2014 01 science slide design ss version

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

Interest

HighHigh

You’re just settling in…

Interest

HighHigh

“Oh, the presentation started!”

Then the mind vacations begin…

Interest

HighHigh

“Oh, that reminds me …”

The speaker continues with bad delivery,

unclear organization, and poorly designed slides…

…the trifecta of horrible presentations!

Interest

HighHigh

…and the speaker drones onand on, and on,and on, and on, and on,and on, and on, and on,and on,

and on…

Interest

HighHigh

Interest

HighHigh

…until the two magic words

Interest

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).

Two line phrases at most

51% Text too small to read

(Pardi, 2013)

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

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

Consider the science

Prune and condense

(Suzuki, et al. 2002)

Wildtype Mutant

Skeletal defects found in PcG mutants

Wildtype Mutant

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?

Wildtype Mutant

main point per slide

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

Arrest of protein translation suggested by fading Nissl staining

Assertion-evidence slides led to better recall and understanding of complex

42%59% (p < .01)

Assertion-evidence audiencehad fewer major misconceptions

5% 48%

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 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)

What is the question

that lead to your assertion?

(Pavlov, 1927)

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]

DON’T USE ALL CAPITALS

[It makes it difficult to read!]

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

Use initial caps on bullets

• Use standard bullets

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

16000P sel MFIAnnexin MFI

Control PF4 ADP 10ul TRAP 6 Convulxin PF4 + KKO0

120P sel % +

Ann % +

Before

What is the relative strength KKO in presence of PF4compared to other established platelet agonists?

Control PF4 ADP 10ul TRAP 6 Convulxin PF4 + KKO0

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

N55E(z)

Su(z)12

EscPcl

PRC 1~ 2MDa

zesteScm

Initiation Maintenance

PRC 2~600 kDa

N55E(z)

Su(z)12

EscPcl

PRC 1~ 2MDa

zesteScm

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)

PRC 2~600 kDa

N55E(z)

Su(z)12

EscPcl

PRC 1~ 2MDa

zesteScm

Initiation MaintenanceTitle does not convey

the main point

PRC 2~600 kDa

N55E(z)

Su(z)12

EscPcl

PRC 1~ 2MDa

zesteScm

Initiation MaintenanceSome details not required

to make the main point

PRC 2~600 kDa

N55E(z)

Su(z)12

EscPcl

PRC 1~ 2MDa

zesteScm

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

All sub-units are required – team effort

PRC2PRC1

Both PcG complexes PRC1 and PRC 2 are required for silencing

PRC2PRC1

mTOR (kinase)eIF4E Active

Inactive 4E-BP

eIF4Esequestered

cap-dependent mRNAtranslation inhibited

Akt (kinase)40S

eIF4Ecap AAAAAAA

Rapamycin/hypoxia

cap-independent mRNA translationstimulated (e.g., VEGF, FGF, Bcl2, HIF1α)

cap-dependent mRNAtranslation

UAAAAAAAnCap

growth factorsmitogenic signalshormones, cytokines

4EBP1 acts as a switch between cap-dependent and cap-independent mRNA translation

Inactive 4E-BP

eIF4Esequestered

cap-dependent mRNAtranslation inhibited

Akt (kinase)40S

eIF4Ecap AAAAAAA

Rapamycin/hypoxia

cap-independent mRNA translationstimulated (e.g., VEGF, FGF, Bcl2, HIF1α)

cap-dependent mRNAtranslation

UAAAAAAAnCap

4EBP1 acts as a switch between cap-dependent and cap-independent mRNA translation

Most pathway slides

benefit from a build

Inactive 4E-BP

Akt (kinase)40S

eIF4Ecap AAAAAAA

Rapamycin/hypoxia

4EBP1 acts as a switch

cap-dependent mRNA translation

Inactive 4E-BP

eIF4Esequestered

cap-dependent mRNA

translation inhibited

Akt (kinase)40S

eIF4Ecap AAAAAAA

Rapamycin/hypoxia

cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1α)

