2014 01 science slide design ss version
Post on 15-Sep-2014
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TRANSCRIPT
Do your slides suck?
Based on the live seminar
Mediocre to Memorable Effectively designing slides for science
Originally created for University of Pennsylvania
School of Medicine Faculty and Postdocs
(Lisa’s client for over 15 years)
(She’s also the host of The Public Speaker podcast which has earned over 11 million downloads)
Do you know what happens
to your attention during a presentation?
The speaker is being introduced
Time
Interest
Low
HighHigh
You’re just settling in…
Time
Interest
Low
HighHigh
“Oh, the presentation started!”
Then the mind vacations begin…
Time
Interest
Low
HighHigh
“Oh, that reminds me …”
The speaker continues with bad delivery,
unclear organization, and poorly designed slides…
…the trifecta of horrible presentations!
Time
Interest
Low
HighHigh
Sleep
…and the speaker drones onand on, and on,and on, and on, and on,and on, and on, and on,and on,
and on…
Time
Interest
Low
HighHigh
Coma
Time
Interest
Low
HighHigh
Coma
…until the two magic words
Time
Interest
Low
HighHigh
“In conclusion…”
Unfortunately this isn’t far
from the truth!
Top 5 Annoyances
(Pardi, 2013)
Top 5 presentation annoyances
72% Reading slides aloud
(Pardi, 2013)
The Redundancy Principle:Redundant material interferes with learning
(Hoffman, 2006)
Pathogenesis of HIT
1. Caused by ultralarge immune complexes composed of IgG antibodies against complexes between platelet factor 4 secreted from activated platelets and heparin or glyscosaminoglycans
2. Thrombocytopenia and thrombosis arise as a result of platelet activation through FcgRIIA, activation of monocytes, and endothelium which together generates a thrombin-mediated feed-forward pathway.
3. Treatment with direct thrombin inhibitors provides incompletebenefit and is associated with major bleeding that approximates1% per day.
Pathogenesis of HIT
1. Caused by ultralarge immune complexes composed of IgG antibodies against complexes between platelet factor 4 secreted from activated platelets and heparin or glyscosaminoglycans
2. Thrombocytopenia and thrombosis arise as a result of platelet activation through FcgRIIA, activation of monocytes, and endothelium which together generates a thrombin-mediated feed-forward pathway.
3. Treatment with direct thrombin inhibitors provides incompletebenefit and is associated with major bleeding that approximates1% per day.
Yes, this is a REAL slide from someone here at Penn!
Look! Speak don’t read!
Pathogenesis of HIT(Heparin-induced thrombocytopenia)
Don’t use slide text
as notes for yourself!
[Put text in notes section if necessary]
Pathogenesis of HIT• Caused by ultralarge immune complexes
• Thrombocytopenia and thrombosis arise from platelets, monocytes, and endothelium
• Treatment with direct thrombin inhibitors provides incomplete benefit
…or at least shorten !
48% Full sentences
(Pardi, 2013)
Observation/Hypothesis
Hypothesis: Inhibition of complement will attenuatethrombocytopenia and thrombosis, increase the benefitof direct thrombin inhibitors, and permit lower and safer doses to be used.
Observation: Platelets from patients with HIT carry increased C3, the third component of complement, and HIT plasma contains complement fixing anti-endothelial cell antibodies that induce expression of tissue factor (NEJM, 1987).
Observation/Hypothesis
Hypothesis: Inhibition of complement will attenuatethrombocytopenia and thrombosis, increase the benefitof direct thrombin inhibitors, and permit lower and safer doses to be used.
Observation: Platelets from patients with HIT carry increased C3, the third component of complement, and HIT plasma contains complement fixing anti-endothelial cell antibodies that induce expression of tissue factor (NEJM, 1987).
Two line phrases at most
51% Text too small to read
(Pardi, 2013)
Observation/Hypothesis
Hypothesis: Inhibition of complement will attenuatethrombocytopenia and thrombosis, increase the benefitof direct thrombin inhibitors, and permit lower and safer doses to be used.
Observation: Platelets from patients with HIT carry increased C3, the third component of complement, and HIT plasma contains complement fixing anti-endothelial cell antibodies that induce expression of tissue factor (NEJM, 1987).
