F5a3bc98-8b28-4a25-8b6d-5f10ef0fce80 - samples
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ABSTRACT:
PROVIDER: EGAD00001007991 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:BAM files containing paired-end mtDNA sequencing data from morphologically normal human liver. CCO-proficient hepatocytes acquired from livers in which clonal CCO-deficient hepatocyte patches had been previously identified. Individual BAM files are named according to their patch, line and sample location, where PT denotes tissue near to the portal triad (PT), central hepatic vein (CV) and midway between these two structures (Mid). "Stroma" control samples were used for identifying germ-line variants. Sequenced on NextSeq 500 platform.
| EGAS00001006962 | EGA
Project description:BAM files containing paired-end mtDNA sequencing data from morphologically normal human liver. CCO-proficient hepatocytes acquired from human livers in which clonal CCO-deficient hepatocyte patches had been previously identified. Individual BAM files are named according to their patch, line and sample location, where PT denotes tissue near to the portal triad (PT), central hepatic vein (CV) and midway between these two structures (Mid). "Stroma" control samples were used for identifying germ-line variants. Sequenced on NextSeq 500 platform.
| EGAD00001010016 | EGA
Project description:RNAseq data from Passman et al 2023. Clonal CCO-deficient hepatocyte patches and nearby CCO-proficient hepatocytes were identified in morphologically normal human livers and sampled at varying distances along the PT-CV axis. Samples are characterised according to their location within the liver lobule, with "PT" denoting samples abutting the portal triad, "CV" denoting samples abutting the central hepatic vein, and "Mid" sampled acquired midway between these structures. Analysis was performed on an Illumina Nextseq using a high output kit and 100 single-end cycles.
| EGAD00001010033 | EGA
Project description:RNAseq data from Passman et al 2023. Clonal CCO-deficient hepatocyte patches and nearby CCO-proficient hepatocytes were identified in morphologically normal human livers and sampled at varying distances along the PT-CV axis. Samples are named according to their location within the liver lobule, with "PT" denoting samples abutting the portal triad, "CV" denoting samples abutting the central hepatic vein, and "Mid" sampled acquired midway between these structures.
Normal human liver is thought to be generally quiescent, however clonal hepatocyte expansions have been observed but neither their cellular source nor their expansion dynamics have been determined. Knowing the hepatocyte cell of origin, and their subsequent dynamics and trajectory within the human liver will provide an important basis to understand disease-associated dysregulation.
Here we use in vivo lineage tracing and a combination of methylation sequence analysis to demonstrate normal human hepatocyte ancestry. We exploit next generation mitochondrial sequencing to determine hepatocyte clonal expansion dynamics across spatially-distinct areas of laser-capture microdissected clones, in tandem with computational modelling in morphologically-normal human liver.
| EGAS00001006984 | EGA
Project description:Lipid A (a hexaacylated 1,4 bis-phosphate) is a potent immune stimulant for TLR4/MD-2. Upon lipid A ligation, the TLR4/MD-2 complex dimerizes and initiates signal transduction. Historically, studies also suggested the existence of TLR4/MD-2-independent LPS signaling. Here we define the role of TLR4 and MD-2 in LPS signaling by using genome wide expression profiling in TLR4- and MD-2-deficient macrophages after stimulations with peptidoglycan-free LPS and synthetic E.coli lipid A. Of the 1,396 genes found significantly induced or repressed by any one of the treatments in the wildtype macrophages, none was present in the TLR4- or MD-2-deficient macrophages, confirming that the TLR4/MD-2 complex is the only receptor for endotoxin, and are both absolutely required for responses to LPS. Using a molecular genetics approach, we investigated the mechanism of TLR4/MD-2 activation by combining the known crystal structure of TLR4/MD-2 with computer modeling. We used lipid IVa, a defined lipid A mimetic to model the activation of mouse TLR4/MD2. The two phosphates on lipid A were predicted to interact extensively with the two positively charged patches mouse TLR4 according to our dimeric murine TLR4/MD-2/lipid IVa model. These two patches are composed of K263, R337, and K360 (Positive Patch 1), and K367 and R434 (Positive Patch 2). When either Positive Patch was abolished by mutagenesis into Ala, the responses to LPS and lipid A were almost abrogated. Thus, ionic interactions between the two phosphates on lipid A and the two positively charged patches on murine TLR4 appear to be essential for LPS receptor activation. The gene expression profile of macrophages from C57BL/6 and MD-2-deficient mice following either 10 ng LPS /mL, 100 ng lipid A/mL or 10 nM Pam2 stimulation for 2 hours were compared to PBS-stimulated control cells . In vitro differentiated macrophages from two individual WT and MD-2-deficient mice were cultured and stimulated with agonists separately, comparing the gene expression to PBS-stimulated control cells from the same mouse. Comparisons of PBS-stimulated WT cells to PBS-stimulated MD-2-deficient cells were performed to directly compare basal gene expression in the two genotypes.
