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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?
You’re just settling in…
High

Interest

Low

The speaker is being introduced

Time
High

“Oh, the presentation started!”
Interest

Low

Time
Then the mind vacations begin…
High

Interest

“Oh, that reminds me …”
Low

Time
The speaker continues
with bad delivery,
unclear organization, and
poorly designed slides…
…the trifecta of horrible presentations!
High

Interest

Low

Sleep

Time
…and the speaker drones on

and on,
and on,
and on,
and on,
and on,
and on,
and on,
and on,
and on,
and on…
High

Interest

Low

Time

Coma
…until the two magic words
High

Interest

Low

Time

Coma
High

Interest

“In conclusion…”

Low

Time
Unfortunately
this isn’t far
from the truth!
Top 5 presentation annoyances

Top 5
Annoyances
(Pardi, 2013)
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 incomplete
benefit and is associated with major bleeding that approximates
1% 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

Yes, this is a REAL slide
from someone
here at Penn!

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 incomplete
benefit and is associated with major bleeding that approximates
1% per day.
Look! Speak don’t read!
Pathogenesis of HIT
(Heparin-induced thrombocytopenia)
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
48%
Full sentences

(Pardi, 2013)
Observation/Hypothesis
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 complement will attenuate
thrombocytopenia and thrombosis, increase the benefit
of direct thrombin inhibitors, and permit lower and
safer doses to be used.
Observation/Hypothesis
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 complement will attenuate
thrombocytopenia and thrombosis, increase the benefit
of direct thrombin inhibitors, and permit lower and
safer doses to be used.
51%
Text too small to read

(Pardi, 2013)
Observation/Hypothesis

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 complement will attenuate
thrombocytopenia and thrombosis, increase the benefit
of direct thrombin inhibitors, and permit lower and
safer doses to be used.
Hypothesis:
Inhibition of C3 complement
will attenuate
thrombocytopenia and thrombosis
26%
Poor color choices

(Pardi, 2013)
Complement staining appears to be specific and
correlates with binding of platelets and KKO

Anti-CD41 (Platelets)

Anti-C3b

KKO

HIT Mouse: Uninvolved Vessels, 20 Min. Post-KKO
NKCC co-localizes with ACIII on the cilia
AC III Ab

Cilia

Overlay

NKCC Ab T4
31%
Overly complex diagrams
NKCC1 and olfactory transduction (I)

Nkcc1 Is Expressed in
50mM [Cl]ex

150mM [Cl]ex

Rat Olfactory Epithelium

Determination of [Cl]in in dendritic knobs
using 2P-FLIM in rat OE
Changes of [Cl]in in dendritic knobs of mouse OE

Cl uptake mechanism happens in the cilia

Kaneko et al., 2004
CL uptake mechanism happens in cilia

50mM [Cl]ex

150mM [Cl]ex

Kaneko et al., 2004
O

O
Photos: Brandon Rossen Photography
Minimum
Essential
Data
Only data
to make
your point
Remember
your paper
contains
all data
Your
presentation
is to generate
interest and
discussion
Let’s look
at
an example
Skeletal Defects in PcG Mutants
wildtype

Mutant 1

Suzuki, et al. (2002) Development 129(18):4171-83

Mutant 2

Mutant 3
Skeletal Defects in PcG Mutants
wildtype

Mutant 1

Suzuki, et al. (2002) Development 129(18):4171-83

Mutant 2

Mutant 3
Skeletal Defects in PcG Mutants
wildtype

Mutant 1

Suzuki, et al. (2002) Development 129(18):4171-83

Mutant 2

Mutant 3
Skeletal defects found in PcG mutants
Wildtype

(Suzuki, et al. 2002)

Mutant
Skeletal defects found in PcG mutants
Wildtype

(Suzuki, et al. 2002)

Mutant
Is silencing PcG important in mammals?
Wildtype

Mutant

Skeletal defects found in PcG mutants
(Suzuki, et al. 2002)
1

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
(Alley et. al, 2007)
Assertion-evidence structure
Assertion-evidence slides led to better
recall and understanding of complex
ideas

59%
(Alley et. al, 2013)

(p < .01)

42%
Assertion-evidence audience
had fewer major misconceptions
5%

(Alley et. al, 2013)

48%
Students that use assertion-evidence
think and learn more deeply

(Aippersbach, Alley, & Garner, 2013)
Results (1/4)
Photo of mouse with helmet
Photo of mouse with helmet
Never give up!
Helmets save lives???
Success =
creativity + determination!
Let’s look
at
an example
Assertion-evidence structure
Assertion-evidence structure
Let’s look
at another
example
How do neutral stimulus
come to symbolize threats?

(Pavlov, 1927)
How do neutral stimulus
come to symbolize threats?

(Pavlov, 1927)
How do neutral stimulus
come to symbolize threats?

(Pavlov, 1927)
A
What is the best font for science?
The quick brown fox…Georgia
The quick brown fox…Times New Roman
The quick brown fox...Verdana
The quick brown fox…Tahoma
The quick brown fox…Arial
The quick brown fox...Trebuchet

The quick brown fox…Calibri

The quick brown fox...Century Gothic
The quick brown fox…Comic Sans
What is the best font for science?
The quick brown fox…Georgia
The quick brown fox…Times New Roman
The quick brown fox...Verdana
The quick brown fox…Tahoma
The quick brown fox…Arial
The quick brown fox...Trebuchet

The quick brown fox…Calibri

The quick brown fox...Century Gothic
The quick brown fox…Comic Sans
94
95
What leads to motor neuron degeneration
in SMARD1?
3 weeks

4 weeks

Fading Nissl staining suggests
arrest of protein translation
97
98
Observation/Hypothesis
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 complement will attenuate
thrombocytopenia and thrombosis, increase the benefit
of direct thrombin inhibitors, and permit lower and
safer doses to be used.
HIT
Mouse, Uni
nvolved
Vessels, 20
Min. PostKKO

Blue= Anti-CD41 (Platelets)
Green= Anti-C3b
Red= KKO
Complement staining appears to be specific and
correlates with binding of platelets and KKO

Anti-CD41 (Platelets)

Anti-C3b

KKO

HIT Mouse: Uninvolved Vessels, 20 Min. Post-KKO
Minimum
Essential
Graphs
Example of bad graph
from 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 graph
by Jean-Luc Dumount, Principae

(Principae, 2009)
Minimum essentials graphs
by Jean-Luc Dumount

(Principiae, 2009)
Let’s look
at examples
from you!
Platelet activation in WB with KKO agonist
16000

P sel MFI

120

P sel % +
Ann % +

Annexin MFI

14000

100
12000
80

10000
8000

60

6000
40
4000
20

2000
0

0
Control

PF4

ADP 10ul

TRAP 6 Convulxin PF4 + KKO

Control

PF4

ADP 10ul

TRAP 6

Convulxin PF4 + KKO
What is the relative strength KKO in presence of PF4
compared to other established platelet agonists?
Mean fluorescence

