How to write abstract

1
How to write abstract
2
How to Write an Abstract
What the reader needs to know to understand why
you did the experiment Why you did the
experiment How you did the experiment What you
saw How you interpret the data The Good and
the Bad
3
How to Write an Abstract
What the reader needs to know to understand why
you did the experiment Why you did the
experiment How you did the experiment What you
saw How you interpret the data The Good and the
Bad
Significance/importance Data from the
literature Previous results
4
How to Write an Abstract
What the reader needs to know to understand why
you did the experiment Why you did the
experiment How you did the experiment What you
saw How you interpret the data The Good and
the Bad
Hypothesis or aim To determine or To define
5
How to Write an Abstract
What the reader needs to know to understand why
you did the experiment Why you did the
experiment How you did the experiment What you
saw How you interpret the data The Good and
the Bad
Methods in brief One sentence or possibly a
phrase, unless the abstract defines/characterizes
a new technique
6
How to Write an Abstract
What the reader needs to know to understand why
you did the experiment Why you did the
experiment How you did the experiment What you
saw How you interpret the data The Good and
the Bad
Results Sometimes includes graphs or
figures Often includes numbers with SEMs or SDs
7
How to Write an Abstract
What the reader needs to know to understand why
you did the experiment Why you did the
experiment How you did the experiment What you
saw How you interpret the data The Good and
the Bad
Conclusions and interpretation Meaning and/or
significance May include speculations or
proposal of a model
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example
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
9
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
10
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
11
Method, animals, group separation can be ignored,
if it is not special.
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
12
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
13
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
14
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
Off course, rational of the results is
important. Observe your results till you can make
the hole on the printed result.
15
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
Conclusion must be simple as much as possible.
You can include perspectives if it fits for the
interest of the meeting.
16
One more,
You should note by active voice, not by passive
voice, as much as possible (because passive
sentence is complicated even for native English
speaker, I heard).
We have previously reported that the renal
medullary ETB receptor inhibits sodium
reabsorption via nitric oxide synthase (NOS) 1.
In addition, we have also demonstrated that
endothelin (ET)-1-induced diuresis and
natriuresis in female rats are mediated not only
by the ETB receptor, but surprisingly, also by
the ETA receptor. Therefore, the present study
was conducted to determine the involvement of
NOS1 in ET-1/ETA-dependent diuretic and
natriuretic responses in renal medulla of female
ETB-deficient rats. Infusion of ET-1 (0.45
µg/kg/h n8) directly into the renal medulla of
anesthetized rats markedly increased urine flow
(UV 4.6 0.2 µl/min during baseline and 9.2
0.4 µl/min during ET-1 infusion plt0.01) and
urinary sodium excretion (UNaV 0.40 0.03
µmol/min during baseline and 0.98 0.09 µmol/min
during ET-1 infusion plt0.01). Pretreatment with
NG-propyl-l-arginine (NPA 10 µg/kg/h, n4), a
selective inhibitor of NOS1, suppressed
ET-1-induced increases in UV and UNaV (5.4 0.4
µl/min and 0.60 0.05 µmol/min, respectively
plt0.01). Neither NPA nor ET-1 affected renal
medullary blood flow at these doses
(laser-Doppler flowmetry). These results suggest
that NOS1 is responsible for the ETA
receptor-dependent water and sodium excretion in
rats, and that these responses do not result from
a change in medullary hemodynamics.
For example
active
or
Urine flow and urinary sodium excretion were
markedly increased by infusion of ET-1 directly
into the renal medulla of anesthetized rats.
passive
17
Abstract
You usually have word limitation, usually it is
250 words.
(Possible) bad example
May be better
Background and hypothesis
Background and hypothesis
Figure 1 2
Figure 1 2
Figure 3, 4, 5, 6 and 7
Figure 3, 4, 5, 6 and 7
conclusion
conclusion
18
When you submit, the system sometimes asks..
category?
Aldosterone and adrenal mechanisms Angiotensin
receptors and signal transduction Cardiac
hypertrophy and dysfunction Cardiovascular-renal
axis Central neural mechanisms Clinical
hypertension Endothelial function and
interactions Epidemiological aspects of
hypertension etc.
who are going to be excited about your abstract?
oral or poster?
Choose oral. Even if you choose poster, the
committee will put your excellent abstract as oral