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POSTER PRESENTATIONS

POSTER PRESENTATIONS. 9.30-9.45 Welcome and Introduction 9.45-10.15 Viewing of posters 10.15-11.00 Discussion of important aspects of poster design Summing up. POSTER PRESENTATIONS. 3.00-3.15 Welcome and Introduction 3.15-3.45 Viewing of posters

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POSTER PRESENTATIONS

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  1. POSTER PRESENTATIONS 9.30-9.45 Welcome and Introduction 9.45-10.15 Viewing of posters 10.15-11.00 Discussion of important aspects of poster design Summing up

  2. POSTER PRESENTATIONS 3.00-3.15 Welcome and Introduction 3.15-3.45 Viewing of posters 3,45-4.30 Discussion of important aspects of poster design Summing up

  3. POSTER PRESENTATION

  4. Modes of Communication • Written – good for detail; time to digest; possible to include complex material Clear beginning, middle and end; Reader can combine with other sources of information to clarify anything that is not clear • Verbal – good for explaining; can get feedback from listener(s) Limited attention span but possible to repeat or explain technical jargon appropriate to audience • Visual – initial impact; memorable image No personal contact; limited viewing time; competing for attention

  5. Verbal or poster presentation? VERBAL • Large audience • High visibility of speaker • Opportunity to stress specific points • Easier to prepare • Last-minute changes possible • Slides reusable • Nerve-wracking • Not all audience interested • Often few questions/little discussion

  6. Verbal or poster presentation? POSTER • Good for certain kinds of data • Attracts interested viewers • Opportunity for discussion • Good if you are a nervous speaker • Good if English is not your first language • Time consuming to make • Cost • May miss viewing parallel posters

  7. POSTER SESSIONS (for the viewer) • Can be selective • Opportunity to meet presenter - ask detailed questions - ask simple questions • Can eavesdrop / join in discussions • Time to think about content • Can take notes, get methods, references • Chance to mention your own interests

  8. Poster definition: A large, usually printed placard, bill, or announcement, often illustrated, that is posted to advertise or publicize something

  9. A good poster will rapidly allow the reader to answer the questions: • What is this about? • What are the authors trying to do? • What is the take-home message?

  10. Questions the viewer asks: • What is this about? Title, picture • What are they doing? Aims • What is the bottom line ? Conclusion • How did they do it? Methods, Results • Who are these guys? Names, Presenter • How can I find out more? Contact address, references

  11. Conference layout

  12. Look at Me!!!!! 400 posters 90 mins 0.225 min/poster 13.5 sec/poster

  13. What makes a good poster?

  14. Grab attention • Give information • Memorable message

  15. First Impressions Count!

  16. ‘…an unattractive poster with high scientific merit risked being overlooked on first impression’

  17. STYLE • Visual impact, Title, Layout, Readability CONTENT • Authors, Aims, Methods, Results, Conclusions

  18. Title Choose your wording carefully and remember that the more words you have, the more space they will take up.

  19. An Investigation Into The Contributory Factors That Improve The Visual Presentation Of Scientific Results In A Conference Scenario. An Investigation Into The Contributory Factors That Improve The Visual Presentation Of Scientific Results In A Conference Scenario. AN INVESTIGATION INTO THE CONTRIBUTORY FACTORS THAT IMPROVE THE VISUAL PRESENTATION OF SCIENTIFIC RESULTS IN A CONFERENCE SCENARIO. An Investigation Into The Contributory Factors That Improve The Visual Presentation of Scientific Results In a Conference Scenario An investigation into the contributory factors that improve the visual presentation of scientific results in a conference scenario

  20. An investigation into the contributory factors that improve the visual presentation of scientific results in a conference scenario Remove redundant words Factors that improve visual presentation of scientific results (note how you can now make the text bigger)

  21. Factors that improve visual presentation

  22. Factors that improve visual presentation FACTORS THAT IMPROVE VISUAL PRESENTATION

  23. Optimum font size for readability is 26 pt Fig. 1. relationship between size of font used in a figure and the ease with which it can be read at a distance of 1 m assessed using a ten-point scale (readability )