Percent Positivity

16000
120

14000
12000

P Sel

100

P Sel %

10000
80
8000

6000
4000

60
40

2000
0

20
0
Control

PF4

ADP 10ul

TRAP 6

PF4/KKO second to Convulxin

Convulxin PF4 + KKO
Minimum
essential
graphs require
“builds”
(sometimes)
Meet the PcG Complexes
PRC 2
~600 kDa

RPD3

E(z)

Pcl

PRC 1
~ 2MDa
Su(z)12

N55

Pc

Ph
Psc

zeste
Scm

Esc

Sce

Initiation

Maintenance
Meet the PcG Complexes
PRC 2
~600 kDa

Points speaker made:

PRC 1
~ 2MDa

RPD3
•

Su(z)12
Each protein complex is made up
E(z)
Pc
Ph
N55
Psc
of multiple distinct subunits
zeste
• All subunits are required
Pcl
Scm
Esc
• Silencing requires both Sce
complexes
(this was the main point)

Initiation

Maintenance
Meet the PcG Complexes
PRC 2
~600 kDa

RPD3

E(z)

Pcl

PRC 1
~ 2MDa
Su(z)12

N55

Pc

Ph
Psc

zeste
Scm

Esc

Sce

Initiation

Maintenance
Meet the PcG Complexes
PRC 2
~600 kDa

RPD3

E(z)

Pcl

PRC 1
~ 2MDa
Su(z)12

N55

Pc

Ph
Psc

zeste
Scm

Esc

Sce

Initiation

Maintenance
Meet the PcG Complexes
PRC 2
~600 kDa

RPD3

E(z)

Pcl

PRC 1
~ 2MDa
Su(z)12

N55

Pc

Ph
Psc

zeste
Scm

Esc

Sce

Initiation

Maintenance
Let’s look
at the
“re-do”
PcG complexes PRC1 and PRC2
PRC1

PRC2

Multiple distinct sub-units
PcG complexes PRC1 and PRC2
PRC1

PRC2

All sub-units are required – team effort
PcG complexes PRC1 and PRC2
PRC1

PRC2

All sub-units are required – team effort
Both PcG complexes PRC1 and PRC 2
are required for silencing
PRC1

PRC2
4EBP1 acts as a switch between cap-dependent and capindependent mRNA translation
eIF4G

eIF4E
cap

growth factors
mitogenic signals
hormones, cytokines

AAAAAAA

eIF4G
40S

Akt (kinase)
mTOR (kinase)
eIF4E

Active
4E-BP

Rapamycin/hypoxia

4E-BP
eIF4E
sequestered

cap-dependent mRNA
translation

P
P Inactive 4E-BP
P

cap-dependent mRNA
translation inhibited
40S

Cap

AUG

UAA

AAAAAn

cap-independent mRNA translation
stimulated (e.g., VEGF, FGF, Bcl2, HIF1)
4EBP1 acts as a switch between cap-dependent and capindependent mRNA translation
eIF4G

eIF4E
cap

growth factors
mitogenic signals
hormones, cytokines

AAAAAAA

eIF4G
40S

Akt (kinase)
mTOR (kinase)
eIF4E

Active
4E-BP

Rapamycin/hypoxia

4E-BP
eIF4E
sequestered

cap-dependent mRNA
translation

P
P Inactive 4E-BP
P

cap-dependent mRNA
translation inhibited
40S

Cap

AUG

UAA

AAAAAn

cap-independent mRNA translation
stimulated (e.g., VEGF, FGF, Bcl2, HIF1)
4EBP1 acts as a switch
eIF4G

eIF4E
cap

growth factors
mitogenic signals
hormones, cytokines

AAAAAAA

eIF4G

40S

Akt (kinase)
mTOR (kinase)
eIF4E

Active
4E-BP

Rapamycin/hypoxia

4E-BP

P
P
P
Inactive 4E-BP

cap-dependent mRNA translation
4EBP1 acts as a switch
eIF4G

eIF4E
cap

growth factors
mitogenic signals
hormones, cytokines

AAAAAAA

eIF4G

40S

Akt (kinase)
mTOR (kinase)
eIF4E

Active
4E-BP

Rapamycin/hypoxia

4E-BP

eIF4E
sequestered

cap-dependent mRNA
translation inhibited

P
P
P
Inactive 4E-BP

40S

Cap

AUG

UAA

AAAAAn

cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1)
Cap-independent mRNA translation
stimulated (e.g., VEGF, FGF, Bcl2, HIF1α)
eIF4G

eIF4E
cap

growth factors
mitogenic signals
hormones, cytokines

AAAAAAA

eIF4G

40S

Akt (kinase)
mTOR (kinase)
Active
4E-BP

eIF4E

Rapamycin/hypoxia

4E-BP

eIF4E
sequestered

P
P
P
Inactive 4E-BP

cap-dependent mRNA
translation inhibited
40S

Cap

AUG

UAA

AAAAAn
Experimental Design
Aversive Olfactory learning
Session 1
Olfactory
Screening

Specific
anosmia

Anxiety
STICSA

Baseline

Set Shock

State–Trait Inventory for Cognitive and Somatic Anxiety
(Ree et al., 2000)
Experimental Design
Aversive Olfactory learning
Session 1
Olfactory
Screening

Specific
anosmia

Anxiety
STICSA

Baseline

Set Shock

State–Trait Inventory for Cognitive and Somatic Anxiety
(Ree et al., 2000)
State-Trait inventory for
cognitive and somatic anxiety
Session1

Olfactory
Screening

(Ree et al., 2000)

Specific
anosmia

Anxiety
STICSA

Baseline

Set Shock
Visual analogous scale used
to collect perceptual ratings
Session1

Olfactory
Screening

Specific
anosmia

Anxiety
STICSA

Baseline

Set Shock
Visual analogous scale used
to collect perceptual ratings
Session1

Olfactory
Screening

Specific
anosmia

Anxiety
STICSA

Baseline

Set Shock
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
The fear of smelling
Odors and Anxiety

Charles Marshall
The fear of smelling
Odors and Anxiety

Charles Marshall
The fear of smelling
Odors and anxiety

Charles Marshall
Monell Chemical Senses Center
Fear vs. Anxiety
Outline
FEAR
real stimulus

ANXIETY
anticipation

signal of
threat
HIT needs more therapeutic modalities
•
•
•
•

Mortality 10-20%
Amputations 10%
New thromboembolic events 20-75%
Therapy reduces new events by 60%
does not reduce amputations
or increase survival
Firestein, 2001
Lower motor neurons in the spinal cord
and their motor units
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
Outline
1. Background: structure
2. Methods: active site
3. Results: our design
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
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
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
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
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
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
Computer-aided detection in DOT
drbusch@physics.upenn.edu

• Automated, fast data analysis scheme
• Improved diagnosis uses multiple
– Measurements
– Subjects
– Chromophores

• Pilot study of chemotherapy monitoring trending
Computer-aided detection in DOT
drbusch@physics.upenn.edu

• 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?
Results (2), Characteristics
Variable

CC
(N=199)
Age
58 (47-70)
Gender
67 (33.7%)
BMI: <25,
59 (29.8%)
25-30,
54 (27.3%)
>30
85 (42.9%)
CYP2C9, any *2 or *3 29 (14.9%)
APOE, any E4
67 (34.2%)
Vitamin K intake
44 (20-112)

