gene_test.p1.out

Third I-GENE
, O
consistent O
with O
these O
data O
, O
N I-GENE
- I-GENE
acetylcysteine I-GENE
reduced O
the O
stimulatory I-GENE
effect O
of O
HGF I-GENE
on O
stress O
kinase I-GENE
activities O
, O
while O
p42 I-GENE
/ I-GENE
44 I-GENE
mitogen I-GENE
activated I-GENE
kinase I-GENE
( O
MAPK I-GENE
) O
was O
unmodified I-GENE
, O
suggesting O
an O
involvement O
of O
c I-GENE
- I-GENE
Jun I-GENE
- I-GENE
N I-GENE
- I-GENE
terminal I-GENE
kinase I-GENE
( O
JNK I-GENE
) O
and O
p38 I-GENE
MAPK I-GENE
in O
HIF I-GENE
- I-GENE
1 I-GENE
activation O
. O

The O
Sox I-GENE
gene I-GENE
family I-GENE
( O
Sry I-GENE
like I-GENE
HMG I-GENE
box I-GENE
gene I-GENE
) O
is O
characterised I-GENE
by O
a O
conserved O
DNA I-GENE
sequence I-GENE
encoding O
a O
domain I-GENE
of O
approximately O
80 O
amino O
acids O
which O
is O
responsible O
for O
sequence I-GENE
specific I-GENE
DNA I-GENE
binding I-GENE
. O

Respiratory I-GENE
parameters O
suggested O
that O
M6G I-GENE
produced O
less O
respiratory O
depression O
than O
morphine O
. O

This O
slow O
progression O
through O
the O
early I-GENE
G1 I-GENE
- I-GENE
phase O
resulted O
in O
decreased O
phosphorylation O
of O
the O
RB I-GENE
protein I-GENE
and O
subsequent O
delay O
into O
the O
S I-GENE
phase O
transition O
. O

Responses I-GENE
of O
TLD I-GENE
Mg2SiO4 I-GENE
: O
Tb I-GENE
and O
radiophotoluminescent I-GENE
glass O
to O
heavy I-GENE
charged O
particles O
and O
space O
radiation O
. O

In O
the O
meantime I-GENE
, O
one O
has O
succeeded I-GENE
to O
establish O
the O
deammonification I-GENE
processes O
in O
a O
continuous O
flow O
moving I-GENE
- I-GENE
bed I-GENE
pilot I-GENE
plant O
. O

An O
18 O
- I-GENE
kb O
genomic O
clone O
including O
sequences I-GENE
encoding O
for O
the O
two O
GHS I-GENE
- I-GENE
R I-GENE
variants I-GENE
was O
isolated O
. O

In O
the O
further O
development O
of O
bladder O
neck O
suspension I-GENE
according O
to O
Stamey I-GENE
- I-GENE
Pereyra I-GENE
, O
the O
use O
of O
miniature I-GENE
bone O
anchors I-GENE
received O
considerable O
support O
. O

CHAP I-GENE
and O
the O
Department I-GENE
of O
Veterans I-GENE
Affairs I-GENE
. O

Finally O
, O
a O
chromogenic I-GENE
method O
was O
used O
, O
based O
on O
thrombin I-GENE
inhibition O
and O
the O
substrate I-GENE
S I-GENE
- I-GENE
2238 I-GENE
. O

As O
an O
oral O
, O
nontoxic I-GENE
compound O
with O
a O
mechanism O
of O
action O
distinct O
from O
that O
of O
ABL I-GENE
tyrosine I-GENE
kinase I-GENE
inhibition O
, O
FTI I-GENE
SCH66336 I-GENE
shows O
promise I-GENE
for O
the O
treatment O
of O
BCR I-GENE
/ I-GENE
ABL I-GENE
- I-GENE
induced O
leukemia I-GENE
. O

Recruitment I-GENE
of O
an O
RNA I-GENE
polymerase I-GENE
II I-GENE
complex I-GENE
is O
mediated O
by O
the O
constitutive O
activation O
domain I-GENE
in O
CREB I-GENE
, O
independently O
of O
CREB I-GENE
phosphorylation O
. O

Our O
results O
are O
reassuring I-GENE
and O
we O
therefore O
advise I-GENE
that O
in O
patients O
undergoing O
free O
jejunum I-GENE
flap O
reconstruction O
of O
the O
hypopharyngo I-GENE
- I-GENE
esophageal O
tract O
voice I-GENE
restoration I-GENE
should O
be O
attempted I-GENE
by O
placing I-GENE
a O
voice I-GENE
prosthesis I-GENE
through O
a O
secondary O
tracheo I-GENE
- I-GENE
esophageal O
puncture I-GENE
and O
providing O
intensive O
speech O
training O
. O

Regarding I-GENE
gestational O
risk O
, O
3 I-GENE
, O
243 I-GENE
drugs O
used O
( O
34 O
%) O
belonged I-GENE
to O
category O
A I-GENE
risk O
, O
1 I-GENE
, O
923 I-GENE
( O
22 O
. O
6 I-GENE
%) O
to O
category O
B I-GENE
, O
3 I-GENE
, O
798 I-GENE
( O
39 O
. O
7 O
%) O
to O
category O
C I-GENE
, O
289 I-GENE
( O
3 I-GENE
. O
0 O
%) O
to O
category O
D I-GENE
, O
and O
55 O
( O
0 O
. O
6 I-GENE
%) O
to O
category O
X I-GENE
. O

The O
human I-GENE
ABCG1 I-GENE
gene I-GENE
encodes O
a O
member O
of O
the O
ATP I-GENE
- I-GENE
binding I-GENE
cassette I-GENE
( O
ABC I-GENE
) O
superfamily I-GENE
of O
transporter I-GENE
proteins I-GENE
and O
is O
highly O
induced O
when O
macrophages O
are O
incubated O
with O
oxysterols I-GENE
. O

At O
the O
end O
of O
each O
day O
of O
migration O
the O
pulmonary O
hemolymph I-GENE
PO2 O
decreased O
by O
1 I-GENE
- I-GENE
2 I-GENE
. O
5 I-GENE
kPa I-GENE
, O
but O
the O
hemocyanin I-GENE
remained O
saturated I-GENE
with O
O2 O
and O
the O
venous O
reserve O
was O
largely O
unchanged O
( O
O2 O
> O
0 O
. O
4 I-GENE
mmol O
x O
l O
(- O
1 I-GENE
)). I-GENE

We O
have O
investigated O
the O
role O
of O
NGF I-GENE
in O
regulating O
gene I-GENE
transcription I-GENE
in O
PC12 O
and O
INS I-GENE
- I-GENE
1 I-GENE
cells O
, O
in O
order O
to O
define O
if O
there O
are O
NGF I-GENE
- I-GENE
regulated O
genes I-GENE
per O
se I-GENE
. O

Thus O
, O
through O
a O
change O
in O
conformation O
upon O
repair I-GENE
of O
the O
6RG I-GENE
lesion O
, O
MGMT I-GENE
switches I-GENE
from O
a O
DNA I-GENE
repair I-GENE
factor I-GENE
to O
a O
transcription I-GENE
regulator I-GENE
( O
R I-GENE
- I-GENE
MGMT I-GENE
), O
enabling I-GENE
the O
cell O
to O
sense O
as O
well O
as O
respond O
to O
mutagens I-GENE
. O

TaqMan I-GENE
analysis O
of O
gene I-GENE
expression O
following O
chronic O
FA I-GENE
treatment O
showed O
neither O
a O
decrease O
in O
the O
amount O
of O
leptin I-GENE
receptor I-GENE
( O
Ob I-GENE
- I-GENE
R I-GENE
) O
mRNA I-GENE
, O
nor O
an O
increase O
in O
the O
negative O
regulators O
of O
STAT I-GENE
signalling O
, O
SOCS3 I-GENE
( O
suppressors O
of O
cytokine O
signalling O
) O
or O
cytokine O
inducible I-GENE
sequence I-GENE
( O
CIS I-GENE
). O

Nine I-GENE
animals O
served I-GENE
as O
control O
animals O
, O
whereas O
20 O
animals O
received O
a O
focal I-GENE
arachnoid I-GENE
scar I-GENE
at O
C1 I-GENE
- I-GENE
C2 I-GENE
, O
which O
was O
produced O
by O
placement O
of O
a O
kaolin I-GENE
- I-GENE
soaked I-GENE
fibrin I-GENE
sponge I-GENE
on O
the O
posterior O
surface O
of O
the O
spinal O
cord O
. O

A I-GENE
comparison O
of O
the O
duplicated O
Vkappa I-GENE
genes I-GENE
suggests O
positive O
selection O
on O
the O
complementarity I-GENE
- I-GENE
determining O
regions O
of O
the O
duplicated O
genes I-GENE
by O
point O
mutations O
. O

They O
have O
not O
been O
previously O
reported O
as O
a O
reaction O
to O
i O
. O
v I-GENE
. O
contrast O
material O
. O

The O
presence O
of O
AS I-GENE
- I-GENE
oligo I-GENE
had O
no O
further O
effect O
on O
the O
FSH I-GENE
- I-GENE
mediated O
activation O
of O
the O
EB I-GENE
*- I-GENE
mTf I-GENE
- I-GENE
CAT I-GENE
construct I-GENE
but O
reduced O
cAMP I-GENE
- I-GENE
mediated O
activation O
. O

The O
homologous O
active O
- I-GENE
site I-GENE
framework I-GENE
of O
these O
enzymes O
with O
distinct O
structures O
suggests O
convergent I-GENE
evolution O
of O
a O
common O
catalytic O
mechanism O
. O

Additional I-GENE
education O
and O
research O
is O
needed O
to O
provide O
further O
direction O
for O
intervention O
and O
incorporation O
into O
practice O
. O

Many O
of O
the O
important O
genes I-GENE
associated I-GENE
with O
G1 I-GENE
regulation O
have O
been O
shown O
to O
play O
a O
key O
role O
in O
proliferation O
, O
differentiation O
and O
oncogenic I-GENE
transformation O
and O
programmed O
cell O
death O
( O
apoptosis O
). O

Drug O
interactions O
have O
been O
found O
with O
drugs O
that O
compete O
for O
the O
same O
CYP450 I-GENE
isoenzymes I-GENE
as O
statins I-GENE
. O

Regulation O
of O
laminin I-GENE
beta2 I-GENE
chain I-GENE
gene I-GENE
expression O
in O
human I-GENE
cancer O
cell O
lines O
. O

Mutation O
of O
the O
NF I-GENE
- I-GENE
kappaB I-GENE
site I-GENE
in O
the O
Mdr1b I-GENE
promoter I-GENE
prevents O
its O
induction O
by O
TNF I-GENE
- I-GENE
alpha I-GENE
. O

Effect O
of O
heat I-GENE
treatments O
on O
the O
meltability I-GENE
of O
cheeses I-GENE
. O

In O
vitro O
binding I-GENE
studies O
demonstrate O
that O
eIF I-GENE
- I-GENE
5A I-GENE
is O
required O
for O
efficient O
interaction O
of O
Rev I-GENE
- I-GENE
NES I-GENE
with O
CRM1 I-GENE
/ I-GENE
exportin1 I-GENE
and O
that O
eIF I-GENE
- I-GENE
5A I-GENE
interacts O
with O
the O
nucleoporins I-GENE
CAN I-GENE
/ I-GENE
nup214 I-GENE
, O
nup153 I-GENE
, O
nup98 I-GENE
, O
and O
nup62 I-GENE
. O

Forced I-GENE
expression O
of O
BZAP45 I-GENE
strongly O
stimulates O
H4 I-GENE
promoter I-GENE
( O
nt O
- I-GENE
215 O
to O
- I-GENE
1 I-GENE
)/ O
CAT I-GENE
reporter I-GENE
gene I-GENE
activity O
. O

Copyright O
2001 I-GENE
Academic O
Press O
. O

The O
diagnosis O
of O
HCV I-GENE
arthritis O
in O
patients O
with O
positive O
rheumatoid I-GENE
factor I-GENE
and O
chronic O
inflammatory O
polyarthritis I-GENE
may O
be O
difficult O
. O

The O
UBA I-GENE
domains I-GENE
of O
RAD23 I-GENE
and O
DDI1 I-GENE
are O
required O
for O
these O
interactions O
. O

E47 I-GENE
protein I-GENE
levels O
remain I-GENE
high O
until O
the O
double O
positive O
developmental O
stage O
, O
at O
which O
point O
they O
drop O
to O
relatively O
moderate O
levels O
, O
and O
are O
further O
downregulated I-GENE
upon O
transition O
to O
the O
single O
positive O
stage O
. O

By O
Caveman I-GENE
. O

These O
findings O
suggest O
that O
the O
adapter I-GENE
Gab1 I-GENE
may O
redirect I-GENE
c I-GENE
- I-GENE
Met I-GENE
signaling O
through O
PI3K I-GENE
away I-GENE
from O
a O
c I-GENE
- I-GENE
Akt I-GENE
/ I-GENE
Pak1 I-GENE
cell O
survival O
pathway O
. O

Another O
mutant I-GENE
, O
T255A I-GENE
, O
lost O
the O
ability O
to O
bind O
E4orf6 I-GENE
, O
but O
unexpectedly I-GENE
, O
viral I-GENE
late O
- I-GENE
gene I-GENE
expression O
was O
not O
affected O
. O