2011-07-30 | E-GEOD-31067 | biostudies-arrayexpress
Project description:Lipid A (a hexaacylated 1,4 bis-phosphate) is a potent immune stimulant for TLR4/MD-2. Upon lipid A ligation, the TLR4/MD-2 complex dimerizes and initiates signal transduction. Historically, studies also suggested the existence of TLR4/MD-2-independent LPS signaling. Here we define the role of TLR4 and MD-2 in LPS signaling by using genome wide expression profiling in TLR4- and MD-2-deficient macrophages after stimulations with peptidoglycan-free LPS and synthetic E.coli lipid A. Of the 1,396 genes found significantly induced or repressed by any one of the treatments in the wildtype macrophages, none was present in the TLR4- or MD-2-deficient macrophages, confirming that the TLR4/MD-2 complex is the only receptor for endotoxin, and are both absolutely required for responses to LPS. Using a molecular genetics approach, we investigated the mechanism of TLR4/MD-2 activation by combining the known crystal structure of TLR4/MD-2 with computer modeling. We used lipid IVa, a defined lipid A mimetic to model the activation of mouse TLR4/MD2. The two phosphates on lipid A were predicted to interact extensively with the two positively charged patches mouse TLR4 according to our dimeric murine TLR4/MD-2/lipid IVa model. These two patches are composed of K263, R337, and K360 (Positive Patch 1), and K367 and R434 (Positive Patch 2). When either Positive Patch was abolished by mutagenesis into Ala, the responses to LPS and lipid A were almost abrogated. Thus, ionic interactions between the two phosphates on lipid A and the two positively charged patches on murine TLR4 appear to be essential for LPS receptor activation. Bone marrow-derived macrophages were pooled from four individual WT or TLR4-deficient mice and stimulated with either 10 ng LPS /mL, 100 ng lipid A/mL or 10 nM Pam2 for 2 hours and compared to PBS-stimulated control cells. We also compared PBS-stimulated WT cells directly to PBS-stimulated TLR4-deficient cells to compare the basal expression of genes in the two genotypes. This experiment was repeated once in its entirety.
2011-07-30 | E-GEOD-31066 | biostudies-arrayexpress
Project description:Microneedle patches are widely employed in pain-free drug delivery, biosensing, and cosmetic applications. However, weak tissue adhesion remains a major challenge in clinical translation of microneedle patches. Here, mimicking the structural features of honeybee stingers, stiff polymeric microneedles with unidirectionally backward facing barbs were fabricated and embedded into various elastomer films to produce self-interlocking microneedle patches. The spirality of the barbing pattern was adjusted to increase interlocking efficiency. In the challenging working condition of animal hearts beat with large cyclic strains, the barbs provided 0.4 N interlocking force, which resulted in firm fixation of the bioinspired microneedle patch. In addition, the minimal bleeding caused by microneedle puncturing adhered the porous surface of the patch substrate between microneedles to the epicardium via coagulation. In the demonstrative application of myocardial infarction treatment, the microneedle patches significantly reduced cardiac wall stress and strain in the infarct and border zone, maintaining left ventricular function and morphology. In addition, the microneedle patch was minimally invasively implanted onto beating porcine heart free of sutures and adhesives, and the fixation step only took 2 minutes. Therefore, the honeybee stinger inspired microneedles could provide an adaptive and convenient means to adhere patches for various medical applications.
