Other Seminars

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Wed 18 Jul 2018 from 12:30 to 13:30

WHG Lunchtime Lab Talks

Wellcome Trust Centre for Human Genetics, Rooms A&B, Headington OX3 7BN

Grimes and Knight Lunchtime Lab Talks

Dr Hai Fang, Dr Katie Burnham, Loic Carrique, Jeremy Keown

Grimes Group: Speaker: Loic Carrique Title: Investigating the transcriptional activity of influenza virus polymerase Speaker: Jeremy Keown Title: Structural studies of the Influenza Polymerase Knight Group: Speaker: Dr Katie Burnham Title: Exploring variation in the sepsis response through a... Read more

Grimes Group: Speaker: Loic Carrique Title: Investigating the transcriptional activity of influenza virus polymerase Speaker: Jeremy Keown Title: Structural studies of the Influenza Polymerase Knight Group: Speaker: Dr Katie Burnham Title: Exploring variation in the sepsis response through a combined -omics approach Speaker: Dr Hai Fang Title: Building infrastructures for genetics-led drug target discovery

Audience: Members of the University only

Organisers: Isabel Schmidt

Thu 19 Jul 2018 from 11:00 to 12:00

Ludwig Institute Seminar Series

NDM Building, Basement seminar room, TDI, Headington OX3 7FZ

Microfluidics with fluid walls; a simple technology for everyone in cell and molecular biology

Professor Peter Cook

Workflows in cell and molecular biology often use microliter volumes and containers with solid walls (e.g., microcentrifuge tubes, microplates). An accessible technology that provides an easy entrée into the use of nanoliter volumes will be described. In this case, liquids are confined by fluid... Read more

Workflows in cell and molecular biology often use microliter volumes and containers with solid walls (e.g., microcentrifuge tubes, microplates). An accessible technology that provides an easy entrée into the use of nanoliter volumes will be described. In this case, liquids are confined by fluid (not solid) walls. Aqueous circuits with any 2D shape, or grids containing thousands of identical chambers, are made in seconds using standard cell-growth media on polystyrene Petri dishes; then, interfacial forces pin liquids to substrates, and an immiscible overlay prevents evaporation. The confining fluid walls are pliant, resilient, and optically transparent; they self-heal when liquids are pipetted through them, and they can even drive flows through circuits without the need for external pumps. The technology will be illustrated using some common cell-based workflows (e.g., cell feeding, replating, cloning, cryopreservation, lysis plus RT-PCR, transfection plus genome-editing, fixation plus immuno-labeling, and the response of human cells to cytokines and drugs, worms to osmotic stress, and bacterial biofilms to chemotactic gradients).

Audience: Members of the University only

Organisers: Christina Woodward

Mon 23 Jul 2018 from 12:00 to 13:00

WTCHG High Profile Seminars

Wellcome Trust Centre for Human Genetics, Rooms A&B, Headington OX3 7BN

B cells biology in sepsis

Dr Manu Shankar-Hari

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis is common, with an extrapolated critical care treated incidence of 103 per 100,000 population in 2014 in England. As critical care incidence represents a small proportion of sepsis... Read more

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis is common, with an extrapolated critical care treated incidence of 103 per 100,000 population in 2014 in England. As critical care incidence represents a small proportion of sepsis cases treated within a health care system, making it more common than some cancers, with an estimated global case load of 16 million cases per year. The improving in hospital mortality generates more sepsis survivors, with longer-term sequelae such as increased health care use and greater risk of death compared to general population. Immunologically, the transition from infection to sepsis represents an inflection point in the race between the human immune system devised to detect danger signals and overwhelm pathogens, ideally without causing a non-homeostatic systemic activation of immune cells. The consequence of such non-homeostatic immune system activation, characterised using whole blood leukocyte transcriptome, highlight changes in major canonical signalling pathways of cellular function, metabolism, in both innate and adaptive immune systems. Either a consequence or primary manifestation of this allostatic overload is accelerated lymphocyte apoptosis, contributing to lymphopenia seen in sepsis patients. In contrast to T cell biology in sepsis, B cell biology is poorly characterised, despite the likely inevitability of B cell changes when there are T cell changes such as loss of helper T cells and impaired ability of T cells to respond to new antigen challenge. We measured key aspects of B cell biology in community acquired sepsis, in adults without any documented immune co-morbidity, prior to critical care admission. In this cohort, B cells are lower than normal at critical care admission, despite normal levels of B cell survival factors (BAFF and APRIL). As a proportion of total B cells, the transitional and naïve B cell subsets were similar, whilst plasmablasts and memory B cells were significantly lower, compared to age-matched health controls. The greater loss of memory loss was secondary to higher apoptosis and the apoptotic cells had greater phosphosrylated-erk mean fluorescent intensity (MFI). In addition, there was reciprocal lower MFI for CD22 without concomitant higher MFI for Bruton’s tyrosine kinase (BTK) and spleen tyrosine kinase (SYK). Using micro-array on negatively selected CD19 positive B cells, the apoptosis networks highlighted by the Ingenuity pathways analysis involved intrinsic pathway with higher expression of CASP2, CASP6, pro-apoptotic BCL2 proteins (APAF1, HTRA2, HIP1 and BOK) and death Receptor pathway with higher expression of plasma membrane death receptor (DR) genes (FAS, TNFRSF25, TNFRSF10B, TNFRSF10A, DR4, DR5 and Trail-R), DR adaptor proteins (CRADD, PIDD1 and FADD), CFLAR, CASP8 and CASP10. Thus, in sepsis, there are major alternations in B cell biology. These findings highlight potential interventions for improving both acute and for longer-term sequalae to sepsis such re-infections related to immunosuppression.

