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579 results for “cell death”
Data from: Reduced internalization of TNF-ɑ/TNFR1 down-regulates caspase dependent phagocytosis induced cell death (PICD) in neonatal monocytes
Phagocytosis-induced cell death (PICD) is diminished in cord blood monocytes (CBMO) as compared to cells from adults (PBMO) due to differences in the CD95-pathway. This may support a prolonged pro-inflammatory response with sequels of sustained inflammation as seen in neonatal sepsis. Here we hypothesized that TNF-α mediated induction of apoptosis is impaired in CBMO due to differences in the TNFR1-dependent internalization. Monocytes were infected with Escherichia coli-GFP (E. coli-GFP). Monocyte phenotype, phagocytic activity, induction of apoptosis, and TNF-α/TNF-receptor (TNFR) -expression were analysed. In the course of infection TNF-α-secretion of CBMO was reduced to 40% as compared to PBMO (p<0.05). Neutralization of TNF-α by an αTNF-α antibody reduced apoptotic PICD in PBMO four-fold (p < 0.05 vs. infection with E. coli). PICD in CBMO was reduced 5-fold compared to PBMO and showed less responsiveness to αTNF-α antibody. CBMO expressed less pro-apoptotic TNFR1, which, after administration of TNF-α or infection with E. coli was internalized to a lesser extent. With similar phagocytic capacity, reduced TNFR1 internalization in CBMO was accompanied by lower activation of caspase-8 (p < 0.05 vs. PBMO). Stronger caspase-8 activation in PBMO caused more activation of effector caspase-3 and apoptosis (all p < 0.05 vs. PBMO). Our results demonstrate that TNFR1 internalization is critical in mediating PICD in monocytes after infection with E.coli and is reduced in CBMO.
Data from: Cell death and survival due to cytotoxic exposure modeled as a two-state Ising system
<p>Cancer chemotherapy agents are assessed for their therapeutic utility primarily by their ability to cause apoptosis of cancer cells and their potency is given by an IC50 value. Chemotherapy uses both target-specific and systemic-action drugs and drug combinations to treat cancer. It is important to judiciously choose a drug type, its dosage, and schedule for optimized drug selection and administration. Consequently, the precise mathematical formulation of cancer cells response to chemotherapy may assist in the selection process. In this paper, we propose a mathematical description of the cancer cell response to chemotherapeutic agent exposure based on a time-tested physical model of two-state multiple-component systems near criticality. We describe the Ising model methodology and apply it to a diverse panel of cytotoxic drugs administered against numerous cancer cell lines in a dose-response manner. The analyzed dataset was generated by the Netherlands Translational Research Center B.V.(Oncolines). This approach allows for an accurate and consistent analysis of cytotoxic agents' effects on cancer cell lines and reveals the presence or absence of the bystander effect through the interaction constant. By calculating the susceptibility function, we see the value of IC50 coinciding with the peak of this measure of the system's sensitivity to external perturbations.</p>
Parthenolide induces ROS-dependent cell death in human gastric cancer cells
<p>Excel 1 - The original data-Parthenolide induces ROS-dependent cell death in human gastric cancer cellanalysis.</p><p>Supplemental Table 1 - Post-hoc Dunn's test for the effect of PN on the cell viability of MGC-803 cell.</p><p>Supplemental Table 2 - Post-hoc Dunn's test for the effect of PN on the cell colonies of MGC-803 cells.</p><p>Supplemental Table 3 - Post-hoc Dunn's test for the effect of PN and catalase on ROS Generation of MGC-803 cells</p><p>Supplemental Table 4 - Post-hoc Dunn's test for the effect of PN and catalase on cell viability of MGC-803 cells</p><p>Excel 2 - gene_sample_count from MGC-803 cells treated with DMSO compared with counterparts treated with PN </p>
DNA damage and reticular stress in cytotoxicity and oncotic cell death of MCF-7 cells treated with fluopsin C
<p>DNA damage and reticular stress in cytotoxicity and oncotic cell death of MCF-7 cells treated with fluopsin C</p>
CLEC-1 is a death sensor that limits antigen cross-presentation by dendritic cells and represents a target for cancer immunotherapy
<p>Tumors exploit numerous immune checkpoints including those deployed by myeloid cells to curtail anti-tumor immunity. Here, we show that the C-type lectin receptor CLEC-1 expressed by myeloid cells senses dead cells killed by programmed necrosis. Moreover, we identified TRIM21 as an endogenous ligand over-expressed in various cancers. Interestingly, we observed that in mice CLEC-1 blockade combined with chemotherapy to prolong survival in tumor models. Loss of CLEC-1 reduced the accumulation of immunosuppressive myeloid cells in tumors and invigorated the activation state of dendritic cells (DCs), thereby increasing T cell responses. Mechanistically, we found that the absence of CLEC-1 increased the cross-presentation of dead-cell associated antigens by conventional type-1 DCs. Importantly, we identified anti-human CLEC-1 antagonist antibodies able to enhance anti-tumor immunity in CLEC-1 humanized mice. Altogether, our results demonstrate that CLEC-1 acts as an immune checkpoint in myeloid cells and support CLEC-1 as a novel target for cancer immunotherapy.</p>
Dataset to "Collagen I Increases Palmitate-Induced Lipotoxicity in HepG2 Cells via Integrin-Mediated Death"
Open the record for dataset details and reuse information.