However O
, O
the O
N63S I-GENE
mutation I-GENE
in O
the O
wild I-GENE
- I-GENE
type I-GENE
VP5 I-GENE
background O
increased O
the O
interaction O
, O
as O
judged O
by O
the O
beta I-GENE
- I-GENE
galactosidase I-GENE
activity O
, O
by O
a O
factor I-GENE
of O
9 O
relative O
to O
when O
the O
PR7 I-GENE
mutation I-GENE
was O
present O
. O

Here O
we O
report O
the O
isolation O
and O
characterization O
of O
the O
forkhead I-GENE
homologue I-GENE
in O
rhabdomyosarcoma I-GENE
( O
FKHR I-GENE
), O
a O
recently O
described O
member O
of O
the O
hepatocyte I-GENE
nuclear I-GENE
factor I-GENE
3 I-GENE
/ I-GENE
forkhead I-GENE
homeotic I-GENE
gene I-GENE
family I-GENE
, O
as O
a O
nuclear I-GENE
hormone I-GENE
receptor I-GENE
( O
NR I-GENE
) O
intermediary I-GENE
protein I-GENE
. O

Unlike O
other O
progenitor I-GENE
cells O
of O
the O
brain O
, O
SVZa I-GENE
progenitor I-GENE
cells O
have O
the O
capacity O
to O
divide I-GENE
even O
though O
they O
express O
a O
neuronal O
phenotype O
. O

We O
previously O
reported O
that O
Tax I-GENE
induced O
cell O
cycle O
progression O
from O
G0 I-GENE
/ I-GENE
G1 I-GENE
phase O
to O
S I-GENE
and O
G2 I-GENE
/ I-GENE
M I-GENE
phases O
in O
human I-GENE
T I-GENE
- I-GENE
cell O
line O
Kit I-GENE
225 I-GENE
cells O
. O

Phosphotyrosyl I-GENE
peptides I-GENE
block O
Stat3 I-GENE
- I-GENE
mediated O
DNA I-GENE
binding I-GENE
activity O
, O
gene I-GENE
regulation O
, O
and O
cell O
transformation O
. O

In O
Exp I-GENE
. O

Human I-GENE
brain O
cDNA I-GENE
library O
screening O
and O
5 I-GENE
' O
rapid O
amplification O
of O
cDNA I-GENE
ends O
yielded O
full I-GENE
- I-GENE
length I-GENE
DENTT I-GENE
cDNA I-GENE
containing O
an O
1899 I-GENE
- I-GENE
bp O
open O
reading O
frame O
encoding O
a O
predicted O
633 I-GENE
- I-GENE
amino O
- I-GENE
acid I-GENE
protein I-GENE
with O
four O
potential O
nuclear I-GENE
localization O
signals O
( O
NLSs I-GENE
) O
and O
two O
coiled O
- I-GENE
coil O
regions O
. O

NaeI I-GENE
, O
a O
novel O
DNA I-GENE
endonuclease I-GENE
, O
shows O
topoisomerase I-GENE
and O
recombinase I-GENE
activities O
when O
a O
Lys O
residue O
is O
substituted O
for O
Leu I-GENE
43 I-GENE
. O

We O
used O
a O
rev I-GENE
- I-GENE
and O
RRE I-GENE
- I-GENE
defective O
HIV I-GENE
type I-GENE
1 I-GENE
( O
HIV I-GENE
- I-GENE
1 I-GENE
) O
molecular O
clone O
in O
complementation O
experiments O
to O
establish O
a O
method O
for O
the O
rapid O
isolation O
of O
posttranscriptional O
regulatory I-GENE
elements O
from O
the O
mammalian I-GENE
genome O
by O
selecting I-GENE
for O
rescue O
of O
virus I-GENE
replication O
. O

OBJECTIVES O
: O
The O
objective O
of O
this O
review O
was O
to O
compare O
the O
effectiveness O
, O
safety O
and O
acceptability I-GENE
of O
the O
diaphragm O
with O
and O
without O
spermicide I-GENE
. O

DESIGN O
: O
Retrospective I-GENE
study O
. O

Considering I-GENE
that O
the O
reactor I-GENE
is O
thoroughly I-GENE
mixed O
during O
each O
discharge O
and O
that O
LD50 O
= O
0 O
. O
9 O
values O
are O
nearly O
independent O
of O
E I-GENE
. O
coli I-GENE
concentrations O
in O
the O
range O
of O
2 I-GENE
x O
10 O
( O
3 I-GENE
) O
< O
or O
= O
E I-GENE
coli I-GENE
/ I-GENE
cfu I-GENE
mL O
(- O
1 I-GENE
) O
< O
or O
= O
3 I-GENE
x O
10 O
( O
6 I-GENE
), O
we O
ascribe I-GENE
the O
nonexponential I-GENE
Pn I-GENE
decay O
of O
single O
- I-GENE
strain O
E I-GENE
. O
coli I-GENE
colonies O
to O
a O
shielding I-GENE
phenomenon O
where O
inactive O
cells O
protect O
the O
successively I-GENE
smaller O
numbers O
of O
viable O
cells O
in O
the O
EHD I-GENE
. O

These O
genes I-GENE
encode O
a O
tryptophanyl I-GENE
tRNA I-GENE
, O
the O
protein I-GENE
translocase I-GENE
component O
SecE I-GENE
, O
the O
antiterminator I-GENE
protein I-GENE
NusG I-GENE
, O
and O
the O
ribosomal I-GENE
proteins I-GENE
L11 I-GENE
and O
L1 I-GENE
in O
addition O
to O
PkwR I-GENE
, O
a O
putative O
regulatory I-GENE
protein I-GENE
of O
the O
LacI I-GENE
- I-GENE
GalR I-GENE
family I-GENE
. O

Body I-GENE
fat O
distribution O
was O
determined O
by O
abdominal O
computed O
tomography O
. O

The O
telomerase I-GENE
RNA I-GENE
- I-GENE
protein I-GENE
complex I-GENE
responsible O
for O
maintenance O
of O
telomeric O
DNA I-GENE
at O
chromosome O
ends O
, O
is O
usually O
inactive O
in O
most O
primary O
somatic O
human I-GENE
cells O
, O
but O
is O
specifically O
activated I-GENE
with O
in O
vitro O
immortalization I-GENE
and O
during O
tumorigenesis O
. O

This O
is O
a O
challenging I-GENE
task O
insofar I-GENE
as O
direct O
measures O
of O
ISF I-GENE
glucose O
are O
not O
readily O
available O
. O

SELECTION I-GENE
CRITERIA I-GENE
: O
All O
randomised O
controlled O
trials O
comparing O
IUSs I-GENE
with O
other O
forms O
of O
reversible O
contraceptives I-GENE
and O
reporting I-GENE
on O
pre I-GENE
- I-GENE
determined O
outcomes O
in O
women O
of O
reproductive O
years O
. O

There O
was O
a O
statistically O
significant O
correlation O
between O
simultaneous O
weekly O
average O
pollen O
levels O
in O
Philadelphia I-GENE
and O
in O
Cherry I-GENE
Hill I-GENE
( O
Acer I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
987 I-GENE
, O
Quercus I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
645 I-GENE
, O
Betula I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
896 I-GENE
, O
Pinus I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
732 I-GENE
, O
Cupressaceae I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
695 I-GENE
, O
Poaceae I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
950 I-GENE
, O
Ambrosia I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
903 I-GENE
, O
and O
Rumex I-GENE
, O
r O
( O
p O
) O
= O
0 O
. O
572 I-GENE
, O
P I-GENE
< O
0 O
. O
001 O
). O

Through I-GENE
two O
novel O
mechanisms O
, O
Arf I-GENE
inhibits O
the O
oncoprotein I-GENE
Hdm2 I-GENE
, O
a O
negative O
regulator I-GENE
of O
p53 I-GENE
. O

2 I-GENE
: O
The O
dynamic O
moduli I-GENE
of O
microcrystalline I-GENE
cellulose I-GENE
. O

Such O
knowledge O
could O
advance I-GENE
diagnosis O
and O
treatment O
of O
the O
patient O
and O
counseling I-GENE
of O
the O
affected O
family I-GENE
. O

Here O
we O
show O
that O
independent O
of O
uncertainties I-GENE
in O
the O
models O
, O
terrestrial I-GENE
planets I-GENE
with O
dense I-GENE
atmosphere I-GENE
like I-GENE
Venus I-GENE
can O
evolve I-GENE
into O
one O
of O
only O
four O
possible O
rotation I-GENE
states O
. O

Our O
results O
suggest O
that O
WASP I-GENE
activates O
transcription I-GENE
following O
TCR I-GENE
stimulation O
in O
a O
manner O
that O
is O
independent O
of O
its O
role O
in O
Arp2 I-GENE
/ I-GENE
3 I-GENE
- I-GENE
directed O
actin I-GENE
polymerization I-GENE
. O

In O
contrast O
, O
the O
ubiquitous O
expression O
of O
p19 I-GENE
( O
INK4d I-GENE
) O
has O
not O
been O
previously O
described O
in O
human I-GENE
or O
murine I-GENE
B I-GENE
- I-GENE
lineage O
cells O
. O

This O
animal O
model O
of O
dystonia I-GENE
appears O
to O
be O
a O
model O
of O
NAD I-GENE
in O
man O
from O
the O
viewpoint I-GENE
of O
treatment O
- I-GENE
response O
. O

These O
results O
indicate O
that O
evaluation O
of O
exposure O
to O
S I-GENE
. O
neurona I-GENE
by O
WB I-GENE
analysis O
of O
serum I-GENE
may O
be O
misleading I-GENE
in O
young O
horses O
. O

The O
Delta6CCI I-GENE
virus I-GENE
was O
extremely O
attenuated O
in O
replication O
capacity O
yet O
retained O
infectiousness I-GENE
for O
CEMx174 I-GENE
and O
MT4 I-GENE
cells O
. O

OBJECTIVE O
: O
To O
determine O
the O
association O
of O
depressive I-GENE
symptoms O
with O
HIV I-GENE
- I-GENE
related I-GENE
mortality O
and O
decline O
in O
CD4 I-GENE
lymphocyte I-GENE
counts O
among O
women O
with O
HIV I-GENE
. O

Phase O
II I-GENE
study O
of O
paclitaxel I-GENE
and O
oral O
etoposide I-GENE
in O
patients O
with O
locally O
advanced O
or O
metastatic O
non O
- I-GENE
small I-GENE
cell O
lung O
cancer O
. O

Analyses I-GENE
revealed O
that O
scale O
matters I-GENE
above O
and O
beyond O
the O
effect O
of O
quadrat I-GENE
area O
. O

Rind I-GENE
et O
al O
.' I-GENE
s O
study O
' O
s O
main O
conclusions O
were O
not O
supported O
by O
the O
original O
data O
. O

Not I-GENE
Available I-GENE

Lactate I-GENE
accumulation O
peak O
was O
unaffected O
by O
supplementation O
( O
HMB I-GENE
, O
8 O
. O
1 I-GENE
+/- O
1 I-GENE
. O
1 I-GENE
mM O
; O
LEU I-GENE
, O
6 I-GENE
. O
2 I-GENE
+/- O
0 O
. O
8 O
mM O
; O
CON I-GENE
, O
7 O
. O
5 I-GENE
+/- O
1 I-GENE
. O
3 I-GENE
mM O
). O

However O
, O
the O
abi1 I-GENE
- I-GENE
1 I-GENE
gene I-GENE
product I-GENE
has O
no O
effect O
on O
the O
ABA I-GENE
suppression O
of O
a O
GA I-GENE
- I-GENE
responsive I-GENE
alpha I-GENE
- I-GENE
amylase I-GENE
gene I-GENE
. O

Polyclonal I-GENE
antibodies I-GENE
against O
the O
N I-GENE
- I-GENE
terminal I-GENE
part O
( O
amino O
acids O
12 O
- I-GENE
363 I-GENE
) O
and O
the O
C I-GENE
- I-GENE
terminal I-GENE
part O
( O
amino O
acids O
330 I-GENE
- I-GENE
730 I-GENE
) O
of O
rainbow I-GENE
trout I-GENE
HIF I-GENE
- I-GENE
1alpha I-GENE
protein I-GENE
recognized O
rainbow I-GENE
trout I-GENE
and O
chinook I-GENE
salmon I-GENE
HIF I-GENE
- I-GENE
1alpha I-GENE
protein I-GENE
in O
Western O
blot O
analysis O
. O

Southern O
blot O
analysis O
of O
genomic O
DNA I-GENE
from O
somatic O
cell O
hybrids O
showed O
that O
endothelial I-GENE
- I-GENE
TACC I-GENE
- I-GENE
related I-GENE
cDNA I-GENE
maps O
to O
chromosome O
10 O
. O

PABP I-GENE
is O
a O
modular I-GENE
protein I-GENE
, O
with O
four O
N I-GENE
- I-GENE
terminal I-GENE
RNA I-GENE
- I-GENE
binding I-GENE
domains I-GENE
and O
an O
extensive O
C I-GENE
terminus O
. O

9 O
. O
7 O
( O
95 O
% O
CI O
: O
9 O
. O
6 I-GENE
- I-GENE
9 O
. O
7 O
) O
micromol I-GENE
/ I-GENE
L I-GENE
among O
women O
( O
P I-GENE
= O
0 O
. O
003 I-GENE
). O

