Calcium Imaging in DRG Neurones

Primary cultures of DRG neurones are used to measure changes in intracellular calcium ([Ca2+]I). The following method was used:

  • DRG neurones were kept at 37oC in humidified air with 5% CO2. Cells up to 1-week-old in culture were used for imaging experiments. The neurones were loaded with a membrane permeable form of the calcium-sensitive fluorescent dye Fura-2-AM (5µM, Molecular Probes) in culture medium for 30 minutes at room temperature (21 – 23oC) in the dark.
  • The neurones were washed with an extracellular bathing solution for a further 30 minutes to allow complete cytoplasmic dye de-esterfication. The bathing solution consisted of (in mM): 107 NaCl, 6 KCl, 1.2 MgSO4, 2 CaCl2, 1.2 KH2PO4, 11.5 glucose, 20 HEPES, pH 7.3 and 320 mOsm, adjusted with NaOH and sucrose, respectively.
  • Neurones were viewed under an inverted Olympus BX50WI microscope with an Olympix Peltier cooled CCD camera (PerkinElmer Life Sciences). Regions containing between 20 and 40 cells were selected, and intracellular free Ca2+ concentration was evaluated by measurement of Fura-2 fluorescence.
  • The estimated [Ca2+]I measurement was made by the ratio method using dual excitation. Excitation was performed with a commercially available monochromator-based microfluorimetry system (Olympus). Excitation light from the mercury-xenon lamp of the microfluorimetry system is passed through a rotating filter wheel and the fluorescence intensity at 510nm, caused by alternate excitation at 340nm and 380nm, was used to estimate the mean [Ca2+]I.
  • Neurones were imaged using a Plan x 40 (1.30 NA) oil-immersion lens (Nikon) and analysed using Ultraview software (PerkinElmer Life Sciences). Data acquisition was typically at 3.9s intervals. Experiments were performed at room temperature (Riccio et al., 2002).

Changes in intracellular free Ca2+ concentration were expressed as the rate of emission (510nm) for 340nm/380nm excitation (f340/380). Data were accumulated under each condition from three to five experiments. The index of fluorescence variations ΔF/F0 used to quantify the relative changes of intracellular Ca2+ was calculated as follows:

ΔF/F0 = [(f340/f380)i – (f340/f380)max] / (f340/f380)i

Where (f340/f380)i is the initial fluorescence ratio measured before application of the relevant drug or toxin and ((f340/f380)max is the maximal fluorescence ratio taken at the peak of the effect (Meunier et al., 2002).

The figures below are calcium imaging results for a test compound and ionomycin (an ionophore used in research to raise [Ca2+]I) control. Figure 1, is a sample Fura-2 imaging trace and figure 2, sample (A) normalised fluorescence ratio, and (B) index of the fluorescence variation ΔF/F0, data.

Picture2 fig7.5

Figure 1: Test compound does not alter intracellular calcium levels in DRGs measured using Fura-2 imaging techniques. Fluorescent ratio changes from plate 1 n = 48 cells labelled with Fura-2, Test compound superfused between 240 – 540 seconds, and ionomycin between 1140 – 1260 seconds.

Figure 2: Test compound does not alter intracellular calcium levels in DRG neurones measured using Fura-2 imaging techniques. A) Normalised fluorescence ratio data from 3 plates of DRGs (plate 1 n=48, plate 2 n=35 and plate 3 n=27). B) The index of the fluorescence variations ΔF/F0 show that the Test compound does not significantly alter intracellular calcium levels whereas ionomycin does ΔF/F0 = 1.33 ** p < 0.005. Student’s paired t-test.


Meunier, F. A., Feng, Z. P., Molgo, J., Zamponi, G. W., & Schiavo, G. (2002). Glycerotoxin from Glycera convoluta stimulates neurosecretion by up-regulating N-type Ca2+ channel activity. EMBO J. 21[24], 6733-6743.

Riccio, A., Mattei, C., Kelsell, R. E., Medhurst, A. D., Calver, A. R., Randall, A. D., Davis, J. B., Benham, C. D., & Pangalos, M. N. (2002). Cloning and functional expression of human short TRP7, a candidate protein for store-operated Ca2+ influx. J. Biol. Chem. 277[14], 12302-12309.