Any T
(N=118)
60 (51-72)
32 (27.1%)
37 (31.9%)
45 (38.8%)
34 (29.3%)
42 (35.6%)
35 (29.7%)
35 (20-85)

P-value
0.23
0.22
0.03
<0.001
0.40
0.49
CCEB
Which? Results
Variable

(2), Characteristics

CC
What are these? (N=199)
Age
58 (47-70)
Gender Which ?
67 (33.7%)
BMI: <25,
59 (29.8%)
25-30,
54 (27.3%)
>30
85 (42.9%)
CYP2C9, any *2 or *3 29 (14.9%)
APOE, any E4
67 (34.2%)
Vitamin K intake
44 (20-112)

Any T
(N=118)
60 (51-72)
32 (27.1%)
37 (31.9%)
45 (38.8%)
34 (29.3%)
42 (35.6%)
35 (29.7%)
35 (20-85)

P-value
0.23
0.22
0.03
<0.001
0.40
0.49
CCEB
Results (2), Characteristics
Variable

CC
Any T
P-value
(N=199)
(N=118)
Age
58 (47-70) 60 (51-72) 0.23
Gender
67 (33.7%) 32 (27.1%) 0.22
N values?
BMI: <25,
59 (29.8%) 37 (31.9%) 0.03
Percentage45 (38.8%)
of group?
25-30,
54 (27.3%)
Precision of percentage?
>30
85 (42.9%) 34 (29.3%)
CYP2C9, any *2 or *3 P-values? 42 (35.6%) <0.001
29 (14.9%)
APOE, any E4
67 (34.2%) 35 (29.7%) 0.40
Vitamin K intake
44 (20-112) 35 (20-85) 0.49
CCEB
Results (2), Characteristics
Variable

CC
(N=199)
Ag
58 (47-70)
Gender
67 (33.7%)
BMI: <25,
59 (29.8%)
25-30,
54 (27.3%)
>30
85 (42.9%)
CYP2C9, any *2 or *3 29 (14.9%)
APOE, any E4
67 (34.2%)
Vitamin K intake
44 (20-112)

Any T
(N=118)
60 (51-72)
32 (27.1%)
37 (31.9%)
45 (38.8%)
34 (29.3%)
42 (35.6%)
35 (29.7%)
35 (20-85)

P-value
0.23
0.22
0.03
<0.001
0.40
0.49
CCEB
Results (2), Characteristics
Variable

CC
(N=199)
Age
58 (47-70)
Gender
67 (33.7%)
BMI: <25,
59 (29.8%)
25-30,
54 (27.3%)
>30
85 (42.9%)
CYP2C9, any *2 or *3 29 (14.9%)
APOE, any E4
67 (34.2%)
Vitamin K intake
44 (20-112)

Any T
(N=118)
60 (51-72)
32 (27.1%)
37 (31.9%)
45 (38.8%)
34 (29.3%)
42 (35.6%)
35 (29.7%)
35 (20-85)

P-value
0.23
0.22
0.03
<0.001
0.40
0.49
CCEB
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)

Avg. Age (years)

60

58

% Male
% CYP2C9 *2 or *3

27%
36%

34%
15%

<0.001

% BMI >30

29%

43%

0.03

% APOE4
Avg. Vit.K intake

30%
35

34%
44

p value
Minimum
Essential
Data
Billboard
Design
…from Mediocre
O

O
…to memorable
www.lisabmarshall.com

www.morefromlisa.com

Featured on:
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to deliver a full seminar
for your organization.
Contact us for details.
Programs for science /engineering:

Art of Speaking Science 1
Art of Speaking Science 2
Designing Science Slides
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2014 01 science slide design ss version