The O
mean O
waiting I-GENE
time O
to O
receive O
the O
pancreas O
transplant O
was O
244 I-GENE
days O
for O
SPK I-GENE
and O
167 I-GENE
days O
for O
PAK I-GENE
recipients O
( O
P I-GENE
= O
0 O
. O
001 O
). O

Zarix I-GENE
expected O
patient O
enrollment I-GENE
in O
Canadian I-GENE
clinical O
sites I-GENE
to O
begin O
in O
Spring I-GENE
2001 I-GENE
[ O
397955 I-GENE
], O
[ O
405928 I-GENE
]. O

The O
isoform I-GENE
, O
designated O
HDAC9a I-GENE
, O
is O
132 O
aa O
shorter O
at O
the O
C I-GENE
terminus O
than O
HDAC9 I-GENE
. O

Long I-GENE
- I-GENE
range O
comparison O
of O
human I-GENE
and O
mouse I-GENE
SCL I-GENE
loci I-GENE
: O
localized O
regions O
of O
sensitivity O
to O
restriction I-GENE
endonucleases I-GENE
correspond O
precisely O
with O
peaks O
of O
conserved O
noncoding O
sequences I-GENE
. O

In O
Saccharomyces I-GENE
cerevisiae I-GENE
, O
eIF6 I-GENE
is O
encoded I-GENE
by O
a O
single O
- I-GENE
copy O
essential O
gene I-GENE
. O

Three O
patients O
received O
additional O
cycles O
of O
5 I-GENE
- I-GENE
fluorouracil O
+/- O
leucovorin I-GENE
as O
maintenance O
chemotherapy O
. O
RESULTS O
: O
Thirty O
males O
and O
21 O
females O
with O
a O
median O
age O
of O
55 O
years O
( O
range O
31 O
-- O
73 O
years O
) O
were O
treated O
. O

RESULTS O
: O
Within O
7 O
days O
, O
all O
groups O
re O
- I-GENE
acquired O
responding O
for O
heroin I-GENE
under O
CRF I-GENE
at O
rates O
similar O
to O
their O
pre I-GENE
- I-GENE
lesion O
performance O
. O

The O
application O
of O
the O
biotechnology I-GENE
at O
the O
plants O
for O
treatment O
of O
the O
surface O
storm I-GENE
waters I-GENE
from O
the O
industrial I-GENE
zone O
Telychka I-GENE
of O
the O
city I-GENE
of O
Kyiv I-GENE
has O
allowed O
the O
content O
of O
petroleum I-GENE
in O
water O
dropped I-GENE
to O
the O
Dnieper I-GENE
to O
be O
constantly I-GENE
reduced O
50 O
- I-GENE
100 O
times O
. O

Using O
immunochemical I-GENE
co O
- I-GENE
precipitation O
methods O
, O
we O
also O
found O
that O
the O
two O
proteins I-GENE
are O
bound O
in O
vivo O
. O

Utility I-GENE
of O
OAE I-GENE
screener I-GENE
( O
GSI I-GENE
70 I-GENE
) O
for O
the O
evaluation O
of O
distortion I-GENE
product I-GENE
otoacoustic I-GENE
emissions I-GENE
] O
The O
purpose O
of O
this O
study O
was O
to O
investigate O
the O
ability O
of O
the O
OAE I-GENE
screener I-GENE
GSI I-GENE
70 I-GENE
to O
evaluate O
of O
cochlea I-GENE
function O
in O
neonates O
, O
infants O
and O
adults O
. O

Our O
results O
demonstrated O
that O
50 O
% O
of O
the O
hepatic I-GENE
artery O
- I-GENE
alone O
ALT I-GENE
graft O
showed O
almost O
normal O
structure O
histologically O
at O
1 I-GENE
month O
after O
grafting I-GENE
, O
with O
bile O
secretion O
preserved I-GENE
. O

Mean O
Hg O
concentrations O
in O
the O
livers I-GENE
of O
mice O
at O
some O
sites I-GENE
in O
Isle I-GENE
Royale I-GENE
are O
not O
significantly O
lower O
( O
P I-GENE
= O
0 O
. O
62 O
) O
than O
Hg O
concentrations O
considered O
by O
some O
government I-GENE
agencies I-GENE
to O
be O
unhealthy I-GENE
for O
human I-GENE
consumption O
. O

We O
show O
here O
that O
the O
in O
vitro O
transcription I-GENE
extract O
contains O
a O
binding I-GENE
activity O
that O
is O
specific I-GENE
for O
the O
initiator O
element I-GENE
and O
thus O
may O
participate O
in O
recruiting I-GENE
RNA I-GENE
polymerase I-GENE
II I-GENE
to O
the O
SL I-GENE
RNA I-GENE
gene I-GENE
promoter I-GENE
. O

The O
desirability I-GENE
function O
is O
based O
on O
the O
search O
for O
a O
global O
optimum I-GENE
[ O
D I-GENE
= O
f I-GENE
( O
Y1 I-GENE
, O
Y2 I-GENE
, O
..., I-GENE
Yn I-GENE
)] O
by O
the O
transformation O
of O
the O
measured O
property I-GENE
to O
a O
dimensionless I-GENE
scale O
for O
each O
criterion O
. O

Naltrexone I-GENE
hydrochloride I-GENE
is O
a O
synthetic O
opioid I-GENE
receptor I-GENE
antagonist O
recently O
used O
in O
efforts I-GENE
to O
provide O
rapid O
opioid I-GENE
detoxification I-GENE
. O

We O
mapped O
the O
DGCR6 I-GENE
gene I-GENE
to O
chromosome O
22q11 I-GENE
within O
a O
low O
copy O
repeat I-GENE
, O
termed O
sc11 I-GENE
. O
1a I-GENE
, O
and O
identified O
a O
second O
copy O
of O
the O
gene I-GENE
, O
DGCR6L I-GENE
, O
within O
the O
duplicate I-GENE
locus I-GENE
, O
termed O
sc11 I-GENE
. O
1b I-GENE
. O

Proliferative I-GENE
vasculopathy I-GENE
and O
cutaneous O
hemorrhages I-GENE
in O
porcine I-GENE
neonates O
infected O
with O
the O
porcine I-GENE
reproductive O
and O
respiratory O
syndrome O
virus I-GENE
. O

The O
child O
left O
behind O
. O

Using O
the O
two O
- I-GENE
hybrid O
system O
, O
we O
show O
that O
nonprenylated I-GENE
Rac1 I-GENE
interacts O
very O
weakly O
with O
Rho I-GENE
- I-GENE
GDI I-GENE
, O
pointing I-GENE
to O
the O
predominant O
role O
of O
protein I-GENE
- I-GENE
isoprene I-GENE
interaction O
in O
complex I-GENE
formation O
. O

In O
contrast O
, O
neither O
I I-GENE
. O
argentina I-GENE
nor O
I I-GENE
. O
theezans I-GENE
exerted I-GENE
any O
effect O
on O
BF I-GENE
or O
intestinal O
propulsion I-GENE
. O

The O
region O
containing O
both O
serines I-GENE
is O
homologous O
to O
the O
N I-GENE
- I-GENE
terminal I-GENE
destruction I-GENE
box I-GENE
of O
IkappaBalpha I-GENE
, O
- I-GENE
beta I-GENE
, O
and O
- I-GENE
epsilon I-GENE
. O

No O
dominant I-GENE
clinical O
factor I-GENE
of O
risk O
was O
found O
, O
but O
multiple O
regression O
analysis O
identified O
age O
, O
body O
surface O
area O
, O
valve O
size O
, O
shop I-GENE
order O
fracture O
rate O
, O
and O
manufacturing I-GENE
period O
as O
risk O
factors I-GENE
for O
OSF I-GENE
. O

A I-GENE
novel O
growth I-GENE
- I-GENE
related I-GENE
nuclear I-GENE
protein I-GENE
binds O
and O
inhibits O
rat I-GENE
aldolase I-GENE
B I-GENE
gene I-GENE
promoter I-GENE
. O

Northern O
blot O
analysis O
revealed O
that O
mlt I-GENE
1 I-GENE
is O
normally O
expressed O
in O
brain O
, O
spleen O
, O
stom I-GENE
ach I-GENE
, O
and O
liver O
. O

NO O
metabolites O
were O
determined O
by O
the O
measurement O
of O
nitrate I-GENE
/ I-GENE
nitrite I-GENE
( O
NOx I-GENE
, O
micromol I-GENE
/ I-GENE
mmol O
creatinine O
) O
and O
cyclic I-GENE
guanosine I-GENE
monophosphate O
( O
cGMP I-GENE
, O
nmol O
/ I-GENE
mmol O
creatinine O
) O
in O
plasma I-GENE
and O
urine O
. O

As O
a O
complement I-GENE
to O
genome O
- I-GENE
wide O
mapping O
and O
sequencing O
efforts I-GENE
, O
it O
is O
often O
important O
to O
generate O
detailed O
maps O
and O
sequence I-GENE
data O
for O
specific I-GENE
regions O
of O
interest O
. O

The O
observed O
phenotypes O
may O
be O
explained O
by O
( O
i O
) O
a O
selective O
disruption O
of O
very O
- I-GENE
low O
- I-GENE
density I-GENE
lipoprotein I-GENE
secretion O
due O
to O
decreased O
expression O
of O
genes I-GENE
encoding O
apolipoprotein I-GENE
B I-GENE
and O
microsomal I-GENE
triglyceride I-GENE
transfer I-GENE
protein I-GENE
, O
( O
ii O
) O
an O
increase O
in O
hepatic I-GENE
cholesterol I-GENE
uptake O
due O
to O
increased O
expression O
of O
the O
major I-GENE
high O
- I-GENE
density I-GENE
lipoprotein I-GENE
receptor I-GENE
, O
scavenger I-GENE
receptor I-GENE
BI I-GENE
, O
and O
( O
iii O
) O
a O
decrease O
in O
bile O
acid I-GENE
uptake O
to O
the O
liver O
due O
to O
down O
- I-GENE
regulation O
of O
the O
major I-GENE
basolateral I-GENE
bile O
acid I-GENE
transporters I-GENE
sodium O
taurocholate I-GENE
cotransporter I-GENE
protein I-GENE
and O
organic O
anion I-GENE
transporter I-GENE
protein I-GENE
1 I-GENE
. O

Effects O
of O
aerosol I-GENE
- I-GENE
vapor I-GENE
JP I-GENE
- I-GENE
8 O
jet I-GENE
fuel I-GENE
on O
the O
functional O
observational I-GENE
battery O
, O
and O
learning O
and O
memory O
in O
the O
rat I-GENE
. O

In O
mouse I-GENE
, O
Mmip1 I-GENE
( O
Mad I-GENE
member O
interacting I-GENE
protein I-GENE
1 I-GENE
) O
and O
Smc3 I-GENE
share O
99 O
% O
sequence I-GENE
identity O
and O
are O
products I-GENE
of O
the O
same O
gene I-GENE
. O

To O
identify O
the O
important O
cis O
- I-GENE
DNA I-GENE
regulatory I-GENE
element I-GENE
( O
s O
) O
involved O
in O
the O
tissue I-GENE
-, I-GENE
region O
-, I-GENE
and O
cell O
- I-GENE
specific I-GENE
expression O
of O
the O
mE I-GENE
- I-GENE
RABP I-GENE
gene I-GENE
, O
the O
5 I-GENE
- I-GENE
kb O
DNA I-GENE
fragment I-GENE
was O
sequenced O
. O

Regional I-GENE
blood O
blow I-GENE
was O
measured O
by O
means O
of O
microspheres O
in O
predefined I-GENE
regions O
of O
the O
C6 I-GENE
, O
T11 I-GENE
, O
and O
L6 I-GENE
vertebrae I-GENE
. O

Breast I-GENE
cancer O
risk O
assessment O
: O
Who I-GENE
holds I-GENE
the O
magic I-GENE
crystal O
ball I-GENE
? O

The O
frameshift O
initiated O
by O
ADEx2 I-GENE
is O
believed O
to O
alter O
the O
regular O
coding O
sequence I-GENE
, O
acting O
as O
a O
loss O
- I-GENE
of O
- I-GENE
function O
ASIP I-GENE
mutation I-GENE
. O

CONCLUSIONS O
: O
Adding I-GENE
MMF I-GENE
, O
a O
potent O
topical I-GENE
corticosteroid I-GENE
, O
to O
an O
emollient I-GENE
cream O
is O
statistically O
significantly O
more O
effective O
than O
emollient I-GENE
cream O
alone O
in O
reducing O
acute O
radiation O
dermatitis O
. O

Copyright O
2001 I-GENE
Academic O
Press O
. O

CONCLUSIONS O
: O
Although O
the O
levels O
of O
oxLDL I-GENE
antibodies I-GENE
might O
be O
modified O
in O
early I-GENE
hypertension O
, O
once O
advanced O
coronary O
artery O
disease O
has O
developed O
the O
presence O
of O
hypertension O
does O
not O
affect O
anti I-GENE
- I-GENE
oxLDL I-GENE
levels O
. O

As O
an O
application O
of O
reverse I-GENE
genetics I-GENE
, O
we O
introduced O
one O
nucleotide I-GENE
change O
( O
UCU I-GENE
to O
ACU I-GENE
) O
to O
immediate I-GENE
downstream O
of O
the O
RNA I-GENE
- I-GENE
editing I-GENE
site I-GENE
of O
the O
V I-GENE
gene I-GENE
in O
the O
full I-GENE
- I-GENE
length I-GENE
hPIV2 I-GENE
cDNA I-GENE
and O
were O
able O
to O
obtain O
infectious O
viruses O
[ O
rPIV2V I-GENE
(-)] I-GENE
from O
the O
cDNA I-GENE
. O