Audience: Members of the University only

Mon 23 Jul 2018 from 12:00 to 13:00

Kennedy Institute Seminars

Kennedy Institute of Rheumatology, Bernard Sunley Lecture Theatre, Headington OX3 7LF

Happy and healthy blood vessels: Keep ‘em quiescent

Prof Hellmut Augustin

Vascular dysfunction is the primary cause of human mortality. The molecular analysis of endothelial activation mechanisms has therefore been focus of intense research during the last three decades. Conversely, vascular quiescence is not just the absence of activation programs. Instead, it is only... Read more

Vascular dysfunction is the primary cause of human mortality. The molecular analysis of endothelial activation mechanisms has therefore been focus of intense research during the last three decades. Conversely, vascular quiescence is not just the absence of activation programs. Instead, it is only recognized in recent years that vascular quiescence is an active process that needs to be actively maintained in order to avoid vascular dysfunction. The presentation will discuss the state-of-the-art of vascular quiescence research and focus on recent systems biology approaches to study the transcriptomic program and epigenetic regulation of vascular quiescence. ---- Trained as veterinary surgeon (DVM, Hannover, Germany) and as experimental pathologist (PhD, Cornell University, USA), Hellmut Augustin worked previously as Assistant Professor at the University of Göttingen, Germany (1993-2000) and as Departmant Head at the Tumor Biology Center in Freiburg, Germany (2001-2006). Since 2006, he is Professor of Vascular and Tumor Biology at Heidelberg University and Division Head at the German Cancer Research Center in Heidelberg. His laboratory (www.augustinlab.de) studies 1.) the molecular mechanisms of physiological blood vessel formation, assembly, and maturation focusing on angiogenesis regulating receptor tyrosine kinases, most notably on the Angiopoietin-Tie ligand-receptor system as well as on other selected novel candidate molecules, 2.) the mechanisms of organotypic vascular differentiation and angiocrine signaling studying the lung and liver vasculature as prototypic vascular beds, 3.) the molecular mechanisms of tumor progression focusing on tumor-vessel interactions during metastasis, and 4.) translational tumor microenvironment experiments aimed at defining the therapeutic window of stromal targeted therapies.

Audience: Members of the University only

Organisers: Laura Sánchez Lazo

Wed 25 Jul 2018 from 10:30 to 11:30

Nuffield Department of Primary Care Health Sciences - Department research seminars

St Luke's Chapel, Woodstock Road OX2 6GG

Using the UK Biobank cohort study for biomedical research

Dr Carmen Piernas

The UK Biobank study has recruited 500,000 volunteers from all around the UK aged 40-69 at enrolment. This age group is being studied because it involves people at risk over the next few decades of developing a wide range of important diseases (including cancer, heart disease, stroke, diabetes,... Read more

The UK Biobank study has recruited 500,000 volunteers from all around the UK aged 40-69 at enrolment. This age group is being studied because it involves people at risk over the next few decades of developing a wide range of important diseases (including cancer, heart disease, stroke, diabetes, dementia). The purpose of this talk is to provide an introduction to this resource for health research and guidance on how to access and handle this data.

Audience: Members of the University only

Organisers: Dr Jenny Hirst