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5,016 results for “THERAPEUTICS”
Safety and Efficacy of Romidepsin and the Therapeutic Vaccine Vacc-4x for Reduction of the Latent HIV-1 Reservoir
ClinicalTrials.gov study NCT02092116. IPD Sharing: NO. Countries: 1. Publications: 2.
Study of Relationship Between Vedolizumab Therapeutic Drug Monitoring, Biomarkers of Inflammation and Clinical Outcomes
ClinicalTrials.gov study NCT04567628. IPD Sharing: YES. Countries: 1. Publications: 1.
Caplacizumab and Immunosuppressive Therapy Without Firstline Therapeutic Plasma Exchange in Adults With Immune-mediated Thrombotic Thrombocytopenic Purpura
ClinicalTrials.gov study NCT05468320. IPD Sharing: YES. Countries: 11. Publications: 1.
Phylogeny explains why less therapeutically redundant plant species are not necessarily facing greater use pressure
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Data from: Bayesian estimation of muscle mechanisms and therapeutic targets using variational autoencoders
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An imaging flow cytometry dataset for profiling the immunological synapse of therapeutic antibodies
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Intracellular delivery of nitric oxide enhances the therapeutic efficacy of mesenchymal stem cells for myocardial infarction
<p>Cell therapy by autologous mesenchymal stem cells (MSCs) is a clinically acceptable strategy for treating various diseases. Unfortunately, the therapeutic efficacy is largely affected by the low quality of MSCs collected from patients. Herein, we showed that the gene expression of MSCs from patients with diabetes was differentially regulated compared to that of MSCs from healthy controls. Then, MSCs were genetically engineered to catalyse an NO prodrug to release NO intracellularly. Compared to extracellular NO conversion, intracellular NO delivery effectively prolonged survival and enhanced the paracrine function of MSCs, as demonstrated by in vitro and in vivo assays. The enhanced therapeutic efficacy of engineered MSCs combined with intracellular NO delivery was further confirmed in mouse and rat models of myocardial infarction, and a clinically relevant cell administration paradigm through secondary thoracotomy has been attempted.</p>
Sustained liver HBsAg loss and clonal T and B cell expansion upon therapeutic DNA vaccination require low HBsAg levels
<p>C57BL/6 mice samples transduced with AAV-HBV, followed by treatment with siRNA+TxTv, control siRNA+TxVx or control siRNA+empty plasmid. 10x genomics (VDJ) was performed in liver IHIC.</p><p>An rds object with the raw and normalised counts, the annotations is available.</p>
Multiomics analyses reveal a Type III-associated immune response in immunotherapy-induced toxicity in melanoma and identifies potential new therapeutic targets
<p>Immune checkpoint inhibitors (ICIs) are standard-of-care for the treatment of advanced melanoma, but their use is limited by immune-related adverse events (irAEs). Proteomic analyses and multiplex cytokine/chemokine assays from serum at baseline and at irAEs onset in melanoma patients indicated aberrant T-cell activity with differential expression of Type I and III immune signatures. This was in line with an increase in the proportions of monocytes and decrease of IL-17A-producing CD4+ T-cells in the peripheral blood using single cell RNA sequencing. Multiplex immunohistochemistry and spatial transcriptomics on ICI-induced skin rash and colitis showed an increase in the proportion of CD4+ T-cells with IL-17A expression. </p> <p>Anti-IL-17A mAbs were administered in two patients with myocarditis, colitis and skin rash with resolution of the irAE. This study highlights the potential role of Type III CD4+ T-cells in irAEs development and provides proof-of-principle evidence for a corresponding clinical trial using anti-IL17A for treating irAEs.</p> <p>Code to generate the figures are located at https://github.com/pcheng84/AE_analysis/</p> <p> </p>
Feasibility and metabolic outcomes of a well-formulated ketogenic diet as an adjuvant therapeutic intervention for women with stage IV metastatic breast cancer: The Keto-CARE trial
