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90 results for “Interleukin-6”
Organic electrochemical transistor aptasensor for interleukin-6 detection
<p>Explanation of included data for following publication:</p><p>-------------------------------------------------------------------------------------</p><p><strong>Organic electrochemical transistor aptasensor for interleukin-6 detection</strong></p><p>Chiara Diacci (1,2), Bernhard Burtscher (1), Marcello Berto (2), Tero Petri Ruoko (1), Samuel Lienemann (1), Pierpaolo Greco (3,4), Magnus Berggren (1), Marco Borsari (5), Daniel T. Simon (1), Carlo A. Bortolotti (2), Fabio Biscarini (2,4)</p><p> </p><p>1) Laboratory of Organic Electronics, Department of Science and Technology, ITN, Linköping University, 601 74, Norrköping, Sweden.</p><p>2) Dipartimento di Scienze della Vita, Università di Modena e Reggio Emilia, via Campi 103, 41125 Modena, Italy.</p><p>3) Department of Neuroscience and Rehabilitation, Università di Ferrara, Via Borsari 46, 44121 Ferrara, Italy.</p><p>4) Center for Translational Neurophysiology of Speech and Communication, Istituto Italiano di Tecnologia, via Fossato di Mortara 17-193, 44100 Ferrara, Italy.</p><p>5) Dipartimento di Scienze Chimiche e Geologiche, Università di Modena e Reggio Emilia, via Campi 103, 41125 Modena, Italy.</p><p>-------------------------------------------------------------------------------------</p><p><strong>Manuscript</strong></p><p> </p><p>Figure 2:</p><ul><li>SEM pictures</li></ul><p> </p><p>Figure 3:</p><ul><li>CV for aptamer deposition (Time, Voltage, Current) in 1µM aptamer solution from 0V to -1V, 50mV/s for 30 cycles</li><li>Impedance data for AuNP/PEDOT:PSS electrode (before aptamer deposition) and after aptamer deposition (Aptamer/AuNP/PEDOT:PSS); (Freq/Hz, Re(Z)/Ohm, -Im(Z)/Ohm, |Z|/Ohm, Phase/deg) in ferricyanide 5mM</li></ul><p> </p><p>Figure 4: Fluorescent images (LSM, as czi format) for</p><ul><li>4a: AuNP/PEDOT:PSS (no Cy3-tag, control)</li><li>4b: Cy3-aptamer/AuNP/PEDOT:PSS (sample)</li><li>4c: Cy3-aptamer/PEDOT:PSS (no AuNP, control)</li></ul><p> </p><p>Figure 5: Data sets of transfer curves for multiple OECTs for various concentrations of IL6/TNF</p><ul><li>One sheet refers to one OECT sample with either IL6 or TNF</li><li>The first coloumn indicates the gate voltage and the others the drain current with various concentration except the second column (Tween) with is without any analyte</li><li>VDS = -0.3V</li><li>VGS swept from 0 to 0.6V</li></ul><p> </p><p> </p><p> </p><p>Supporting Information:</p><p> </p><p>Figure S1: AuNP/PEDOT:PSS electrical characteristics</p><ul><li>S1a: CV in 5mM ferricyanide from -0.5V to 0.5V at 50mV/s</li><li>S1b: Transconductance for bare Au, PEDOT:PSS in PBS 10mM</li><li>S1c: Transfer curves in PBS 10mM</li></ul><p> </p><p>Figure S2: FTIR-ATR measurements</p><ul><li>Raw exported files from the FTIR (Au+PEDOT, Au+DNA, Au+PEDOT+NP, Au+PEDOT+NP+DNA) as txt file.</li><li>For Au+DNA the normalized with the maximum and for the others the 1010cm-1 peak used for normalization. This is shown in the ATR.xlsx file.</li></ul><p> </p><p>Figure S3: IL6 detection on AuNP/PEDOT:PSS gate</p><ul><li>Transfer Charasteristics of the AuNP/PEDOT:PSS electrode with increasing IL6 concentration with VDS=-0.3V and VGS from 0V to 0.6V</li></ul><p> </p><p>Figure S4: Transconductance of OECT based aptasensor</p><ul><li>Datasets used for S4 are identical with the ones from Figure 5</li></ul><p> </p><p>Figure S5: Impedance of functionalized device with IL6</p><ul><li>Each sheet is for a IL6 concentration. The normalized OECT concentration is the same as in Figure 5.</li></ul>
Simulations from "Mechanistic computational modeling of monospecific and bispecific antibodies targeting interleukin-6/8 receptors"