2023-01-01 | GSE201196 | GEO
Project description:S. coelicolor spore stocks were diluted to 2x108 cfu/mL and 0.5ul was spotted onto a 60x15mm petri dish with 4ml ISP2 agar, resulting in agar approximately 2 mm thick. For interactions, 0.5 ul of an Amycolatopsis sp. AA4 stock (8x108 cfu/mL) was spotted 0.75 cm away from the S. coelicolor spot. Interactions were grown for 4 days at 30°C, then imaged or harvested for RNA isolation. Biomass was collected after 4 days of growth at 30°C using a cell scraper. For the patches growing alone, the entire patch was collected and one sample consists of three whole patches combined. For the patches in interactions, only half of the patch, the side closest to the initiator strain, was collected and one sample consists of five half patches. Precaution was taken to not scrape up any of the interacting strain.
2021-09-08 | GSE167965 | GEO
Project description:S. coelicolor spore stocks were diluted to 2x108 cfu/mL and 0.5ul was spotted onto a 60x15mm petri dish with 4ml ISP2 agar, resulting in agar approximately 2 mm thick. For interactions, 0.5 ul of an Amycolatopsis sp. AA4 stock (8x108 cfu/mL) was spotted 0.75 cm away from the S. coelicolor spot. Interactions were grown for 4 days at 30°C, then imaged or harvested for RNA isolation. Biomass was collected after 4 days of growth at 30°C using a cell scraper. For the patches growing alone, the entire patch was collected and one sample consists of three whole patches combined. For the patches in interactions, only half of the patch, the side closest to the initiator strain, was collected and one sample consists of five half patches. Precaution was taken to not scrape up any of the interacting strain.
2021-09-08 | GSE167964 | GEO
Project description:Lipid A (a hexaacylated 1,4 bis-phosphate) is a potent immune stimulant for TLR4/MD-2. Upon lipid A ligation, the TLR4/MD-2 complex dimerizes and initiates signal transduction. Historically, studies also suggested the existence of TLR4/MD-2-independent LPS signaling. Here we define the role of TLR4 and MD-2 in LPS signaling by using genome wide expression profiling in TLR4- and MD-2-deficient macrophages after stimulations with peptidoglycan-free LPS and synthetic E.coli lipid A. Of the 1,396 genes found significantly induced or repressed by any one of the treatments in the wildtype macrophages, none was present in the TLR4- or MD-2-deficient macrophages, confirming that the TLR4/MD-2 complex is the only receptor for endotoxin, and are both absolutely required for responses to LPS. Using a molecular genetics approach, we investigated the mechanism of TLR4/MD-2 activation by combining the known crystal structure of TLR4/MD-2 with computer modeling. We used lipid IVa, a defined lipid A mimetic to model the activation of mouse TLR4/MD2. The two phosphates on lipid A were predicted to interact extensively with the two positively charged patches mouse TLR4 according to our dimeric murine TLR4/MD-2/lipid IVa model. These two patches are composed of K263, R337, and K360 (Positive Patch 1), and K367 and R434 (Positive Patch 2). When either Positive Patch was abolished by mutagenesis into Ala, the responses to LPS and lipid A were almost abrogated. Thus, ionic interactions between the two phosphates on lipid A and the two positively charged patches on murine TLR4 appear to be essential for LPS receptor activation.
2011-07-31 | GSE31067 | GEO