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Cell culture: Dorsal root ganglion (DRG) preparation

DRG sensory neurones were dissociated by a prolonged trypsin/collagenase treatment. They were then plated onto tissue culture plastic coated with poly-L-lysine and laminin. Nerve growth factor (NGF) was added to the medium because it affects cell phenotype. For example, NGF regulates the capsaicin-sensitivity of DRG neurones (Winter et al., 1988). The following method was modified from Lindsay, 1988. DRG were collected in calcium/magnesium-free Hank’s balanced salt solution (HBSS). Following removal of meninges and roots, the ganglia were trypsinized (normal tissue culture aliquots, 5ml) for 15 minutes at 37°C. An equal volume of Dulbecco’s modified Eagle’s medium (DMEM; high glucose) + 10 % fetal calf serum (FCS) 5ml + Penicillin 100U/ml and Streptomycin 100 µg/ml, was added to block the action of trypsin. The ganglia were collected by centrifugation at 100 g for 3 minutes. The solution was carefully removed before adding 0.1 % collagenase (500 ml of 0.5 % stock plus 2 ml HBSS) to the ganglia which were then incubated for 30 minutes at 37 °C. An equal volume of DMEM + 10% FCS (2.5ml) was used to block collagenase activity. Ganglia were again collected by centrifugation at 100 g for 30 minutes. 2 ml DMEM + FCS was added and the ganglia were then mechanically dissociated by trituration 20 times using a Pasteur pipette with a fire-polished tip. The resulting suspension was made up to 10ml with DMEM + 10% FCS and then plated onto a 100mm tissue culture dish for 1 hour at 37°C. Medium containing unattached neurones was collected, centrifuged at 200g for 5 minutes, and the medium was removed using a vacuum aspirator. The cell pellet was re-suspended with 2 ml serum-free DMEM plus 50 ng/ml NGF and 0.05% bovine serum albumin (BSA). Cells were counted with a haemacytometer. For prolonged storage, the medium was changed every 3 days with fresh DMEM plus 50 ng/ml NGF and 0.05% BSA but normally ganglia were used within a 5 days. Cells were plated at a density of ~ 200,000 cells per coverslip / 35mm dish in 2ml medium for electrophysiological recordings, see figure 1. For calcium imaging 70,000 – 100,000 DRG in 100µl medium were spotted onto a coverslip, incubated for 1hr to allow neurones to attach before flooding the dish with 2ml medium for imaging.

Picture1Figure 1: An IR-DIC micrograph of cultured DRG neurones plated on a coverslip. N.B. DRGs shown >48 hrs post culture. At this stage, cells exhibited extensive neurite outgrowth, bar = 20 μm.


Lindsay, R. M. (1988). Nerve growth factors (NGF, BDNF) enhance axonal regeneration but are not required for survival of adult sensory neurons. J. Neurosci. 8[7], 2394-2405.

Winter, J., Forbes, C. A., Sternberg, J., & Lindsay, R. M. (1988). Nerve growth factor (NGF) regulates adult rat cultured dorsal root ganglion neuron responses to the excitotoxin capsaicin. Neuron 1[10], 973-981.


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The incidence of kidney cancer found in the UK

Kidney cancer is the 8th most common cancer in the UK.1-4 The number of cases are outlined in table 1. Kidney cancer rates are reportedly higher than average in the South West and Northern England, Wales and parts of Scotland.5 Lower than average rates are documented in areas of the West Midlands, South East England and London.6,7 In terms of age 75% of cases diagnosed were aged 60 and over; with 35% of cases reported in men and women aged 75 and over.1-4 Kidney cancers are also linked to obesity and smoking which are more prevalent in deprived communities. The most recent England-wide data for 2000-2004 shows European AS incidence rates are around 11% higher for men and 30% higher for women living in more deprived areas compared with the least deprived.8 The incidence of kidney cancer also shows variation with ethnicity. In age-standardised rates, the males’ kidney cancer ranges from 11.2 to 11.8 per 100,000. This rate is significantly lower in Asian (5.3 to 9.2) and Black (5.9 to 10.8) males. The range for White females’ is 5.7 to 6.0 (per 100,000). Again the rate is lower in Black (3.0 to 6.0) and Asian (1.9 to 3.8) females’.9

Kidney cancer

Table 1: Kidney Cancer, Number of New Cases, Crude and European Age-Standardised (AS) Incidence Rates per 100,000 Population, UK, 2011. Abbreviations: LCL, Lower confidence limit; UCL, Upper confidence limit.