At O
both O
companies I-GENE
sites I-GENE
Salmonella I-GENE
enteritidis I-GENE
and O
Salmonella I-GENE
typhimurium I-GENE
Tr104 I-GENE
were O
also O
isolated O
occasionally I-GENE
from O
various O
locations O
. O

Most O
yeast I-GENE
peroxisomal I-GENE
matrix I-GENE
proteins I-GENE
contain O
a O
type I-GENE
1C I-GENE
- I-GENE
terminal I-GENE
peroxisomal I-GENE
targeting O
signal I-GENE
( O
PTS1 I-GENE
) O
consisting O
of O
the O
tripeptide I-GENE
SKL I-GENE
or O
a O
conservative O
variant I-GENE
thereof I-GENE
. O

Tumor I-GENE
- I-GENE
like I-GENE
accumulation O
on O
Tl O
- I-GENE
201 O
SPECT O
in O
subacute O
hemorrhagic O
cerebral O
infarction O
. O

WRN I-GENE
helicase I-GENE
resolves I-GENE
alternate O
DNA I-GENE
structures O
including O
tetraplex I-GENE
and O
triplex I-GENE
DNA I-GENE
, O
and O
Holliday I-GENE
junctions O
. O

The O
increase O
in O
number O
of O
terminal I-GENE
hairs I-GENE
, O
which O
are O
defined O
as O
hairs I-GENE
more O
than O
60 O
microm O
in O
diameter O
, O
in O
the O
designated O
area O
( O
0 O
. O
5 I-GENE
cm O
square O
= O
0 O
. O
25 O
cm2 O
area O
) O
of O
the O
procyanidin I-GENE
B I-GENE
- I-GENE
2 I-GENE
group O
subjects O
after O
the O
6 I-GENE
- I-GENE
month O
trial O
was O
significantly O
greater O
than O
that O
of O
the O
placebo O
control O
group O
subjects O
( O
procyanidin I-GENE
B I-GENE
- I-GENE
2 I-GENE
, O
1 I-GENE
. O
99 O
+/- O
2 I-GENE
. O
58 O
( O
mean O
+/- O
SD O
)/ O
0 O
. O
25 O
cm2 O
; O
placebo O
, O
- I-GENE
0 O
. O
82 O
+/- O
3 I-GENE
. O
40 I-GENE
( O
mean O
+/- O
SD O
)/ O
0 O
. O
25 O
cm2 O
; O
P I-GENE
< O
0 O
. O
02 O
, O
two O
- I-GENE
sample O
t I-GENE
test O
). O

SKP1 I-GENE
- I-GENE
SnRK I-GENE
protein I-GENE
kinase I-GENE
interactions O
mediate O
proteasomal I-GENE
binding I-GENE
of O
a O
plant O
SCF I-GENE
ubiquitin I-GENE
ligase I-GENE
. O

Based O
on O
the O
hypothesis O
that O
evolutionarily O
conserved O
regions O
are O
functionally O
important O
and O
likely O
to O
interact O
with O
coactivators I-GENE
, O
we O
compared O
the O
amino O
acid I-GENE
sequence I-GENE
of O
C I-GENE
/ I-GENE
EBPalpha I-GENE
from O
different O
species O
( O
frog I-GENE
to O
human I-GENE
) O
and O
identified O
four O
highly O
conserved O
regions O
( O
CR1 I-GENE
- I-GENE
CR4 I-GENE
) O
within O
the O
transactivation O
domain I-GENE
. O

Colorectal I-GENE
cancer O
was O
shown O
to O
disproportionately I-GENE
overburden I-GENE
Ashkenazi I-GENE
Jews I-GENE
, O
who O
may O
also O
be O
at O
increased O
risk O
for O
ovarian O
, O
pancreatic O
and O
stomach O
cancer O
, O
and O
non O
- I-GENE
Hodgkin O
' O
s O
lymphoma O
. O

Percentages I-GENE
of O
recovery O
for O
overload O
and O
dilution O
tests O
were O
between O
87 O
and O
120 O
%. O

This O
shows O
that O
in O
situations O
of O
separated O
breaks I-GENE
, O
NHEJ I-GENE
deficiency O
leads O
to O
genomic O
rearrangements O
, O
in O
agreement O
with O
chromosomal I-GENE
studies O
. O

Copyright O
2001 I-GENE
S I-GENE
. O

After O
nerve I-GENE
injury O
, O
the O
nociceptive I-GENE
responses O
through O
type I-GENE
I I-GENE
neurons O
, O
which O
are O
polymodal I-GENE
C I-GENE
- I-GENE
fibers O
and O
drive O
NK1 I-GENE
- I-GENE
receptor I-GENE
mechanisms O
in O
spinal O
pain O
transmission O
, O
were O
completely O
lost O
, O
but O
without O
changes O
in O
type I-GENE
II I-GENE
ones O
, O
which O
are O
polymodal I-GENE
C I-GENE
- I-GENE
fibers O
and O
drive O
NMDA I-GENE
receptor I-GENE
- I-GENE
mechanisms O
, O
while O
type I-GENE
III I-GENE
ones O
, O
which O
are O
capsaicin I-GENE
- I-GENE
insensitive I-GENE
( O
possibly O
A I-GENE
- I-GENE
fibers O
) O
and O
drive O
NMDA I-GENE
- I-GENE
receptor I-GENE
mechanisms O
, O
were O
markedly O
enhanced O
. O

SV1 I-GENE
has O
a O
33 O
- I-GENE
amino O
acid I-GENE
insert O
in O
the O
S1 I-GENE
transmembrane I-GENE
domain I-GENE
that O
does O
not O
alter O
S1 I-GENE
overall O
hydrophobicity I-GENE
, O
but O
makes O
the O
S0 I-GENE
- I-GENE
S1 I-GENE
linker I-GENE
longer O
. O

A I-GENE
variety O
of O
receptor I-GENE
- I-GENE
mediated O
signaling O
pathways O
are O
controlled O
by O
both O
positive O
and O
negative O
extracellular I-GENE
regulators O
. O

A I-GENE
20 O
- I-GENE
base O
pair O
oligonucleotide I-GENE
containing O
this O
nonamer I-GENE
confers O
up O
- I-GENE
regulation O
by O
hypoxia O
and O
inhibition O
by O
unsaturated I-GENE
fatty I-GENE
acids O
when O
placed O
upstream O
of O
a O
heterologous O
promoter I-GENE
in O
a O
lacZ I-GENE
reporter I-GENE
construct I-GENE
. O

Our O
results O
indicate O
that O
D I-GENE
( O
4 I-GENE
) O
and O
D I-GENE
( O
2L I-GENE
) O
receptors I-GENE
activate O
the O
ERK I-GENE
kinase I-GENE
cascade O
by O
first O
mobilizing I-GENE
signaling O
by O
the O
PDGF I-GENE
receptor I-GENE
, O
followed O
by O
the O
subsequent O
activation O
of O
ERK1 I-GENE
/ I-GENE
2 I-GENE
by O
pathways O
associated I-GENE
with O
this O
receptor I-GENE
tyrosine I-GENE
kinase I-GENE
. O

Raes I-GENE
, O
P I-GENE
. O

Finally O
, O
we O
compared O
the O
differential O
screening O
techniques O
in O
terms O
of O
sensitivity O
, O
efficiency O
and O
occurrence O
of O
false O
positives I-GENE
. O

C I-GENE
/ I-GENE
EBPbeta I-GENE
LIP I-GENE
overexpressing O
HC11 I-GENE
cells O
did O
not O
express O
beta I-GENE
- I-GENE
casein I-GENE
mRNA I-GENE
( O
mammary O
epithelial O
cell O
differentiation O
marker O
) O
in O
response O
to O
lactogenic I-GENE
hormones O
. O

NF I-GENE
- I-GENE
kappaB I-GENE
is O
involved O
in O
the O
regulation O
of O
CD154 I-GENE
( O
CD40 I-GENE
ligand O
) O
expression O
in O
primary O
human I-GENE
T I-GENE
cells O
. O

Subacute I-GENE
diencephalic I-GENE
angioencephalopathy I-GENE
( O
SDAE I-GENE
) O
is O
a O
rare O
and O
fatal O
disease O
of O
unknown O
etiology O
that O
involves O
the O
thalami I-GENE
bilaterally I-GENE
. O

NGF I-GENE
elicits I-GENE
a O
more O
delayed O
and O
sustained O
ERK I-GENE
phosphorylation O
than O
EGF I-GENE
, O
consistent O
with O
previous O
reports O
. O

TBARS I-GENE
levels O
, O
oxygen O
- I-GENE
radical O
absorbing I-GENE
capacity O
assay O
and O
AFR I-GENE
release O
assessed O
by O
electron O
paramagnetic I-GENE
resonance O
( O
EPR I-GENE
) O
were O
used O
to O
explore O
the O
existence O
of O
oxidative O
stress O
in O
diabetes O
. O

Pulmonary I-GENE
vein O
varix I-GENE
in O
association O
with O
bilateral O
pulmonary O
vein O
stenosis O
. O

Derivation I-GENE
and O
initial O
characterization O
of O
a O
mouse I-GENE
mammary O
tumor I-GENE
cell O
line O
carrying O
the O
polyomavirus I-GENE
middle I-GENE
T I-GENE
antigen I-GENE
: O
utility I-GENE
in O
the O
development O
of O
novel O
cancer O
therapeutics I-GENE
. O

The O
images O
showed O
rapid O
, O
predominantly O
urinary O
excretion O
of O
99mTc O
ciprofloxacin I-GENE
, O
with O
low O
to O
absent O
brain O
, O
lung O
and O
bone O
marrow O
uptake O
and O
low O
liver O
uptake O
and O
excretion O
. O

Thus O
, O
the O
anti I-GENE
- I-GENE
interferon I-GENE
functions O
of O
vIRF I-GENE
- I-GENE
2 I-GENE
may O
contribute O
to O
the O
establishment O
of O
a O
chronic O
or O
latent I-GENE
infection O
. O

Topological I-GENE
and O
mutational O
analysis O
of O
Saccharomyces I-GENE
cerevisiae I-GENE
Ste14p I-GENE
, O
founding I-GENE
member O
of O
the O
isoprenylcysteine I-GENE
carboxyl O
methyltransferase I-GENE
family I-GENE
. O

Two O
remotely I-GENE
situated O
exons O
within O
the O
complement I-GENE
C3 I-GENE
gene I-GENE
locus I-GENE
encode O
an O
alternate O
5 I-GENE
' O
end O
and O
proximal I-GENE
ORF I-GENE
under O
the O
control O
of O
a O
bidirectional I-GENE
promoter I-GENE
. O

Although O
there O
was O
a O
high O
correlation O
between O
sap I-GENE
flux I-GENE
densities I-GENE
registered I-GENE
by O
the O
old O
and O
new O
sensors I-GENE
, O
significant O
differences O
in O
sap I-GENE
flux I-GENE
densities I-GENE
between O
the O
duplicated O
sensors I-GENE
were O
detected O
. O

Their O
numbers O
have O
regularly I-GENE
increased O
since O
the O
mid O
- I-GENE
1970s I-GENE
. O

The O
hcKrox I-GENE
gene I-GENE
family I-GENE
regulates O
multiple O
extracellular I-GENE
matrix I-GENE
genes I-GENE
. O

NB I-GENE
- I-GENE
506 I-GENE
completely O
inhibits O
the O
capacity O
of O
topoisomerase I-GENE
I I-GENE
to O
phosphorylate O
, O
in O
vitro O
, O
the O
human I-GENE
splicing O
factor I-GENE
2 I-GENE
/ I-GENE
alternative O
splicing O
factor I-GENE
( O
SF2 I-GENE
/ I-GENE
ASF I-GENE
). O

Recent O
studies O
using O
isolated O
rat I-GENE
adipocytes O
and O
chemically I-GENE
synthesized O
PIG I-GENE
compounds O
point O
to O
IRS1 I-GENE
/ I-GENE
3 I-GENE
tyrosine I-GENE
phosphorylation O
by O
p59Lyn I-GENE
kinase I-GENE
as O
the O
site I-GENE
of O
cross O
- I-GENE
talk I-GENE
, O
the O
negative O
regulation O
of O
which O
by O
interaction O
with O
caveolin I-GENE
is O
apparently O
abrogated O
by O
PIG I-GENE
. O

To O
investigate O
the O
effects O
of O
exogenous O
hyaluronic I-GENE
acid I-GENE
, O
the O
development O
of O
port I-GENE
- I-GENE
site I-GENE
metastasis O
was O
examined O
using O
mouse I-GENE
adenocarcinoma O
cell O
- I-GENE
line O
colon O
26 O
cells O
. O