<p><em>Purpose:</em></p> <p>Ketogenic diets may positively influence cancer through pleiotropic mechanisms, but only a few small and short-term studies have addressed feasibility and efficacy in cancer patients. The primary goals of this study were to evaluate the feasibility and the sustained metabolic effects of a personalized well-formulated ketogenic diet (WFKD) designed to achieve consistent blood beta-hydroxybutyrate (<span>β</span>HB) >0.5 mM in women diagnosed with stage IV metastatic breast cancer (MBC) undergoing chemotherapy.</p> <p><em>Methods: </em></p> <p>Women (n = 20) were enrolled in a six-month two-phase, single-arm WFKD intervention (NCT03535701). Phase I was a highly-supervised, ad libitum, personalized WFKD, where women were provided with ketogenic-appropriate food daily for three-months. Phase II transitioned women to a self-administered WFKD with ongoing coaching for an additional three-months. Fasting capillary <span>β</span>HB and glucose were collected daily; weight, body composition, plasma insulin, and insulin resistance were collected at baseline, three- and six-months. </p> <p><em>Results:</em></p> <p>Capillary <span>β</span>HB indicated women achieved nutritional ketosis (Phase I mean: 0.8 mM (n = 15); Phase II mean: 0.7 mM (n = 9)). Body weight decreased 10% after three-months, primarily from body fat. Fasting plasma glucose, plasma insulin, and insulin resistance also decreased significantly after three-months (p < 0.01), an effect that persisted at six-months.</p> <p><em>Conclusions</em>:</p> <p>Women diagnosed with MBC undergoing chemotherapy can safely achieve and maintain nutritional ketosis, while improving body composition and insulin resistance, out to six-months.</p>
Data from: Quantitative PCR as a marker for preemptive therapy and its role in therapeutic control in Trypanosoma cruzi/HIV coinfection
<p><strong>Background: </strong><em>Trypanosoma cruzi</em> and HIV coinfection can evolve with depression of cellular immunity and increased parasitemia. We applied quantitative PCR (qPCR) as a marker for preemptive antiparasitic treatment to avoid fatal Chagas disease reactivation and analyzed the outcome of treated cases.</p> <p><strong>Methodology:</strong> This mixed cross-sectional and longitudinal study included 171 Chagas disease patients, 60 coinfected with HIV. Of these 60 patients, ten showed Chagas disease reactivation, confirmed by parasites identified in the blood, cerebrospinal fluid, or tissues, 12 exhibited high parasitemia but no reactivation, and 38 had low parasitemia and no reactivation.</p> <p><strong>Results</strong>: We showed, for the first time, the success of the timely introduction of benznidazole in the non-reactivated group with high levels of parasitemia detected by qPCR and the absence of parasites in reactivated cases with at least 58 days of benznidazole. HIV+ and HIV+ without reactivation had a 4.0 – 5.1 higher chance of having parasitemia than HIV seronegative cases. A positive correlation was found between parasite and viral loads. Remarkably, treated <em>T. cruzi/</em>HIV-coinfected patients had 77.3% conversion from positive to negative parasitemia compared to 19.1% of untreated patients. Additionally, untreated patients showed ~13.6 times higher odds of having positive parasitemia in the follow-up period compared with treated patients. Treated and untreated patients showed no differences regarding the evolution of Chagas disease. The main factors associated with all-cause mortality were higher parasitemia, lower CD4 counts/µL, higher viral load, and absence of antiretroviral therapy.</p> <p><strong>Conclusion</strong>: We recommend qPCR prospective monitoring of <em>T. cruzi</em> parasitemia in HIV+ patients and point out the value of pre-emptive therapy for patients with temporary high parasitemia. In parallel, an early antiretroviral therapy introduction is advisable, aiming at viral load control, immune response restoration, and major survival. We also suggest an earlier antiparasitic treatment for all coinfected patients, followed by effectiveness analysis alongside antiretroviral therapy.</p>
Liver-targeted polymeric prodrugs delivered subcutaneously improve tafenoquine therapeutic window for malaria radical cure