1. Data were provided by the Office for National Statistics on request, July 2013. Similar data can be found here:–england–series-mb1-/index.html.

2. Data were provided by ISD Scotland on request, May 2013. Similar data can be found here:

3. Data were provided by the Welsh Cancer Intelligence and Surveillance Unit on request, June 2013. Similar data can be found here:

4. Data were provided by the Northern Ireland Cancer Registry on request, June 2013. Similar data can be found here:

5. Quinn M, Wood H, Cooper N, et al. Cancer Atlas of the United Kingdom and Ireland 1991-2000. Office for National Statistics: Newport; 2005.

6. National Cancer Intelligence Network (NCIN). Cancer Incidence and Mortality by Cancer Network, UK, 2005. NCIN; London: 2008.

7. National Cancer Intelligence Network (NCIN). Cancer e-Atlas. Accessed January 2014

8. National Cancer Intelligence Network (NCIN). Cancer incidence by deprivation England, 1995-2004. NCIN; London: 2008.

9. National Cancer Intelligence Network and Cancer Research UK. Cancer Incidence and Survival by Major Ethnic Group, England, 2002-2006. 2009.

Sources of data found:

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Esomeprazole 40mg provides more effective acid control than rabeprazole 20mg

Wilder-Smith1, K. Röhss2, C. Claar-Nilsson2

1Gastrointestinal Unit & GI Physiology Lab, Bern, Switzerland; 2AstraZeneca R&D Mölndal, Mölndal, Sweden.

Introduction: In patients with symptoms of gastro-oesophageal reflux disease (GORD), the proton pump inhibitor, esomeprazole has demonstrated advantages over omeprazole, including (a) achieving more sustained acid control and (b) healing erosive oesophagitis in more patients.

Aim: To compare the effects of repeated once-daily oral dosing of esomeprazole 40 mg and rabeprazole 20 mg on intragastric pH in healthy subjects.

Methods: This was an open-label, randomized, two-way cross-over study that included 23 Helicobacter pylori-negative healthy subjects. Subjects received esomeprazole 40 mg or rabeprazole 20 mg for 5 days. The main outcome measures were time with intragastric pH>4 and pH>3 over 24 hours and median pH over 24 hours.

Results: One subject was excluded during the first treatment period. The proportion of time with intragastric pH>4 and pH>3 was significantly higher with esomeprazole compared to rabeprazole (Table 1). The mean (SD) value of the 24-hour median intragastric pH was significantly higher with esomeprazole (4.3 ± 0.7) than with rabeprazole (3.5 ± 1.1; p=0.005). The proportion of subjects with intragastric pH>4 for ≥12 hours (77% vs. 36%, p=0.04) and ≥16 hours (32% vs. 5%, p=0.03) was significantly higher in the esomeprazole, compared to the rabeprazole group. Repeated dose administration of both study drugs was well tolerated with no adverse events observed.

Table 1: Mean percentage of time with intragastric pH>4 and pH>3 on Day 5 (n=22)

Variable Treatment group* Difference
Esomeprazole 40 mg Rabeprazole 20 mg
pH>4 Estimated mean % time (95% CI) 61.0 (53.6–68.3) 45.1 (37.7–52.5) 15.8 (5.4–26.3)†
pH>3 Estimated mean % time (95% CI) 73.8 (66.4–81.1) 59.7 (52.4–67.0) 14.0 (3.8–24.3)‡

*All doses given once daily.

CI, confidence interval; †p<0.005; ‡p<0.010

Conclusion: Esomeprazole 40 mg provides significantly more effective acid control than rabeprazole 20 mg in healthy male and female subjects after repeated dosing, suggesting improved clinical efficacy in the treatment of acid-related diseases. Tolerability profiles for both drugs were comparable.