METHODS O
: O
Thyroid I-GENE
status O
was O
measured O
at O
baseline O
( O
1990 O
- I-GENE
93 O
), O
through O
assessment O
of O
serum I-GENE
antibodies I-GENE
to O
thyroid I-GENE
peroxidase I-GENE
( O
TPO I-GENE
- I-GENE
Abs I-GENE
, O
positive O
: O
> O
10 O
IU O
/ I-GENE
ml O
), O
serum I-GENE
TSH I-GENE
levels O
, O
and O
when O
TSH I-GENE
was O
abnormal O
(< O
0 O
. O
4 I-GENE
or O
> O
4 I-GENE
. O
0 O
mU I-GENE
/ I-GENE
l O
), O
serum I-GENE
thyroxin I-GENE
levels O
( O
T4 I-GENE
). O

Mechanical I-GENE
ventilation O
in O
control O
lungs O
produced O
a O
47 O
% O
decrease O
in O
chord I-GENE
compliance O
, O
an O
increase O
in O
lung O
lavage I-GENE
levels O
of O
tumor I-GENE
necrosis I-GENE
factor I-GENE
( O
TNF I-GENE
)- I-GENE
alpha I-GENE
( O
722 I-GENE
+/- O
306 I-GENE
pg O
/ I-GENE
ml O
), O
interleukin I-GENE
( O
IL I-GENE
)- I-GENE
1beta I-GENE
( O
902 I-GENE
+/- O
322 I-GENE
pg O
/ I-GENE
ml O
), O
and O
macrophage I-GENE
inflammatory O
protein I-GENE
- I-GENE
2 I-GENE
( O
MIP I-GENE
- I-GENE
2 I-GENE
) O
( O
363 I-GENE
+/- O
104 O
pg O
/ I-GENE
ml O
) O
as O
compared O
with O
low O
levels O
of O
cytokines O
detected O
in O
preventilation I-GENE
data O
, O
and O
no O
change O
in O
percentage O
of O
surfactant I-GENE
large O
aggregates O
( O
LA O
). O

Autoregulation I-GENE
enables O
different O
pathways O
to O
control O
CCAAT I-GENE
/ I-GENE
enhancer I-GENE
binding I-GENE
protein I-GENE
beta I-GENE
( O
C I-GENE
/ I-GENE
EBP I-GENE
beta I-GENE
) O
transcription I-GENE
. O

In O
the O
past O
decade I-GENE
, O
there O
have O
been O
enormous I-GENE
advances I-GENE
in O
the O
use O
of O
Bayesian I-GENE
methodology I-GENE
for O
analysis O
of O
epidemiologic I-GENE
data O
, O
and O
there O
are O
now O
many O
practical I-GENE
advantages O
to O
the O
Bayesian I-GENE
approach O
. O

In O
strains O
lacking O
tup11 I-GENE
and O
tup12 I-GENE
, O
the O
atf1 I-GENE
- I-GENE
pcr1 I-GENE
transcriptional O
activator I-GENE
continues I-GENE
to O
play O
a O
central O
role O
in O
fbp1 I-GENE
- I-GENE
lacZ I-GENE
expression O
; O
however O
, O
spc1 I-GENE
MAPK I-GENE
phosphorylation O
of O
atf1 I-GENE
is O
no O
longer O
essential O
for O
its O
activation O
. O

Single I-GENE
amino O
acid I-GENE
substitutions O
at O
the O
acyl I-GENE
- I-GENE
CoA I-GENE
- I-GENE
binding I-GENE
domain I-GENE
interrupt I-GENE
14 O
[ O
C I-GENE
] O
palmitoyl I-GENE
- I-GENE
CoA I-GENE
binding I-GENE
of O
ACBP2 I-GENE
, O
an O
Arabidopsis I-GENE
acyl I-GENE
- I-GENE
CoA I-GENE
- I-GENE
binding I-GENE
protein I-GENE
with O
ankyrin I-GENE
repeats I-GENE
. O

RESULTS O
: O
Sixty I-GENE
per O
cent O
of O
African O
Americans I-GENE
exposed O
in O
26 O
community O
outbreaks I-GENE
were O
TST I-GENE
positive O
compared O
to O
only O
40 I-GENE
% O
of O
whites I-GENE
following O
comparable O
exposures O
. O

For O
immunological I-GENE
methods O
, O
identification O
of O
such O
antigens I-GENE
with O
intermolecular I-GENE
variability O
, O
e O
. O
g O
., O
the O
structural O
aescin I-GENE
analogs I-GENE
, O
is O
of O
unknown O
validity O
. O

It O
was O
found O
that O
intrathecal I-GENE
administration O
( O
i O
. O
t I-GENE
.) O
of O
D2 I-GENE
receptor I-GENE
agonist O
LY171555 I-GENE
or O
D1 I-GENE
/ I-GENE
D2 I-GENE
receptor I-GENE
agonist O
apomorphine I-GENE
increased O
pain O
threshold O
and O
had O
a O
potentiating I-GENE
effect O
on O
AA O
. O

Interactions I-GENE
between O
the O
checkpoint I-GENE
abrogator I-GENE
UCN I-GENE
- I-GENE
01 O
and O
several O
pharmacological O
inhibitors O
of O
the O
mitogen I-GENE
- I-GENE
activated I-GENE
protein I-GENE
kinase I-GENE
( O
MAPK I-GENE
) O
kinase I-GENE
( O
MEK I-GENE
)/ O
MAPK I-GENE
pathway O
have O
been O
examined O
in O
a O
variety O
of O
human I-GENE
leukemia I-GENE
cell O
lines O
. O

Analysis O
of O
regulatory I-GENE
regions O
in O
the O
promoter I-GENE
of O
the O
ctr4 I-GENE
(+) I-GENE
copper I-GENE
transporter I-GENE
gene I-GENE
in O
fission I-GENE
yeast I-GENE
Schizosaccharomyces I-GENE
pombe I-GENE
reveals O
the O
identity O
of O
a O
conserved O
copper I-GENE
- I-GENE
signaling O
element I-GENE
( O
CuSE I-GENE
), O
which O
is O
recognized O
by O
the O
transcription I-GENE
factor I-GENE
Cuf1 I-GENE
. O

However O
, O
during O
our O
work O
with O
a O
replication O
- I-GENE
deficient O
virus I-GENE
expressing O
the O
ASF I-GENE
/ I-GENE
SF2 I-GENE
splicing O
factor I-GENE
from O
a O
progesterone I-GENE
antagonist O
- I-GENE
inducible I-GENE
gene I-GENE
cassette I-GENE
, O
we O
discovered O
that O
ASF I-GENE
/ I-GENE
SF2 I-GENE
was O
expressed O
at O
a O
significant O
level O
in O
the O
293 O
producer I-GENE
cell O
line O
, O
even O
in O
the O
absence O
of O
inducer I-GENE
. O

This O
study O
suggests O
that O
PSP I-GENE
is O
more O
common O
than O
previously O
considered O
, O
is O
commonly O
misdiagnosed I-GENE
and O
that O
the O
majority O
of O
cases O
are O
not O
initially O
referred O
to O
neurologists I-GENE
. O

Between I-GENE
1967 I-GENE
and O
1994 O
, O
495 I-GENE
patients O
underwent O
surgery O
for O
primary O
PTC I-GENE
at O
the O
Department I-GENE
of O
Surgery I-GENE
, O
Helsinki I-GENE
University O
Central I-GENE
Hospital I-GENE
. O

The O
described O
results O
show O
that O
DTD I-GENE
is O
fast O
, O
simple O
, O
and O
easy I-GENE
to O
automate I-GENE
; O
requires O
only O
a O
small I-GENE
amount O
of O
sample O
( O
approximately O
50 O
mg O
); O
and O
affords I-GENE
quantitative O
information O
about O
the O
main O
groups O
of O
compounds O
present O
in O
cheeses I-GENE
. O

Srb10 I-GENE
is O
a O
physiological O
regulator I-GENE
of O
Gcn4 I-GENE
stability O
because O
both O
phosphorylation O
and O
turnover O
of O
Gcn4 I-GENE
are O
diminished O
in O
srb10 I-GENE
mutants I-GENE
. O

The O
promoter I-GENE
activity O
of O
the O
proximal I-GENE
region O
was O
found O
to O
be O
restricted O
to O
a O
subset O
of O
prestalk I-GENE
cells O
. O

Two O
nuclear I-GENE
medicine O
physicians O
blinded I-GENE
to O
the O
surgical O
findings O
interpreted O
all O
available O
images O
and O
various O
Tc O
- I-GENE
99m O
MIBI I-GENE
image O
combinations O
at O
15 O
minutes O
alone O
; O
15 O
minutes O
and O
2 I-GENE
hours O
, O
15 O
minutes O
and O
4 I-GENE
hours O
; O
and O
15 O
minutes O
and O
2 I-GENE
and O
4 I-GENE
hours O
each O
with O
and O
without O
correlative I-GENE
pertechnetate I-GENE
thyroid I-GENE
imaging O
. O

We O
demonstrated O
that O
, O
under O
serum I-GENE
- I-GENE
starved I-GENE
conditions O
, O
KMS I-GENE
- I-GENE
11 O
and O
OPM I-GENE
- I-GENE
2 I-GENE
cells O
express O
appreciable I-GENE
levels O
of O
phosphorylated O
FGFR3 I-GENE
mutants I-GENE
indicating O
a O
constitutive O
activation O
of O
the O
Y373C I-GENE
and O
K650E I-GENE
receptors I-GENE
; O
the O
addition O
of O
the O
aFGF I-GENE
ligand O
further O
increased O
the O
level O
of O
receptor I-GENE
phosphorylation O
. O

Identical I-GENE
effects O
were O
obtained O
when O
inhibitors O
and O
dominant I-GENE
negative O
mutants I-GENE
were O
tested O
on O
the O
- I-GENE
29 O
to O
+ I-GENE
139 O
bp O
region O
of O
the O
cyclin I-GENE
D1 I-GENE
promoter I-GENE
. O

In O
this O
paper O
the O
tyrosine I-GENE
dephosphorylating I-GENE
enzymes O
, O
the O
protein I-GENE
- I-GENE
tyrosine I-GENE
phosphatases I-GENE
( O
PTPs I-GENE
), O
are O
studied O
which O
can O
be O
grouped I-GENE
into O
two O
subfamilies I-GENE
, O
the O
soluble I-GENE
PTPs I-GENE
and O
the O
receptor I-GENE
PTPs I-GENE
( O
RPTPs I-GENE
). O

Coexposure I-GENE
to O
FP I-GENE
also O
resulted O
in O
a O
more O
pronounced O
and O
sustained O
activation O
of O
the O
mitogen I-GENE
- I-GENE
activated I-GENE
protein I-GENE
kinase I-GENE
kinase I-GENE
/ I-GENE
extracellular I-GENE
signal I-GENE
- I-GENE
regulated O
protein I-GENE
kinase I-GENE
cascade O
after O
PMA O
treatment O
, O
although O
disruption O
of O
this O
pathway O
by O
the O
mitogen I-GENE
- I-GENE
activated I-GENE
protein I-GENE
kinase I-GENE
kinase I-GENE
1 I-GENE
inhibitor I-GENE
U0126 I-GENE
did O
not O
prevent O
potentiation O
of O
apoptosis O
. O

The O
LA O
50s I-GENE
derived O
from O
this O
combined O
data O
when O
compared O
with O
our O
earlier O
series O
from O
1965 I-GENE
to O
1970 I-GENE
also O
did O
not O
show O
a O
significant O
change O
in O
mortality O
. O

Most O
patients O
harboring O
metronidazole I-GENE
- I-GENE
and O
clarithromycin I-GENE
- I-GENE
resistant O
strains O
were O
eradicated I-GENE
at O
an O
equal O
rate O
by O
each O
of O
the O
three O
regimens O
. O

Responses I-GENE
of O
single O
- I-GENE
unit I-GENE
carotid O
body O
chemoreceptors I-GENE
in O
adult O
rats O
. O

Thus O
, O
MKK7 I-GENE
is O
an O
essential O
and O
specific I-GENE
regulator I-GENE
of O
stress O
- I-GENE
induced O
SAPK I-GENE
/ I-GENE
JNK I-GENE
activation O
in O
mast I-GENE
cells O
and O
MKK7 I-GENE
negatively O
regulates O
growth I-GENE
factor I-GENE
and O
antigen I-GENE
receptor I-GENE
- I-GENE
driven O
proliferation O
in O
hematopoietic I-GENE
cells O
. O

The O
N I-GENE
- I-GENE
terminal I-GENE
portion O
of O
Notch I-GENE
( O
IC I-GENE
) O
inhibited O
p50 I-GENE
DNA I-GENE
binding I-GENE
and O
interacted O
specifically O
with O
p50 I-GENE
subunit I-GENE
, O
not O
p65 I-GENE
of O
NF I-GENE
- I-GENE
kappaB I-GENE
. O

To O
account O
for O
this O
observation O
, O
other O
possible O
causes O
include O
increased O
CSF I-GENE
pulsation I-GENE
in O
children O
creating I-GENE
motion O
artifact I-GENE
, O
changes O
in O
arterial O
oxygen O
concentration O
intrinsic O
to O
propofol I-GENE
or O
related I-GENE
to O
the O
supplemental I-GENE
oxygen O
normally O
administered O
, O
or O
changes O
in O
CSF I-GENE
protein I-GENE
levels O
related I-GENE
to O
propofol I-GENE
binding I-GENE
to O
proteins I-GENE
for O
uptake O
into O
CSF I-GENE
. O

Molecular O
cloning O
and O
characterization O
of O
OsPSK I-GENE
, O
a O
gene I-GENE
encoding O
a O
precursor I-GENE
for O
phytosulfokine I-GENE
- I-GENE
alpha I-GENE
, O
required O
for O
rice I-GENE
cell O
proliferation O
. O

