acids. Microbiota transfer from intestinal clock-deficient mice into germ-free mice altered intestinal gene expression, enhanced lymphoid organ weights and suppressed immune cell recruitment. These results highlight the importance of functional intestinal clocks for circadian microbiota composition and function, which is required to balance the host’s gastrointestinal homeostasis. </strong></p>
DNA Methyltransferase regulates nitric oxide homeostasis and virulence in a chronically adapted Pseudomonas aeruginosa strain
<p><span>Opportunistic pathogens such as <em>Pseudomonas aeruginosa </em>adapt their genomes rapidly during chronic infections. Understanding their epigenetic regulation may provide biomarkers for diagnosis and reveal novel regulatory mechanisms. We performed single-molecule real-time sequencing (SMRT-seq) to characterize the methylome of a chronically adapted P. aeruginosa clinical strain TBCF10839. Two </span><span>N6-methyl-adenine (6mA) methylation recognition motifs (RCC<strong>A</strong>NNNNNNN<strong>T</strong>GAR and </span><span>TRG<strong>A</strong>NNNNNN<strong>T</strong>GC)</span><span> were identified and predicted as </span><span>new type I methylation sites using REBASE analysis. We confirmed that motif </span><span>TRG<strong>A</strong>NNNNNN<strong>T</strong>GCwas methylated by MTase M.PaeTBCFII, according to methylation sensitivity assays <em>in vivo </em>and <em>vitro</em>. Transcriptomic analysis showed that <em>Δ</em></span><em><span>M.PaeTBCFII</span></em><span><em> </em>knockout mutant significantly downregulated nitric oxide reductase (NOR) regulating and coding gene expression such as </span><span>nosR </span><span>and norB,</span><span> which contain</span><span> methylated motifs in their promoters or coding regions.</span><span> Δ</span><span>M.PaeTBCFII </span><span>exhibited </span><span>reduced intercellular survival capacity in NO-producing RAW 264.7 macrophages and attenuated virulence in <em>Galleria mellonella</em> infection model; the </span><span>complemented strain recovered these defective phenotypes</span><span>. Further phylogenetic analysis demonstrated that homologs of M.PaeTBCFII occur frequently in P. aeruginosa sp as well as other bacterial species. Our work therefore provided new insights on the relationship between DNA methylation, NO detoxification, and bacterial virulence, </span><span>laying a foundation for further exploring the molecular mechanism of DNA methyltransferase in regulating the pathogenicity of <em>P. aeruginosa</em></span><span>.</span></p>
Raw data for the paper entitled "Astrocytic GLUT1 Reduction Paradoxically Improves Central and Peripheral Glucose Homeostasis"
<p>This files contains the raw data for all the figures contained in the paper entitled "Astrocytic GLUT1 Reduction Paradoxically Improves Central and Peripheral Glucose Homeostasis".</p>
Supplementary Figure 1 - Debulking surgery after muscular paraffin oil injections: Effects on calcium homeostasis and patient satisfaction
<p><strong><span>Figure legend</span></strong><span>: A-B: Plot for serum concentration of 1,25 dihydroxyvitamin D from baseline, and 1, 3, 6, and 12 months after surgery. Plot A is for normocalcemic men, while plot B is for hypercalcemic men.</span></p>
Constriction rate modulation can drive cell size control and homeostasis in C. crescentus. Data part 2.
<p>This data corresponds to the publication "Constriction rate modulation can drive cell size control and homeostasis in <em>C. crescentus</em>".</p> <p>This is part 2 out of 2.</p> <p>Part 1: 10.5281/zenodo.1172042</p> <p>See metadata.docx for more information.</p>
Constriction rate modulation can drive cell size control and homeostasis in C. crescentus. Data part 1.
