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X-ORIGINAL-URL:https://qcb.ucla.edu
X-WR-CALDESC:Events for Institute for Quantitative and Computational Biosciences
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BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230303T160000
DTEND;TZID=America/Los_Angeles:20230303T170000
DTSTAMP:20260517T015938
CREATED:20230217T151413Z
LAST-MODIFIED:20230217T151518Z
UID:24018-1677859200-1677862800@qcb.ucla.edu
SUMMARY:QCBio/Center for Biological Physics: Gregoire Altan-Bonnet\, Principal Investigator – Immunodynamics group Laboratory of Integrative Cancer Immunology NCI\, NIH\, Bethesda MD
DESCRIPTION:TITLE: “Stochasticity in cancer immunotherapies: identifying the T cell subset that sparks tumor eradication” \nABSTRACT: We use an ex vivo model of tumor eradication to dissect the fundamental variability of clinical outcomes in cancer immunotherapies. We demonstrate that there exists an inherent stochastic variability in immune responses\, based on the low abundance of hyper-responsive naïve T cells (so-called Spark T cells) and feedback regulations amongst leukocytes. We introduce a methodology (combining hierarchical clustering of single-cell measurements and statistical matching with functional outcomes)  to identify Spark T cells. We then carry out functional tests to model the mechanics of Spark T cells igniting global immune responses and tumor rejection.
URL:https://qcb.ucla.edu/event/qcbio-the-center-for-biological-physics-gregoire-altan-bonnet-principal-investigator-immunodynamics-group-laboratory-of-integrative-cancer-immunology-nci-nih-bethesda-md/
LOCATION:Boyer Hall 130
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/02/Altan-Bonnet.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230306T140000
DTEND;TZID=America/Los_Angeles:20230306T150000
DTSTAMP:20260517T015938
CREATED:20230305T183912Z
LAST-MODIFIED:20230305T183912Z
UID:24502-1678111200-1678114800@qcb.ucla.edu
SUMMARY:QCBio Research Seminar: Gregoire Altan-Bonnet\, Principal Investigator – Immunodynamics group Laboratory of Integrative Cancer Immunology NCI\, NIH\, Bethesda MD
DESCRIPTION:TITLE: “Stochasticity in cancer immunotherapies: identifying the T cell subset that sparks tumor eradication” \nABSTRACT: We use an ex vivo model of tumor eradication to dissect the fundamental variability of clinical outcomes in cancer immunotherapies. We demonstrate that there exists an inherent stochastic variability in immune responses\, based on the low abundance of hyper-responsive naïve T cells (so-called Spark T cells) and feedback regulations amongst leukocytes. We introduce a methodology (combining hierarchical clustering of single-cell measurements and statistical matching with functional outcomes) to identify Spark T cells. We then carry out functional tests to model the mechanics of Spark T cells igniting global immune responses and tumor rejection.
URL:https://qcb.ucla.edu/event/qcbio-research-seminar-gregoire-altan-bonnet-principal-investigator-immunodynamics-group-laboratory-of-integrative-cancer-immunology-nci-nih-bethesda-md/
LOCATION:Boyer 159
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/02/Altan-Bonnet.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230306T160000
DTEND;TZID=America/Los_Angeles:20230306T170000
DTSTAMP:20260517T015938
CREATED:20230103T165103Z
LAST-MODIFIED:20230103T165103Z
UID:23257-1678118400-1678122000@qcb.ucla.edu
SUMMARY:QCBio/Bioinformatics/Human Genetics seminar: Zoltán Kutalik\, PhD\, Associate Professor\, University of Lausanne
DESCRIPTION:TITLE: “Pushing the boundaries of causal inference.”