The O
present O
study O
was O
initiated O
to O
explore O
the O
potential O
of O
a O
hybrid O
biological O
reactor I-GENE
, O
combining I-GENE
trickling I-GENE
filter O
( O
TF I-GENE
) O
and O
activated I-GENE
sludge I-GENE
process O
( O
ASP I-GENE
), O
to O
treat O
wastewater I-GENE
containing O
trichloroethylene I-GENE
( O
TCE I-GENE
) O
at O
ambient I-GENE
temperature O
at O
different O
hydraulic I-GENE
retention O
time O
( O
HRT I-GENE
). O

If O
you I-GENE
think I-GENE
education O
is O
expensive I-GENE
-- O
try I-GENE
ignorance I-GENE
-- O
Bok I-GENE
' O
s O
Law I-GENE
. O

The O
COD I-GENE
and O
color O
removals I-GENE
were O
both O
more O
than O
90 O
% O
when O
FeCl3 I-GENE
was O
used O
as O
the O
coagulation I-GENE
( O
dosages I-GENE
of O
two O
- I-GENE
step O
coagulation I-GENE
were O
0 O
. O
031 I-GENE
and O
0 O
. O
012 I-GENE
mol O
/ I-GENE
L I-GENE
respectively O
) O
after O
a O
ferrous I-GENE
hydrogen O
peroxide I-GENE
oxidation O
pretreatment O
at O
a O
H2O2 I-GENE
dosage O
of O
0 O
. O
06 O
mol O
/ I-GENE
L I-GENE
. O

An O
element I-GENE
within O
the O
5 I-GENE
' O
untranslated O
region O
of O
human I-GENE
Hsp70 I-GENE
mRNA I-GENE
which O
acts O
as O
a O
general O
enhancer I-GENE
of O
mRNA I-GENE
translation I-GENE
. O

The O
selective O
alteration O
of O
the O
genome O
using O
Cre I-GENE
recombinase I-GENE
to O
target O
the O
rearrangement O
of O
genes I-GENE
flanked O
by O
LOX I-GENE
recognition I-GENE
sequences I-GENE
has O
required O
the O
use O
of O
two O
separate O
genetic O
constructs I-GENE
in O
trans O
, O
one O
containing O
cre I-GENE
and O
the O
other O
containing O
the O
gene I-GENE
of O
interest O
flanked O
by O
LOX I-GENE
sites I-GENE
. O

It O
has O
been O
suggested O
that O
members O
of O
this O
protein I-GENE
family I-GENE
exhibit O
both O
prolyl I-GENE
isomerase I-GENE
and O
chaperone I-GENE
activity O
. O

Newcastle I-GENE
disease O
antibody I-GENE
titre I-GENE
is O
dependent I-GENE
on O
serum I-GENE
calcium O
concentration O
. O

In O
three O
cases O
( O
21 O
. O
4 I-GENE
%), O
the O
MR O
imaging O
was O
interpreted O
as O
negative O
, O
but O
microscopic O
tumor I-GENE
was O
shown O
around O
seroma I-GENE
on O
reexcision I-GENE
. O

2 I-GENE
were O
nonviable I-GENE
, O
and O
the O
mutant I-GENE
Vp1s I-GENE
unexpectedly I-GENE
failed O
to O
localize O
to O
the O
nucleus O
though O
Vp2 I-GENE
and O
Vp3 I-GENE
did O
, O
suggesting O
that O
the O
mutated O
NLS1 I-GENE
acted I-GENE
as O
a O
dominant I-GENE
signal I-GENE
for O
the O
cytoplasmic I-GENE
localization O
of O
Vp1 I-GENE
. O

Compared I-GENE
with O
normal O
control O
subjects O
, O
all O
74 O
TOF O
patients O
had O
decreased O
systolic O
and O
diastolic O
myocardial O
velocities I-GENE
and O
a O
longer O
isovolumic I-GENE
relaxation O
time O
. O

The O
corresponding O
orifice I-GENE
voltages I-GENE
for O
the O
three O
instruments O
were O
20 O
/ I-GENE
50 O
/ I-GENE
80 O
V I-GENE
( O
API I-GENE
365 I-GENE
), O
30 O
/ I-GENE
90 O
/ I-GENE
130 I-GENE
V I-GENE
( O
API I-GENE
2000 O
) O
and O
40 I-GENE
/ I-GENE
80 O
/ I-GENE
120 O
V I-GENE
( O
API I-GENE
3000 I-GENE
). O

We O
compared O
previously O
the O
methylation O
status O
between O
normal O
liver O
and O
liver O
tumors O
in O
SV40 I-GENE
T I-GENE
/ I-GENE
t I-GENE
antigen I-GENE
transgenic O
mice O
( O
MT I-GENE
- I-GENE
D2 I-GENE
mice O
) O
using O
Restriction O
Landmark I-GENE
Genomic O
Scanning I-GENE
for O
Methylation I-GENE
( O
RLGS I-GENE
- I-GENE
M I-GENE
) O
and O
identified O
several O
loci I-GENE
/ I-GENE
spots O
that O
appeared O
to O
be O
methylated I-GENE
frequently O
in O
liver O
tumors O
. O

We O
have O
cloned O
a O
novel O
mouse I-GENE
protein I-GENE
, O
TAF I-GENE
( O
II I-GENE
) O
140 I-GENE
, O
containing O
an O
HFD I-GENE
and O
a O
plant O
homeodomain I-GENE
( O
PHD I-GENE
) O
finger I-GENE
, O
which O
we O
demonstrated O
by O
immunoprecipitation O
to O
be O
a O
mammalian I-GENE
TFIID I-GENE
component O
. O

3D I-GENE
image O
- I-GENE
processing O
permits O
to O
analyse I-GENE
ultrasound O
data O
interactively I-GENE
in O
three O
orthogonal I-GENE
planes I-GENE
( O
section O
mode O
) O
or O
in O
realistic I-GENE
3D I-GENE
views I-GENE
( O
rendering I-GENE
mode O
). O

A I-GENE
proposal I-GENE
of O
50 O
performance O
indicators O
divided O
into O
five O
different O
groups O
is O
presented O
here O
, O
namely O
structural O
indicators O
, O
operational I-GENE
indicators O
, O
water O
and O
service I-GENE
quality O
indicators O
, O
personnel I-GENE
indicators O
and O
economic I-GENE
indicators O
. O

These O
analyses O
re O
- I-GENE
open O
the O
question O
whether O
all O
the O
CesA I-GENE
genes I-GENE
encode O
cellulose I-GENE
synthases I-GENE
or O
whether O
some O
of O
the O
sub O
- I-GENE
class I-GENE
members O
may O
encode O
other O
non O
- I-GENE
cellulosic I-GENE
( O
1 I-GENE
--> I-GENE
4 I-GENE
) O
beta I-GENE
- I-GENE
glycan I-GENE
synthases I-GENE
in O
plants O
. O

The O
relationship O
of O
the O
factor I-GENE
V I-GENE
Leiden I-GENE
mutation I-GENE
or O
the O
deletion O
- I-GENE
deletion O
polymorphism O
of O
the O
angiotensin I-GENE
converting I-GENE
enzyme I-GENE
to O
postoperative O
thromboembolic I-GENE
events O
following O
total O
joint O
arthroplasty I-GENE
. O

In O
contrast O
, O
exogenous O
PTHrP1 I-GENE
- I-GENE
34 O
and O
1 I-GENE
- I-GENE
86 I-GENE
peptides I-GENE
did O
not O
significantly O
affect O
IL I-GENE
- I-GENE
8 O
production O
; O
moreover I-GENE
, O
PTHrP I-GENE
- I-GENE
neutralizing I-GENE
antibodies I-GENE
did O
not O
inhibit O
the O
production O
of O
IL I-GENE
- I-GENE
8 O
by O
transfected O
PTHrP I-GENE
. O

Furthermore O
, O
this O
kinase I-GENE
- I-GENE
deficient O
mutant I-GENE
inhibited O
2 I-GENE
- I-GENE
MeSADP I-GENE
- I-GENE
induced O
caspase I-GENE
- I-GENE
3 I-GENE
stimulation O
and O
the O
associated I-GENE
decrease O
in O
cell O
number O
. O

Against I-GENE
gram O
- I-GENE
positive O
organisms O
, O
E I-GENE
- I-GENE
4767 I-GENE
and O
E I-GENE
- I-GENE
5065 I-GENE
were O
, O
in O
general O
, O
eight O
- I-GENE
and O
fourfold O
more O
active O
than O
tosufloxacin I-GENE
, O
which O
is O
the O
most O
potent O
of O
the O
reference O
compounds O
. O

The O
results O
presented O
here O
show O
that O
AR1 I-GENE
of O
the O
promoter I-GENE
- I-GENE
proximal I-GENE
CAP I-GENE
subunit I-GENE
was O
required O
for O
papBA I-GENE
transcription I-GENE
even O
in O
the O
absence O
of O
the O
histone I-GENE
- I-GENE
like I-GENE
protein I-GENE
H I-GENE
- I-GENE
NS I-GENE
. O

CONCLUSIONS O
: O
Under O
current O
immunization O
practices I-GENE
, O
the O
authors O
estimate O
that O
nearly O
13 O
, O
000 O
Asian I-GENE
and O
Pacific I-GENE
Islander I-GENE
children O
living O
in O
the O
United O
States I-GENE
today I-GENE
will O
become O
infected O
with O
HBV O
in O
the O
future O
, O
resulting O
in O
more O
than O
600 O
liver O
carcinoma O
deaths O
. O

METHODS O
: O
A I-GENE
structured O
interview I-GENE
was O
undertaken O
at O
the O
time O
of O
initial O
consultation I-GENE
and O
at O
subsequent O
1 I-GENE
- I-GENE
year O
intervals O
regarding O
type I-GENE
of O
BHS I-GENE
, O
frequency O
of O
spells I-GENE
, O
associated I-GENE
phenomenon O
, O
sequelae I-GENE
, O
family I-GENE
history O
, O
and O
age O
at O
termination O
of O
spells I-GENE
. O

Cell O
. O

Rapid I-GENE
evolution O
of O
the O
DNA I-GENE
- I-GENE
binding I-GENE
site I-GENE
in O
LAGLIDADG I-GENE
homing I-GENE
endonucleases I-GENE
. O

These O
mutations O
, O
when O
placed O
in O
a O
wild I-GENE
- I-GENE
type I-GENE
fliF I-GENE
background O
, O
had O
no O
mutant I-GENE
phenotype O
. O

Inhibition O
of O
JNK1 I-GENE
and O
ERK I-GENE
kinase I-GENE
activities O
either O
by O
expression O
of O
the O
dominant I-GENE
negative O
mutant I-GENE
JNK1 I-GENE
or O
by O
treatment O
with O
a O
selective O
chemical O
inhibitor I-GENE
of O
ERK I-GENE
( O
PD098059 I-GENE
) O
substantially O
abrogates I-GENE
the O
UV O
induction O
of O
the O
GADD45 I-GENE
promoter I-GENE
. O

At O
termination O
( O
gd I-GENE
20 O
), O
confirmed O
- I-GENE
pregnant O
females O
( O
21 O
to O
25 O
per O
group O
) O
were O
evaluated O
for O
clinical O
status O
and O
gestational O
outcome O
; O
live O
fetuses I-GENE
were O
examined O
for O
external O
, O
visceral O
, O
and O
skeletal I-GENE
malformations O
. O

In O
mammals O
, O
the O
transcriptional O
repressors I-GENE
in O
the O
Wnt I-GENE
pathway O
are O
not O
well O
defined O
. O

Intravenous O
L I-GENE
- I-GENE
carnitine I-GENE
treatment O
increased O
plasma I-GENE
carnitine I-GENE
concentrations O
, O
improved O
patient O
- I-GENE
assessed O
fatigue I-GENE
, O
and O
may O
prevent O
the O
decline O
in O
peak O
exercise O
capacity O
in O
hemodialysis O
patients O
. O

The O
Van I-GENE
der I-GENE
Hoeve I-GENE
' O
s O
syndrome O
lesions O
as O
poorly O
mineralized I-GENE
, O
with O
low O
calcium O
salt O
and O
apparent O
increase O
of O
phosphates I-GENE
. O

A I-GENE
computerized O
method O
of O
determining O
the O
focal I-GENE
point O
of O
electrical O
activity O
in O
the O
pallidum I-GENE
of O
parkinsonian I-GENE
patients O
was O
developed O
using O
on O
- I-GENE
line O
quantitative O
physiological O
data O
analysis O
. O

The O
first O
hypothesis O
was O
supported O
in O
the O
sense O
that O
stimulus O
differences O
might O
affect O
behaviour O
even O
without O
their O
successful O
attentive I-GENE
processing O
in O
normal O
participants I-GENE
. O

We O
interpret I-GENE
these O
data O
as O
further O
evidence O
that O
interaction O
with O
a O
small I-GENE
GTPase I-GENE
is O
the O
main O
regulatory I-GENE
function O
of O
the O
C1 I-GENE
domain I-GENE
in O
yeast I-GENE
. O

This O
effect O
was O
observed O
in O
the O
absence O
of O
de O
novo I-GENE
protein I-GENE
synthesis O
and O
was O
independent O
of O
histone I-GENE
deacetylase I-GENE
activity O
. O