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Zoledronate – Preclinical Pharmacology

Preclinical studies indicate the zoledronate is a highly potent inhibitor of bone resorption. Indirect evidence of bone resorption was provided from a thyroparathyroidectomied (TPTx) rat model with vitamin D3-induced hypercalcaemia.  Zoledronate (ED50 of 0.07µg/kg) was more potent than earlier generation bisphosphates, including pamidronate (ED50 of 60µg/kg), at reducing hypercalcaemia. The direct effect on bone metabolism was assessed in vitamin D3-induced calcium release from mouse calvarial cultures. Zoledronate proved to be a more potent inhibitor of bone resorption (IC50 of 0.002µM) compared to pamidronate (IC50 of 0.2µM). There is a strong linear correlation between the values of the two assays.

These data were supported by studies of bone resorption in vivo. Zoledronate and pamidronate (1.7 and 390µg/kg/day sc, respectively) resulted in 50% increases in bone density in young growing rats. Zoledronate, at intermediate and high doses (0.3 and 3.0µg/kg) restored bone calcium and hydroxyproline to at over above control levels, in a rat model of bone loss induced by ovariectomy. The potency of zoledronate (0.03, 0.3 and 3.µg/kg/day) was 100 times that of pamidronate (4, 40 and 400µg/kg/day) on histomorphometric parameters of young rats. The increase in bone mass was apparent in micrographs after von Kassa staining.

The increased potency of zoledronate as an inhibitor of bone resorption was not associated with increased intolerability in the kidney or intestine. In acute in vivo screen for renal tolerability in rats, the effect of zoledronate on serum urea levels was less marked than that of pamidronate, indicating a dissociation of bone and renal effects. Despite the increased potency of zoledronate over pamidronate, tests of renal (serum urea levels) and intestinal (human intestinal and rat mucosal permeability tests) tolerability were similar in the former and less in the latter.

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Tailoring the treatment of renal anaemia to the individual – a patient-centred approach

Recombinant human erythropoietin (rh-EPO, epoetin) has been used for over two decades to treat renal anaemia. Nevertheless, there is still considerable uncertainty as to the optimal target haemoglobin (Hb) levels. A US study highlighted that higher Hb levels resulted in increased mortality in patients with pre-existing cardiac disease. This outcome was counterbalanced by three later studies in healthier dialysis patients in which normalized Hb levels improved exercise tolerance, quality of life and reduced left ventricular dilatation. These studies suggest that healthier patients, without pre-existing heart disease, could benefit from normalized Hb levels. Despite the presence of US and European guidelines, there is no clear scientific justification for a single targeted approach. Individualized treatment targets have the potential to provide better outcomes for renal anaemia patients.

Keywords anaemia; dialysis; end-stage renal disease; erythropoietin; hematocrit; target haemoglobin.


As a result of inadequate renal production of erythropoietin, anaemia is developed in patients with chronic renal failure (CRF). This results in a number of physiological abnormalities, such as left ventricular hypertrophy (LVH) and congestive heart failure (CHF), which affect the well-being of CRF patients. Patients undergo epoetin therapy to aid the reversal of anaemia. Current treatments based on US and European guidelines recommend a target Hb concentration of approximately 11–12 g/dl.2,4 This level is lower than the normal concentrations of Hb that are in the range of 13–15 g/dl for women and 14–16 g/dl for men. There are risks and benefits to the different Hb levels obtained from epoetin therapy. For example, at the subnormal concentration, there is a link with cardiovascular disease. It may, therefore, be more appropriate to use higher or normalized Hb concentrations enabling the complete correction of anaemia. However, this level of Hb can result in hypertension and advancement of renal disease.7 The concerns relating to Hb concentration and adverse effects emphasize the need for individualized treatment targets in the management of patients with renal anaemia.12


A survey of nephrologists and specialists in the field of renal anaemia generally agreed that a lower target Hb (10–12 g/dl) might be appropriate for an elderly patient with multiple medical problems including cardiac dysfunction, resulting in a limited life expectancy.7

Advantages of this subnormal Hb approach are reduced iron deficiency, treatment cost, vascular access problems and cardiac morbidity and mortality. The presence of co-morbid conditions may influence the target Hb concentration. A US Normal Hematocrit Trial consisted of subjects with CHF or ischemic heart disease. Here subnormal hematocrit (hct) levels were recommended for patients with heart disease, as the higher hct group had an increased incidence of death or non-fatal myocardial infarction (risk ratio 1.3).3 Safety concerns over anaemia correction with epoetin have seen an increase in the rate of vascular access thrombosis.1 Hence making the choice of subnormal Hb levels a safer option. The use of low Hb targets also reduces the economic burden. This can be considerable as renal anaemia is a long-term problem, persisting until death or a kidney transplant.12 However this subnormal Hb level would not achieve maximal clinical benefit for all patients.


