A few tips on writing a successful research Grant.
Remember, of all grants submitted, some 30% will be significantly flawed because they are not feasible, or they are too speculative, or there are other specific issues in the work planned that make them non-competitive.
However, few funding bodies fund more than 25% and most rather fewer, so your task is to make sure that your grant is not fundamentally flawed, and that it appeals to the people assessing it to the extent that it is the top 1/3 of those not fatally flawed. Otherwise you will be facing the sort of feedback that is very frustrating “No significant criticisms, but not in the funding range”.
Here are a few areas where many people make mistakes, so learn from theirs!
1Read the funder's guidance notes before completing the application form
You need to check such things as your eligibility to apply, and that of any co-Is. Check the levels of costs permitted under specific headings. Do not ask for more than is permitted: for example maximum travel budgets are often specified. Check the way you can write your application – pages or words permitted, whether you can append figures of pilot data, or if they can go into the body of the text. As an example, Wellcome allows you 3,500 words of text in the main case for support, and you can either append up to 5 pages of figures OR embed them in the text, where they and any contained figure legends do not count towards the word limit. BBSRC has specific page limits instead. This can lead to temptation to cram in as much text as possible in the smallest permitted font size. Resist that temptation and see the examples later on in the document.
Even if you have applied before to this funder, read the notes again. They do change from time to time. If you do something that is wrong, it may result in the application being returned to you, which is bad enough, or it may mean that the reviewers read it and on seeing your inappropriate request for 3x as much travel funding as is permitted, think immediately “These people did not read the notes. I wonder what else is wrong with this grant?” Just what you need to avoid if you are trying to get into the funding range.
2Make sure that your abstract and lay summary (or equivalents) are clear informative, interesting and understandable by the target audience.
A lay summary should be understandable by someone without higher degree levels of scientific experience. Try it out on someone appropriately inexpert in the subject.
3 If possible, state your hypothesis or research question in clear unequivocal terms.
Some research is not based on testing a hypothesis, but the much is. Reviewers like to know your underlying rationale for the work.
4 Give a global aim for the work and a series of SMART objectives.
SMART is an acronym for:
Specific
This is the difference between 'Answer the phone quickly' which is not specific, and ‘answer the phone within 3 rings' , which is.
Measurable
Can success be assessed after the event? "Investigate glutamate signalling in bone" is not measurable. "Determine the effect of glutamate receptor antagonist drugs x&y on bone cell proliferation and viability" is measurable. Essentially your objectives should imply a criterion for success and failure within the wording. If at the end of 3 years, you have investigated x, explored y, and characterised z, you could have met your objectives (and spent all the money), but discovered nothing whatever.
Achievable
Can the objective be accomplished?
Realistic Can the objective be met with a reasonable amount of effort by the applicants with the resources they request?
Time Based / Time limited Set specific goals for completion of milestone activities. Does the work proposed fit into the available time?
I tend to write my aim and objectives in a rather specific way to include a global hypothesis. Here is a real scientific example (Ignore the acronyms – they have been spelled out earlier in the text)
Aim and objectives of the proposed project
The aim of this project is to test two hypotheses: 1) that RAMPs 1, 2 and 3 regulate the signalling function of receptors for parathyroid hormone, vasoactive intestinal peptide, N-ethylmaleimide-sensitive factor, extracellular calcium and glucagon, 2) that RAMPs regulate expression, trafficking or function of additional group A, and C G-protein coupled receptors.
The specific objectives are to:-
1)Determine the ability of PTH, VIP, NSF, glucagon and calcium to activate downstream signaling pathways in the presence or absence of novel RAMP 1,2 and 3 ECD domain antibodies by measurement of intracellular calcium and cAMP activation.
2)Determine the ability of RAMPs 1, 2 and 3 to regulate intracellular trafficking of those receptors by siRNA knockdown and confocal microscopy.
