publishing and presenting clinical research 2011 warren browner, md, mph [email protected]
TRANSCRIPT
Today's agenda
Talks and slides
Posters
2
Making Slides
A few easy lessons
Do’s and don’ts
3
PowerPoint Rules
Keep the distractions to a minimum– Fonts, animation, graphics, colors (4-5)
Remember the color-blind
Minimum font size (this is 28)– This is 24
This is 20– This is 18
4
Use Explanatory (Results) Titles
Life is Tough
Life is Really Tough for Fellows
Life is Even Tougher for Junior Faculty
Life is Piece of Cake for Senior Faculty
5
A Few Points about Figures
Avoid baked goods
Make the message clear
Don’t “distort”
Easy colors
6
Alcohol abuse
Diabetes
B12 deficiency
Paraneoplastic
Medication-related
Other
Idiopathic
Causes of neuropathy in 112 primary care patients
Pies = good in bakeries7
40-4950-59
60-6970+
None
1 - 3 drinks per day
3 - 5 drinks per day6 or more drinks per day0
20
40
60
80
100
120
Hepatoma risk per 100,000
Age (years)
Annual risk of hepatoma by age and alcohol consumption.
3D = hard to read
8
0
20
40
60
80
100
120
140
40-49 50-59 60-69 70+
Age (years)
Hepatoma risk per 100,000
None
1 - 3 drinks per day
3 - 5 drinks per day
6 or more drinks per day
Hepatoma risk increase with age and alcohol use
A better version
9
Mortality by age and sex
Makes modeled results look too real
10
Mortality modeled as a function of age and sex
Legend informs the reader11
MediCal is Increasing with Time
12 Warning: Red/green confusion
MediCal is Increasing with Time
13
What Do You See?
14
More Rules
Maximum of 4-5 colors
Don’t forget the color-blind (cross-hatch)
15
Clues that Something is Wrong
It takes you > 10 minutes to make a slide
You have 20 minutes to talk and 40 slides– One slide per minute
16
What This Slide Says
I don’t have a point to make I do have too much time my hands I learned how to use animation You're going to have to sit through it
Now what was I trying to say?
17
Practicing the Talk
First aim for overall message and time
Then seek input about the slides– Fix slides as you do so
Then seek suggestions about the talk– Get “style” comments in private
18
Always
Spell check (F7)
Then print slides (hand-out) and proof-read
19
The PowerPoint Show
F5 = start; ESC = end; “X” enter = slide “X”
During the show – B = blackout; W = whiteout– Next = Spacebar, right or up arrow, N, enter, or
left click– Previous = Backspace, down or left arrow, or P
20
The Talk Itself
Arrive early Meet the chairs Position friends in the front of the audience Bring a glass of water Don’t get spontaneous until you get good Chuck the laser pointer
21
Don’t Read Your Slides
Reading slides is boring and turns people off Most will realize they don't have to pay
attention to what the speaker is saying, and they will stop doing so
People can also read faster than someone can speak (can’t you?)
But don’t ignore what you’ve written
22
Responding to Questions
ESL: “Thanks for your attention. I will try to respond to your questions, but English is not my first language. Please speak slowly and simply.”
All: “I'm sorry; I don't understand your question. Perhaps we can discuss this after the session.”
23
Responding to Nasty Questioners
Multi-part questions:– Answer what you want to– Then say “What was the other question?”
Hostile or argumentative:– “Perhaps we can discuss this later. Next
question?”
24
Posters
Almost always contain WAY too much data and too little information– The abstract is not needed unless mandatory
Put the key stuff at eye level in big fonts or simple tables and figures
Use a (good) template
25
Posters, Panel by Panel
Introduction and background Subjects and methods (2-4) Results (3-5)
– With explanatory titles
Limitations Conclusions and implications
26
Poster Fonts
Title = 85 point Your name = 56 point Sub-headers = 36 point Text = 24 point Legends, tables = 18 point
Use upper and lower case; left-justified
27
Prettifying: Fonts
Two per document or presentation– Serifs (doohickeys) for text– Sans serif for tables, figures, legends, headers
Garamond, Times New Roman, Book Antiqua, Bookman
Arial Narrow, Arial, Tahoma, Trebuchet MS, Verdana
Courier lines up verticallyOne line is under another
28
What To Do at a Poster Session
As a presenter: It’s your party!– Meet your neighbors– Invite (famous) strangers– Greet your guests– Offer them a drink– Hang in there
29
What To Do at a Poster Session
As a visitor– Spend 5 min. identifying which homes to visit– Don’t look and then decide the party is boring
“I’m a vegetarian”
– Introduce yourself to the host
30
That’s all folks…
Questions?
31
ConclusionsThe majority of men on active surveillance will be free of treatment at five years. Grade progression is relatively common. Of those who undergo radical prostatectomy, a minority will have adverse pathology. However, early biochemical recurrence free survival appears excellent.
Outcomes of Active Surveillance for Early Stage Prostate Cancer
BackgroundGiven concern about prostate cancer over diagnosis due to the use of PSA – based screening practices, there has been a renewed interest in active surveillance in lieu of immediate treatment. The safety and efficacy of such an approach requires validation.
PurposeThe aim of this study was to describe the results of an ongoing prospective cohort of men with early stage prostate cancer who chose active surveillance as their initial management strategy.
Results (cont)
Jared M Whitson , Sima P Porten, Janet E Cowan, and Peter R Carroll
MethodsThis is a prospective cohort study at a single academic institution of men with prostate cancer who chose active surveillance as their initial management strategy. Men were excluded if they had not yet reached 6 months follow-up after diagnostic biopsy.