Hypothesis:Inhibition of C3 complement
will attenuatethrombocytopenia and thrombosis
Large simple
plain language
26% Poor color choices
(Pardi, 2013)
High contrast is best
for text and background
Consider the science
HIT Mouse: Uninvolved Vessels, 20 Min. Post-KKO
Anti-CD41 (Platelets) Anti-C3b KKO
Complement staining appears to be specific and correlates with binding of platelets and KKO
AC III Ab NKCC Ab T4
NKCC co-localizes with ACIII on the ciliaCilia
Overlay
Consider psychology
Consider color blindness
Red/green blindness
is very common…
[Change red dots to red X’s]
31% Overly complex diagrams
NKCC1 and olfactory transduction (I)
Kaneko et al., 2004
Determination of [Cl]in in dendritic knobs using 2P-FLIM in rat OE
Nkcc1 Is Expressed in
Rat Olfactory Epithelium 150mM [Cl]ex50mM [Cl]ex
Cl uptake mechanism happens in the cilia
Changes of [Cl]in in dendritic knobs of mouse OE
CL uptake mechanism happens in cilia
Kaneko et al., 2004
150mM [Cl]ex50mM [Cl]ex
Include only what
you plan to talk about!
F OH E
L LO WT
Photos: Brandon Rossen Photography
MinimumEssential
Data
Only datato make
your point
Rememberyour papercontains all data
Your presentationis to generate interest and discussion
Let’s look at
an example
Skeletal Defects in PcG Mutants
Suzuki, et al. (2002) Development 129(18):4171-83
wildtype Mutant 1 Mutant 2 Mutant 3
Skeletal Defects in PcG Mutants
Suzuki, et al. (2002) Development 129(18):4171-83
wildtype Mutant 1 Mutant 2 Mutant 3
Consider the science
Prune and condense
Skeletal Defects in PcG Mutants
Suzuki, et al. (2002) Development 129(18):4171-83
wildtype Mutant 1 Mutant 2 Mutant 3
(Suzuki, et al. 2002)
Wildtype Mutant
Skeletal defects found in PcG mutants
(Suzuki, et al. 2002)
Wildtype Mutant
Skeletal defects found in PcG mutants
Additions needed for clarity
• Does the title make the main point?
• Where do I want the eyes to go?
Is silencing PcG important in mammals?
(Suzuki, et al. 2002)
Wildtype Mutant
Skeletal defects found in PcG mutants
main point per slide
1
Use “billboard” design
“Headline” titles and takeaways
Guide eyes to important stuff
Mix of image and text
[Mostly image and only some text]
High contrast color
[Blue writing on white background]
[Red as highlight color]
Sans-serif font
Assertion-evidence structure
Assertion in the form of a sentence headline title
(Alley et. al, 2007)
Visual
Evidence
Assertion-evidence structure
Arrest of protein translation suggested by fading Nissl staining
Assertion-evidence slides led to better recall and understanding of complex
ideas
42%59% (p < .01)
(Alley et. al, 2013)
Assertion-evidence audiencehad fewer major misconceptions
5% 48%
(Alley et. al, 2013)
Students that use assertion-evidence think and learn more deeply
(Aippersbach, Alley, & Garner, 2013)
Most people start with
visual evidence,
then add a title…
Results (1/4)
Unfortunately this type
of title is common, right?
Photo of mouse with helmet
…and this type is
even more common
Photo of mouse with helmet
But…descriptive titles don’t
communicate the meaning!
Never give up!
Instead, use the title
to make your point…
Helmets save lives???
…or your audience
may make the
wrong conclusion!
Express the “so what?”
(not the what)
Success =creativity + determination!
Start with a blank slate
What do you want the
audience to remember?
Let’s look at
an example
Assertion-evidence structure
Assertion-evidence structureStart with the “so what”
Next, choose the best
possible visual evidence
Let’s look at another
example
Sometimes you need to
discuss and explain
before you make an assertion
(Pavlov, 1927)
How do neutral stimuluscome to symbolize threats?
