Elizabeth UnniSep 29, 2011

Why?• Opportunity to exchange ideas

Clinical problemsResearch outcomes Research ideas (Work in progress)

Where?• Conferences (Eg: Diabetes Summit)• Professional Association Annual Meetings

National – APhALocal – UPhA

• Capitol HillPolicy making

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TitleAbstract (Optional)Introduction/BackgroundGoals/ObjectivesMethodsResultsDiscussion & LimitationsClinical ImplicationsConclusionAcknowledgementsReferences

It is not necessary to have all these components in

a poster

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Use the 10–10 rule• Attendees spend only 10 seconds scanning

posters as they stroll by from a distance of 10 feet

• Essential that the poster capture their attentionBlend between manuscript and oral presentation• Use content judiciously

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Clarity & Simplicity• Concise and neat layout

Keep the words to a minimum• Busy attendees do not have time to read a lot

Use pictures, graphs, and diagrams• But not in a distractive way

Main message should be clear and visible• Resist the urge to fill voids with clutter that might

discourage attendees from approaching your poster

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Use phrases, not sentencesUse bullet points, not paragraphsAvoid jargon and acronymsUse consistent wording, especially between text and visualsEnsure that the content is self-explanatory

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Ensure that the text is legible and appealing• Use the same type-font throughout the poster

Times New Roman or Arial is usually used

• Distinguish between headers and textSize of font

Headers can be read from 5m and text can be read from 2m.

Type of fontUniversal for headers

• Top to bottom & left to right readingLogical sequence of presentation

• Softer colors (pastel or gray) as background 9/29/2011

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Suggested font sizes:

• Title: 96 pt• Authors: 72 pt• Affiliations: 36-48 pt• Section headings: 36 pt• Text: 24 pt• Acknowledgements: 18 pt

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Editing• Proofread

ColleaguesPeople familiar with your topicPeople not so familiar with your topic

• Spell check

Very very.. important• Get feedback

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Components• Title

Interesting – to capture attention of the audienceIf too long, shorten it; do not reduce font size

• AuthorsIf too many authors, use last and first name

Omit middle initials & titles

Include academic affiliationOmit city and state if there are too many authors & gives a crowded look

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Components• Introduction/background

Research gap What is the research question?Why is this research question important?

Should lead to the goals/objectives

• MethodsWhat was the strategy used?Why was this strategy used?

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Components• Results

The most important part of a posterDo not assume everyone is an expert in your field

What are the results?Use graphs, tables, and diagramsInclude only the most important & unique results

• Discussion/conclusionSummary of findings in a sentence or twoHow does your results compare with existing research?What is the next step of the study?

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Components• References

Omit if possibleInclude it in the handout

• AcknowledgementsResearch partners, funding source

If space allows, provide your email ID or QRC code, or a website where they can access the poster

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Usually 3 to 4 columns Either• Equal distribution of columns• Middle column wider than the other two columns

Depending on content

• Equal spacing between columns• All the top headers on the same level

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Know your poster and contents well• Should be able to explain the complete poster in

3 to 5 minutesPractice it and time it!

• Have a good opening sentenceExplains why your poster is importantFocus on the major question you are answering with the study

• Explain your results & conclusions well and its importance

What is the implication of your results?In clinical applicationIn scientific world

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Presentation style• Dress business casual/formals• Eye contact• Posture• Speak slowly and clearly

Avoid jargons and acronymsRemember, not everyone is an expert in your field

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Frame possible questions • prepare answers

Listen to the question• Wait until they finish the question

Answer the question• Ask whether you answered their question

Have handouts with contact information

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Budget it! Posters are expensive!

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Thermal and Mechanical Responses in TRPV1-/- Mice with Site Specific Expression of TRPV1

Graduate Program in Physical Therapy & Rehabilitation

Science

Results

Summary and Conclusions

Transient receptor potential vanilloid 1 (TRPV1) is aCa2+ permeable nonselective cation channel that isactivated by both exogenous and endogenousstimuli, including heat, low pH, anandamide, andcapsaicin. TRPV1 channels are found in the centraland the peripheral nervous system and are involvedin the transmission and modulation of pain, as wellas the integration of diverse painful stimuli. TRPV1antagonists have shown efficacy in reducingnociception from inflammatory and neuropathicanimal models of pain.

Introduction

Methods

Animals:All animal experiments were approved by the University of Iowa Animal Care and UseCommittee and were conducted in accordance with National Institutes of Health guidelines.Congenic TRPV1-/- on a C57Bl/6 background and C57Bl/6 (WT) mice were bred at theUniversity of Iowa Animal Care Facility. Male mice, 6-10 weeks of age, were used in thesestudies.

Induction of Inflammation:Mice were briefly anesthetized with 4% isofluorane and the left gastrocnemius muscle wasinjected with 20 μl of 3% carrageenan. Behavior measurements were made before and 24, 48,72 hours, 1 week and 2 weeks after carrageenan injection. In the re-expresssion experiments,behavior measurements were made before and 24 hours after carrageenan injection.