A second case study was considered in a survey of nephrologists. It was generally agreed that a higher target Hb concentration (12–14 g/dl) might be appropriate for a fit young man with a physically demanding job who has no significant co-morbidity and a very active lifestyle.7

A number of studies showed that patients with a higher Hb (and Hct) had a significantly improved quality of life,1,3,5 and a reduced probability of requiring a blood transfusion compared with patients with a low Hct. Symptoms of fatigue and depression showed improvements those of patients with a low Hb target after 24 weeks.5 It was also noted that there was no significant difference in the incidence of vascular access thrombosis, cardiac events or death between the two patient groups, although patients with higher Hb levels were more likely to require antihypertensive medication.5 More recent studies have now shown that increasing the Hb target in certain patient populations can produce benefits without an unacceptable increase in adverse effects.

A large number of studies have evaluated the benefits arising from treatment of anaemia in patients with end-stage renal disease (ESRD) undergoing dialysis. These patients often present with cardiac abnormalities, such as LVH, which show improvement but not normalization following epoetin treatment.6,8 They observed a slower progression of left ventricular (LV) dilatation in patients with asymptomatic LV hypertrophy when on a higher Hb target. When LV dilatation was already established, no benefit of a higher Hb level was observed. Furthermore, there was no significant difference in the incidence of vascular access thrombosis, cardiac events or death between the low and normalized Hb groups.5

An Australian study investigated the effect of normalizing Hb levels in 14 hem dialysis (HD) patients who were in otherwise good health.9,10 Patients with a high Hb target experienced significant improvements over lower target patients in cardiac output, LV end diastolic diameter and quality of life. In addition, LV mass index was significantly lower in patients with a high Hb target compared with baseline. Furthermore, those with the 14 g/dl Hb target could perform more work and consumed 18% more oxygen than those on the lower target. In a second Australian study in HD patients excluding diabetics, the elderly and patients with severe co-morbidities, increasing the Hb target improved quality of life.11 There was also a decrease in the number and duration of hospitalizations in this patient group which may help offset the cost of the increase in epoetin required to normalize Hb levels.

There no significant increase in the incidence of arterial hypertension when Hb levels were increased. Thus, younger, healthier patients seem to gain significant benefits from higher Hb levels without experiencing an increase in adverse effects.12


When considering epoetin treatment for CRF patients with anaemia, studies of Hb levels have shown conflicting results. Outcomes depend upon the health status of patients studied. Normalized Hb levels may be unfavourable to patients with pre-existing cardiac disease, whereas healthier patients could attain an improved exercise capacity, better quality of life and some protection against developing serious cardiac morbidities. Hence, a single Hb target will not achieve a maximal clinical benefit for all renal anaemia conditions. Evidence-based criteria for individualizing renal anaemia treatment are likely to yield better outcomes for patients.