<p>This data corresponds to the publication "Constriction rate modulation can drive cell size control and homeostasis in <em>C. crescentus</em>".</p> <p>This is part 1 out of 2.</p> <p>Part 2: 10.5281/zenodo.1241005 </p> <p>See metadata.docx for more information.</p>
Automated Model Discovery for Tensional Homeostasis: Constitutive Machine Learning in Growth and Remodeling (Source code and data)
<p>This dataset contains</p> <ul> <li>the source code</li> <li>the data and examples</li> <li>the material subroutine with examples of uniaxial strain and stress</li> </ul> <p>of the inelastic Constitutive Artificial Neural Network (iCANN) enhanced by the concept of homeostatic surfaces to discover tensional homeostasis.</p> <p>The corresponding publication is:</p> <p>Holthusen, H., Brepols, T., Linka, K., & Kuhl, E..<em> </em></p> <p><em>Automated Model Discovery for Tensional Homeostasis: Constitutive Machine Learning in Growth and Remodeling.</em></p> <p> </p> <p><strong>Standalone_Materialroutine</strong></p> <ul> <li>00_Materialroutine: Contains the material subroutine implemented in FORTRAN</li> <li>01_uniaxial_strain: Example of the material subroutine in a uniaxial strain driven manner</li> <li>02_uniaxial_stress: Example of the material subroutine in a uniaxial stress driven manner</li> </ul> <p> </p> <p><strong>TensorFlow</strong></p> <ul> <li> <p>iCANN:</p> <ul> <li> <p>01_Biax/biax_l1: Keras/TensorFlow implementation of the iCANN. Example of the cross specimen with L1 (Lasso) regularization</p> </li> <li> <p>01_Biax/biax_l2: Keras/TensorFlow implementation of the iCANN. Example of the cross specimen with L2 (ridge) regularization</p> </li> <li> <p>02_Uniax/uniax_l1: Keras/TensorFlow implementation of the iCANN. Example of the stripe specimen with L1 (Lasso) regularization</p> </li> <li>02_Uniax/uniax_l1: Keras/TensorFlow implementation of the iCANN. Example of the stripe specimen with L2 (ridge) regularization</li> </ul> </li> <li> <p>iCANN_ABS_activation: Same four examples as above, however, with the absolute value activation function</p> </li> <li> <p>installed_packages: File containing a list of installed Python modules used to implement the iCANN</p> </li> </ul> <p>The TensorFlow implementations in all 01_Biax/ and 02_Uniax/ sub-directories are the same.</p> <p>The implementation in iCANN_ABS_activation is different with respect to the activation functions of the pseudo potential.</p> <p> </p> <p>The experimental data for the cross and stripe specimen are taken from the literature:</p> <p>Eichinger, J. F., Paukner, D., Szafron, J. M., Aydin, R. C., Humphrey, J. D., & Cyron, C. J. (2020).</p> <p>Computer-controlled biaxial bioreactor for investigating cell-mediated homeostasis in tissue equivalents. <em>Journal of biomechanical engineering</em>, <em>142</em>(7), 071011.</p> <p><a href="https://doi.org/10.1115/1.4046201">https://doi.org/10.1115/1.4046201</a></p>
Lipidomic datasets for: Transmembrane protein 135 regulates lipid homeostasis through its role in peroxisomal DHA metabolism
<p>Transmembrane protein 135 (TMEM135) is thought to participate in the cellular response to increased intracellular lipids yet no defined molecular function for TMEM135 in lipid metabolism has been identified. In this study, we performed a lipid analysis of tissues from <em>Tmem135</em> mutant mice and found striking reductions of docosahexaenoic acid (DHA) across all <em>Tmem135</em> mutant tissues, indicating a role of TMEM135 in the production of DHA. Since all enzymes required for DHA synthesis remain intact in <em>Tmem135</em> mutant mice, we hypothesized that TMEM135 is involved in the export of DHA from peroxisomes. The <em>Tmem135</em> mutation likely leads to the retention of DHA in peroxisomes, causing DHA to be degraded within peroxisomes by their beta-oxidation machinery. This may lead to generation or alteration of ligands required for the activation of peroxisome