Mutation O
analyses O
identified O
the O
cobalt I-GENE
- I-GENE
responsive I-GENE
sequences I-GENE
as O
the O
stress O
- I-GENE
response O
elements O
( O
StREs I-GENE
). O

In O
order O
to O
quantify I-GENE
these O
effects O
, O
tests O
were O
conducted O
in O
the O
NASA I-GENE
MSFC I-GENE
Neutral I-GENE
Buoyancy I-GENE
Simulator I-GENE
, O
in O
the O
NASA I-GENE
KC I-GENE
- I-GENE
135 O
in O
parabolic I-GENE
flight I-GENE
, O
and O
in O
space O
with O
the O
EASE I-GENE
program O
during O
the O
Shuttle I-GENE
Atlantis I-GENE
mission I-GENE
61 O
- I-GENE
B I-GENE
. O

OBJECTIVE O
: O
To O
investigate O
the O
association O
between O
complete O
congenital O
heart O
block O
( O
CCHB I-GENE
) O
in O
the O
fetus O
and O
adult O
disease O
. O

The O
present O
chemotherapy O
of O
AE I-GENE
is O
based O
on O
the O
administration O
of O
benzimidazole I-GENE
carbamate I-GENE
derivatives O
, O
such O
as O
mebendazole I-GENE
and O
albendazole I-GENE
. O

The O
uptake O
of O
fluorine I-GENE
- I-GENE
18 O
fluorodeoxyglucose I-GENE
( O
F I-GENE
- I-GENE
18 O
FDG O
) O
by O
a O
malignant O
tumor I-GENE
depends O
on O
the O
blood O
glucose O
level O
. O

Deterministic I-GENE
effects O
. O

DESIGN O
: O
A I-GENE
retrospective O
chart I-GENE
review O
of O
9 O
, O
322 I-GENE
patients O
undergoing O
surgical O
procedures O
in O
the O
period O
January O
1993 O
to O
December I-GENE
1998 O
. O

Peripheral I-GENE
and O
preemptive I-GENE
opioid I-GENE
antinociception I-GENE
in O
a O
mouse I-GENE
visceral O
pain O
model O
. O

METHODS O
: O
We O
studied O
the O
clinical O
benefit O
of O
depth O
- I-GENE
dependent I-GENE
RR O
, O
nonuniform I-GENE
AC I-GENE
using O
a O
scanning O
line O
source O
, O
and O
scatter I-GENE
correction O
( O
photon O
energy O
recovery O
[ O
PER I-GENE
]) I-GENE
compared O
with O
filtered I-GENE
backprojection I-GENE
alone O
. O

Cloning O
and O
characterization O
of O
the O
murine I-GENE
beta I-GENE
( O
3 I-GENE
) O
integrin I-GENE
gene I-GENE
promoter I-GENE
: O
identification O
of O
an O
interleukin I-GENE
- I-GENE
4 I-GENE
responsive I-GENE
element I-GENE
and O
regulation O
by O
STAT I-GENE
- I-GENE
6 I-GENE
. O

DNA I-GENE
binding I-GENE
assays O
confirmed O
the O
interference O
of O
p30 I-GENE
( O
II I-GENE
) O
with O
the O
assembly O
of O
CREB I-GENE
- I-GENE
Tax I-GENE
- I-GENE
p300 I-GENE
/ I-GENE
CBP I-GENE
multiprotein I-GENE
complexes I-GENE
on O
21 O
- I-GENE
bp O
repeat I-GENE
oligonucleotides O
in O
vitro O
. O

Transient O
transfections O
showed O
that O
a O
single O
mutation I-GENE
( O
556M I-GENE
) O
decreased O
TBLV I-GENE
enhancer I-GENE
activity O
at O
least O
20 O
- I-GENE
fold O
in O
two O
different O
T I-GENE
- I-GENE
cell O
lines O
. O

In O
conclusion O
, O
tube O
size O
estimated O
by O
Cole I-GENE
' O
s O
formula O
tends I-GENE
to O
be O
smaller O
than O
practically I-GENE
appropriate O
tube O
size O
for O
pediatric O
cardiac O
anesthesia O
, O
and O
therefore O
we O
suggest O
new O
formula O
to O
estimate O
the O
tube O
size O
. O

Thus O
, O
in O
T47D I-GENE
breast O
carcinoma O
cells O
, O
IL I-GENE
- I-GENE
6 I-GENE
acts O
in O
synergy I-GENE
with O
EGF I-GENE
receptor I-GENE
autocrine O
activity O
to O
signal I-GENE
through O
the O
MAPK I-GENE
/ I-GENE
PI3K I-GENE
pathways O
. O

Nerve I-GENE
growth I-GENE
factor I-GENE
( O
NGF I-GENE
) O
and O
retinoic I-GENE
acid I-GENE
( O
RA O
) O
exert O
important O
actions O
on O
PC12 O
cells O
. O

HexA71 I-GENE
negatively O
affects O
RpoS I-GENE
, O
as O
the O
levels O
of O
this O
alternative O
sigma I-GENE
factor I-GENE
are O
higher O
in O
the O
HexA I-GENE
- I-GENE
mutant I-GENE
than O
in O
the O
HexA I-GENE
+ I-GENE
strain O
. O

Moreover O
, O
elderly O
men O
with O
bioavailable I-GENE
estradiol O
levels O
below O
the O
median O
[ O
40 I-GENE
pmol I-GENE
/ I-GENE
liter O
( O
11 O
pg O
/ I-GENE
ml O
)] O
had O
significantly O
higher O
rates O
of O
bone O
loss O
and O
levels O
of O
bone O
resorption O
markers O
than O
men O
with O
bioavailable I-GENE
estradiol O
levels O
above O
40 I-GENE
pmol I-GENE
/ I-GENE
liter O
. O

The O
histamine O
H1 I-GENE
receptor I-GENE
antagonists O
( O
antihistamines I-GENE
) O
are O
an O
important O
class I-GENE
of O
medications I-GENE
used O
for O
the O
relief I-GENE
of O
common O
symptoms O
associated I-GENE
with O
hyperhistaminic I-GENE
conditions O
occurring O
in O
children O
and O
adults O
. O

The O
production O
of O
ceramide I-GENE
is O
emerging I-GENE
as O
a O
fixture I-GENE
of O
programmed O
cell O
death O
. O

The O
flux I-GENE
rates O
of O
p O
- I-GENE
toluidine I-GENE
decreased O
as O
the O
pH O
value O
in O
the O
donor O
solution O
increased O
. O

Managing I-GENE
HIV I-GENE
. O

BACKGROUND O
: O
There O
is O
increasing O
interest O
on O
the O
part O
of O
investigators I-GENE
and O
the O
public I-GENE
at O
large O
in O
finding O
ways O
to O
study O
and O
improve O
treatments O
for O
the O
seriously I-GENE
mentally I-GENE
ill I-GENE
without O
exposing I-GENE
such O
individuals O
to O
unnecessary I-GENE
risks I-GENE
. O

Multidrug I-GENE
resistance O
in O
Saccharomyces I-GENE
cerevisiae I-GENE
mainly O
results O
from O
the O
overexpression O
of O
genes I-GENE
coding O
for O
the O
membrane I-GENE
efflux I-GENE
pumps I-GENE
, O
the O
major I-GENE
facilitators I-GENE
and O
the O
ABC I-GENE
binding I-GENE
cassette I-GENE
transporters I-GENE
, O
under O
the O
control O
of O
key O
transcription I-GENE
regulators O
encoded I-GENE
by O
the O
PDR1 I-GENE
and O
PDR3 I-GENE
genes I-GENE
. O

Serum I-GENE
PTH I-GENE
tended O
to O
increase O
in O
the O
WL I-GENE
group O
but O
not O
in O
the O
WM I-GENE
group O
( O
P I-GENE
< O
0 O
. O
06 O
). O

Bandshift I-GENE
experiments O
demonstrate O
that O
BmHR3A I-GENE
binds O
specifically O
to O
RORE I-GENE
( O
Retinoic I-GENE
acid I-GENE
- I-GENE
related I-GENE
Orphan I-GENE
receptor I-GENE
Response O
Element I-GENE
)- I-GENE
like I-GENE
sequences I-GENE
in O
the O
promoters I-GENE
of O
both O
genes I-GENE
, O
thus O
suggesting O
a O
direct O
role O
for O
BmHR3A I-GENE
in O
regulating O
the O
expression O
of O
BmGATAbeta I-GENE
and O
ESP I-GENE
genes I-GENE
during O
vitellogenesis I-GENE
. O

Efficacy I-GENE
of O
first O
- I-GENE
generation O
Cavermap I-GENE
to O
verify I-GENE
location O
and O
function O
of O
cavernous I-GENE
nerves O
during O
radical O
prostatectomy I-GENE
: O
a O
multi I-GENE
- I-GENE
institutional I-GENE
evaluation O
by O
experienced O
surgeons I-GENE
. O

During O
most O
of O
the O
cell O
cycle O
, O
separase I-GENE
is O
kept O
inactive O
by O
binding I-GENE
to O
an O
inhibitory I-GENE
protein I-GENE
called O
securin I-GENE
. O

In O
conclusion O
, O
obesity O
, O
alcohol O
intake O
, O
and O
multimetabolic I-GENE
disorders O
were O
determined O
to O
be O
independent O
predictors O
for O
the O
development O
of O
hyperuricemia I-GENE
. O

This O
study O
examined O
the O
role O
of O
cholesteryl I-GENE
ester O
transfer I-GENE
( O
CET I-GENE
), O
cholesteryl I-GENE
ester O
transfer I-GENE
protein I-GENE
( O
CETP I-GENE
) O
activity O
, O
and O
phospholipid I-GENE
transfer I-GENE
protein I-GENE
( O
PLTP I-GENE
) O
activity O
in O
the O
increased O
prevalence O
of O
coronary O
artery O
calcification I-GENE
( O
CAC I-GENE
) O
in O
diabetic O
subjects O
compared O
with O
nondiabetic I-GENE
subjects O
and O
in O
the O
loss O
of O
the O
sex I-GENE
difference O
in O
CAC I-GENE
in O
diabetes O
. O

In O
the O
mouse I-GENE
, O
both O
genes I-GENE
reside O
in O
the O
syntenic I-GENE
region O
8E1 I-GENE
on O
chromosome O
8 O
. O

We O
observed O
NP I-GENE
/ I-GENE
NMP4 I-GENE
/ I-GENE
CIZ I-GENE
expression O
in O
osteocytes I-GENE
, O
osteoblasts I-GENE
, O
and O
chondrocytes I-GENE
in O
rat I-GENE
bone O
. O

Following O
baseline O
clinical O
examination O
and O
initial O
periodontal O
therapy O
, O
32 O
patients O
received O
mucogingival I-GENE
surgery O
with O
free O
gingival I-GENE
grafts O
for O
treatment O
of O
insufficient O
attached O
gingiva I-GENE
. O

In O
contrast O
, O
the O
failure O
of O
the O
QKTT I-GENE
motif I-GENE
and O
TGN46 I-GENE
cytoplasmic I-GENE
tail O
to O
induce O
steady O
- I-GENE
state O
ER I-GENE
localization O
of O
vesicular O
stomatitis I-GENE
virus I-GENE
glycoprotein I-GENE
( O
VSVG I-GENE
) O
chimeras I-GENE
in O
HeLa O
and O
NRK I-GENE
cells O
indicates O
that O
significant O
differences O
in O
early I-GENE
secretory I-GENE
trafficking O
also O
exist O
. O

We O
previously O
showed O
that O
this O
proteolysis O
1 I-GENE
) O
can O
be O
acutely I-GENE
promoted O
by O
the O
phorbol O
ester O
phorbol O
12 O
- I-GENE
myristate O
13 O
- I-GENE
acetate O
( O
PMA O
), O
2 I-GENE
) O
requires O
a O
metalloprotease I-GENE
activity O
, O
3 I-GENE
) O
generates O
both O
shed I-GENE
GHBP I-GENE
and O
a O
membrane I-GENE
- I-GENE
associated I-GENE
GHR I-GENE
transmembrane I-GENE
/ I-GENE
cytoplasmic I-GENE
domain I-GENE
remnant I-GENE
, O
and O
4 I-GENE
) O
results O
in O
down O
- I-GENE
regulation O
of O
GHR I-GENE
abundance O
and O
GH I-GENE
signaling O
. O

Our O
data O
indicate O
that O
SIP1 I-GENE
is O
required O
to O
confine I-GENE
XBra I-GENE
gene I-GENE
expression O
to O
the O
mesoderm O
. O

Changes O
of O
the O
DB I-GENE
sequence I-GENE
without O
affecting O
the O
postulated O
stem O
structure O
led O
to O
drastic I-GENE
losses I-GENE
of O
translation I-GENE
efficiency O
. O

This O
subfamily I-GENE
of O
genes I-GENE
all O
have O
a O
single O
ATP I-GENE
- I-GENE
binding I-GENE
domain I-GENE
at O
the O
N I-GENE
- I-GENE
terminus O
and O
a O
single O
C I-GENE
- I-GENE
terminal I-GENE
set O
of O
transmembrane I-GENE
segments O
. O

Subsequently I-GENE
, O
these O
coordinates I-GENE
must O
be O
interpreted O
to O
define O
particular O
tissues O
and O
organs O
. O

