Modes of Communication Written ie paper article 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 ID: 495763
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Slide1
Poster PresentationSlide2
Modes of Communication
Written (i.e. paper / article)
– 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
Oral/Spoken/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/Poster
– initial impact; memorable image
No personal contact; limited viewing time; competing for attentionSlide3
When posters are used
Meetings/Conferences
General, Specialist, Clinical
Large, Small
National, International
Open days
Entertaining fundraisers
Attracting staff, students
Informing general public
Site Visits / Visits from Funding Bodies
Corridor decorationSlide4
PROS
Large audience
High visibility of speaker
Opportunity to stress specific points
Easier to prepare
Last-minute changes possibleSlides reusableCONSNerve-wrackingNot all audience interestedOften few questions/little discussion
Pros and Cons of the Spoken
PresentationSlide5
Pros and Cons of the Poster Presentation
PROS
Good for certain kinds of data
Attracts interested viewers
Opportunity for discussion
Good if you are a nervous speakerGood if English is not your first languageCONSTime consuming to makeCostMay miss viewing parallel postersSlide6
Poster Sessions – What is in it 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 contentCan take notes, get methods, referencesChance to mention your own interestsSlide7
What is a poster?
A
large, usually printed placard, bill, or announcement,
often illustrated
, that is posted to advertise or publicize somethingSlide8Slide9
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?Slide10
Questions the viewer asks:
What is this about?
Title, picture
What are they doing?
Aims
What is the bottom line ? ConclusionHow did they do it? Methods, ResultsWho are these guys? Names, Presenter How can I find out more? Contact address, referencesSlide11
What makes a good poster?Slide12
Grab attention
Give information
Memorable messageSlide13Slide14
Know your audience
Expert, semi-expert, patients, fund-raisers general public
THINK about content, text and terminology
Avoid acronyms – even ones that seems obvious to you
No jargon / Do not assume knowledge
Always ask yourself - do they need to know this piece of information in order to understand my message?Slide15
Avoid acronymsSlide16
Poster Style
Visual impact
Title
Layout
ReadabilitySlide17
Poster Layout
Landscape better than portrait
3 columns – reduces line lengthSlide18
Poster Content
Authors
Aims
Methods
Results
Conclusions? ReferencesSlide19
Title
Possibly the most important aspect of the poster.
First thing viewers will read.
Short but needs to capture the essence of the poser
Choose your wording carefully and remember that the more words you have, the more space they will take up.Slide20
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 scenarioSlide21
An investigation into the contributory factors that improve the visual presentation of scientific results in a conference scenario
Factors that improve visual presentation of scientific results
(note how you can now make the text bigger)
Remove redundant wordsSlide22
Factors that improve visual presentation
FACTORS THAT IMPROVE VISUAL PRESENTATION
The case for lower-caseSlide23
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 )
Optimum font size for readability is 26 pt
Size mattersSlide24
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.
2020
IL-18 and Immune Responses to Periodontal Pathogens
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: L.M.Jamieson@ncl.ac.uk
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
Discussion
Conclusions
Acknowledgements
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
Introduction
Aims
Methods
Results
This project was supported by a Wellcome Trust Vacation Scholarship
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 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)
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)
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)
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.
*
*
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.
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 addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4).
Clinical signs of destructive periodontal disease
PBS
PMA
Pg
Ec
*
*
*
*
*Slide25
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.
2020
IL-18 and Immune Responses to Periodontal Pathogens
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: L.M.Jamieson@ncl.ac.uk
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
Discussion
Conclusions
Acknowledgements
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
Introduction
Aims
Methods
Results
This project was supported by a Wellcome Trust Vacation Scholarship
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 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)
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)
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)
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.
*
*
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.
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 addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4).
Clinical signs of destructive periodontal disease
PBS
PMA
Pg
Ec
*
*
*
*
*Slide26
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.
2020
IL-18 and Immune Responses to Periodontal Pathogens
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: L.M.Jamieson@ncl.ac.uk
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
Discussion
Conclusions
Acknowledgements
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
Introduction
Aims
Methods
Results
This project was supported by a Wellcome Trust Vacation Scholarship
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 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)
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)
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)
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.
*
*
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.
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 addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4).
Clinical signs of destructive periodontal disease
PBS
PMA
Pg
Ec
*
*
*
*
*Slide27
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.
2020
IL-18 and Immune Responses to Periodontal Pathogens
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: L.M.Jamieson@ncl.ac.uk
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
Discussion
Conclusions
Acknowledgements
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
Introduction
Aims
Methods
Results
This project was supported by a Wellcome Trust Vacation Scholarship
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 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)
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)
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)
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.
*
*
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.
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 addition of anti-IL-18 BPa significantly (P <0.05) increased the concentration of IL-18 assayed by the ELISA (Figure 4).
Clinical signs of destructive periodontal disease
PBS
PMA
Pg
Ec
*
*
*
*
*Slide28
Corporate Visual Identity
Newcastle University Policy and Regulations
http://www.ncl.ac.uk/cvi-support/Slide29
Do NOT forgot your sponsor!Slide30Slide31
Conference layoutSlide32Slide33Slide34
400 posters
90
mins
13.5 sec/poster
0.225 min/poster
Look at Me!!!!!Slide35
First Impressions Count!Slide36
‘…an unattractive poster with high scientific merit risked being overlooked on first impression’Slide37
Typical Instructions
for Poster Presentations
One poster board will be provided for you. The poster board is approximately 4 feet high and 8 feet wide.
Prepare a title board for the top of your poster, indicating the title and author(s) of your presentation. Ideally, the lettering for the title should not be less than 1-1/2 inches high.
Do not use normal "typewriter-size" type (10–12 point font size).
We will provide a printed “number,” identifying each poster board. Push pins will also be provided. Display of commercial/product sales posters is prohibited. Any poster that is deemed to be a commercial advertisement is unacceptable and will be removed from the poster hall. Slide38
Typical Instructions
for Poster Presentations
All illustrations should be made up beforehand. Remember that your illustrations must be read from a distance of at least 3-5 feet.
Charts
, drawings, and illustrations should be similar to those you would use for slide presentations, but more heavily drawn. Remember to keep illustrated and written material simple.
Do not mount illustrations on a heavy board because they may be difficult to keep in position on the poster boards. One or two authors should be in attendance at each poster during the entire presentation time. Slide39
Typical Instructions
for Poster Presentations
Do not allow yourself to be monopolized for an inordinate period of time by a single individual.
Please remove your materials from the poster board immediately after the session.
Materials left on the boards after the session will be discarded.
The only handouts allowed in the Poster Hall include exact copies of your poster or business cards; all other types of handouts are not allowed in the Poster Hall. Slide40
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
?
Methods
Are these appropriately presented
?
Results
Have table, graphs and figures been used well?
Is it easy for the reader to understand the
data?
Conclusions
How are these presented?Slide41
Final Points
…
Why are you doing a poster?
to
communicate
resultsto advertise your work, yourself, your departmentBe 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