<p>Approximately 3.3 billion people live with the threat of Plasmodium vivax malaria. Infection can result in liver-localized hypnozoites, which when reactivated cause relapsing malaria. This is the first demonstration of an enzyme-cleavable polymeric prodrug of tafenoquine (TQ) that addresses key requirements for a mass administration, eradication campaign: excellent subcutaneous bioavailability, complete parasite control after a single dose, improved therapeutic window compared to the parent oral drug, and low Cost of Goods Sold (COGS) at less than $1.50/dose. Liver-targeting and subcutaneous dosing resulted in improved liver:plasma exposure profiles, with increased efficacy and reduced Glucose 6-Phosphate Dehydrogenase (G6PD)-dependent hemotoxicity in validated preclinical models. A COGS and manufacturability analysis demonstrated global scalability, affordability, and the ability to redesign this fully synthetic polymeric prodrug specifically to increase global equity and access. Taken together, this polymer prodrug platform is a candidate for evaluation in human patients and shows potential for P. vivax eradication campaigns.</p>
Generative AI in the Advancement of Viral Therapeutics for Predicting and Targeting Immune-Evasive SARS-CoV-2 Mutations
<p>This dataset <strong>encompasses</strong> and describes the following features:</p> <ul> <li>Mutations in viruses like SARS-CoV-2 can make them escape vaccines and treatments.</li> <li>Accurately predicting these mutations is crucial for developing effective countermeasures.</li> <li>The study uses a type of AI called a Generative Adversarial Network (GAN) to analyze the virus's spike protein, which plays a key role in infection.</li> <li>The GAN generates protein sequences similar to natural ones, but which are also likely to evade immune responses.</li> <li>By analyzing these generated sequences, the researchers improve their AI model's ability to predict real-world escape mutations.</li> <li>This improved prediction could help design better vaccines and treatments, and prepare for future viral threats.</li> </ul>
Replication Data for: Precision Oncology, Cell Signaling and Targeted Therapy: A Holistic Approach to Molecular Cancer Therapeutics
<p>In recent decades, there has been a deluge in the large-scale production of anticancer agents, primarily due to advances in genomic technologies enabling precise targeting of oncogenic pathways involved in disease progression. This initiated a paradigm shift in cancer research and therapeutics based on the ability to study molecular changes throughout the genome. It provided a unique opportunity in the field of translational cancer research and have led to the concept of precision medicine in cancer therapy, raising hopes of developing better diagnostic and therapeutic means for the management of cancer. The purpose of this article is to briefly review the tools and techniques involved in precision oncology research and their applications in the field of cancer treatment. </p>
BRAT1 - a new therapeutic target for glioblastoma
<p>Proteomic and phosphoproteomic raw data files (Excel) used for further analysis of the research on BRAT1 as a new therapeutic target for glioblastoma.</p>
Single-cell RNA-Seq-based deconvolution of hairy cell leukemia reveals novel disease drivers and identifies DUSP1 as potential therapeutic target
<p>Microwell-based (BD Rhapsody) scRNA-seq of Hairy Cell Leukemia Patients published in </p> <blockquote> <p><strong>Single-cell RNA-Seq-based deconvolution of hairy cell leukemia reveals novel disease drivers and identifies DUSP1 as potential therapeutic target, Jan-Paul Bohn et al. Submitted.</strong></p> </blockquote> <p>The files will be made available upon publication. <br></p> <h4><strong>Description of the files</strong></h4> <ul> <li><strong>01_raw_counts: </strong>count matrices as CSV as generated by the BD Rhapsody WTA analysis pipeline</li> <li><strong>10_prepare_adata</strong>: Load BD Rhapsody WTA analysis pipeline outputs into AnnData objects and add metadata.</li> <li><strong>20_scrnaseq_qc</strong>: Use a nextflow pipeline (stored in lib/single-cell-analysis-nf) to perform threshold-based filtering of single-cell data and apply SOLO for doublet detection.</li> <li><strong>30_merge_adata</strong>: Merge samples into a single AnnData object, train a scVI model for batch effect removal, and annotate cell-types based on unsupervised clustering</li> <li><strong>40_cluster_analysis</strong>: Identify and investigate subclusters representing cell-states that go beyond the major cell-types</li> <li><strong>50_de_analysis</strong>: Generate pseudobulk and perform differential gene expression analysis using DESeq2 (based on a wrapper script stored in lib/deseq2_workflow)</li> <li><strong>70_downstream_analysis</strong>: Perform pathway analyses and generate figures for publication based on the data generated in the previous steps</li> <li><strong>containers:</strong> Conda environments used for the analysis packed up as singularity containers. </li> </ul>
