Transcript POSTER PRESENTATIONS - Newcastle University

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
3,45-4.30
Discussion of important
aspects of poster design
Summing up
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
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
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
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
Poster definition:
A large, usually printed placard, bill, or announcement, often
illustrated, that is posted to advertise or publicize something
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?
Questions the viewer asks:
• What is this about?
• What are they doing?
• What is the bottom line ?
Title, picture
• How did they do it?
• Who are these guys?
• How can I find out more?
Methods, Results
Aims
Conclusion
Names, Presenter
Contact address,
references
Conference layout
Look at Me!!!!!
400 posters
90 mins
0.225 min/poster
13.5 sec/poster
What makes a good poster?
• Grab attention
• Give information
• Memorable message
First Impressions Count!
‘…an unattractive poster with high scientific merit risked being overlooked on first impression’
STYLE
• Visual impact, Title, Layout, Readability
CONTENT
• Authors, Aims, Methods, Results, Conclusions
Title
Choose your wording carefully and remember that the
more words you have, the more space they will take up.
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
Remove redundant words
Factors that improve visual presentation of scientific results
(note how you can now make the text bigger)
Factors that improve visual presentation
Factors that improve visual presentation
FACTORS THAT IMPROVE VISUAL PRESENTATION
Optimum font size for readability is 26 pt
12
8
10
6
Series1
8
50
38
44
Font size
32
0
26
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 )
2
20
Font size
4
14
50
44
38
32
26
20
14
8
2
0
6
8
2
2
4
Readability
Readability
10
S1
IL-18 and Immune Responses to Periodontal Pathogens
2020
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: [email protected]
Aims
Introduction
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.
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).
3000
Results
IL-18 concentration (pg/ml)
•
To establish whether human THP-1 monocytes produce IL18 when stimulated with Porphyromonas gingivalis LPS
To examine the relationship between pro-inflammatory
IL-18 and anti-inflammatory IL-18 BPa
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).
2500
*
*
1.5
15
2000
1500
1000
500
0
0
1800
IL-18 concentration (pg/ml)
•
*
1600
1400
0.15
Anti-IL-18 BPa antibody conc (μg/m l)
*
1200
* *
1000
800
*
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)
6h
*
24h
600
400
200
Discussion
0
Pg
Ec
PMA
Unstimulated
control
Treatment
Clinical signs of destructive periodontal disease
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 THP1 cells exposed to LPS from P. gingivalis and E. coli (6h)
0.7
*
*
0.6
*
*
IL-18BPa (620nm)
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.
Conclusions
*
0.5
Methods
The results indicate that significant concentrations of IL-18 and IL18BPa 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.
0.4
6Hr
24 Hr
0.3
•
The balance between IL-18 and IL-18 BPa may be important in
immune responses to periodontal bacteria
0.2
•
0.1
0
PBS
Pg
Ec
PMA
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 system may represent a novel immunoregulatory circuit in
periodontal disease and a potential therapuetic target
Acknowledgements
This project was supported by a Wellcome Trust Vacation Scholarship
IL-18 and Immune Responses to Periodontal Pathogens
2020
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: [email protected]
Aims
Introduction
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.
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).
3000
Results
IL-18 concentration (pg/ml)
•
To establish whether human THP-1 monocytes produce IL18 when stimulated with Porphyromonas gingivalis LPS
To examine the relationship between pro-inflammatory
IL-18 and anti-inflammatory IL-18 BPa
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).
2500
*
*
1.5
15
2000
1500
1000
500
0
0
1800
IL-18 concentration (pg/ml)
•
*
1600
1400
0.15
Anti-IL-18 BPa antibody conc (μg/m l)
*
1200
* *
1000
800
*
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)
6h
*
24h
600
400
200
Discussion
0
Pg
Ec
PMA
Unstimulated
control
Treatment
Clinical signs of destructive periodontal disease
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 THP1 cells exposed to LPS from P. gingivalis and E. coli (6h)
0.7
*
*
0.6
*
*
IL-18BPa (620nm)
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.