<h1>IL6R/IL8R Antibody Binding Model Code</h1> <p>Christina M.P. Ray, Huilin Yang, Jamie B. Spangler, Feilim Mac Gabhann</p> <p>This dataset contains all simulation output files generated for the article "Mechanistic computational modeling of monospecific and bispecific antibodies targeting interleukin-6/8 receptors". The model is comprised of a coupled set of ordinary differential equations (ODEs) where each individual ODE describes one molecule (antibody or receptor) or molecular complex (antibody + receptor). The terms in the ODEs represent each binding interaction (binding and unbinding processes) in the system.</p> <p>The code for the binding model and for the analysis and visualization results is available on GitHub at <a href="https://github.com/christyray/bispecific-binding-model">christyray/bispecific-binding-model</a>.</p> <h2>Specific Simulations</h2> <p>The <code>.csv</code> and <code>.rds</code> files in the correspond to the results from the simulations performed for the article "Mechanistic computational modeling of monospecific and bispecific antibodies targeting interleukin-6/8 receptors". These files can be read into R using the <code>import_data()</code> function included in the <a href="https://github.com/christyray/bispecific-binding-model">GitHub repository</a>.</p> <p>The <code>id</code> files contain simulation IDs to link the molecule concentrations (<code>yin</code>) and parameter values (<code>params</code>) with the simulation results (<code>out</code>). When applicable, the <code>norm</code> files contain normalized simulation output, and the <code>occupied</code> files contain receptor fractional occupancy values calculated from the simulation output.</p> <ul> <li><code>optimization</code>: Optimization of binding rate constants (association and dissociation) to experimental <em>in vitro</em> flow cytometry data; results displayed in Figure 2</li> <li><code>binding-curve</code>: Model simulations using the best-fit parameter set for comparison to the experimental data used to fit the model parameters; results displayed in Figure 3</li> <li><code>compare-opt</code>: Model simulations using each of the optimized parameter sets; results displayed in the Supplemental Information</li> <li><code>time</code>: Simulations of antibody binding dynamics over time; results displayed in Figure 4</li> <li><code>concentration</code>: Simulations with varying antibody concentrations and receptor expression levels; results displayed in Figure 5</li> <li><code>monovalent</code>: Simulations restricted to monovalent antibody binding only; results displayed in Figure 6</li> <li><code>compare-ab</code> and <code>compare-recep</code>: Simulations of both the bispecific antibody BS1 and the combination of monospecific antibodies tocilizumab and 10H2 for comparsion; results displayed in Figure 7</li> <li><code>local</code> and <code>global</code>: Local and global univariate sensitivity analyses; results displayed in Figure 8</li> </ul> <h2>References</h2> <blockquote> <p>H. Yang, M. N. Karl, W. Wang, B. Starich, H. Tan, A. Kiemen, A. B. Pucsek, Y.-H. Kuo, G. C. Russo, T. Pan, E. M. Jaffee, E. J. Fertig, D. Wirtz, and J. B. Spangler. Engineered bispecific antibodies targeting the interleukin-6 and -8 receptors potently inhibit cancer cell migration and tumor metastasis. Molecular Therapy, 30(11):3430–3449, Nov. 2022. doi:<a href="https://doi.org/10.1016/j.ymthe.2022.07.008">10.1016/j.ymthe.2022.07.008</a></p> </blockquote>
A Phase II Study of the Interleukin-6 Receptor Inhibitor Tocilizumab in Combination With Ipilimumab and Nivolumab in Patients With Unresectable Stage III or Stage IV Melanoma
ClinicalTrials.gov study NCT03999749. IPD Sharing: YES. Countries: 1. Publications: 1.