  1.  Association between recombinant human erythropoietin and quality of life and exercise capacity of patients receiving haemodialysis. Canadian Erythropoietin Study Group. BMJ 1990; 300:573-578.
  2.  NKF-DOQI clinical practice guidelines for the treatment of anemia of chronic renal failure. National Kidney Foundation-Dialysis Outcomes Quality Initiative. Am.J.Kidney Dis. 1997; 30:S192-S240.
  3. Besarab A, Bolton WK, Browne JK, et al. The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin. N.Engl.J.Med. 1998; 339:584-590.
  4. Eknoyan G, Levin NW, Eschbach JW, et al. Continuous quality improvement: DOQI becomes K/DOQI and is updated. National Kidney Foundation’s Dialysis Outcomes Quality Initiative. Am.J.Kidney Dis. 2001; 37:179-194.
  5. Foley RN, Parfrey PS, Morgan J, et al. Effect of hemoglobin levels in hemodialysis patients with asymptomatic cardiomyopathy. Kidney Int. 2000; 58:1325-1335.
  6. Jeren-Struji’c B, Raos V, Jeren T, et al. Morphologic and functional changes of left ventricle in dialyzed patients after treatment with recombinant human erythropoietin (r-HuEPO). Angiology 2000; 51:131-139.
  7. Macdougall IC. Individualizing target hemoglobin concentrations–tailoring treatment for renal anemia. Nephrol.Dial.Transplant. 16 Suppl 2001; 7:9-14.
  8. Massimetti C, Pontillo D, Feriozzi S, et al. Impact of recombinant human erythropoietin treatment on left ventricular hypertrophy and cardiac function in dialysis patients. Blood Purif. 1998; 16:317-324.
  9. McMahon LP, Mason K, Skinner SL, et al. Effects of hemoglobin normalization on quality of life and cardiovascular parameters in end-stage renal failure. Nephrol.Dial.Transplant 2000; 15:1425-1430.
  10. McMahon LP, McKenna MJ, Sangkabutra T, et al. Physical performance and associated electrolyte changes after hemoglobin normalization: a comparative study in haemodialysis patients. Nephrol.Dial.Transplant 1999; 14:1182-1187.
  11. Moreno F, Sanz-Guajardo D, Lopez-Gomez JM, et al. Increasing the hematocrit has a beneficial effect on quality of life and is safe in selected hemodialysis patients. Spanish Cooperative Renal Patients Quality of Life Study Group of the Spanish Society of Nephrology. J.Am.Soc.Nephrol. 2000; 11:335-342.
  12. Muirhead N. A rationale for an individualized hemoglobin target. Nephrol.Dial.Transplant 17 Suppl 2002; 6:2-7.


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How to Structure and Present a Scientific Poster

Congratulations! You have had your abstract accepted, and you can now develop a poster to present at a conference. This article describes what type of information you should include and how it should be structured into a poster format.

Why is there a need to present a poster?

Posters enable a larger number of scientist to present their data than would be viable through oral presentations. It provides the presenter with an opportunity to present their current data to the scientific community. The posters can be displayed before the authors are present, this gives the attendees the chance to read the information, and get an understanding of the data prior to discussions with the presenter. A poster enables the researcher to:

  • Showcase data from a current project to experts in the field.
  • Enable discussion of the data from an ongoing project with colleagues.
  • Develop collaborations with colleagues/labs to progress the work.
  • A networking opportunity to learn about job opportunities.
  • Attendees can ask in-depth questions into the presenter.

A starting point

You need to start compiling resources to develop a poster well in advance of the conference, maybe up to six months in advance. Experiments/data collection can be ongoing and added nearer the submission date, but knowing you have the majority of the information in place will reduce stress and need to rush, which can result in errors. Useful information to starts with:

  • The title and abstract submitted and accepted by the conference.
  • Availability of supervisor/colleagues to check and discuss project/data and poster.
  • Institutions resources to print poster, in good time to be ready for conference.

Planning the poster

When planning the poster you need to adhere to the guidelines for poster presentation at the conference you are attending. It is also important to make the poster understandable on its own. This is because it may be viewed by an attendee when you are not present at the poster, or you are speaking to another colleague. The poster is likely to be displayed in the hallway of you institution post-conference, and passer-by will need to understand the work on its own. Other considerations are:

  • Select a clear, specific topic and present only the highlights.
  • Choose interesting images and figures that will present the key messages to attract viewers.
  • Only use a small amount of text, in a large clear font (about 500-1000 words).

Development of poster

Start designing and developing the poster well in advance of the conference presentation day. Even if you haven’t got all the data yet for the poster. Keep the poster simple. This is by having a simple story for the data, have a lot of white space, with a small amount of text and clear simple figures. High-quality figures can attract readers to the poster, and make complex data more coherent and easier to understand. Other considerations:

  • Make sure the text and images are big enough for attendees to read easily.
  • Draft the writing well in advance, in order to revise, grammar, sentence structure and data points. Get feedback on your writing from a colleague.
  • View your poster from the perspective of a conference attendee. Is it a presentation that you could understand and enjoy reading?