"Global Functional Genomics Reveals GRK5 as a Therapeutic Target for Cystic Fibrosis", CFTR interactomes
<p><em>A tidy selection of published CFTR interactomes (or CFTR-related omics datasets)</em></p> <p>Collects data from the original online sources, converts gene/protein identifiers into a standard tidy format and updates the identifiers. The Uniprot ID is taken as reference and all other identifiers are genereated from them. This causes some datasets to end up with less genes/proteins than reported.</p> <p>Datasets included</p> <ul> <li><strong>Botelho (2021)</strong> - CFTR traffic regulators <ul> <li>Botelho <em>et al</em> (2022), submitted</li> </ul> </li> <li><strong>Pankow (2015)</strong> - CFTR interactome <ul> <li>Pankow <em>et al</em> (2015) deltaF508 CFTR interactome remodelling promotes rescue of cystic fibrosis. <em>Nature</em>. 528, 510--516. <a href="https://doi.org/10.1038/nature15729">https://doi.org/10.1038/nature15729</a></li> </ul> </li> <li><strong>Canato (2018)</strong> - CFTR interactome <ul> <li>Canato <em>et al</em> (2018) Proteomic interaction profiling reveals KIFC1 as a factor involved in early targeting of F508del-CFTR to degradation. <em>Cell Mol Life Sci</em>. 75(24):4495-4509. <a href="https://doi.org/10.1007/s00018-018-2896-7">https://doi.org/10.1007/s00018-018-2896-7</a></li> </ul> </li> <li><strong>Santos (2019)</strong> - CFTR interactome <ul> <li>Santos <em>et al</em> (2019) Folding Status Is Determinant over Traffic-Competence in Defining CFTR Interactors in the Endoplasmic Reticulum. <em>Cells</em>. 8(4):353. <a href="https://doi.org/10.3390/cells8040353">https://doi.org/10.3390/cells8040353</a></li> </ul> </li> <li><strong>Hutt (2018)</strong> - CFTR interactome <ul> <li>Hutt <em>et al</em> (2018) A Proteomic Variant Approach (ProVarA) for Personalized Medicine of Inherited and Somatic Disease. <em>J Mol Biol</em>. 430: 2951-2973. <a href="https://doi.org/10.1016/j.jmb.2018.06.017">https://doi.org/10.1016/j.jmb.2018.06.017</a></li> </ul> </li> <li><strong>Rauniyar (2014)</strong> - CFTR proteome <ul> <li>Rauniyar <em>et al</em> (2014) Quantitative Proteomic Profiling Reveals Differentially Regulated Proteins in Cystic Fibrosis Cells. <em>J Proteome Res</em>. 13(11): 4668-4675. <a href="https://doi.org/10.1021/pr500370g">https://doi.org/10.1021/pr500370g</a></li> </ul> </li> <li><strong>Almaça (2013)</strong> - ENaC regulome <ul> <li>Almaça <em>et al</em> (2013) High-content siRNA screen reveals global ENaC regulators and potential cystic fibrosis therapy targets. <em>Cell</em>. 154(6):1390-400. <a href="https://doi.org/10.1016/j.cell.2013.08.045">https://doi.org/10.1016/j.cell.2013.08.045</a></li> </ul> </li> <li><strong>Tomati (2018)</strong> - CFTR regulome <ul> <li>Tomati <em>et al</em> (2018) High-throughput screening identifies FAU protein as a regulator of mutant cystic fibrosis transmembrane conductance regulator channel. <em>J Biol Chem</em>. 293(4):1203-1217. <a href="https://doi.org/10.1074/jbc.m117.816595">https://doi.org/10.1074/jbc.m117.816595</a></li> </ul> </li> <li><strong>Simpson (2012)</strong> - Secretome <ul> <li>Simpson <em>et al</em> (2012) Genome-wide RNAi screening identifies human proteins with a regulatory function in the early secretory pathway. <em>Nature Cell Biology</em>. 14, 764-774. <a href="https://doi.org/10.1038/ncb2510">https://doi.org/10.1038/ncb2510</a></li> </ul> </li> <li><strong>Wang (2006)</strong> - CFTR interactome <ul> <li>Wang <em>et al</em> (2006) Hsp90 Cochaperone Aha1 Downregulation Rescues Misfolding of CFTR in Cystic Fibrosis. <em>Cell</em>. 127(4):803-815. <a href="https://doi.org/10.1016/j.cell.2006.09.043">https://doi.org/10.1016/j.cell.2006.09.043</a></li> </ul> </li> <li><strong>Reilly (2017)</strong> - CFTR interactome <ul> <li>Reilly <em>et al</em> (2017) Targeting the PI3K/Akt/mTOR signalling pathway in Cystic Fibrosis. <em>Sci Rep</em>. 