(Pavlov, 1927)
How do neutral stimuluscome to symbolize threats?
What is the question
that lead to your assertion?
(Pavlov, 1927)
How do neutral stimuluscome to symbolize threats?
Questions more closely
follow scientific process…
Observation, question,
then assertion
B A S I C
The quick brown fox...Verdana
The quick brown fox…ArialThe quick brown fox…Tahoma
The quick brown fox...Trebuchet
The quick brown fox…Times New Roman
The quick brown fox...Century GothicThe quick brown fox…Calibri
The quick brown fox…Comic Sans
The quick brown fox…Georgia
What is the best font for science?
The quick brown fox...Verdana
The quick brown fox…ArialThe quick brown fox…Tahoma
The quick brown fox...Trebuchet
The quick brown fox…Times New Roman
The quick brown fox...Century GothicThe quick brown fox…Calibri
The quick brown fox…Comic Sans
The quick brown fox…Georgia
What is the best font for science?
Lisa’s choice = Calibri
[Fits more text but still readable from distance]
94
DON’T USE ALL CAPITALS
[It makes it difficult to read!]
95
Don’t mix font types
What leads to motor neuron degeneration in SMARD1?
3 weeks 4 weeks
Fading Nissl staining suggests arrest of protein translation
Use sentence case
97
Use initial caps on bullets
98
• Use standard bullets
Observation/Hypothesis
Hypothesis: Inhibition of complement will attenuatethrombocytopenia and thrombosis, increase the benefitof direct thrombin inhibitors, and permit lower and safer doses to be used.
Observation: Platelets from patients with HIT carry increased C3, the third component of complement, and HIT plasma contains complement fixing anti-endothelial cell antibodies that induce expression of tissue factor (NEJM, 1987).Don’t repeat
HIT Mouse, Uninvolved Vessels, 20 Min. Post-KKO
Blue= Anti-CD41 (Platelets)Green= Anti-C3bRed= KKO
Layout is important
HIT Mouse: Uninvolved Vessels, 20 Min. Post-KKO
Anti-CD41 (Platelets) Anti-C3b KKO
Complement staining appears to be specific and correlates with binding of platelets and KKO
MinimumEssentialGraphs
(Principae, 2009)
Example of bad graphfrom Jean-Luc Dumount, Principae
(Principae, 2009)
Principae pruning process
• Data lines better contrasted• Non-data lines grey • Position labels near data• Relevant ticks marks only
(Principae, 2009)
Minimum essential graphby Jean-Luc Dumount, Principae
(Principiae, 2009)
Minimum essentials graphsby Jean-Luc Dumount
Let’s look at examples
from you!
Platelet activation in WB with KKO agonist
Control PF4 ADP 10ul TRAP 6 Convulxin PF4 + KKO
0
2000
4000
6000
8000
10000
12000
14000
16000P sel MFIAnnexin MFI
Control PF4 ADP 10ul TRAP 6 Convulxin PF4 + KKO0
20
40
60
80
100
120P sel % +
Ann % +
Before
What is the relative strength KKO in presence of PF4compared to other established platelet agonists?