  • 2. 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)
  • 3. Do you know what happens to your attention during a presentation?
  • 4. You’re just settling in… High Interest Low The speaker is being introduced Time
  • 5. High “Oh, the presentation started!” Interest Low Time
  • 6. Then the mind vacations begin…
  • 8. The speaker continues with bad delivery, unclear organization, and poorly designed slides… …the trifecta of horrible presentations!
  • 10. …and the speaker drones on and on, and on, and on, and on, and on, and on, and on, and on, and on, and on…
  • 12. …until the two magic words High Interest Low Time Coma
  • 15. Top 5 presentation annoyances Top 5 Annoyances (Pardi, 2013)
  • 17. The Redundancy Principle: Redundant material interferes with learning (Hoffman, 2006)
  • 18. 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 incomplete benefit and is associated with major bleeding that approximates 1% per day.
  • 19. 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 Yes, this is a REAL slide from someone here at Penn! 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 incomplete benefit and is associated with major bleeding that approximates 1% per day.
  • 22. 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
  • 24. Observation/Hypothesis 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 complement will attenuate thrombocytopenia and thrombosis, increase the benefit of direct thrombin inhibitors, and permit lower and safer doses to be used.
  • 25. Observation/Hypothesis 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 complement will attenuate thrombocytopenia and thrombosis, increase the benefit of direct thrombin inhibitors, and permit lower and safer doses to be used.
  • 26. 51% Text too small to read (Pardi, 2013)
  • 27. Observation/Hypothesis 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 complement will attenuate thrombocytopenia and thrombosis, increase the benefit of direct thrombin inhibitors, and permit lower and safer doses to be used.
  • 28. Hypothesis: Inhibition of C3 complement will attenuate thrombocytopenia and thrombosis
  • 30.
  • 31.
  • 32.
  • 33. Complement staining appears to be specific and correlates with binding of platelets and KKO Anti-CD41 (Platelets) Anti-C3b KKO HIT Mouse: Uninvolved Vessels, 20 Min. Post-KKO
  • 34. NKCC co-localizes with ACIII on the cilia AC III Ab Cilia Overlay NKCC Ab T4
  • 35.
  • 36.
  • 37.
  • 39. NKCC1 and olfactory transduction (I) Nkcc1 Is Expressed in 50mM [Cl]ex 150mM [Cl]ex Rat Olfactory Epithelium Determination of [Cl]in in dendritic knobs using 2P-FLIM in rat OE Changes of [Cl]in in dendritic knobs of mouse OE Cl uptake mechanism happens in the cilia Kaneko et al., 2004
  • 40. CL uptake mechanism happens in cilia 50mM [Cl]ex 150mM [Cl]ex Kaneko et al., 2004
  • 41. O O
  • 42. Photos: Brandon Rossen Photography
  • 48. Skeletal Defects in PcG Mutants wildtype Mutant 1 Suzuki, et al. (2002) Development 129(18):4171-83 Mutant 2 Mutant 3
  • 49. Skeletal Defects in PcG Mutants wildtype Mutant 1 Suzuki, et al. (2002) Development 129(18):4171-83 Mutant 2 Mutant 3
  • 50. Skeletal Defects in PcG Mutants wildtype Mutant 1 Suzuki, et al. (2002) Development 129(18):4171-83 Mutant 2 Mutant 3
  • 51. Skeletal defects found in PcG mutants Wildtype (Suzuki, et al. 2002) Mutant
  • 52. Skeletal defects found in PcG mutants Wildtype (Suzuki, et al. 2002) Mutant
  • 53. Is silencing PcG important in mammals? Wildtype Mutant Skeletal defects found in PcG mutants (Suzuki, et al. 2002)
  • 57. Guide eyes to important stuff
  • 58. Mix of image and text
  • 59. [Mostly image and only some text]
  • 61. [Blue writing on white background]
  • 66. Assertion-evidence slides led to better recall and understanding of complex ideas 59% (Alley et. al, 2013) (p < .01) 42%
  • 67. Assertion-evidence audience had fewer major misconceptions 5% (Alley et. al, 2013) 48%
  • 68. Students that use assertion-evidence think and learn more deeply (Aippersbach, Alley, & Garner, 2013)
  • 69.
  • 71. Photo of mouse with helmet
  • 72. Photo of mouse with helmet
  • 75. Success = creativity + determination!
  • 76.
  • 77.
  • 81.
  • 82.
  • 83.
  • 85.
  • 86.
  • 87. How do neutral stimulus come to symbolize threats? (Pavlov, 1927)
  • 88. How do neutral stimulus come to symbolize threats? (Pavlov, 1927)
  • 89. How do neutral stimulus come to symbolize threats? (Pavlov, 1927)
  • 90.
  • 91. A
  • 92. What is the best font for science? The quick brown fox…Georgia The quick brown fox…Times New Roman The quick brown fox...Verdana The quick brown fox…Tahoma The quick brown fox…Arial The quick brown fox...Trebuchet The quick brown fox…Calibri The quick brown fox...Century Gothic The quick brown fox…Comic Sans
  • 93. What is the best font for science? The quick brown fox…Georgia The quick brown fox…Times New Roman The quick brown fox...Verdana The quick brown fox…Tahoma The quick brown fox…Arial The quick brown fox...Trebuchet The quick brown fox…Calibri The quick brown fox...Century Gothic The quick brown fox…Comic Sans
  • 94. 94
  • 95. 95
  • 96. What leads to motor neuron degeneration in SMARD1? 3 weeks 4 weeks Fading Nissl staining suggests arrest of protein translation
  • 97. 97
  • 98. 98
  • 99. Observation/Hypothesis 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 complement will attenuate thrombocytopenia and thrombosis, increase the benefit of direct thrombin inhibitors, and permit lower and safer doses to be used.
  • 100. HIT Mouse, Uni nvolved Vessels, 20 Min. PostKKO Blue= Anti-CD41 (Platelets) Green= Anti-C3b Red= KKO
  • 101. Complement staining appears to be specific and correlates with binding of platelets and KKO Anti-CD41 (Platelets) Anti-C3b KKO HIT Mouse: Uninvolved Vessels, 20 Min. Post-KKO
  • 103. Example of bad graph from Jean-Luc Dumount, Principae (Principae, 2009)
  • 104. Principae pruning process • Data lines better contrasted • Non-data lines grey • Position labels near data • Relevant ticks marks only (Principae, 2009)
  • 105. Minimum essential graph by Jean-Luc Dumount, Principae (Principae, 2009)
  • 106. Minimum essentials graphs by Jean-Luc Dumount (Principiae, 2009)
  • 108. Platelet activation in WB with KKO agonist 16000 P sel MFI 120 P sel % + Ann % + Annexin MFI 14000 100 12000 80 10000 8000 60 6000 40 4000 20 2000 0 0 Control PF4 ADP 10ul TRAP 6 Convulxin PF4 + KKO Control PF4 ADP 10ul TRAP 6 Convulxin PF4 + KKO
  • 109. What is the relative strength KKO in presence of PF4 compared to other established platelet agonists? Mean fluorescence Percent Positivity 16000 120 14000 12000 P Sel 100 P Sel % 10000 80 8000 6000 4000 60 40 2000 0 20 0 Control PF4 ADP 10ul TRAP 6 PF4/KKO second to Convulxin Convulxin PF4 + KKO
  • 111. Meet the PcG Complexes PRC 2 ~600 kDa RPD3 E(z) Pcl PRC 1 ~ 2MDa Su(z)12 N55 Pc Ph Psc zeste Scm Esc Sce Initiation Maintenance
  • 112. Meet the PcG Complexes PRC 2 ~600 kDa Points speaker made: PRC 1 ~ 2MDa RPD3 • Su(z)12 Each protein complex is made up E(z) Pc Ph N55 Psc of multiple distinct subunits zeste • All subunits are required Pcl Scm Esc • Silencing requires both Sce complexes (this was the main point) Initiation Maintenance
  • 113. Meet the PcG Complexes PRC 2 ~600 kDa RPD3 E(z) Pcl PRC 1 ~ 2MDa Su(z)12 N55 Pc Ph Psc zeste Scm Esc Sce Initiation Maintenance
  • 114. Meet the PcG Complexes PRC 2 ~600 kDa RPD3 E(z) Pcl PRC 1 ~ 2MDa Su(z)12 N55 Pc Ph Psc zeste Scm Esc Sce Initiation Maintenance