9;7(1):7642. <a href="https://doi.org/10.1038/s41598-017-06588-z">https://doi.org/10.1038/s41598-017-06588-z</a></li> </ul> </li> <li><strong>Gilchrist (2006)</strong> - Secretome <ul> <li>Gilchrist <em>et al</em> (2006) Quantitative Proteomics Analysis of the Secretory Pathway. <em>Cell</em>. 127(6):1265-1281. <a href="https://doi.org/10.1016/j.cell.2006.10.036">https://doi.org/10.1016/j.cell.2006.10.036</a></li> </ul> </li> <li><strong>Pankow (2019)</strong> - CFTR interactome <ul> <li>Pankow <em>et al</em> (2019) A posttranslational modification code for CFTR maturation is altered in cystic fibrosis. <em>Science Signaling</em>. 12(562):eaan7984. <a href="https://doi.org/10.1126/scisignal.aan7984">https://doi.org/10.1126/scisignal.aan7984</a></li> </ul> </li> <li><strong>Dang (2020)</strong> - CF lung disease modifier genes <ul> <li>Dang <em>et al</em> (2020) Mining GWAS and eQTL data for CF lung disease modifiers by gene expression imputation. <em>PLoS One</em>. 15(11):e0239189. <a href="https://doi.org/10.1371/journal.pone.0239189">https://doi.org/10.1371/journal.pone.0239189</a></li> </ul> </li> <li><strong>Hodos (2020)</strong> - CF genomic meta-analysis <ul> <li>Hodos <em>et al</em> (2020) Integrative genomic meta-analysis reveals novel molecular insights into cystic fibrosis and deltaF508-CFTR rescue. <em>Sci Rep</em> 10(1):20553. <a href="http://dx.doi.org/10.1038/s41598-020-76347-0">http://dx.doi.org/10.1038/s41598-020-76347-0</a></li> </ul> </li> </ul>
Molcular Dynamics Data for Therapeutic High Affinity T Cell Receptor Targeting a KRAS G12D Cancer Neoantigen
<p>This folder contains the starting structures and input scripts required to simulate the wild-type and G12D KRAS peptide bound TCR-pHLA complexes, as performed in this study.</p> <p><br> Starting_Structures - This folder contains the amber parameter/topology files used to simulate each system (.prmtop) and the coordinates of the starting structure both as amber coordinate file (.rst) and PDB file (.pdb).<br> MD_Inputs - This folder contains the amber MD inputs used to run the md simulations. <br> MMPBSA_inputs - This folder contains the input files for running MMPBSA with the MMPBSA.py script in amber. The mmpbsa.in script was used for calculating overall binding energy whereas the mmpbsa_decomp.in script was used for calculating the per-residue contribution to binding energy. </p>
Amplicon structure creates collateral therapeutic vulnerability in cancer
<p>Raw RNA sequencing data expressed in KELLY cells with vs. without ectopic DDX1 expression</p> <p>AH_YB_021 DDX1, AH_YB_023 DDX1, AH_YB_025 DDX1, : DDX1 -</p> <p>AH_YB_022 DDX1, AH_YB_024 DDX1, AH_YB_026 DDX1, : DDX1 +</p>
PAM-altering SNP-based allele-specific CRISPR-Cas9 therapeutic strategies for Huntington's disease
<p>Huntington's disease (HD) is caused by an expanded CAG repeat in huntingtin (<em>HTT</em>). Since HD is dominant, and loss of <em>HTT </em>leads to neurological abnormalities, safe therapeutic strategies require selective inactivation of mutant <em>HTT</em>. Previously, we proposed a concept of CRISPR-Cas9 using mutant-specific PAM sites generated by SNPs to selectively inactivate mutant <em>HTT</em>. Aiming at revealing suitable targets for clinical development, we analyzed the largest HD genotype dataset to reveal target <strong>P</strong>AM-<strong>a</strong>ltering <strong>S</strong>NPs (PAS) and subsequently evaluated their allele specificities. The gRNAs based on the PAM sites generated by rs2857935, rs16843804, and rs16843836 showed high levels of allele specificity in patient-derived cells. Simultaneous use of two gRNAs based on rs2857935-rs16843804 or rs2857935-rs16843836 produced selective genomic deletions in mutant <em>HTT </em>and prevented the transcription of mutant <em>HTT </em>mRNA without impacting the expression of normal counterpart or re-integration of the excised fragment elsewhere in the genome. RNAseq and off-target analysis confirmed high levels of allele specificity and the lack of recurrent off-targeting. Approximately 60% of HD subjects are eligible for mutant-specific CRISPR-Cas9 strategies of targeting one of these 3 PAS in conjunction with one non-allele-specific site, supporting high applicability of PAS-based allele-specific CRISPR approaches in the HD patient population.</p>
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.