  24. 2020 IL-18 and Immune Responses to Periodontal PathogensLeah Jamieson (supervisors Neil Foster and John Taylor)Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastleemail: L.M.Jamieson@ncl.ac.uk Aims • To establish whether human THP-1 monocytes produce IL-18 when stimulated with Porphyromonas gingivalis LPS • To examine the relationship between pro-inflammatory • IL-18 and anti-inflammatory IL-18 BPa A novel ELISA was developed to detect IL-18 BPa. Anti-IL-18 BPa was added to the supernatants of P. gingivalis stimulated cells to investigate the effect on IL-18 concentration. The addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4). Results Introduction * * Both P. gingivalis and E. coli LPS induced IL-18 secretion in THP-1 monocytes as demonstrated by ELISA and Western blotting (Figure 1 & 2) as well as IL-18BPa (Figure 3). The latest UK Dental Health Survey revealed that 40-45% of adults have moderate destructive periodontal disease, with 5-10% of cases being severe. Periodontal disease is a result of excessive immune responses to dental plaque bacteria which destroy the supporting tissues of the teeth, leading to loss of dental function. Cytokines play a central role in inflammatory processes that influence the progression of periodontal disease and its clinical outcome. Interleukins (IL) are a group of cytokines produced primarily by leukocytes. IL-18 has pro-inflammatory properties. It induces production of interferon (IFN)-γ which has a major role in the activation of cells of the immune system. IL-18 binding protein (BPa) strictly controls IL-18 activity by blocking binding to the IL-18 receptor on target cells and IL-18 BPa expression is stimulated by IFN-γ. This is an important regulatory circuit as overproduction of IFN-γ causes tissue pathology. However, there is no information on IL-18 in the pathogenesis of this disease. Figure 4: Addition of anti-IL-18 BPa to P. gingivalis LPS stimulated supernatants (6h) significantly increases IL-18 detection by ELISA (N= 3) (* = P< 0.05) Discussion The results indicate that significant concentrations of IL-18 and IL-18BPa are produced by human THP-1 cells within 6 hours of initial exposure to P. gingivalis LPS. Antibodies to IL-18BPa increased the amount of free IL-18 in LPS-stimulated THP-1 cultures indicating that IL-18BPa normally binds IL-18 secreted from THP-1 monocytes. The balance between IL-18 and IL-18 BPa may be important in regulating IL-18 activity and may play a role in the host response to plaque bacteria, and possibly progression and severity of periodontal disease. This work also indicates that antibodies or binding proteins could be used to modify immune responses involving cytokines and therefore be used therapeutically in the treatment of periodontal disease. Clinical signs of destructive periodontal disease Figure 1: ELISA analysis to quantitate IL-18 secreted by THP-1 cells exposed to LPS from P. gingivalis and E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N= 6) (* = P <0.05) P. gingivalis E. coli - ve → Figure 2: Western blot of IL-18 protein in supernatants from THP-1 cells exposed to LPS from P. gingivalis and E. coli (6h) * * * Conclusions * * Methods • The balance between IL-18 and IL-18 BPa may be important in immune responses to periodontal bacteria • This system may represent a novel immunoregulatory circuit in periodontal disease and a potential therapuetic target Cells from the pro-monocyte cell line THP-1 were treated with Vitamin D3 (0.1 μM) to induce differentiation into monocytes. Differentiation was confirmed by the ability of the cells to adhere to the plastic plate. THP-1 monocytes were cultured with lipopolysaccharide (LPS) from the periodontal bacterium P. gingivalisand the enterobacterium E. coli for 6 and 24 hours. The concentration of protein in each sample was determined by a protein assay and IL-18 concentrations were measured using an ELISA assay kit and detected via a Western Blot. PBS Pg PMA Ec Acknowledgements Figure 3: ELISA analysis of IL-18 BPa secreted by THP-1 cells exposed to LPS from P. gingivalis or E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N =3) (*= P< 0.05) This project was supported by a Wellcome Trust Vacation Scholarship