  • 115. Meet the PcG Complexes PRC 2 ~600 kDa RPD3 E(z) Pcl PRC 1 ~ 2MDa Su(z)12 N55 Pc Ph Psc zeste Scm Esc Sce Initiation Maintenance
  • 117. PcG complexes PRC1 and PRC2 PRC1 PRC2 Multiple distinct sub-units
  • 118. PcG complexes PRC1 and PRC2 PRC1 PRC2 All sub-units are required – team effort
  • 119. PcG complexes PRC1 and PRC2 PRC1 PRC2 All sub-units are required – team effort
  • 120. Both PcG complexes PRC1 and PRC 2 are required for silencing PRC1 PRC2
  • 121. 4EBP1 acts as a switch between cap-dependent and capindependent mRNA translation eIF4G eIF4E cap growth factors mitogenic signals hormones, cytokines AAAAAAA eIF4G 40S Akt (kinase) mTOR (kinase) eIF4E Active 4E-BP Rapamycin/hypoxia 4E-BP eIF4E sequestered cap-dependent mRNA translation P P Inactive 4E-BP P cap-dependent mRNA translation inhibited 40S Cap AUG UAA AAAAAn cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1)
  • 122. 4EBP1 acts as a switch between cap-dependent and capindependent mRNA translation eIF4G eIF4E cap growth factors mitogenic signals hormones, cytokines AAAAAAA eIF4G 40S Akt (kinase) mTOR (kinase) eIF4E Active 4E-BP Rapamycin/hypoxia 4E-BP eIF4E sequestered cap-dependent mRNA translation P P Inactive 4E-BP P cap-dependent mRNA translation inhibited 40S Cap AUG UAA AAAAAn cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1)
  • 123. 4EBP1 acts as a switch eIF4G eIF4E cap growth factors mitogenic signals hormones, cytokines AAAAAAA eIF4G 40S Akt (kinase) mTOR (kinase) eIF4E Active 4E-BP Rapamycin/hypoxia 4E-BP P P P Inactive 4E-BP cap-dependent mRNA translation
  • 124. 4EBP1 acts as a switch eIF4G eIF4E cap growth factors mitogenic signals hormones, cytokines AAAAAAA eIF4G 40S Akt (kinase) mTOR (kinase) eIF4E Active 4E-BP Rapamycin/hypoxia 4E-BP eIF4E sequestered cap-dependent mRNA translation inhibited P P P Inactive 4E-BP 40S Cap AUG UAA AAAAAn cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1)
  • 125. Cap-independent mRNA translation stimulated (e.g., VEGF, FGF, Bcl2, HIF1α) eIF4G eIF4E cap growth factors mitogenic signals hormones, cytokines AAAAAAA eIF4G 40S Akt (kinase) mTOR (kinase) Active 4E-BP eIF4E Rapamycin/hypoxia 4E-BP eIF4E sequestered P P P Inactive 4E-BP cap-dependent mRNA translation inhibited 40S Cap AUG UAA AAAAAn
  • 126.
  • 127.
  • 128.
  • 129.
  • 130.
  • 131. Experimental Design Aversive Olfactory learning Session 1 Olfactory Screening Specific anosmia Anxiety STICSA Baseline Set Shock State–Trait Inventory for Cognitive and Somatic Anxiety (Ree et al., 2000)
  • 132. Experimental Design Aversive Olfactory learning Session 1 Olfactory Screening Specific anosmia Anxiety STICSA Baseline Set Shock State–Trait Inventory for Cognitive and Somatic Anxiety (Ree et al., 2000)
  • 133. State-Trait inventory for cognitive and somatic anxiety Session1 Olfactory Screening (Ree et al., 2000) Specific anosmia Anxiety STICSA Baseline Set Shock
  • 134. Visual analogous scale used to collect perceptual ratings Session1 Olfactory Screening Specific anosmia Anxiety STICSA Baseline Set Shock
  • 135. Visual analogous scale used to collect perceptual ratings Session1 Olfactory Screening Specific anosmia Anxiety STICSA Baseline Set Shock
  • 136.
  • 137.
  • 138.
  • 139.
  • 140.
  • 141.
  • 142. 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
  • 143. The fear of smelling Odors and Anxiety Charles Marshall
  • 144. The fear of smelling Odors and Anxiety Charles Marshall
  • 145. The fear of smelling Odors and anxiety Charles Marshall Monell Chemical Senses Center
  • 146. Fear vs. Anxiety Outline FEAR real stimulus ANXIETY anticipation signal of threat
  • 147.
  • 148.
  • 149.
  • 150. HIT needs more therapeutic modalities • • • • Mortality 10-20% Amputations 10% New thromboembolic events 20-75% Therapy reduces new events by 60% does not reduce amputations or increase survival
  • 151.
  • 152.
  • 154. Lower motor neurons in the spinal cord and their motor units
  • 155.
  • 156.
  • 157.
  • 158. 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
  • 159. Outline 1. Background: structure 2. Methods: active site 3. Results: our design
  • 160. 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
  • 161. 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
  • 162. 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
  • 163. 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
  • 164. 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
  • 165.
  • 166. 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
  • 167.
  • 168.
  • 169.
  • 170.
  • 171.
  • 172.
  • 173. Computer-aided detection in DOT drbusch@physics.upenn.edu • Automated, fast data analysis scheme • Improved diagnosis uses multiple – Measurements – Subjects – Chromophores • Pilot study of chemotherapy monitoring trending
  • 174. Computer-aided detection in DOT drbusch@physics.upenn.edu • 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
  • 176.
  • 177.
  • 178.
  • 179.
  • 180.
  • 181.
  • 182. Results (2), Characteristics Variable CC (N=199) Age 58 (47-70) Gender 67 (33.7%) BMI: <25, 59 (29.8%) 25-30, 54 (27.3%) >30 85 (42.9%) CYP2C9, any *2 or *3 29 (14.9%) APOE, any E4 67 (34.2%) Vitamin K intake 44 (20-112) Any T (N=118) 60 (51-72) 32 (27.1%) 37 (31.9%) 45 (38.8%) 34 (29.3%) 42 (35.6%) 35 (29.7%) 35 (20-85) P-value 0.23 0.22 0.03 <0.001 0.40 0.49 CCEB
  • 183. Which? Results Variable (2), Characteristics CC What are these? (N=199) Age 58 (47-70) Gender Which ? 67 (33.7%) BMI: <25, 59 (29.8%) 25-30, 54 (27.3%) >30 85 (42.9%) CYP2C9, any *2 or *3 29 (14.9%) APOE, any E4 67 (34.2%) Vitamin K intake 44 (20-112) Any T (N=118) 60 (51-72) 32 (27.1%) 37 (31.9%) 45 (38.8%) 34 (29.3%) 42 (35.6%) 35 (29.7%) 35 (20-85) P-value 0.23 0.22 0.03 <0.001 0.40 0.49 CCEB
  • 184. Results (2), Characteristics Variable CC Any T P-value (N=199) (N=118) Age 58 (47-70) 60 (51-72) 0.23 Gender 67 (33.7%) 32 (27.1%) 0.22 N values? BMI: <25, 59 (29.8%) 37 (31.9%) 0.03 Percentage45 (38.8%) of group? 25-30, 54 (27.3%) Precision of percentage? >30 85 (42.9%) 34 (29.3%) CYP2C9, any *2 or *3 P-values? 42 (35.6%) <0.001 29 (14.9%) APOE, any E4 67 (34.2%) 35 (29.7%) 0.40 Vitamin K intake 44 (20-112) 35 (20-85) 0.49 CCEB
  • 185. Results (2), Characteristics Variable CC (N=199) Ag 58 (47-70) Gender 67 (33.7%) BMI: <25, 59 (29.8%) 25-30, 54 (27.3%) >30 85 (42.9%) CYP2C9, any *2 or *3 29 (14.9%) APOE, any E4 67 (34.2%) Vitamin K intake 44 (20-112) Any T (N=118) 60 (51-72) 32 (27.1%) 37 (31.9%) 45 (38.8%) 34 (29.3%) 42 (35.6%) 35 (29.7%) 35 (20-85) P-value 0.23 0.22 0.03 <0.001 0.40 0.49 CCEB
  • 186. Results (2), Characteristics Variable CC (N=199) Age 58 (47-70) Gender 67 (33.7%) BMI: <25, 59 (29.8%) 25-30, 54 (27.3%) >30 85 (42.9%) CYP2C9, any *2 or *3 29 (14.9%) APOE, any E4 67 (34.2%) Vitamin K intake 44 (20-112) Any T (N=118) 60 (51-72) 32 (27.1%) 37 (31.9%) 45 (38.8%) 34 (29.3%) 42 (35.6%) 35 (29.7%) 35 (20-85) P-value 0.23 0.22 0.03 <0.001 0.40 0.49 CCEB
  • 187. 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) Avg. Age (years) 60 58 % Male % CYP2C9 *2 or *3 27% 36% 34% 15% <0.001 % BMI >30 29% 43% 0.03 % APOE4 Avg. Vit.K intake 30% 35 34% 44 p value
  • 191. O O
  • 194. Lisa would be delighted to deliver a full seminar for your organization. Contact us for details.
  • 195. Programs for science /engineering: Art of Speaking Science 1 Art of Speaking Science 2 Designing Science Slides Networking for Academics Interviewing Skills Poster Presentations More…
  • 196. very politely asks… Share this Deck Follow Me [Help your colleagues!] [Learn more. Grow more.]