UAAAAAAAnCap

4EBP1 acts as a switch

Inactive 4E-BP

eIF4Esequestered

cap-dependent mRNA translation inhibited

Akt (kinase)40S

eIF4Ecap AAAAAAA

Rapamycin/hypoxia

UAAAAAAAnCap

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

Anxiety STICSA

Specific anosmia

Use expanded callouts to

highlight important details

Visual analogous scale used to collect perceptual ratings

Session1 Olfactory

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

Notice the “headline” title

“Foundation figure” is used

Sections are numbered

Key words are highlighted

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

drbusch@physics.upenn.edu

Computer-aided detection in DOT

• Automated, fast data analysis scheme• Improved diagnosis uses multiple

– Measurements– Subjects– Chromophores

• Pilot study of chemotherapy monitoring trending

drbusch@physics.upenn.edu

• 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

Variable CC (N=199)

Any T (N=118)

P-value

Age 58 (47-70)

60 (51-72)

Gender 67 (33.7%)

32 (27.1%)

BMI: <25, 25-30, >30

59 (29.8%) 54 (27.3%) 85 (42.9%)

37 (31.9%)45 (38.8%)34 (29.3%)

CYP2C9, any *2 or *3

29 (14.9%)

42 (35.6%)

<0.001

APOE, any E4 67 (34.2%)

35 (29.7%)

Vitamin K intake 44 (20-112)

35 (20-85)

Table slide

Variable CC (N=199)

Any T (N=118)

P-value

Age 58 (47-70)

60 (51-72)

Gender 67 (33.7%)

32 (27.1%)

BMI: <25, 25-30, >30

59 (29.8%) 54 (27.3%) 85 (42.9%)

37 (31.9%)45 (38.8%)34 (29.3%)

29 (14.9%)

42 (35.6%)

<0.001

APOE, any E4 67 (34.2%)

35 (29.7%)

35 (20-85)

Clarify and clearly annotate Which ?

Which?

What are these?

Variable CC (N=199)

Any T (N=118)

P-value

Age 58 (47-70)

60 (51-72)

Gender 67 (33.7%)

32 (27.1%)

BMI: <25, 25-30, >30

59 (29.8%) 54 (27.3%) 85 (42.9%)

37 (31.9%)45 (38.8%)34 (29.3%)

29 (14.9%)

42 (35.6%)

<0.001

APOE, any E4 67 (34.2%)

35 (29.7%)

35 (20-85)

Which data and

what precision is meaningful?

N values? Percentage of group?Precision of percentage?P-values?

Variable CC (N=199)

Any T (N=118)

P-value

Ag 58 (47-70)

60 (51-72)

Gender 67 (33.7%)

32 (27.1%)

BMI: <25, 25-30, >30

59 (29.8%) 54 (27.3%) 85 (42.9%)

37 (31.9%)45 (38.8%)34 (29.3%)

29 (14.9%)

42 (35.6%)

<0.001

APOE, any E4 67 (34.2%)

35 (29.7%)

35 (20-85)

Which results are relevant and

in what order will you present?

[Highlight and reorder if necessary]

Variable CC (N=199)

Any T (N=118)

P-value

Age 58 (47-70)

60 (51-72)

Gender 67 (33.7%)

32 (27.1%)

BMI: <25, 25-30, >30

59 (29.8%) 54 (27.3%) 85 (42.9%)

37 (31.9%)45 (38.8%)34 (29.3%)

29 (14.9%)

42 (35.6%)

<0.001

APOE, any E4 67 (34.2%)

35 (29.7%)

35 (20-85)

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

BillboardDesign

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F OH E

L LO WT

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2014 01 science slide design ss version

chemotherapy

borne disease

story telling

hiperphosforelated

subsequently

added enzymatic

arousing physical

de novo proteins

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