URL:https://qcb.ucla.edu/event/qcbio-bioinformatics-human-genetics-seminar-zoltan-kutalik-phd-associate-professor-university-of-lausanne/
LOCATION:Boyer 159\, 611 Charles E. Young Dr. E.\, Los Angeles\, CA\, 90095\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/01/ZOLTAN.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230310T120000
DTEND;TZID=America/Los_Angeles:20230310T123000
DTSTAMP:20260517T015938
CREATED:20230304T013617Z
LAST-MODIFIED:20230310T233042Z
UID:24486-1678449600-1678451400@qcb.ucla.edu
SUMMARY:QCBio Research Seminar: Daniel Ha (Yang)\, Postdoc\, Dept. Integrative Biology and Physiology
DESCRIPTION:TITLE: ““Cross-tissue multiomics studies reveal gutbrain interactions mediating the effect of Akkermansia muciniphila in counteracting fructose-induced obesity” \nABSTRACT: The gut bacterium Akkermansia muciniphila (A. muciniphila) has been implicated in anti-obesity effects\, but a systems level understanding of the molecular mechanisms is lacking. We carried out multiomics studies to investigate the molecular cascades mediating the anti-obesity effect of A. muciniphila in a fructoseinduced obesity mouse model. We found that A. muciniphila colonization triggered significant shifts in gut microbiota composition\, gut and plasma metabolites\, and gene expression in hypothalamic neurons. Multiomics integration and network analysis prioritized the metabolite oleoylethanolamide (OEA) in the gut and circulation as a regulator of gut-brain interactions that underlie the A. muciniphila antiobesity effect. Oral administration of OEA counteracted the fructose-induced obesity through the regulation of hypothalamic anorexigenic neuropeptides such as oxytocin and arginine vasopressin. Our multiomics investigation and experimental validation elucidates the molecular regulators and pathways involved in the communication between A. muciniphila in the gut and hypothalamic neurons that counter fructose-induced obesity. \n\nhttps://qcb.ucla.edu/wp-content/uploads/sites/14/2023/03/Daniel-Ha-3.10.23.mp4\n 
URL:https://qcb.ucla.edu/event/qcbio-research-seminar-daniel-ha-yang-postdoc-dept-integrative-biology-and-physiology/
LOCATION:ZOOM\, CA\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/03/headshot_photo-1-180x180-DanHa-copy.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230310T123000
DTEND;TZID=America/Los_Angeles:20230310T130000
DTSTAMP:20260517T015938
CREATED:20230304T013953Z
LAST-MODIFIED:20230310T223250Z
UID:24493-1678451400-1678453200@qcb.ucla.edu
SUMMARY:QCBio Research Seminar: Brandon Tsai (Boutros)\, Grad Student\, Human Genetics
DESCRIPTION:TITLE: “Exercise and tumor genomic landscapes in 2\,702 patients with cancer” \nABSTRACT: Approximately two-thirds of cancer diagnoses globally are attributed to modifiable lifestyle factors such as smoking\, diet and inactivity. Conversely\, regular exercise is linked to decreased risk of multiple cancers. However\, the underlying molecular mechanisms are not fully elucidated. Specifically\, how exercise impacts tumor genomic landscapes has not been considered. To address this gap\, we integrated clinical annotation of exercise exposure with tumor mutational profiling of 2\,702 patients with cancer. Exercise exposure was evaluated by validated questionnaire and tumor genomic profiling of ≥ 505 commonly mutated cancer genes was performed using the Memorial Sloan Kettering Cancer Center Integrated Mutation Profiling of Actional Cancer Targets (MSK-IMPACT) assay. Among the most represented cancer types were breast (n = 629)\, lung (n = 525)\, endometrial (n = 260)\, colorectal (n = 213) and prostate (n = 177). We found that exercise influences the genomic landscapes of tumors in a cancer-type specific manner. For instance\, breast and lung cancers from exercising patients had lower tumor mutation burden (TMB) compared with non-exercisers. A pan-cancer analysis revealed a higher risk ratio among exercisers for mutations in ERBB2 and lower risk ratio for mutations in PIK3CA and CDKN2A. Overall\, this study shows that exercise regulates tumor genomic landscapes in a cancer-site specific manner. \nhttps://qcb.ucla.edu/wp-content/uploads/sites/14/2023/03/Brandon-Tsai-31023.mp4
URL:https://qcb.ucla.edu/event/qcbio-research-seminar-brandon-tsai-boutros-grad-student-human-genetics/
LOCATION:ZOOM\, CA\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/03/KGD_8087.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230313T160000
DTEND;TZID=America/Los_Angeles:20230313T170000
DTSTAMP:20260517T015938
CREATED:20230103T165307Z
LAST-MODIFIED:20230103T165307Z
UID:23261-1678723200-1678726800@qcb.ucla.edu
SUMMARY:QCBio/Bioinformatics/Human Genetics seminar: Min Xu\, PhD\, Assistant Professor\, Computational Biology Department\, Co-Director\, MS in Computational Biology Program\, Carnegie Mellon University
DESCRIPTION:TITLE: “Automatic analysis of cryo-electron tomography using computer vision and machine learning.”