  25. 2020 IL-18 and Immune Responses to Periodontal PathogensLeah Jamieson (supervisors Neil Foster and John Taylor)Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastleemail: L.M.Jamieson@ncl.ac.uk Aims • To establish whether human THP-1 monocytes produce IL-18 when stimulated with Porphyromonas gingivalis LPS • To examine the relationship between pro-inflammatory • IL-18 and anti-inflammatory IL-18 BPa A novel ELISA was developed to detect IL-18 BPa. Anti-IL-18 BPa was added to the supernatants of P. gingivalis stimulated cells to investigate the effect on IL-18 concentration. The addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4). Results Introduction * * Both P. gingivalis and E. coli LPS induced IL-18 secretion in THP-1 monocytes as demonstrated by ELISA and Western blotting (Figure 1 & 2) as well as IL-18BPa (Figure 3). The latest UK Dental Health Survey revealed that 40-45% of adults have moderate destructive periodontal disease, with 5-10% of cases being severe. Periodontal disease is a result of excessive immune responses to dental plaque bacteria which destroy the supporting tissues of the teeth, leading to loss of dental function. Cytokines play a central role in inflammatory processes that influence the progression of periodontal disease and its clinical outcome. Interleukins (IL) are a group of cytokines produced primarily by leukocytes. IL-18 has pro-inflammatory properties. It induces production of interferon (IFN)-γ which has a major role in the activation of cells of the immune system. IL-18 binding protein (BPa) strictly controls IL-18 activity by blocking binding to the IL-18 receptor on target cells and IL-18 BPa expression is stimulated by IFN-γ. This is an important regulatory circuit as overproduction of IFN-γ causes tissue pathology. However, there is no information on IL-18 in the pathogenesis of this disease. Figure 4: Addition of anti-IL-18 BPa to P. gingivalis LPS stimulated supernatants (6h) significantly increases IL-18 detection by ELISA (N= 3) (* = P< 0.05) Discussion The results indicate that significant concentrations of IL-18 and IL-18BPa are produced by human THP-1 cells within 6 hours of initial exposure to P. gingivalis LPS. Antibodies to IL-18BPa increased the amount of free IL-18 in LPS-stimulated THP-1 cultures indicating that IL-18BPa normally binds IL-18 secreted from THP-1 monocytes. The balance between IL-18 and IL-18 BPa may be important in regulating IL-18 activity and may play a role in the host response to plaque bacteria, and possibly progression and severity of periodontal disease. This work also indicates that antibodies or binding proteins could be used to modify immune responses involving cytokines and therefore be used therapeutically in the treatment of periodontal disease. Clinical signs of destructive periodontal disease Figure 1: ELISA analysis to quantitate IL-18 secreted by THP-1 cells exposed to LPS from P. gingivalis and E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N= 6) (* = P <0.05) P. gingivalis E. coli - ve → Figure 2: Western blot of IL-18 protein in supernatants from THP-1 cells exposed to LPS from P. gingivalis and E. coli (6h) * * * Conclusions * * Methods • The balance between IL-18 and IL-18 BPa may be important in immune responses to periodontal bacteria • This system may represent a novel immunoregulatory circuit in periodontal disease and a potential therapuetic target Cells from the pro-monocyte cell line THP-1 were treated with Vitamin D3 (0.1 μM) to induce differentiation into monocytes. Differentiation was confirmed by the ability of the cells to adhere to the plastic plate. THP-1 monocytes were cultured with lipopolysaccharide (LPS) from the periodontal bacterium P. gingivalisand the enterobacterium E. coli for 6 and 24 hours. The concentration of protein in each sample was determined by a protein assay and IL-18 concentrations were measured using an ELISA assay kit and detected via a Western Blot. PBS Pg PMA Ec Acknowledgements Figure 3: ELISA analysis of IL-18 BPa secreted by THP-1 cells exposed to LPS from P. gingivalis or E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N =3) (*= P< 0.05) This project was supported by a Wellcome Trust Vacation Scholarship