Editor's Notes

  1. © 2013 Lisa B. Marshall All rights reserved. For information, address DNA Press, 1400 Berlin Road #126, PO Box 606, Cherry Hill, NJ 08003No form of copying, modifying, publishing, broadcasting, or distributing in any way of any materials is permitted without first obtaining express written permission from DNA Press and Lisa B. Marshall. Presented Feb 5, 2014 @ U PennNotes: The opening needs to be a bit sharper…(no ideas on how to do that) maybe only “in conclusion” is necessary. Tighten the delivery of this. There seemed to be interest in the top five annoyances from presentations – I wonder if I could find other survey data about how audiences feel about presentations – maybe do something specific for scientists? I’d like to learn more about the redudancy principle as it applies to presentations/multi-media Find the real graph (you saw it – I think it’s in the Mcconnell presentation online). Add in a slide that has “figure” text below it – show how that should be modified for a slide
  2. © 2013 Lisa B. Marshall All rights reserved. For information, address DNA Press, 1400 Berlin Road #126, PO Box 606, Cherry Hill, NJ 08003No form of copying, modifying, publishing, broadcasting, or distributing in any way of any materials is permitted without first obtaining express written permission from DNA Press and Lisa B. Marshall. Presented Feb 5, 2014 @ U PennNotes: The opening needs to be a bit sharper…(no ideas on how to do that) maybe only “in conclusion” is necessary. Tighten the delivery of this. There seemed to be interest in the top five annoyances from presentations – I wonder if I could find other survey data about how audiences feel about presentations – maybe do something specific for scientists? I’d like to learn more about the redudancy principle as it applies to presentations/multi-media Find the real graph (you saw it – I think it’s in the Mcconnell presentation online). Add in a slide that has “figure” text below it – show how that should be modified for a slide
  3. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  4. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  5. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  6. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  7. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  8. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  9. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  10. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  11. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  12. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  13. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  14. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  15. To find out why we begin to lose attention, we can turn to surveys of audiences. My favorite survey which mirrors the results of most of them is from my colleague Dave PardiEvery year he surveys audiences to find out what annoys people the most about presentations “Annoying PowerpoInt survey”http://www.thinkoutsidetheslide.com/free-resources/latest-annoying-powerpoint-survey-results/I thought I share with you the top 5 annoyances, and interestingly the the top 3 spots haven’t changes since last year. Let’s take a quick look at them.
  16. 72% of respondents (out of 682) - say that reading a slide aloud is by far the most annoying thing a presenter can do…The Redundancy PrincipleLearners can learn better with just graph and narrationText that is presented verbally at the same time creates cognitive overload EXCEPTIONS: When there is no graphics and the text is very limited When there is enough time to process the graphic and the text is very limited If audio is difficult to understand (foreign language) In case you don’t think this applies to you…https://sites.google.com/site/cognitivetheorymmlearning/redundancy-principle
  17. The Redundancy PrincipleLearners can learn better with just graph and narrationText that is presented verbally at the same time creates cognitive overload EXCEPTIONS: When there is no graphics and the text is very limited When there is enough time to process the graphic and the text is very limited If audio is difficult to understand (foreign language) In case you don’t think this applies to you…https://sites.google.com/site/cognitivetheorymmlearning/redundancy-principle
  18. People read the slide often because they want to be sure they get the words right. Or they want to be sure they don’t skip anything.Put the details the notes section if necessary, but don’t put it on the slide. When you do that you are being YOU focused and not audience focused.
  19. Text is too small (and there’s to much)Relative size of the fonts is also not right
  20. Text is too small (and there’s to much)Relative size of the fonts is also not right
  21. I believe this is primarily result of business presentations—not academic presentations (Many people in industry are moving toward using presentation software to create documents – academia/science create a paper)However, I have seen some fonts that just weren’t readable -- If they can’t see it , there is no point in putting it on the slide Only exception for small fonts are the references which should be small, but readable font for reference.
  22. Text is too small (and there’s to much)Relative size of the fonts is also not right
  23. Size difference -- overall size -- underlines – don’t duplicate
  24. Background colors and text colors – high contrast
  25. This was a submitted slide – good use of contrast and color – BACKGROUND ONLY - CLICKCLICK
  26. This was a submitted slide – good use of contrast and color – BACKGROUND ONLY - CLICKCLICK
  27. Background:High Contrast – Light on dark, dark on light – highest contrast light on dark (some say better for large conference halls)Take science into consideration CLICK– florescence or micrographs then black may be better -- combination is OK—just realize the transition will be jarring so use that to your advantage
  28. Again, this is the same mouse 20 minutes post infusion of KKO. These are uninvolved vessels. Note that the complement staining appears to be specific and correlates with the binding of platelets and KKO.HIT(hPF4+/FcyRIIA+) mouse post KKO injuriesmPlatelets(CD41) – Blue, KKO-568 – Red, mC3b-488 - Green
  29. – florescence or micrographs then black may be better -- combination is OK—just realize the transition will be jarring so use that to your advantage
  30. Psychology of color – colors have meaningColor blindness - most common is red/green – doesn’t meant they see it in black and white or don’t see at all, just can’t distiguish between the twoAre are final top annoyance….CLICK
  31. And this is what we are going to be spending a good amount of our time on…How to data slides
  32. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  33. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  34. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  35. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  36. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  37. Minimum essential data also means only point per slide – you can make as many slides as you need to make your points…don’t worry about how many slides you have ultimately as long don’t go over your time. You’ll need to create slides that are SEPARATE from the data you collect or the figures that you create for your paper. Keeping in mind the purpose of the presentation…
  38. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  39. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  40. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  41. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  42. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  43. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  44. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  45. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  46. Like a billboard design (I’ve been teaching billboard design for close to 20 years here at Penn)What can we learn from the billboard? Headline title and/or takeaway that expresses the one main idea – The message is very clear, Tailgaiting isn’t worth it – and if that’s not enough, it’s against the law. Guides eyes to important stuff (in this case the crash is what we look at)Mixture of text and images (notice it’s mostly image and just a little bit of text)Uses color for text and background well (clear while backgound – notice the colors work together)Fonts are reading from distance (chose a clear readable font that was readable from distance)
  47. The assertion is a sentence headline that states the main message of the slideThe evidence is NOT a bulleted list, but instead visual evidence: photos, drawings, diagrams, graphs, films, or equationsThe main assumption of the assertion-evidence structure assumes the primary purpose of the slide is the help the audience understandRemember the content rather than provide talking points for the speaker.
  48. Here’s an example:The headline is the assertion – image shows the evidence