0
2000
4000
6000
8000
10000
12000
14000
16000
Control PF4 ADP 10ul TRAP 6 Convulxin PF4 + KKO0
20
40
60
80
100
120
Mean fluorescence Percent Positivity
PF4/KKO second to Convulxin
P Sel P Sel %
Minimumessential
graphs require“builds”(sometimes)
Meet the PcG Complexes
PRC 2~600 kDa
RPD3
N55E(z)
Su(z)12
EscPcl
PRC 1~ 2MDa
PcPsc
Sce
zesteScm
Ph
Initiation Maintenance
Meet the PcG Complexes
PRC 2~600 kDa
RPD3
N55E(z)
Su(z)12
EscPcl
PRC 1~ 2MDa
PcPsc
Sce
zesteScm
Ph
Initiation Maintenance
Points speaker made:
• Each protein complex is made up of multiple distinct subunits
• All subunits are required • Silencing requires both complexes (this was the main point)
Meet the PcG Complexes
PRC 2~600 kDa
RPD3
N55E(z)
Su(z)12
EscPcl
PRC 1~ 2MDa
PcPsc
Sce
zesteScm
Ph
Initiation MaintenanceTitle does not convey
the main point
Meet the PcG Complexes
PRC 2~600 kDa
RPD3
N55E(z)
Su(z)12
EscPcl
PRC 1~ 2MDa
PcPsc
Sce
zesteScm
Ph
Initiation MaintenanceSome details not required
to make the main point
Meet the PcG Complexes
PRC 2~600 kDa
RPD3
N55E(z)
Su(z)12
EscPcl
PRC 1~ 2MDa
PcPsc
Sce
zesteScm
Ph
Initiation MaintenanceColor suggests a connection
where there isn’t one
Let’s look at the “re-do”
PcG complexes PRC1 and PRC2
Multiple distinct sub-units
PRC2PRC1
PcG complexes PRC1 and PRC2
PRC2PRC1
All sub-units are required – team effort
PcG complexes PRC1 and PRC2
All sub-units are required – team effort
PRC2PRC1
Both PcG complexes PRC1 and PRC 2 are required for silencing
PRC2PRC1
mTOR (kinase)eIF4E Active
4E-BP
P P P
4E-BP
Inactive 4E-BP
eIF4Esequestered
cap-dependent mRNAtranslation inhibited
Akt (kinase)40S
eIF4G
eIF4G
eIF4Ecap AAAAAAA
Rapamycin/hypoxia
cap-independent mRNA translationstimulated (e.g., VEGF, FGF, Bcl2, HIF1α)
cap-dependent mRNAtranslation
UAAAAAAAnCap
AUG
40S
growth factorsmitogenic signalshormones, cytokines
4EBP1 acts as a switch between cap-dependent and cap-independent mRNA translation
mTOR (kinase)eIF4E Active
4E-BP
P P P
4E-BP
Inactive 4E-BP
eIF4Esequestered
cap-dependent mRNAtranslation inhibited
Akt (kinase)40S
eIF4G
eIF4G
eIF4Ecap AAAAAAA
Rapamycin/hypoxia
cap-independent mRNA translationstimulated (e.g., VEGF, FGF, Bcl2, HIF1α)
cap-dependent mRNAtranslation
UAAAAAAAnCap
AUG
40S
growth factorsmitogenic signalshormones, cytokines
4EBP1 acts as a switch between cap-dependent and cap-independent mRNA translation
Most pathway slides
benefit from a build
mTOR (kinase)eIF4E Active
4E-BP
P P P
4E-BP
Inactive 4E-BP
Akt (kinase)40S
eIF4G
eIF4G
eIF4Ecap AAAAAAA
Rapamycin/hypoxia
growth factorsmitogenic signalshormones, cytokines
4EBP1 acts as a switch
cap-dependent mRNA translation
mTOR (kinase)eIF4E Active
4E-BP
P P P
4E-BP
Inactive 4E-BP
eIF4Esequestered
cap-dependent mRNA
translation inhibited
Akt (kinase)40S
eIF4G
eIF4G
eIF4Ecap AAAAAAA
Rapamycin/hypoxia
cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1α)
UAAAAAAAnCap
AUG
40S
growth factorsmitogenic signalshormones, cytokines
4EBP1 acts as a switch
mTOR (kinase)eIF4E Active
4E-BP
P P P
4E-BP
Inactive 4E-BP
eIF4Esequestered
cap-dependent mRNA translation inhibited
Akt (kinase)40S
eIF4G
eIF4G
eIF4Ecap AAAAAAA
Rapamycin/hypoxia
UAAAAAAAnCap
AUG
40S
growth factorsmitogenic signalshormones, cytokines
Cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1α)
Use builds when
describing a process
Aversive Olfactory learning
Session 1
Experimental Design
Olfactory Screening
Set Shock
Baseline
Anxiety STICSA
Specific anosmia
State–Trait Inventory for Cognitive and Somatic Anxiety(Ree et al., 2000)
Aversive Olfactory learning
Session 1
Experimental Design
Olfactory Screening
Set Shock
Baseline
Anxiety STICSA
Specific anosmia
State–Trait Inventory for Cognitive and Somatic Anxiety(Ree et al., 2000)
Process steps should be
horizontal if possible
State-Trait inventory for cognitive and somatic anxiety
Session1 Olfactory
ScreeningSet ShockBaseline
Anxiety STICSA
Specific anosmia
(Ree et al., 2000)
Visual analogous scale used to collect perceptual ratings
Session1 Olfactory