• TRPV1-/- mice show a higher level of baseline mechanical sensitivity of the paw thanWT mice; re-expression of TRPV1 in the skin restores normal mechanical sensitivity.

• TRPV1-/- mice show a lower level of baseline heat sensitivity than WT mice; re-expressionof TRPV1 in the muscle and the skin restores normal heat sensitivity.

• WT and TRPV1-/- mice develop a similar increase in mechanical sensitivity of the paw aftermuscle inflammation.

• TRPV1-/- mice do not develop heat hyperalgesia after muscle inflammation; re-expression ofTRPV1 in muscle and skin restores the heat hyperalgesia induced by muscle inflammation.

• TRPV1 expression in the skin and muscle play distinct roles in the development ofmechanical and heat sensitivity and response to inflammatory muscle hyperalgesia.

• TRPV1 plays a role in the responsiveness of cutaneous nociceptors to mechanicalstimulation as well as to high intensity heat stimuli.

• TRPV1 expression in the skin and muscle is necessary for the restoration of heatsensitivity in TRPV1-/- mice. This suggests that TRPV1 is both a pH sensor in themuscle and a heat sensor in the skin.

Methods

Behavioral Testing:

Quantitative RT-PCR:RNA was purified from ipsilateral and contralateral L4, L5, and L6 DRGs using the Trizolreagent (Invitrogen, Carlsbad, CA). First strand cDNA was synthesized from 0.2-1µg of eachRNA sample using VILO reverse transcriptase (Invitrogen, Carlsbad, CA). Taqman PCR wascarried out using an ABI prism 7900 sequence detector on cDNA samples (University of Iowa,DNA Facility, Iowa City, IA). Reactions were carried out for 40 cycles in triplicate. Rat TRPV1(Rn01460299_m1), and the mouse control assay for glyceraldehyde-3-P-dehydrogenase(GAPDH) were obtained from Applied Biosystems, Inc. (Foster City, CA). Quantitative RT-PCRdata were normalized with GAPDH mRNA levels.

Results

In the present study, we examined if TRPV1 was a peripheral initiator of muscle inflammatoryhyperalgesia. We hypothesized that removal of TRPV1 would have an effect on thermal but notmechanical hyperalgesia after the development of muscle inflammation. To test if TRPV1 in skinor muscle was necessary for the development of thermal hyperalgesia, we re-introduced theexpression of TRPV1 by injecting recombinant HSV expressing TRPV1 into the skin, muscle,and both skin and muscle of TRPV1-/- mice.

Viral Constructs: NPG (Control) and NPGTRPV1 (TRPV1 re-expressing virus). These vectors do not expressICP34.5 (deletion) or thymidine kinase (TK, UL23, insertional inactivation). Expression of enhanced green fluorescentprotein (EGFP) is driven by the hCMV immediate-early enhancer-promoter. PA, polyadenylation signal; IR, internalrepeat; L, long; S, short. NPGTRPV1 is similar to NPG and a cassette for expression of rat TRPV1 is inserted betweenthe UL36 and UL37 genes. This transcription cassette contains a woodchuck hepatitis virus element (WPRE) to enhanceRNA stability and the hCMV enhancer-promoter.

Mechanical sensitivity was tested bilaterally by assessing the number of responses torepeated application of von Frey filaments (0.4mN, 0.7mN, and 1.6mN) to the plantar surface ofthe paw. The number of withdrawals out of 5 was assessed in 10 trials and an average of all 10trials was determined for each time period. An increase in the number of responses wasinterpreted as increased mechanical sensitivity of the paw.

Thermal sensitivity was tested bilaterally by exposing the plantar surface of the paw to radiantheat with thermal intensities corresponding to 125, 135, and 145V and recording the time in secuntil withdrawal. Withdrawal times are expressed as an average of 3 trials per paw.

IR-LIR-S IR-SIR-L

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TRPV1 consists of 6 transmembrane segments and intracellular NH2- and COOH- termini. The channel is organized as a tetramer of homo or heteromeric subunits.

Purpose and Experimental PlanRe-expression of TRPV1:HSV viruses (NPG or NPGTRPV1) were injected in either A) Skin, B) Muscle, or C) Skin andMuscle. In sets A and C, each mouse was injected intradermally into the left paw with 20µl ofvirus (107PFU/µl). In sets B and C, each mouse was injected with 20µl of virus (107PFU/µl) inthe left gastrocnemius muscle. Animals were allowed to recover for 3-4 weeks before behaviorexperiments were performed.

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Re-expression of TRPV1 in muscle and skin in TRPVI-/- mice restores heat hyperalgesia after muscle inflammation

Re-expression of TRPV1 in the skin of TRPV1-/- mice restoresTRPV1+/+-likemechanical sensitivity

Re-expression of TRPV1 in muscle and skin in TRPV1-/- mice restores heat sensitivity

The number of withdrawals to repeated mechanical stimulation (0.4 mN) was significantly increased after carrageenan-induced muscle inflammation in both TRPV1-/- mice and TRPV1+/+ mice, *, p<0.05, repeated ANOVA. However, thelatency to heat (125V) was unchanged after muscle inflammation in TRPV1-/- mice compared to decreases observed inTRPV1+/+ mice, *, p<0.01, paired t-test from baseline.