  49. In 2013, Michael Alley did a study and the results showedThis style of presentation vs. the topic and bullet point list lead to better better recall and comprehension of complex dataInternational Journal of Engineering Education (accepted 2013)
  50. In the same study he found that people who were exposed to the assertion-evidence slides had fewer major misconceptions about the material
  51. In a separate study, by team, [add in picture of a college student)Students that use this approach to present in class think and learn more deeply about the topic
  52. It’s important to notice using this structure for slides evidence is NOT a bulleted list, but instead visual evidence: photos, drawings, diagrams, graphs, films, or equationsSo let’s say this is your evidence is this photo….What I see (not as much, but still I see it) is the “structure” type of title CLICK
  53. Structure titles do not communicate any meaning…and they simply repeat…Don’t waste valuable real estate on the slide with meaningless words. So in coaching I’ll push someone and say – what are you communicatingAh, I’ve got…CLICK
  54. Although it’s slightly better, the meaning is still missing, rightThe audience can SEE the what! They don’t need text to tell them that! They want to know the meaning…
  55. Although it’s slightly better, the meaning is still missing, rightThe audience can SEE the what! They don’t need text to tell them that! They want to know the meaning…
  56. It could be….
  57. It could be….
  58. So the headings always need to communicate the so what
  59. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  60. Here’s an example of something that is close, but not quite enough…it’s almost a cross between the two…You see the topic heading and the bulleted list in red, but you also see the graphs underneath. It was like the person understood they should be there, but felt like they also had to keep the old structure
  61. Here’s an example of something that is close, but not quite enough…it’s almost a cross between the two…You see the topic heading and the bulleted list in red, but you also see the graphs underneath. It was like the person understood they should be there, but felt like they also had to keep the old structure
  62. When you have an assertion in the title it lets you know what to go looking for in the graph.
  63. When you have an assertion in the title it lets you know what to go looking for in the graph.
  64. Once you have your assertion, add in your images.Then add in labels on the image.Transition: Why should we use this structure?
  65. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  66. Here’s another example from the same presentation – notice the assertion-evidence structure The title is the sentence assertion and the images below are what support it. However, my friend (and colleague) Jean-Luc Lebrun questions the sequence…assertion then evidence or is it better to go with evidence then assertion. Certainly in the opposite direction it more closely models the scientific process: Hypothesis, observation, assertionHe suggest that some might feel more engaged if they were actively involved in probing the visual evidence for answers –he suggest that it the mind is in a moe active let-me-see mode The idea is that the under the guidance of the presenter, they discover the yet-to-appear assertion. When I work with clients I suggest they use upside down evidence-assertion when they want to use a story telling style and use the research questions to guide them through. I also think it’s useful to use the upside structure when you have a controversial result and you want to walk through your observations step-by-step before revealing the assertion.
  67. Here’s another example from the same presentation – notice the assertion-evidence structure The title is the sentence assertion and the images below are what support it. However, my friend (and colleague) Jean-Luc Lebrun questions the sequence…assertion then evidence or is it better to go with evidence then assertion. Certainly in the opposite direction it more closely models the scientific process: Hypothesis, observation, assertionHe suggest that some might feel more engaged if they were actively involved in probing the visual evidence for answers –he suggest that it the mind is in a moe active let-me-see mode The idea is that the under the guidance of the presenter, they discover the yet-to-appear assertion. When I work with clients I suggest they use upside down evidence-assertion when they want to use a story telling style and use the research questions to guide them through. I also think it’s useful to use the upside structure when you have a controversial result and you want to walk through your observations step-by-step before revealing the assertion.
  68. So here is an example, that although it’s not controversial –this would be the example of a more story telling style approach. Notice the question is at the top and the evidence walks through how the question was addressed…this slide then works in conjunction with the second one we already saw…CLICK
  69. So here is an example, that although it’s not controversial –this would be the example of a more story telling style approach. Notice the question is at the top and the evidence walks through how the question was addressed…this slide then works in conjunction with the second one we already saw…CLICK
  70. So here is an example, that although it’s not controversial –this would be the example of a more story telling style approach. Notice the question is at the top and the evidence walks through how the question was addressed…this slide then works in conjunction with the second one we already saw…CLICK
  71. Here’s another example from the same presentation – notice the assertion-evidence structure The title is the sentence assertion and the images below are what support it. However, my friend (and colleague) Jean-Luc Lebrun questions the sequence…assertion then evidence or is it better to go with evidence then assertion. Certainly in the opposite direction it more closely models the scientific process: Hypothesis, observation, assertionHe suggest that some might feel more engaged if they were actively involved in probing the visual evidence for answers –he suggest that it the mind is in a moe active let-me-see mode The idea is that the under the guidance of the presenter, they discover the yet-to-appear assertion. When I work with clients I suggest they use upside down evidence-assertion when they want to use a story telling style and use the research questions to guide them through. I also think it’s useful to use the upside structure when you have a controversial result and you want to walk through your observations step-by-step before revealing the assertion.
  72. Start with the basic rules
  73. Size difference -- overall size -- underline
  74. It means editing down the picture and thinking about color, making it readable and labelling properly
  75. Again, this is the same mouse 20 minutes post infusion of KKO. These are uninvolved vessels. Note that the complement staining appears to be specific and correlates with the binding of platelets and KKO.HIT(hPF4+/FcyRIIA+) mouse post KKO injuriesmPlatelets(CD41) – Blue, KKO-568 – Red, mC3b-488 - Green
  76. What is the absolute least amount of data you need to present?
  77. This graph is directly from Jean-Luc Doumont, from his book Trees, Maps, and theoremsYou can find a download from wwww.treesmapsandtheorems.com
  78. This graph is directly from Jean-Luc Doumont, from his book Trees, Maps, and theoremsYou can find a download from wwww.treesmapsandtheorems.com
  79. JUST FOR A SECOND TO SEE THE CHANGE – Then click to see the stuff that changed….
  80. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  81. We wanted to assess the relative strength of KKO in the presence of PF4 as an activator compared to other established platelet agonists. As you can see when comparing the mean fluorescence intensity and percent positivity, PF4/KKO is second only to convulxin as a platelet activator.
  82. I would have put them in the order of increasing – not just random orderTo make my redo process more efficient and because I didn’t have the original data – I just put boxes over stuff to Not sure how I feel about the only relevent tick marks – also since it’s not me, I wasn’t sure which were relevant
  83. What is the absolute least amount of data you need to present?
  84. Minimum essential data– you need to focus on ONLY what is necessary to make your pointRemember the paper is repository for all the data- the presentation is to generate interest and discussionEXAMPLE to PROCESS
  85. Notice the direction that that moves Notice there aren’t any wipes or animated transitions