Conclusions
*
0.5
Methods
The results indicate that significant concentrations of IL-18 and IL18BPa 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.
0.4
6Hr
24 Hr
0.3
•
The balance between IL-18 and IL-18 BPa may be important in
immune responses to periodontal bacteria
0.2
•
0.1
0
PBS
Pg
Ec
PMA
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 system may represent a novel immunoregulatory circuit in
periodontal disease and a potential therapuetic target
Acknowledgements
This project was supported by a Wellcome Trust Vacation Scholarship
IL-18 and Immune Responses to
Periodontal Pathogens
2020
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: [email protected]
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).
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.
Both P. gingivalis and E. coli LPS induced IL-18 secretion in THP1 monocytes as demonstrated by ELISA and Western blotting
(Figure 1 & 2) as well as IL-18BPa (Figure 3).
2500
*
*
1.5
15
2000
1500
1000
500
0
0
1800
IL-18 concentration (pg/ml)
Introduction
IL-18 concentration (pg/ml)
3000
Results
*
1600
1400
0.15
Anti-IL-18 BPa antibody conc (μg/m l)
*
1200
* *
1000
800
*
6h
*
24h
600
400
200
0
Pg
Ec
PMA
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
Unstimulated
control
Treatment
Clinical signs of destructive periodontal disease
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)
0.7
0.6
0.5
IL-18BPa (620nm)
Methods
*
*
*
*
*
Conclusions
0.4
6Hr
0.3
The results indicate that significant concentrations of IL-18 and IL18BPa 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.
24 Hr
Cells from the pro-monocyte cell line THP-1 were treated with Vitamin
0.2
D3 (0.1 μM) to induce differentiation into monocytes. Differentiation was
0.1
confirmed by the ability of the cells to adhere to the plastic plate. THP-1
monocytes were cultured with lipopolysaccharide (LPS) from the
0
Pg
Ec
PB
PMA
periodontal bacterium P. gingivalis and the enterobacterium E. coli for 6
S
and 24 hours. The concentration of protein in each sample was
determined by a protein assay and IL-18 concentrations were measured
Figure 3: ELISA analysis of IL-18 BPa secreted by THP-1 cells exposed
using an ELISA assay kit and detected via a Western Blot.
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)
•
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
Acknowledgements
This project was supported by a Wellcome Trust Vacation Scholarship
IL-18 and Immune Responses to Periodontal Pathogens
2020
Leah Jamieson (supervisors Neil Foster and John Taylor)
Oral Microbiology and Host Responses Group, School of Dental Sciences, University of Newcastle
email: [email protected]
Aims
Introduction
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.
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).
3000
Results
IL-18 concentration (pg/ml)
•
To establish whether human THP-1 monocytes produce IL18 when stimulated with Porphyromonas gingivalis LPS
To examine the relationship between pro-inflammatory
IL-18 and anti-inflammatory IL-18 BPa
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).
2500
*
*
1.5
15
2000
1500
1000
500
0
0
1800
IL-18 concentration (pg/ml)
•
*
1600
1400
0.15
Anti-IL-18 BPa antibody conc (μg/m l)
*
1200
* *
1000
800
*
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)
6h
*
24h
600
400
200
Discussion
0
Pg
Ec
PMA
Unstimulated
control
Treatment
Clinical signs of destructive periodontal disease
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 THP1 cells exposed to LPS from P. gingivalis and E. coli (6h)
0.7
*
*
0.6
*
*
IL-18BPa (620nm)
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.
Conclusions
*
0.5
Methods
The results indicate that significant concentrations of IL-18 and IL18BPa 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.
0.4
6Hr
24 Hr
0.3
•
The balance between IL-18 and IL-18 BPa may be important in
immune responses to periodontal bacteria
0.2
•
0.1
0
PBS
Pg
Ec
PMA
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 system may represent a novel immunoregulatory circuit in
periodontal disease and a potential therapuetic target
Acknowledgements
This project was supported by a Wellcome Trust Vacation Scholarship
Corporate Visual Identity
Newcastle University Policy and Regulations
http://www.ncl.ac.uk/cvi-support/
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?
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
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