Arrangement of Poster

The abstract submitted to the conference should form the basis of the poster but is not usually included on it.

  • Include substantial white space.
  • Have 3 to 5 columns of content on a poster in landscape format.
  • Organise the poster in a simple manner, for example;
    • Introduction, Methods, Results, Conclusions, References & Acknowledgements.

Preparing the poster

The title:

Keep the title as short as possible, using large type (about 2.5 cm high, 72 point type). It should make the attendee want to read the poster. It should be concise and fascinating. It could highlight a new finding or pose an interesting question. Perhaps, only use capital letters on the ‘main’ words. For example:

  • Enhance the quality and duration of peoples’ lives.
  • Enhance the Quality and Duration of Peoples’ Lives.

The images:

These include graphs, flow charts, photographs. Make sure you use colours effectively and that contrast well. It is usually better to use graphs rather than tables, as they may require less studying.

  • Label all of the images.
  • Make the images simple and uncluttered to increase understanding.

The text:

Proofread the text carefully, and keep the word count low.

  • Use large enough type (at least 18 points).
  • Use bullet-pointed or numbered lists, rather than paragraphs.
    • Keep paragraphs short if needed.

Poster Presentation.

Organisation to be ready for the day:

  • Carry your poster with you, not in your checked luggage. In a heavy duty teletube.
  • Have a backup of the poster on a USB stick and on email.

These tips will enable you to stay calm when travelling to and during the conference. Carry the poster with you will reduce the likelihood of it being lost.

Carrying it in suitable luggage, such as a teletube, which you may be able to borrow from your lab/department, will keep the poster in good condition, without being folded, creased or marked.

Having backup copies of the poster on a USB stick and/or email will enable you to present the work if the poster did get lost. Printing out paper copies would also be a useful option.

Professional and welcoming impression:

  • Dress smartly and avoid a colour clash with the poster.
  • Smile, and be approachable and ready to talk.

Dressing smartly on the day can give you more confidence, and a professional impression to colleagues (who could be potential collaborators/employers) when discussing your work.

Be welcoming to attendees, have an open stance, smile and say hello. Point to the relevant parts of the poster as you talk to your audience, which could be one or a small group of people. I someone new comes along as you are talking, acknowledge them with eye contact, and ask them at the end of your chat it there is anything they missed, or that needs further clarification.

Preparation – know your subject:

  • Make a list of questions you could be asked about your work.
  • Prepare descriptions of your work of different length.
  • Ask questions, to gain more knowledge and information about your project area.

It is important to know your subject, from researching the background to your subject and the classic and current literature. With this information is had, jot down some potential questions and rehearse answers with friend/colleagues prior to the poster presentation. It you do not know the answer to a question it is important to be honest and say so, perhaps asking the attendee for their ideas and thoughts.

Descriptions of various lengths should be prepared for your poster. A short ‘elevator pitch’ this could be a two minute summary of your study, explaining 1) What is the research subject? 2) What have you discovered? 3) Why is that important?

It this information has interested the audience, you can carry on to a longer description of the study described on the poster. They could take in the region of ten minutes, answering the three questions, above, in more detail.

Networking during and after the conference:

  • Take advantage of the opportunity to network and get feedback on your work.
  • Have business cards available.
  • Consider having handouts and/or people signing up for further details.

Business cards and handouts, for examples, an A4 copy of the poster, a synopsis of key findings, or additional data can be useful materials. They enable attendees to consider your work over a longer time scale and contact you after the event, for further discussions. Handouts can prevent some people engaging with you, preferring the ‘easy option’ of taking the handout and moving on.


Erren, T.C. and Bourne, P.E. (2007) Ten simple rules for a good poster presentation. PLoS Comput Biol, 3 (5), e102.

Gastrel, B. and Day, R.A. (2017) How to prepare a poster. In: How to write and publish a scientific paper. 8th edition. Cambridge, pp. 183-187.

Purrington, C. Academic Tips. Designing conference posters. [Online] [Accessed 28th December 2017].

Scientifica. NeuroWire: Tips for presenting your scientific poster at a conference. [Online] [Accessed 28th December 2017].

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