proliferator-activated receptor a (PPARa) signaling, which in turn could result in increased peroxisomal number and beta-oxidation enzymes observed in <em>Tmem135</em> mutant mice. We confirmed this effect of PPARa signaling by detecting decreased peroxisomes and their proteins upon genetic ablation of <em>Ppara</em> in <em>Tmem135</em> mutant mice. Using <em>Tmem135</em> mutant mice, we also validated the protective effect of increased peroxisomes and peroxisomal beta-oxidation on the metabolic disease phenotypes of leptin mutant mice which has been observed in previous studies. Thus, we conclude that TMEM135 has a role in lipid homeostasis through its function in peroxisomes.</p>
Diet-mediated constitutive induction of novel IL4+ ILC2 cells maintains intestinal homeostasis in mice
<p>Group 2 innate lymphoid cells (ILC2s) expressing IL-5 and IL-13 are localized at various mucosal tissues and play critical roles in the induction of type 2 inflammation, response to helminth infection, and tissue repair. Here we reveal a unique ILC2 subset in the mouse intestine that constitutively expresses IL-4 together with GATA3, ST2, KLRG1, IL-17RB, and IL-5. In this subset, IL-4 expression is regulated by mechanisms similar to but distinct from those observed in T cells and is partly affected by IL-25 signaling. Although the absence of the microbiota had marginal effects, feeding mice with a vitamin B1-deficient diet compromised the number of intestinal IL-4+ ILC2s. The decrease in the number of IL-4+ ILC2s caused by the vitamin B1 deficiency was accompanied by a reduction in IL-25-producing tuft cells. Our findings reveal that dietary vitamin B1 plays a critical role in maintaining interaction between tuft cells and IL-4+ ILC2s, a previously uncharacterized immune cell population that may contribute to maintaining intestinal homeostasis.</p>
Parkin regulates amino acid homeostasis at mitochondria-lysosome (M/L) contact sites in Parkinson's disease
<p>Mutations in the E3 ubiquitin ligase parkin are the most common cause of early-onset Parkinson's disease (PD). Although parkin modulates mitochondrial and endolysosomal homeostasis during cellular stress, whether parkin regulates mitochondrial and lysosomal crosstalk under physiologic conditions remains unresolved. Using transcriptomics, metabolomics, and super-resolution microscopy, we identify amino acid metabolism as a disrupted pathway in iPSC-derived dopaminergic neurons from parkin PD patients. Compared to isogenic controls, parkin mutant neurons exhibit decreased mitochondria-lysosome contacts via destabilization of active Rab7. Subcellular metabolomics in parkin mutant neurons reveals amino acid accumulation in lysosomes and their deficiency in mitochondria. Knockdown of the Rab7 GTPase-activating protein TBC1D15 restores mitochondria-lysosome tethering and ameliorates cellular and subcellular amino acid profiles in parkin mutant neurons. Our data thus uncover a function of parkin in promoting mitochondrial and lysosomal amino acid homeostasis through stabilization of mitochondria-lysosome contacts and suggest that modulation of inter-organelle contacts may serve as a potential target for ameliorating amino acid dyshomeostasis in disease.</p>
Aldosterone and Glucose Homeostasis
ClinicalTrials.gov study NCT00732160. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Hemodynamically Guided Home Self-Therapy in Severe Heart Failure Patients (HOMEOSTASIS)
ClinicalTrials.gov study NCT00547729. IPD Sharing: NO. Countries: 3. Publications: 4.
A Study to Determine Acute (After First Dose) and Chronic (After 28 Days) Effects of Empagliflozin (BI 10773) on Pre and Postprandial Glucose Homeostasis in Patients With Impaired Glucose Tolerance an
ClinicalTrials.gov study NCT01248364. IPD Sharing: Not stated. Countries: 3. Publications: 3.
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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.