3)Screen for functional interactions of RAMPs with examples of GPCRs from groups A (Growth Hormone and oxytocin) and C (Metabotropic glutamate, GABA) using siRNA knockdown and ECD domain antibody blockade.
4)Determine the effect of PTH, VIP, NSF, glucagon and calcium on RAMP mRNA and protein expression.
Nb these are not time limited but in this application, we included a Gantt chart to show when things would be done, and also specific time line milestones in with the detailed plan of experiments.
5Remember that reviewers of your grant for the funding body will have others to look at, and other work to do.
Make their job easy by using hierarchy in the main body of the application, using subheadings, bold and different font sizes to give your text visual appeal. If possible within constraints of space, embed figures tables and other non-text items into the main case for support rather than appending as a separate document.
Compare these two bits of text.
2.a.1Background
Bone is a dynamic tissue allowing the healthy organism to adapt its skeletal architecture in response to changes in the mechanical loads placed upon it. Such alterations in bone architecture require the actions of cells, and in bone, the orchestration of different populations responsible for formation and resorption. As a result of perception of external stimuli that include the effects of diet, exercise, systemic osteotropic hormones (whether acting directly on bone cell receptors or centrally in the brain and via the sympathetic nervous system), modified by the effects of ageing and environmental factors (e.g. smoking, caffeine consumption etc), bone may be perceived to be adequate for its function, inadequate or excessively massive. In response to the results of that balance of influences, bone is either formed, or resorbed to tune architecture to current function Of these influences, within each of us as individuals, the most important is probably the effect of exercise or habitual activity. High strain* environments as generated by high impact physical exercise, result in bone formation. In contrast the absence of a load stimulus, for example due to a even relatively short periods of inactivity, lead to bone loss. This adaptation in bone structure, effected by the processes of bone modelling and remodelling, is the result of the orchestrated activity of bone forming osteoblasts and bone resorbing osteoclasts. However, not all parts of the skeleton respond in the same way to loading: Indeed it would be costly and inefficient to design a system for regulation of skeletal structure where that was the case. There are profound differences in bone mass and architecture at different skeletal sites that requires that there is a mechanism for tissue homeostasis that takes account of site-specific or positionally derived cues.
Do you want to read any more?
How about this – even if the topic does not interest you, I hope you see it as more appealing visually
2.a.1Background
Bone is a dynamic tissue allowing the healthy organism to adapt its skeletal architecture in response to changes in the mechanical loads placed upon it. Such alterations in bone architecture require the actions of cells, and in bone, the orchestration of different populations responsible for formation and resorption. As a result of perception of external stimuli that include the effects of diet, exercise, systemic osteotropic hormones (whether acting directly on bone cell receptors or centrally in the brain and via the sympathetic nervous system), modified by the effects of ageing and environmental factors (e.g. smoking, caffeine consumption etc), bone may be perceived to be adequate for its function, inadequate or excessively massive. In response to the results of that balance of influences, bone is either formed, or resorbed to tune architecture to current function
Of these influences, within each of us as individuals, the most important is probably the effect of exercise or habitual activity. High strain environments as generated by high impact physical exercise, result in bone formation. In contrast the absence of a load stimulus, for example due to a even relatively short periods of inactivity, lead to bone loss. This adaptation in bone structure, effected by the processes of bone modelling and remodelling, is the result of the orchestrated activity of bone forming osteoblasts and bone resorbing osteoclasts.
However, not all parts of the skeleton respond in the same way to loading: Indeed it would be costly and inefficient to design a system for regulation of skeletal structure where that was the case. There are profound differences in bone mass and architecture at different skeletal sites that requires that there is a mechanism for tissue homeostasis that takes account of site-specific or positionally derived cues. While bone cells from different regions of the skeleton are similar in their expression of receptors for different osteotropic agents etc., and are exposed to the same levels of circulating osteotropic hormones, their interactions with the major regulator of bone properties (mechanical strain) are radically different.