The number of withdrawals to repeated mechanicalstimulation was significantly increased in TRPV1-/- micecompared to TRPV1+/+ mice. However, mechanicalthresholds were similar between groups (inset). The latencyto high intensity thermal stimuli was increased in TRPV1-/-mice when compared to TRPV1+/+ mice, *, p<0.05.

Quantitative PCR shows that injection of HSV-1 expressingTRPV1 into TRPV1-/- mice results in expression of rat TRPV1mRNA in DRG 4 weeks after injection. The increases areobserved only on the side of injection and not on thecontralateral side, Indicating new expression of TRPV1 inTRPV1-/- mice. Data represent means ± SEM; n=5-7 for allsets.

Re-expression of TRPV1 in the skin of TRPV1-/- mice results in a significant decrease in the number of withdrawalssimilar to that observed in naïve TRPV1+/+ mice, *, p<0.05, repeated ANOVA. Re-expression in the muscle or boththe skin and muscle has no effect on the number of withdrawals.

Re-expression of TRPV1 in both the muscle and skin in TRPV1-/- mice results in a significant decrease in thewithdrawal latency to high intensity heat stimuli *, p=0.04, one-way ANOVA. Re-expression singly in either the skin orthe muscle has no effect on the withdrawal latency.

Re-expression of TRPV1 in both the muscle and skin inTRPV1-/- mice restores the heat hyperalgesia (125V)induced by carrageenan-induced muscle inflammation. Re-expression singly in either the skin or the muscle has noeffect on restoring the decreased withdrawal latencyproduced by carrageenan-induced muscle inflammation. *,p=0.01, one-way ANOVA.

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Supported by National Institutes of Health AR053509 and AR053509-S1.

Increased expressions of TRPV1 mRNA in DRGs of TRPV1-/- mice injected with HSV-1 expressing TRPV1 in skin, muscle, or skin and muscle

Re-expression of TRPV1into Skin

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Loss of heat, but not mechanical hyperalgesia in TRPV1-/- mice with muscle inflammation

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Too much text and too many results!

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Professional?Interest capturing – Yes!!

Strike a balance!

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A poster with inappropriate proportions, spacing, & colors

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Background is distracting!

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Look at the column breaks…

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Different background, but still soft..Logical flow of content

Just enough pictures to keep it attractive

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Graph and table colors not matching with the remaining text (Copy pasted without editing?)

Last minute work?9/29/2011

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Too much text!Will you stand there and read this complete?

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Good pictures..BTW, what is the message?

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THE β4 NICOTINIC RECEPTOR SUBUNIT MODULATES THE ANTIDEPRESSANT ACTION OF BUPROPION

1Radhakrishnan, R., 2DeBiasi, M., and 3Arias, H.R1College of Pharmacy, University of Southern Nevada, South Jordan, UT.,

2Baylor College of Medicine, Houston, TX., 3College of Pharmacy, Midwestern University, Glendale, AZ.

Bupropion (BP) is an antidepressant drug used also as a smoking cessation agent.

AimsTo determine the acute and chronic antidepressanteffects of BP, and the withdrawal effects afterchronic administration in male and female wild-type(β4+/+) and knockout (β4-/-) mice using the forcedswim test.

Methods

Results

The β4 subunit plays a modulatory role in:• the acute antidepressant effect of BP• the chronic antidepressant effect of BP• the residual effect after withdrawal of chronic BP

BP may affect males and females differently.

Conclusions

Results

Bupropion

BP is a noncompetitive inhibitor of severalnicotinic acetylcholine receptors (AChRs).

AChR inhibition could be involved in theantidepressant and anti-nicotinic activity of BP.

i) Acute treatment increased the antidepressant effect ofBP in all mice types. However the kinetics in β4-/- micewas faster than in β4+/+ mice.

ii) The antidepressant effect after chronic treatment wasseen only in the male and female β4+/+ mice, not in β4-/-mice .

iii) Only male β4+/+ mice showed significant antidepressanteffect compared to control mice after 1 week withdrawal.

Background

β4 subunit of AChR is absent in(β4-/-) mice and hence thereceptor is assumed to bedysfunctional. Wild-type (β4+/+)and KO (β4-/-) mice wereseparated by sex, and theninjected (i.p.) with saline (0.9%NaCl; control) or BP (40 mg/kg)every day for two weeks. Todetermine the acute and chroniceffects of BP, forced swimmingtests were performed on the

Ref: Cryan et al., Trends Pharmacol Sci.,.23 (5),2002.

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1st day at 0, 15, 30, 45, and 60 min after theinjection, and after two weeks of treatment,respectively. To determine the withdrawal effect,forced swimming tests were performed on the 1st

and the 2nd weeks after chronic treatment.

A good example of a basic science research poster

Bullet points in methods section

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A good example of a clinical poster9/29/2011

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Not too fancy, but professional!9/29/2011

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Poster presented by P3 students for the Capitol Hill Pharmacy Day presentation

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If you are on a budget issue, this is an option..

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Questions?

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