URL:https://qcb.ucla.edu/event/qcbio-bioinformatics-human-genetics-seminar-min-xu-phd-assistant-professor-computational-biology-department-co-director-ms-in-computational-biology-program-carnegie-mellon-university/
LOCATION:Boyer 159\, 611 Charles E. Young Dr. E.\, Los Angeles\, CA\, 90095\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/01/MIN.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230317T120000
DTEND;TZID=America/Los_Angeles:20230317T123000
DTSTAMP:20260517T015938
CREATED:20230314T170407Z
LAST-MODIFIED:20230319T154301Z
UID:24592-1679054400-1679056200@qcb.ucla.edu
SUMMARY:QCBio Research Seminar: Jessica Ding (Yang)\, Grad Student\, Molecular\, Cellular\, and Integrative Physiology
DESCRIPTION:TITLE: “Multi-tissue single-cell level understanding of Alzheimer’s disease points to the therapeutic potential of nutritional and metabolic modulation.” \nABSTRACT: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by extracellular amyloid plaque deposition and intracellular neurofibrillary tangles. The direct cause of abnormal protein accumulation and aggregation is largely unknown\, and no treatments exist to effectively delay or prevent development of AD. AD onset and progression is affected by many genetic and environmental factors\, and exploration of significant risk factors for AD may help elucidate its complexity. AD is often comorbid with metabolic syndrome\, which includes hypertension\, elevated blood glucose and triglycerides\, and abdominal obesity. We investigate the potential connection between AD and metabolic syndrome by testing the effect of high fructose consumption\, omega-3 fatty acid docosahexaenoic acid (DHA)\, and nicotinamide riboside (NR) on hippocampal and hypothalamic single cell transcriptomes of the 5XFAD mouse model of amyloid accumulation. We report that metabolically challenging 5XFAD mice with fructose promotes expression of certain proinflammatory genes that may further exacerbate neuronal loss. Supplementation of 5XFAD with DHA and NR was shown to downregulate microglial activation genes\, but DHA and NR on 5XFAD with fructose background also enhanced specific aspects of microglial function while downregulating fructose-induced exacerbation of proinflammatory genes\, which may indicate mechanisms to counteract further worsening of AD by fructose. Overlaying differentially expressed genes (DEGs) onto a microglial gene regulatory network showed fructose\, DHA\, and NR target shared and specific aspects of the disease subnetwork. We also observed that fructose led to a depletion of an intermediate activated microglial state which was enhanced by DHA and NR. Transcriptomic signatures derived from this study showed high enrichment of GWAS signals including cell-type specific nutrition DEGs\, regulatory network modules\, and microglia trajectory associated genes. Our study has demonstrated that metabolic modulation impacts AD transcriptomic signatures and has significant implications for the treatment of AD with DHA and NR or modulators that enhance associated mechanisms. \nhttps://qcb.ucla.edu/wp-content/uploads/sites/14/2023/03/Jessica-Ding-3.17.23.mp4
URL:https://qcb.ucla.edu/event/qcbio-research-seminar-jessica-ding-yang-grad-student-molecular-cellular-and-integrative-physiology/
LOCATION:ZOOM\, CA\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/03/Ding-Jessica.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230317T123000
DTEND;TZID=America/Los_Angeles:20230317T130000
DTSTAMP:20260517T015938
CREATED:20230311T171133Z
LAST-MODIFIED:20230319T155440Z
UID:24581-1679056200-1679058000@qcb.ucla.edu
SUMMARY:QCBio Research Seminar: Helena Winata (Boutros)\, Grad Student\, Bioinformatics IDP
DESCRIPTION:TITLE: “Efficient\, Multi Sample Inference of Cancer Phylogeny.” \nABSTRACT: Cancer is characterized by the ongoing accumulation of somatic mutations that may lead to dysregulated cellular proliferation. The selection of advantageous mutations leads to clonal expansions of progressively more aberrant and fit cancer cells. Reconstructing the evolutionary history of a tumor allows us to understand key events in disease progression and mechanisms that lead to disease lethality.  Sequencing multiple tumor samples provide an opportunity to study tumor evolution in much greater detail and accuracy than was previously feasible through single-sample datasets. However\, current reconstruction methods utilize stochastic-search algorithms\, which iterates through a parameter space to jointly infer clone populations and their phylogeny. As tumor phylogenetic topology increases in complexity\, the parameter space grows exponentially\, and stochastic-search algorithms become computationally intractable. To circumvent current computational limitations\, we developed a heuristic-based algorithm for subclonal reconstruction that leverages fundamental principles of cancer biology to encode heuristics that reduce the solution space to biologically plausible phylogenies. Benchmarking on real and simulated datasets are ongoing\, and preliminary results indicate a ten-fold reduction in runtime. We have thus presented a novel method for rapid and optimized reconstruction of tumor evolutionary histories from multi-sample datasets.  \nhttps://qcb.ucla.edu/wp-content/uploads/sites/14/2023/03/Helena-Winata-31723.mp4