Code and Data to recreate figures from: Activation of immune receptor Rx1 triggers distinct immune-responses culminating in cell death after four hours.
<p>Code and Data to recreate figures from: Activation of immune receptor Rx1 triggers distinct immune-responses culminating in cell death after four hours.</p> <p><a href="https://doi.org/10.1111/mpp.12776">https://doi.org/10.1111/mpp.12776</a></p> <p> </p> <p>These files are also on Github:</p> <p>https://github.com/MolPlantPathology/PMID-30537296-</p>
Identification of Predictive Factors for the Response to Anti-Programmed Cell Death Protein 1 (PD1) Immunotherapy in Head and Neck Squamous Cell Carcinoma
ClinicalTrials.gov study NCT05328024. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Study of Pembrolizumab (MK-3475) Versus Platinum-Based Chemotherapy for Participants With Programmed Cell Death-Ligand 1 (PD-L1)-Positive Advanced or Metastatic Non-Small Cell Lung Cancer (MK-3475-042
ClinicalTrials.gov study NCT02220894. IPD Sharing: YES. Countries: 0. Publications: 5.
Immunotherapy Using Pluripotent Killer-Programmed Cell Death 1 (PIK-PD-1) Cells for the Treatment of Advanced Hepatocellular Carcinoma
ClinicalTrials.gov study NCT02632006. IPD Sharing: Not stated. Countries: 1. Publications: 25.
Natural Killer(NK) Cell Combined With Programmed Death-1(PD-1) Antibody as Second Line Therapy for Advanced Driver Mutation Negative Non-small Cell Lung Cancer
ClinicalTrials.gov study NCT03958097. IPD Sharing: NO. Countries: 1. Publications: 2.
Tumor-Infiltrating Lymphocytes and Programmed Cell Death - Ligand 1 in Breast Cancer
ClinicalTrials.gov study NCT05250336. IPD Sharing: UNDECIDED. Countries: 1. Publications: 5.
Epidemiologic Multicenter Prospective Study in Advanced NSCLC (Non Small Cell Lung Cancer) Patients With PDL1 (Protein Death Ligand 1) Expression.
ClinicalTrials.gov study NCT02785562. IPD Sharing: NO. Countries: 1. Publications: 2.
Study of Pembrolizumab (MK-3475) Versus Platinum-Based Chemotherapy for Participants With Programmed Cell Death-Ligand 1 (PD-L1)-Positive Advanced or Metastatic Non-Small Cell Lung Cancer (MK-3475-042
ClinicalTrials.gov study NCT03850444. IPD Sharing: YES. Countries: 0. Publications: 1.
Regorafenib Plus Programmed Cell Death-1 (PD-1) Inhibitors in Patients With Advanced Colorectal Cancer
ClinicalTrials.gov study NCT04771715. IPD Sharing: NO. Countries: 1. Publications: 1.
Mechanisms of Cell Death in Spinal Muscular Atrophy
ClinicalTrials.gov study NCT01754441. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Detection of Human Beta Cell Death in Type 1 Diabetes Mellitus (T1DM) by Methylation Specific Polymerase Chain Reaction (PCR)
ClinicalTrials.gov study NCT01176253. IPD Sharing: Not stated. Countries: 1. Publications: 8.
Anti-programmed Cell Death-1 Ligand 1 (aPDL-1) Antibody Atezolizumab, Bevacizumab and Acetylsalicylic Acid in Recurrent Platinum Resistant Ovarian Cancer
ClinicalTrials.gov study NCT02659384. IPD Sharing: Not stated. Countries: 5. Publications: 1.
Immunogenic Cell Death as a Novel Mechanism of Mitomycin C Activity in Bladder Cancer
ClinicalTrials.gov study NCT04256616. IPD Sharing: NO. Countries: 1. Publications: 1.
Study of TSR-042, an Anti-programmed Cell Death-1 Receptor (PD-1) Monoclonal Antibody, in Participants With Advanced Solid Tumors
ClinicalTrials.gov study NCT02715284. IPD Sharing: YES. Countries: 10. Publications: 11.
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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)
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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.