Interleukin-6 (IL-6) activates the NOTCH1 signaling pathway through E-proteins in endometriotic lesions
<p><b>Context:</b> NOTCH signaling is activated in endometriotic lesions but the exact mechanisms remains unclear. Interleukin-6 (IL-6), which is increased in the peritoneal fluid of women with endometriosis, induces NOTCH1 through E-proteins including E2A and HEB in cancer development.</p> <p><b>Objective:</b> To study the role of E-proteins in inducing NOTCH1 expression under the regulation of IL-6 in endometriosis.</p> <p><b>Setting and Design:</b> The expression of E2A, HEB and NOTCH1 was first investigated in endometrium of women with endometriosis and the baboon model of endometriosis. Regulation of E-proteins and NOTCH1 expression was examined after IL-6 stimulation and siRNA mediated inhibition of E2A or/and HEB in human endometriotic epithelial cells (12Z) <i>in vitro</i>, and subsequent following <i>in vivo </i>IL-6 treatment in the mouse model of endometriosis <i>in vivo</i>.</p> <p><b>Results: </b>E2A, HEB and NOTCH1 were significantly upregulated in glandular epithelium (GE) of ectopic endometrium compared to eutopic endometrium in both women and baboon model. IL-6 treatment upregulated the expression of NOTCH1 together with E2A and HEB in 12Z cells. siRNA inhibition of E2A and HEB or HEB alone decreased NOTCH1 expression. Binding efficiency of both E2A and HEB was significantly higher at the binding sites on the human NOTCH1 promoter after IL-6 treatment. Finally, IL-6 treatment resulted in a significantly increased number of endometriotic lesions along with the increased expression of E2A, HEB and NOTCH1 in GE of the lesions compared with the vehicle treated group in an endometriosis mouse model.</p> <p><span><b>Conclusions:</b> IL-6 induced NOTCH1 expression is mediated by E-proteins in the ectopic GE cells, which may promote endometriotic lesion development. </span></p>
Interleukin-6 (IL-6) activates the NOTCH1 signaling pathway through E-proteins in endometriotic lesions
Open the record for dataset details and reuse information.
Interleukin-6 response to insulin-induced hypoglycemia is associated with hypothalamic-pituitary-adrenal axis activation
<p>Raw data (excel table) concerning 23 patients who underwnt ITT for evaluation of IL-6 and counter-regulatory responses </p>
Demographic data along with a comparison of α1-Antitrypsin, Interleukin-1β and Interleukin -6 levels measured in this study
<p><strong>Serum levels of α-1Antitrypsin, Interleukin-1β, and Interleukin-6 in Iraqi COVID-19 patients: A cross-Sectional Study, data set</strong></p>
Optical Detection of Interleukin-6 using Liquid Janus Emulsions using Hyperthermophilic Affinity Proteins
Open the record for dataset details and reuse information.
Figure 3 in Molecular cloning and sequence analysis of the gene encoding interleukin-6 of the giant panda (Ailuropoda melanoleuca)
Figure 3. Phylogenetic relationships of IL-6 sequences from seven species in Carnivora. (A) Neighbour-joining tree of IL-6 nucleotide sequences based on Kimura's 2-parameter distances. (B) Maximum-parsimony tree of IL-6 mature protein sequences.
Figure 1 in Molecular cloning and sequence analysis of the gene encoding interleukin-6 of the giant panda (Ailuropoda melanoleuca)
Figure 1. RT-PCR of giant panda IL-6. The expected, 700bp fragment of giant panda IL-6 cDNA was amplified.