  26. 2020 IL-18 and Immune Responses to Periodontal PathogensLeah Jamieson (supervisors Neil Foster and John Taylor)Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastleemail: L.M.Jamieson@ncl.ac.uk Aims • To establish whether human THP-1 monocytes produce IL-18 when stimulated with Porphyromonas gingivalis LPS • To examine the relationship between pro-inflammatory • IL-18 and anti-inflammatory IL-18 BPa A novel ELISA was developed to detect IL-18 BPa. Anti-IL-18 BPa was added to the supernatants of P. gingivalis stimulated cells to investigate the effect on IL-18 concentration. The addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4). * * Results Introduction Both P. gingivalis and E. coli LPS induced IL-18 secretion in THP-1 monocytes as demonstrated by ELISA and Western blotting (Figure 1 & 2) as well as IL-18BPa (Figure 3). The latest UK Dental Health Survey revealed that 40-45% of adults have moderate destructive periodontal disease, with 5-10% of cases being severe. Periodontal disease is a result of excessive immune responses to dental plaque bacteria which destroy the supporting tissues of the teeth, leading to loss of dental function. Cytokines play a central role in inflammatory processes that influence the progression of periodontal disease and its clinical outcome. Interleukins (IL) are a group of cytokines produced primarily by leukocytes. IL-18 has pro-inflammatory properties. It induces production of interferon (IFN)-γ which has a major role in the activation of cells of the immune system. IL-18 binding protein (BPa) strictly controls IL-18 activity by blocking binding to the IL-18 receptor on target cells and IL-18 BPa expression is stimulated by IFN-γ. This is an important regulatory circuit as overproduction of IFN-γ causes tissue pathology. However, there is no information on IL-18 in the pathogenesis of this disease. Figure 4: Addition of anti-IL-18 BPa to P. gingivalis LPS stimulated supernatants (6h) significantly increases IL-18 detection by ELISA (N= 3) (* = P< 0.05) Discussion The results indicate that significant concentrations of IL-18 and IL-18BPa are produced by human THP-1 cells within 6 hours of initial exposure to P. gingivalis LPS. Antibodies to IL-18BPa increased the amount of free IL-18 in LPS-stimulated THP-1 cultures indicating that IL-18BPa normally binds IL-18 secreted from THP-1 monocytes. The balance between IL-18 and IL-18 BPa may be important in regulating IL-18 activity and may play a role in the host response to plaque bacteria, and possibly progression and severity of periodontal disease. This work also indicates that antibodies or binding proteins could be used to modify immune responses involving cytokines and therefore be used therapeutically in the treatment of periodontal disease. Figure 1: ELISA analysis to quantitate IL-18 secreted by THP-1 cells exposed to LPS from P. gingivalis and E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N= 6) (* = P <0.05) Clinical signs of destructive periodontal disease P. gingivalis - ve E. coli → Figure 2: Western blot of IL-18 protein in supernatants from THP-1 cells exposed to LPS from P. gingivalis and E. coli (6h) * * * * * Conclusions Methods • The balance between IL-18 and IL-18 BPa may be important in immune responses to periodontal bacteria • This system may represent a novel immunoregulatory circuit in periodontal disease and a potential therapuetic target Cells from the pro-monocyte cell line THP-1 were treated with Vitamin D3 (0.1 μM) to induce differentiation into monocytes. Differentiation was confirmed by the ability of the cells to adhere to the plastic plate. THP-1 monocytes were cultured with lipopolysaccharide (LPS) from the periodontal bacterium P. gingivalis and the enterobacterium E. coli for 6 and 24 hours. The concentration of protein in each sample was determined by a protein assay and IL-18 concentrations were measured using an ELISA assay kit and detected via a Western Blot. Pg Ec PBS PMA Acknowledgements Figure 3: ELISA analysis of IL-18 BPa secreted by THP-1 cells exposed to LPS from P. gingivalis or E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N =3) (*= P< 0.05) This project was supported by a Wellcome Trust Vacation Scholarship