URL:https://qcb.ucla.edu/event/qcbio-research-seminar-helena-wimata-boutros-grad-student-bioinformatics-idp/
LOCATION:ZOOM\, CA\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/03/QCbio_pic-copy.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230324T120000
DTEND;TZID=America/Los_Angeles:20230324T123000
DTSTAMP:20260517T015938
CREATED:20230307T193641Z
LAST-MODIFIED:20230327T173940Z
UID:24514-1679659200-1679661000@qcb.ucla.edu
SUMMARY:QCBio Research Seminar: Dongyuan Song (Li JJ)\, Grad Student\, Bioinformatics IDP
DESCRIPTION:TITLE: “ClusterDE: a post-clustering differentially expressed (DE) gene identification method robust to false-positive inflation caused by double-dipping” \nABSTRACT: In typical single-cell RNA-seq data analysis\, first\, a clustering algorithm is applied to cluster cells; then\, a statistical method is used to identify the differentially expressed (DE) genes between the cell clusters. However\, this common procedure uses the same data twice\,  an issue known as “double dipping”: the same gene expression data are used to define cell clusters and DE genes\, leading to false-positive DE genes even when the cell clusters are spurious. To overcome this challenge\, we propose ClusterDE\, a post-clustering DE method for controlling the false discovery rate (FDR) regardless of clustering quality. The core idea of ClusterDE is to generate in silico negative control data with only one cluster\, which can be used in contrast to real data for evaluating the whole clustering+DE procedure. Using comprehensive simulation and real data analysis\, we show that ClusterDE can not only has solid FDR control but also finds cell-type marker genes that are biologically meaningful. ClusterDE is fast\, transparent\, and adaptive to a wide range of clustering methods and statistical tests. \nhttps://qcb.ucla.edu/wp-content/uploads/sites/14/2023/03/Dongyuan-Song-32423.mp4
URL:https://qcb.ucla.edu/event/qcbio-research-seminar-dongyuan-song-li-jj-grad-student-bioinformatics-idp/
LOCATION:ZOOM\, CA\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/03/UCLA.jpg
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=America/Los_Angeles:20230324T123000
DTEND;TZID=America/Los_Angeles:20230324T130000
DTSTAMP:20260517T015938
CREATED:20230319T153305Z
LAST-MODIFIED:20230327T174010Z
UID:24633-1679661000-1679662800@qcb.ucla.edu
SUMMARY:QCBio Research Seminar: Nicholas Wang (Boutros)\, Grad Student\, Bioinformatics
DESCRIPTION:TITLE: “Germline structural variants shape prostate cancer clinical and molecular evolution.” \nABSTRACT: Inherited genetic variation profoundly influences cancer risk and outcome. While the impact of germline single nucleotide polymorphisms has been well-studied in several cancer types\, the effects of germline structural variants (gSVs) on cancer biology and clinical outcomes is largely unknown. From our cohort of 300 men with localized\, intermediate risk prostate cancer\, we identified 6\,003 gSVs present in at least 3% of patients\, with 48 associated with recurrent somatic alterations or clinical outcome. Of these\, ~50% associated with expression of nearby genes or intersected with exons or regulatory regions. Using external cohorts\, we validated three gSVs that were strongly associated with poor clinical outcomes\, including an inversion at chr14q24.1 present in ~20% of patients. Notably\, a strong synergistic effect on outcome was observed in patients with somatic TP53 alterations or high genomic instability\, defining a new aggressive prostate cancer subtype with chr14INV as a novel\, recurrent biomarker. \nhttps://qcb.ucla.edu/wp-content/uploads/sites/14/2023/03/Nicholas-Wang-32423.mp4
URL:https://qcb.ucla.edu/event/qcbio-research-seminar-nicholas-wang-boutros-grad-student-bioinformatics-p/
LOCATION:ZOOM\, CA\, United States
CATEGORIES:Research Seminars
ATTACH;FMTTYPE=image/jpeg:https://wp-misc.lifesci.ucla.edu/qcb/wp-content/uploads/sites/14/2023/03/Nicholas-Wang.jpg
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