Underlying data for Association between Serum Insulin and Interleukin-6 levels with Breast Cancer in Post-Menopausal Iraqi Women
<p>Underlying data for Association between Serum Insulin and Interleukin-6 levels with Breast Cancer in Post-Menopausal Iraqi Women</p>
Combined immune checkpoint blockade increases myocardial secretion of H-FABP, NT-Pro-BNP, NLRP-3 inflammasome, Interleukin-1β and Interleukin-6: biochemical implications in cardio-immuno-oncology
<p>Background: Immune checkpoint inhibitors have transformed the treatment of several cancers by releasing restrained antitumor immune responses. Ipilimumab, an anti–cytotoxic T-lymphocyte–associated antigen 4 (CTLA-4) antibody, and nivolumab, an anti–programmed death-1 (PD-1) antibody, have individually improved survival in patients with melanoma, and their combination further enhances antitumor activity and survival. More recently, an anti-LAG3 human monoclonal antibody, Relatlimab, has been approved by FDA for combinatorial treatment with Nivolumab for metastatic melanoma and an anti-PD-L1 mAb,Atezolizumab, is undergoing clinical trials evaluation in combination with Ipilimumab for metastatic lung cancer.However,adverse events associated with these agents include dermatitis, endocrinopathies, colitis, hepatitis, and pneumonitis, which are all thought to arise from aberrant activation of autoreactive T cells. These toxic effects are more frequent and severe when immunomodulatory mAbs are used in combination. </p> <p>Methods: human cardiomyocytes co-cultured with hPBMC were exposed to monotherapy and combinatorial ICIs (PD-L1 and CTLA-4 or PD-1 and LAG-3 blocking agents, at 200 nM) for 48 h. After treatments, cardiac cell lysis and secretion of biomarkers of cardiotoxicity (H-FABP, NT-Pro-BNP), NLRP3-inflammasome and Interleukin 1 and 6 were determined through colorimetric and enzymatic assays. <strong>Results:</strong>Both Combinations of immune checkpoint inhibitors exertmore potent cardiotoxic side effects compared to monotherapies against human cardiac cells co-cultured with human lymphocytes. LDH release from cardiac cells was 43% higher in PDL-1/CTLA-4 blocking agents, and 35.7% higher in PD-1/LAG-3 blocking agents compared to monotherapies. Biomarkers of cardiotoxicity, such as H-FABP and NT-Pro-BNP were also strongly increased in combination therapy than monotherapies. NLRP3 inflammasome, IL-1β and IL-6 levels were also increased by PDL-1/CTLA-4 and PD-1/LAG-3 combined blocking agents compared to untreated cells and monotherapies. </p> <p><strong>Conclusions:</strong>Data of the present study, although in vitro, indicate that combinatorial immune checkpoint blockade on co-cultures of hPBMCs and cardiac cells, including for the first time the anti LAG-3 monoclonal antibody, induce a pro- inflammatory phenotype, thus indicating that these therapies should be closely monitored by the multidisciplinary team consisting of oncologists, cardiologists and immunologists.</p>
dataset for paper entitled "Effect of Moringa Oleifera Leaf Extract On Body Length, Malondialadehyd and Interleukin-6 Levels in Zebrafish Larvae (Danio Rerio) Induced Stunting Model with Rotenone"
<p>The dataset consist of:</p> <p>1. Appendices of tools and material used for laboratory research</p> <p>2. Certificate of ethical test </p> <p>3. Data of moringa oleifera controls</p> <p>4. Data of zebrafish growth </p>
Pregabalin on Interleukin-6 Levels in Living Donor Kidney
ClinicalTrials.gov study NCT01529190. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Effects of Interleukin-6 Inhibition on Vascular, Endothelial and Left Ventricular Function in Rheumatoid Arthritis
ClinicalTrials.gov study NCT03288584. IPD Sharing: NO. Countries: 1. Publications: 2.
Interleukin-6 Antagonists in Critically-ill Covid-19 Patients
ClinicalTrials.gov study NCT05218369. IPD Sharing: NO. Countries: 1. Publications: 9.
Role of Interleukin-6 in Exercise
ClinicalTrials.gov study NCT01073826. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Study to Evaluate the Ability of TNFR:Fc to Decrease the Amount of IL-6 (Interleukin-6) and TNF-alpha (Tumor Necrosis Factor) in HIV-Infected Patients
ClinicalTrials.gov study NCT00001116. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Role of Interleukin-1 in the Regulation of Muscle Derived Interleukin-6 During Exercise
ClinicalTrials.gov study NCT01771445. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Plasticity Biomarkers,Interleukin-6 and Motor Performance in Response to Vagus Nerve Stimulation After Stroke
ClinicalTrials.gov study NCT06388954. IPD Sharing: NO. Countries: 1. Publications: 0.
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