  86. 23 participants were tested: 11 LA and 12 HA. Participants’ olfactory abilities, anxiety vulnerability and, the presence of recordable SCR response were tested. One participant was excluded from the final analyses because she did not demonstrate a SCR. Participants set their own shock level subsequently used in Session 2. During session two we simultaneously recorded perceptual ratings, physiological arousal, and neural activations. Perceptual ratings were collected on a Visual analogous scale ranging from not at all to very much. Participants had to answer the questions how intense was the odor. Arousal was measured via skin conductance, or the ease with which electrical current pass through the skin. Skin conductance changes for a variety of reasons mostly tied to how much you&apos;re sweating. The more anxious someone becomes, the more he sweats, the higher the amplitude of her skin conductance response.An event-related design was used to collect neural responses. In order to account for temporal autocorrelations in time series, a 1st order polynomial expansion regressor was applied.
  87. 23 participants were tested: 11 LA and 12 HA. Participants’ olfactory abilities, anxiety vulnerability and, the presence of recordable SCR response were tested. One participant was excluded from the final analyses because she did not demonstrate a SCR. Participants set their own shock level subsequently used in Session 2. During session two we simultaneously recorded perceptual ratings, physiological arousal, and neural activations. Perceptual ratings were collected on a Visual analogous scale ranging from not at all to very much. Participants had to answer the questions how intense was the odor. Arousal was measured via skin conductance, or the ease with which electrical current pass through the skin. Skin conductance changes for a variety of reasons mostly tied to how much you&apos;re sweating. The more anxious someone becomes, the more he sweats, the higher the amplitude of her skin conductance response.An event-related design was used to collect neural responses. In order to account for temporal autocorrelations in time series, a 1st order polynomial expansion regressor was applied.
  88. I wasn’t sure exactly whey the process was there? Perhaps it was to orient the person to where they were in the process?If the process was an important part of the slide, then move it horizontal…our minds more easily process a process horizontallyFirst thing to notice is that the process moves horizontally. Often there are slides that simply don’t let themselves to much of an image—and turning them horizontal will add a visual elementOK- -NOW BACK to the inventory that you couldn’t read…I see this with surveys or variable lists. Show the entire list, but then use animation to highlight the key examples
  89. Now I’m going to cover rules that are associated with certain types of slides that you all create—title slides, aknowledgment slides, etc.
  90. Asnake rattlesnakeappears at your feet. Most likely you’d freeze and start sweating ― a quick, automatic sequence of arousing physical reactions. We areclearly experiencing fear.
  91. Asnake rattlesnakeappears at your feet. Most likely you’d freeze and start sweating ― a quick, automatic sequence of arousing physical reactions. We areclearly experiencing fear.
  92. For those of you not familiar with Heparin induced thrombocytopenia and thrombosis designated HITT, the sentinel clinical features are shown on this slide. This is the leg from someone who donated their saphenous vein for coronary bypass and subsequently developed HITT. Heparin induced thrombocytopenia is a prothrombotic disorder seen in patients receiving heparin approximately 5 days to 14 days after the initiation of heparin therapy. The overall mortality in patients diagnosed with HIT is 10-20%. Approximately 10% of patients suffer amputations and new thromboembolic events occur in 20-75% of people with HIT. Current therapies such as direct thrombin inhibitors or anti-Factor Xa drugs reduce new events by approximately 60%, but do not reduce amputations or increase survival indicating the clear need for additional therapeutic modalities.
  93. For those of you not familiar with Heparin induced thrombocytopenia and thrombosis designated HITT, the sentinel clinical features are shown on this slide. This is the leg from someone who donated their saphenous vein for coronary bypass and subsequently developed HITT. Heparin induced thrombocytopenia is a prothrombotic disorder seen in patients receiving heparin approximately 5 days to 14 days after the initiation of heparin therapy. The overall mortality in patients diagnosed with HIT is 10-20%. Approximately 10% of patients suffer amputations and new thromboembolic events occur in 20-75% of people with HIT. Current therapies such as direct thrombin inhibitors or anti-Factor Xa drugs reduce new events by approximately 60%, but do not reduce amputations or increase survival indicating the clear need for additional therapeutic modalities.
  94. The title is what, not a so what and at the start there may not yet be a so what…better to use the image at the attention getter
  95. Motor neurons are specialized cells, consisting of a soma with short dendrites and a single axon that might extend over one meter in length to reach its targets (show on the figure). Motor neurons directly link the nervous system and muscles and each motor neuron with its associated muscle fibers constitutes a functional entity called the motor unit (show on the figure). Damage to motor neuron cell bodies or their peripheral axons results in paralysis or weakness of the affected muscles and as later effect atrophy due to denervation and disuse of the affected muscles.
  96. CLICK THROUGH JUST TO SEE IT….
  97. TitleSections are numberedKeywords are highlightedOrienting “home” image
  98. TitleSections are numberedKeywords are highlightedOrienting “home” image
  99. TitleSections are numberedKeywords are highlightedOrienting “home” image
  100. TitleSections are numberedKeywords are highlightedOrienting “home” image
  101. TitleSections are numberedKeywords are highlightedOrienting “home” image
  102. Here’s an example from the submitted slidesSpecific Aim or subaim?
  103. For longer presentations using this sort of orienting slide can be helpful
  104. This was created
  105. In this case this slide is pretty good, but the main equation is at the very bottom. May get missed.
  106. What is the absolute least amount of data you need to present?
  107. What is the absolute least amount of data you need to present?
  108. What is the absolute least amount of data you need to present?
  109. And this is what we are going to be spending a good amount of our time on…How to data slides
  110. What is the absolute least amount of data you need to present?
  111. Expert. Practical. Authentic.Most people know Lisa B. Marshall as the host of The Public Speaker podcast which has earned over 9 million downloads. However, primarily she delivers professional development consulting, workshops, and speeches. She specializes in transformations - financial, personal and professional – throughdeveloping and enhancing communication. She&apos;s helped organizations build stronger teams, manage conflict, create stronger, more effective messages, and deliver better presentations. In addition, she&apos;s coached many senior leaders one-on-one to develop stronger executive communication skills. She’s author of Smart Talk, Ace Your Interview, and Expert Presenter.Her clients include Johns Hopkins Medicine, Harvard University, NY Academy of Science, University of Pennsylvania, Genentech, and Roche among many others. Her work has been featured in diverse media: CBS Money Watch, Ragan.com, Woman&apos;s Day, Cosmopolitan, etc. She holds masters with duel degrees in interpersonal/intercultural communication and organizational communication. Visit www.lisabmarshall.com to learn more about Lisa and www.smarttalksuccess.com for info on her latest book.Head Shot (plus bio): http://bit.ly/LisaBInfoPodcast Information: www.morefromlisa.comText Excerpt of Smart Talk: http://bit.ly/STSampleAudio Excerpt of Smart Talk: http://bit.ly/STAudioSmart Talk Challenge:  http://bit.ly/STChallengeSmart Talk Cartoons: http://bit.ly/STCartoonsSmart Talk &quot;Difficult People&quot; Info graphic: http://bit.ly/STInfographicSmart Talk &quot;Marvelous&quot; Trailer: http://bit.ly/STTrailerPrimary Website Links:http://www.lisabmarshall.com (for lisa)http://www.smarttalksuccess.com (for Smart Talk book)http://www.morefromlisa.com (for Public Speaker podcast)Social Media Links:Facebook = http://www.facebook.com/ThePublicSpeakerGoogle+ = http://gplus.to/LisaBMarshallTwitter = http://twitter.com/lisabmarshallLinkedIn = http://linkedin.com/in/lisabmarshallPinterest = http://pinterest.com/SmartTalkLBM/
  112. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  113. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…
  114. Of course, we don’t really die from too many bullet points, but what does happen to audience attention during a talk in important. So I if you look at this graph of audience interest, we have audience interest on the y-axis and time on x-axis….What this graph represents is the attention level of the audience when a speaker is being introduced. Not everyone is paying attention yet, but a good majority are….some people are still thinking about the last speaker, some people are still entering the room, some people may be thinking about lunch or dinner…