ScreeningSet ShockBaseline
Anxiety STICSA
Specific anosmia
Use expanded callouts to
highlight important details
Visual analogous scale used to collect perceptual ratings
Session1 Olfactory
ScreeningSet ShockBaseline
Anxiety STICSA
Specific anosmia
Don’t include verbal transitions
M O R ES L I D E
The title slide
All titles require
manual, natural breaks
Simple presentation title
(not paper title)
Presenter needs
to be obvious
Multi-scale dispersal patterns of Triatoma infestans
Corentin M. Barbu, Karthik Sethuraman, Jen Manne, Javier E. Quintanila Calderon, Michael Z. Levy
University of Pennsylvania – Universidad Peruana Cayetano-Heredia
Charles Marshall
The fear of smellingOdors and Anxiety
Charles Marshall
The fear of smellingOdors and Anxiety
Carefully consider use
of cartoons or photos
The fear of smelling
Odors and anxietyCharles MarshallMonell Chemical Senses Center
Outline
FEAR ANXIETY
real stimulus anticipation
Fear vs. Anxiety
signal of threat
The “hook” slide
[usually the first slide]
Has more impact
when the photo
is full screen
• Mortality 10-20%• Amputations 10%• New thromboembolic events 20-75%• Therapy reduces new events by 60%
does not reduce amputations or increase survival
HIT needs more therapeutic modalities
Firestein, 2001Choose simplistic diagrams
Lower motor neurons in the spinal cord and their motor units
Methods (only if novel)
Again use full screen photo
…with enlarged highlights
How we added enzymatic function to de novo proteins
1.Review analysis of the structure
2.How we created the active site by trimming side chain residues
3.How we stabilized our design by reengineering the turn
The “preview map” slide
(for longer talks)
Outline
1.Background: structure
2.Methods: active site
3.Results: our design
Not a generic outline
How we added enzymatic function to de novo proteins
1.Review analysis of the structure
2.How we created the active site by trimming side chain residues
3.How we stabilized our design by reengineering the turn
Notice the “headline” title
1.Review analysis of the structure
2.How we created the active site by trimming side chain residues
3.How we stabilized our design by reengineering the turn
How we added enzymatic function to de novo proteins
“Foundation figure” is used
How we added enzymatic function to de novo proteins
1.Review analysis of the structure
2.How we created the active site by trimming side chain residues
3.How we stabilized our design by reengineering the turn
Sections are numbered
How we added enzymatic function to de novo proteins
1.Review analysis of the structure
2.How we created the active site by trimming side chain residues
3.How we stabilized our design by reengineering the turn
Key words are highlighted
How we added enzymatic function to de novo proteins
1.Review analysis of the structure
2.How we created the active site by trimming side chain residues
3.How we stabilized our design by reengineering the turn
Aims can work as “map”
Disrupting vector-borne disease transmission in complex environments
1. To improve accuracy of maps of disease vectors based on imperfect and incomplete surveys
2. To improve vector advance through a divided landscape
3. To improve detection of emerging or re-emerging vector-borne disease transmission through sequential spatial sampling strategy
The acknowledgment slide
Use bullets (it’s a list)
Use professional photos only
Put funding on title slide
The conclusion slide
[This “before” slide was presented as a build]
• Automated, fast data analysis scheme• Improved diagnosis uses multiple
– Measurements– Subjects– Chromophores
• Pilot study of chemotherapy monitoring trending
Computer-aided detection in DOT
Computer-aided detection in DOT
• Automated, fast data analysis scheme• Improved diagnosis uses multiple
– Measurements– Subjects– Chromophores
• Pilot study of chemotherapy monitoring trending
• Therapy monitoring• Adding healthy subjects• DOT and other data
– DCS blood flow– MRI: T1 and Gd-Uptake
• Expand data set
Questions?