  27. 2020 IL-18 and Immune Responses to Periodontal PathogensLeah Jamieson (supervisors Neil Foster and John Taylor)Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastleemail: L.M.Jamieson@ncl.ac.uk Aims • To establish whether human THP-1 monocytes produce IL-18 when stimulated with Porphyromonas gingivalis LPS • To examine the relationship between pro-inflammatory • IL-18 and anti-inflammatory IL-18 BPa A novel ELISA was developed to detect IL-18 BPa. Anti-IL-18 BPa was added to the supernatants of P. gingivalis stimulated cells to investigate the effect on IL-18 concentration. The addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4). Results Introduction * * Both P. gingivalis and E. coli LPS induced IL-18 secretion in THP-1 monocytes as demonstrated by ELISA and Western blotting (Figure 1 & 2) as well as IL-18BPa (Figure 3). The latest UK Dental Health Survey revealed that 40-45% of adults have moderate destructive periodontal disease, with 5-10% of cases being severe. Periodontal disease is a result of excessive immune responses to dental plaque bacteria which destroy the supporting tissues of the teeth, leading to loss of dental function. Cytokines play a central role in inflammatory processes that influence the progression of periodontal disease and its clinical outcome. Interleukins (IL) are a group of cytokines produced primarily by leukocytes. IL-18 has pro-inflammatory properties. It induces production of interferon (IFN)-γ which has a major role in the activation of cells of the immune system. IL-18 binding protein (BPa) strictly controls IL-18 activity by blocking binding to the IL-18 receptor on target cells and IL-18 BPa expression is stimulated by IFN-γ. This is an important regulatory circuit as overproduction of IFN-γ causes tissue pathology. However, there is no information on IL-18 in the pathogenesis of this disease. Figure 4: Addition of anti-IL-18 BPa to P. gingivalis LPS stimulated supernatants (6h) significantly increases IL-18 detection by ELISA (N= 3) (* = P< 0.05) Discussion The results indicate that significant concentrations of IL-18 and IL-18BPa are produced by human THP-1 cells within 6 hours of initial exposure to P. gingivalis LPS. Antibodies to IL-18BPa increased the amount of free IL-18 in LPS-stimulated THP-1 cultures indicating that IL-18BPa normally binds IL-18 secreted from THP-1 monocytes. The balance between IL-18 and IL-18 BPa may be important in regulating IL-18 activity and may play a role in the host response to plaque bacteria, and possibly progression and severity of periodontal disease. This work also indicates that antibodies or binding proteins could be used to modify immune responses involving cytokines and therefore be used therapeutically in the treatment of periodontal disease. Clinical signs of destructive periodontal disease Figure 1: ELISA analysis to quantitate IL-18 secreted by THP-1 cells exposed to LPS from P. gingivalis and E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N= 6) (* = P <0.05) P. gingivalis E. coli - ve → Figure 2: Western blot of IL-18 protein in supernatants from THP-1 cells exposed to LPS from P. gingivalis and E. coli (6h) * * * Conclusions * * Methods • The balance between IL-18 and IL-18 BPa may be important in immune responses to periodontal bacteria • This system may represent a novel immunoregulatory circuit in periodontal disease and a potential therapuetic target Cells from the pro-monocyte cell line THP-1 were treated with Vitamin D3 (0.1 μM) to induce differentiation into monocytes. Differentiation was confirmed by the ability of the cells to adhere to the plastic plate. THP-1 monocytes were cultured with lipopolysaccharide (LPS) from the periodontal bacterium P. gingivalisand the enterobacterium E. coli for 6 and 24 hours. The concentration of protein in each sample was determined by a protein assay and IL-18 concentrations were measured using an ELISA assay kit and detected via a Western Blot. PBS Pg PMA Ec Acknowledgements Figure 3: ELISA analysis of IL-18 BPa secreted by THP-1 cells exposed to LPS from P. gingivalis or E. coli. Cultures with PMA and PBS served as positive and negative controls respectively (N =3) (*= P< 0.05) This project was supported by a Wellcome Trust Vacation Scholarship

  28. Corporate Visual IdentityNewcastle University Policy and Regulations http://www.ncl.ac.uk/cvi-support/

  29. Look at posters critically with respect to these points • Impact Is the poster eye-catching? • Title Short, punchy, informative? • Authors Is it clear who is the presenter? Is there "Corporate Visual Identity" for the Institution? • Layout Is it tidy? Is it easy to follow the sequence? • Readability Are print size, font etc. appropriate? • Purpose Is Introduction useful, are Aims clear? • Conclusions How are these presented? • Methods Are these appropriately presented? • Results Have table, graphs and figures been used well? Is it easy for the reader to understand the data?

  30. Other points to consider CONFERENCE FACTORS • Specific instructions on poster preparation from conference organisers • Board size and shape } • Fixing method } don’t rely on these being right! • Location } • Will presenters be present? • Will there be a Discussion session? LOCAL FACTORS • Nature of your material • Departmental policy • Visual Identity • Cost • Re-use of poster

  31. FINAL POINTS … WHY ARE YOU HERE? - to communicate results • to advertise your work, yourself, your department • Be proactive - • identify yourself • (photo on poster, presenter badge, add poster number to badge) • Be remembered - • first name on poster, Email address, take-away handouts, reprints

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