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!

1 Read 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.

2 Make 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.
5 Remember 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.1 Background
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.1 Background

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.