Equation slides
Equations: Labeled and visible
Review / preview slide
Results (2), Characteristics
CCEB
Variable CC (N=199)
Any T (N=118)
P-value
Age 58 (47-70)
60 (51-72)
0.23
Gender 67 (33.7%)
32 (27.1%)
0.22
BMI: <25, 25-30, >30
59 (29.8%) 54 (27.3%) 85 (42.9%)
37 (31.9%)45 (38.8%)34 (29.3%)
0.03
CYP2C9, any *2 or *3
29 (14.9%)
42 (35.6%)
<0.001
APOE, any E4 67 (34.2%)
35 (29.7%)
0.40
Vitamin K intake 44 (20-112)
35 (20-85)
0.49
Table slide
Results (2), Characteristics
CCEB
Variable CC (N=199)
Any T (N=118)
P-value
Age 58 (47-70)
60 (51-72)
0.23
Gender 67 (33.7%)
32 (27.1%)
0.22
BMI: <25, 25-30, >30
59 (29.8%) 54 (27.3%) 85 (42.9%)
37 (31.9%)45 (38.8%)34 (29.3%)
0.03
CYP2C9, any *2 or *3
29 (14.9%)
42 (35.6%)
<0.001
APOE, any E4 67 (34.2%)
35 (29.7%)
0.40
Vitamin K intake 44 (20-112)
35 (20-85)
0.49
Clarify and clearly annotate Which ?
Which?
What are these?
Results (2), Characteristics
CCEB
Variable CC (N=199)
Any T (N=118)
P-value
Age 58 (47-70)
60 (51-72)
0.23
Gender 67 (33.7%)
32 (27.1%)
0.22
BMI: <25, 25-30, >30
59 (29.8%) 54 (27.3%) 85 (42.9%)
37 (31.9%)45 (38.8%)34 (29.3%)
0.03
CYP2C9, any *2 or *3
29 (14.9%)
42 (35.6%)
<0.001
APOE, any E4 67 (34.2%)
35 (29.7%)
0.40
Vitamin K intake 44 (20-112)
35 (20-85)
0.49
Which data and
what precision is meaningful?
N values? Percentage of group?Precision of percentage?P-values?
Results (2), Characteristics
CCEB
Variable CC (N=199)
Any T (N=118)
P-value
Ag 58 (47-70)
60 (51-72)
0.23
Gender 67 (33.7%)
32 (27.1%)
0.22
BMI: <25, 25-30, >30
59 (29.8%) 54 (27.3%) 85 (42.9%)
37 (31.9%)45 (38.8%)34 (29.3%)
0.03
CYP2C9, any *2 or *3
29 (14.9%)
42 (35.6%)
<0.001
APOE, any E4 67 (34.2%)
35 (29.7%)
0.40
Vitamin K intake 44 (20-112)
35 (20-85)
0.49
Which results are relevant and
in what order will you present?
[Highlight and reorder if necessary]
Results (2), Characteristics
CCEB
Variable CC (N=199)
Any T (N=118)
P-value
Age 58 (47-70)
60 (51-72)
0.23
Gender 67 (33.7%)
32 (27.1%)
0.22
BMI: <25, 25-30, >30
59 (29.8%) 54 (27.3%) 85 (42.9%)
37 (31.9%)45 (38.8%)34 (29.3%)
0.03
CYP2C9, any *2 or *3
29 (14.9%)
42 (35.6%)
<0.001
APOE, any E4 67 (34.2%)
35 (29.7%)
0.40
Vitamin K intake 44 (20-112)
35 (20-85)
0.49
Before (again)
T-allele carriers have increased risk of CYP2C9 *2 or *3 & decreased risk of elevated BMI
T allele carriers (N=118)
Non T-allele carriers (N=199)
p value
Avg. Age (years) 60 58
% Male 27% 34%% CYP2C9 *2 or *3 36% 15% <0.001
% BMI >30 29% 43% 0.03
% APOE4 30% 34%
Avg. Vit.K intake 35 44
MinimumEssential
Data
BillboardDesign
…from Mediocre
F OH E
L LO WT
…to memorable
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