Results (cont)
Results
Total no. 83Gleason Grade -- no. (%)
≤6 25 (31)7 (3+4) 43 (54)7 (4+3) 9 (11)
8-10 3 (4)Pathologic T Stage -- no (%)
pT2 55 (68)pT3 26 (32)
Extracapsular Extension -- no (%) 22 (27)Seminal Vesical Invasion -- no (%) 6 (7)Positive Surgical Margin -- no (%) 12 (14)
T able 3. Pathology at R adical Prostatectomy
Total no. 532Mean Age ± SD (years) 62.5 ± 8.2Year of Diagnosis -- no. (%)
≤ 2000 74 (14)2001-2005 283 (53)
≥2006 175 (32)PSA at Diagnosis -- no. (%)
≤6 175 (52)>6-10 164 (31)
>10 66 (12)Clinical T Stage -- no. (%)
T1 346 (66)T2 180 (34)
Gleason Grade -- no. (%)≤6 484 (93)
7 (3+4) 31 (6)7 (4+3) 4 (1)
8-10 1 (<1)Biopsy Cores Positive -- no. (%)
≤33% 411 (77)>33% 58 (11)
T able 1. B aseline clinical information
Methods (cont.)Data from the entire cohort are presented and additionally from just those men who underwent radical prostatectomy. The primary outcome in this subset was biochemical recurrence free survival which was defined as PSA < 0.2ng/ml and no second treatment.
PSA Measurements -- no. (%)≤3 84 (16)
4-7 106 (20)>7 342 (64)
Number of Biopsies -- no. (%)Diagnostic Only 112 (21)
1 Repeat 194 (37)≥2 Repeats 226 (42)
Gleason Upgrade -- no. (%) 144 (27)Treatment -- no. (%)
None 369 (69)Radical Prostatectomy 83 (16)
Radiation 58 (11)Androgen Deprivation 22 (4)
Survival -- no (%)Alive 518 (97)
Died of Other Cause 8 (2)Died of Unknown Cause 6 (1)
T able 2. Follow-Up D uring Surveillance
Low Leptin is Associated with Increased Mortality and Cardiovascular Events Low Leptin is Associated with Increased Mortality and Cardiovascular Events in Patients with Stable Coronary Artery Disease:in Patients with Stable Coronary Artery Disease:
The Heart and Soul StudyThe Heart and Soul StudyIvy Ku MD, Ramin Farzaneh-Far MD, Beeya Na MPH, Mary Whooley MD
University of California, San Francisco; and San Francisco VA Medical Center
BackgroundBackground
Research QuestionResearch Question
MethodMethodss
ConclusionsConclusions
• Leptin is an adipokine with both protective and harmful effects on the cardiovascular (CV) system
• Studies of association between leptin levels and CV outcomes have yielded conflicting results
Design:Design:Prospective cohort study
Subjects:Subjects: 981 outpatients with stable coronary disease recruited from 12 clinics in the San Francisco Bay Area between 9/00 and 12/02
Predictor:Predictor:Baseline Baseline serum serum leptin levelsleptin levels
Outcomes:Outcomes: Death, myocardial infarction, stroke, adjudicated by review of medical records during 6.3 years of follow-up
PotentialPotentialConfounders: Confounders:
Sex, body Sex, body mass index mass index (BMI), co-(BMI), co-morbidities, morbidities, physical physical activity, activity, smoking, smoking, insulin insulin resistance, resistance, HDL, C-HDL, C-reactive reactive proteinprotein
Potential Potential Interaction:Interaction:
Sex, BMI, Sex, BMI, diabetesdiabetes
Analysis:Analysis: Cox proportional hazards models, adjusted for potential confounders associated with leptin (p < 0.1)
Baseline characteristics of 981 participantsBaseline characteristics of 981 participants Kaplan Meier event-free survival curveKaplan Meier event-free survival curve
LimitationsLimitations
Covariates in model
Hazard Ratio (95% CI)
Low versus High Leptin
P value
Adjusted for age, sex, race
1.30 (1.05 – 1.59) 0.01
Add body mass index
1.26 (0.99 – 1.60) 0.06
Add medical history
1.36 (1.05 – 1.76) 0.02
Add biomarkers 1.40 (1.09 – 1.81) 0.009
• 6397 person-years of follow up, 314 deaths, 118 myocardial infarctions, 56 strokes.
• Low leptin associated with 40% increased rate of CV outcomes (HR 1.40, CI 1.09 – 1.81, p = 0.009)
• Low leptin associated with 37% increased mortality (HR 1.37, CI 1.03 – 1.81, p = 0.03)
• Association between leptin and mortality strongest among patients in lowest BMI tertile (IQR 22 – 25 kg/m2)
ResultsResults
Leptin and mortality stratified by Leptin and mortality stratified by BMIBMI
Association between leptin and combined CV Association between leptin and combined CV outcomesoutcomes
Per SD decrease in log-leptin*
Hazard Ratio (95% CI)
P value
BMI tertile I(IQR 22 – 25)
1.70 (1.30 – 2.24)
< 0.001
BMI tertile II(IQR 27 – 29)
0.91 (0.66 – 1.26)
0.57
BMI tertile III(IQR 31 – 36)
1.07 (0.79 – 1.46)
0.66
• Are leptin levels associated with adverse outcomes in coronary artery disease?
High High leptinleptin
Low Low leptinleptin
Log-rank test p = Log-rank test p = 0.010.01
• Most participants urban men, results may not generalize
• All subjects had stable CAD, leptin effects may differ in healthy and post-MI patients
• Only used baseline leptin levels, does not capture effect of fluctuating levels over time
*(p = 0.01 for leptin*BMI interaction)
• Low leptin predicts subequent CV events and mortality in stable CAD
• This association is independent of known factors affecting leptin, including gender and obesity
• Whether leptin has direct effects on CAD, or functions as a marker of other protective pathways, deserves further study
34