The O
cyclins I-GENE
bind O
to O
and O
activate O
the O
CDK I-GENE
, O
which O
leads O
to O
phosphorylation O
( O
and O
then O
inhibition O
) O
of O
the O
tumor I-GENE
suppressor I-GENE
protein I-GENE
, O
pRb I-GENE
. O
pRb I-GENE
controls O
commitment I-GENE
to O
progress O
from O
the O
G1 I-GENE
to O
S I-GENE
phase O
, O
at O
least O
in O
part O
by O
repressing O
the O
activity O
of O
the O
E2F I-GENE
transcription I-GENE
factors I-GENE
known O
to O
promote O
cell O
proliferation O
. O

The O
mean O
serum I-GENE
creatinine O
level O
did O
not O
change O
during O
the O
first O
6 I-GENE
months O
after O
withdrawal O
of O
MMF I-GENE
. O

The O
severity O
of O
pathologic O
changes O
increased O
with O
the O
magnitude O
of O
percussion I-GENE
. O

Patients O
with O
antibody I-GENE
peaks O
, O
defined O
as O
fivefold I-GENE
or O
higher O
increase O
in O
antibody I-GENE
titer O
compared O
to O
the O
lowest O
antibody I-GENE
titer O
over O
the O
course O
of O
GBS I-GENE
, O
had O
higher O
disability I-GENE
scores O
during O
the O
first O
two O
weeks O
of O
GBS I-GENE
and O
a O
worse I-GENE
clinical O
outcome O
( O
anti I-GENE
- I-GENE
GM1 I-GENE
IgG I-GENE
and O
anti I-GENE
- I-GENE
GD1a I-GENE
IgM I-GENE
antibody I-GENE
peaks O
) O
and O
axonal I-GENE
damage O
( O
anti I-GENE
- I-GENE
GD1a I-GENE
IgM I-GENE
antibody I-GENE
peaks O
), O
compared O
to O
patients O
without O
peak O
antibody I-GENE
titers I-GENE
. O

At O
20 O
days O
( O
D I-GENE
) O
and O
at O
3 I-GENE
months O
post O
- I-GENE
TBI I-GENE
, O
irradiated O
rats O
had O
a O
significantly O
lower O
percentage O
of O
avoidance I-GENE
than O
controls O
but O
no O
statistical O
difference O
was O
found O
at O
5 I-GENE
months O
post O
- I-GENE
TBI I-GENE
. O
b I-GENE
/ I-GENE
Two O
- I-GENE
way O
avoidance I-GENE
test O
: O
this O
test O
was O
performed O
only O
after O
TBI I-GENE
. O

TE I-GENE
- I-GENE
671 I-GENE
cells O
that O
were O
transfected O
with O
cAMP I-GENE
response O
element I-GENE
mutant I-GENE
constructs I-GENE
demonstrated O
a O
diminished O
basal O
activity O
of O
the O
GnRH I-GENE
- I-GENE
II I-GENE
promoter I-GENE
. O

The O
severity O
of O
clinical O
course O
was O
expressed O
by O
means O
of O
SOFA I-GENE
score O
( O
group O
A I-GENE
0 O
. O
3 I-GENE
- I-GENE
1 I-GENE
- I-GENE
1 I-GENE
. O
3 I-GENE
point O
, O
group O
B I-GENE
2 I-GENE
. O
2 I-GENE
- I-GENE
2 I-GENE
. O
9 O
- I-GENE
2 I-GENE
. O
6 I-GENE
point O
, O
group O
C I-GENE
7 O
. O
4 I-GENE
- I-GENE
8 O
. O
3 I-GENE
- I-GENE
7 O
. O
7 O
point O
) O
and O
APACHE I-GENE
II I-GENE
score O
( O
group O
A I-GENE
3 I-GENE
. O
7 O
- I-GENE
7 O
. O
6 I-GENE
- I-GENE
8 O
. O
1 I-GENE
point O
, O
group O
B I-GENE
8 O
. O
6 I-GENE
- I-GENE
11 O
. O
1 I-GENE
- I-GENE
10 O
. O
5 I-GENE
point O
, O
group O
C I-GENE
16 O
. O
3 I-GENE
- I-GENE
15 O
. O
2 I-GENE
- I-GENE
14 O
. O
3 I-GENE
point O
). O

A I-GENE
novel O
potential O
effector O
of O
M I-GENE
- I-GENE
Ras I-GENE
and O
p21 I-GENE
Ras I-GENE
negatively O
regulates O
p21 I-GENE
Ras I-GENE
- I-GENE
mediated O
gene I-GENE
induction O
and O
cell O
growth I-GENE
. O

Promoter O
transcriptional O
activity O
was O
determined O
for O
a O
wide O
5 I-GENE
' O
portion O
of O
the O
human I-GENE
annexin I-GENE
A5 I-GENE
gene I-GENE
, O
from O
bp O
- I-GENE
1275 I-GENE
to O
+ I-GENE
79 O
relative O
to O
the O
most O
5 I-GENE
' O
of O
several O
discrete O
transcription I-GENE
start O
points O
. O

Structure O
of O
the O
EMAPII I-GENE
domain I-GENE
of O
human I-GENE
aminoacyl I-GENE
- I-GENE
tRNA I-GENE
synthetase I-GENE
complex I-GENE
reveals O
evolutionary O
dimer O
mimicry I-GENE
. O

Adding I-GENE
10 O
mmol O
SDS O
/ I-GENE
l O
led O
to O
transient O
inhibition O
of O
acidification O
, O
metal O
solubilization I-GENE
and O
sulfur O
oxidation O
. O

Competition O
electrophoretic O
mobility I-GENE
shift O
and O
immunoshift I-GENE
assays O
confirmed O
that O
NF1 I-GENE
factors I-GENE
present O
in O
nuclear I-GENE
extracts O
of O
HeLa O
and O
CV I-GENE
- I-GENE
1 I-GENE
cells O
bind O
to O
the O
BKV I-GENE
- I-GENE
MLP I-GENE
. O

Northern O
and O
Western O
blot O
analyses O
demonstrated O
that O
Graf2 I-GENE
is O
expressed O
in O
several O
tissues O
, O
with O
the O
highest O
expression O
in O
skeletal I-GENE
muscle O
. O

A I-GENE
minimal I-GENE
ER3 I-GENE
sequence I-GENE
of O
DNA I-GENE
was O
further O
demonstrated O
to O
function O
as O
a O
FXR I-GENE
HRE I-GENE
and O
was O
bound O
in O
vitro O
by O
FXR I-GENE
- I-GENE
expressing O
yeast I-GENE
extracts O
. O

In O
Ka13 I-GENE
cells O
, O
CoCl I-GENE
( O
2 I-GENE
) O
stimulated O
expression O
of O
a O
luciferase I-GENE
reporter I-GENE
gene I-GENE
under O
the O
control O
of O
a O
15 O
- I-GENE
kilobase O
pair O
mouse I-GENE
ho I-GENE
- I-GENE
1 I-GENE
promoter I-GENE
( O
pHO15luc I-GENE
). O

Nine I-GENE
strains O
were O
subtyped I-GENE
as O
Camp I-GENE
. O
jejuni I-GENE
subsp I-GENE
. O
jejuni I-GENE
biotype I-GENE
II I-GENE
and O
the O
remaining O
ones O
as O
biotype I-GENE
I I-GENE
. O

The O
Ig I-GENE
- I-GENE
related I-GENE
, O
typical O
metazoan I-GENE
, O
module I-GENE
is O
classified O
to O
the O
disulphide I-GENE
lacking O
Ig I-GENE
members O
and O
represents O
the O
phylogenetic O
earliest I-GENE
member O
of O
this O
group O
. O

In O
budding I-GENE
yeast I-GENE
, O
this O
latter O
checkpoint I-GENE
response O
involves O
the O
proteins I-GENE
Mad1 I-GENE
, O
2 I-GENE
, O
3 I-GENE
, O
Bub1 I-GENE
and O
Bub3 I-GENE
, O
whose O
vertebrate I-GENE
counterparts O
localize O
to O
unattached I-GENE
kinetochores I-GENE
. O

We O
investigated O
the O
production O
of O
hyaluronan I-GENE
( O
HA I-GENE
) O
and O
its O
effect O
on O
cell O
motility O
in O
cells O
expressing O
the O
v I-GENE
- I-GENE
src I-GENE
mutants I-GENE
. O

Oral I-GENE
supplementation O
of O
L I-GENE
- I-GENE
arginine I-GENE
significantly O
increased O
plasma I-GENE
L I-GENE
- I-GENE
citrulline I-GENE
, O
which O
indicated O
enhancement O
of O
NO O
production O
. O

We O
can O
classify I-GENE
antibiotics O
into O
two O
groups O
based O
on O
initial O
bactericidal O
activity O
against O
P I-GENE
. O
aeruginosa I-GENE
; O
one O
class I-GENE
is O
antibiotics O
having O
rapid O
initial O
killing I-GENE
such O
as O
AMK I-GENE
, O
IPM I-GENE
and O
PAPM I-GENE
, O
the O
other O
is O
CAZ I-GENE
, O
MEPM I-GENE
showing O
slow O
initial O
killing I-GENE
. O

The O
presence O
of O
truncated I-GENE
receptor I-GENE
isoforms I-GENE
in O
diverse O
species O
suggests O
that O
these O
proteins I-GENE
may O
have O
important O
functional O
roles O
in O
regulating O
EGFR I-GENE
activity O
. O

Of O
its O
gene I-GENE
products I-GENE
, O
E6 I-GENE
binds O
to O
and O
inactivates I-GENE
p53 I-GENE
tumor I-GENE
suppressor I-GENE
protein I-GENE
by O
ubiquitin I-GENE
/ I-GENE
proteasome I-GENE
- I-GENE
dependent I-GENE
degradation O
. O

Low O
affinity O
binding I-GENE
of O
Rab6A I-GENE
- I-GENE
GTP I-GENE
was O
also O
observed O
( O
K I-GENE
( O
d O
) O
= O
16 O
microm O
), O
whereas O
Rab1B I-GENE
, O
- I-GENE
5 I-GENE
, O
- I-GENE
7 O
, O
- I-GENE
8 O
, O
or O
- I-GENE
11A I-GENE
did O
not O
bind O
. O

( O
1997 O
) O
Nature I-GENE
387 I-GENE
, O
370 I-GENE
- I-GENE
376 I-GENE
)], I-GENE
we O
suggest O
that O
the O
metal O
fluoride O
ions O
replaced O
phosphate I-GENE
at O
the O
two O
ATP I-GENE
- I-GENE
binding I-GENE
sites I-GENE
of O
the O
iron O
protein I-GENE
, O
Kp2 I-GENE
. O

A I-GENE
1 I-GENE
- I-GENE
base O
pair O
mismatch I-GENE
within O
the O
corresponding O
region O
of O
the O
CYP3A4 I-GENE
gene I-GENE
was O
sufficient O
for O
a O
differential O
enhancer I-GENE
activity O
. O

AIMS I-GENE
: O
To O
establish O
a O
baseline O
and O
intraindividual I-GENE
fluctuations O
of O
the O
tumour I-GENE
markers O
CEA I-GENE
, O
CA I-GENE
50 O
and O
CA I-GENE
242 I-GENE
in O
patients O
cured I-GENE
from O
colorectal I-GENE
cancer O
, O
and O
to O
test O
the O
hypothesis O
that O
serum I-GENE
concentrations O
and O
intraindividual I-GENE
fluctuations O
do O
not O
differ O
from O
the O
concentrations O
in O
cancer O
- I-GENE
free O
individuals O
. O

Substitution O
of O
serine I-GENE
residues O
at O
the O
C I-GENE
- I-GENE
terminus O
indicated O
that O
loss O
of O
phosphorylation O
sites I-GENE
did O
not O
appear O
to O
have O
any O
effect O
on O
transcription I-GENE
and O
replication O
. O

Molecular O
analysis O
of O
the O
pRA2 I-GENE
partitioning I-GENE
region O
: O
ParB I-GENE
autoregulates I-GENE
parAB I-GENE
transcription I-GENE
and O
forms O
a O
nucleoprotein I-GENE
complex I-GENE
with O
the O
plasmid O
partition I-GENE
site I-GENE
, O
parS I-GENE
. O

Tumor I-GENE
cell O
lines O
transduced I-GENE
at O
an O
MOI I-GENE
of O
8 O
for O
3 I-GENE
days O
led O
to O
> O
90 O
% O
gene I-GENE
transfer I-GENE
efficiency O
. O

No O
ISREs I-GENE
could O
be O
identified O
in O
the O
mouse I-GENE
promoter I-GENE
. O

GABA I-GENE
( O
B I-GENE
) O
R1g I-GENE
was O
expressed O
in O
both O
brain O
and O
peripheral O
tissues O
. O

Granulocyte I-GENE
colony I-GENE
- I-GENE
stimulating I-GENE
factor I-GENE
( O
G I-GENE
- I-GENE
CSF I-GENE
) O
administration O
in O
vivo O
has O
been O
shown O
to O
improve O
the O
defence I-GENE
mechanisms O
against O
infection O
by O
different O
microbes I-GENE
. O

Use O
of O
a O
dual O
- I-GENE
pulse O
lithotripter I-GENE
to O
generate O
a O
localized O
and O
intensified I-GENE
cavitation I-GENE
field O
. O

The O
best O
regression O
model O
for O
predicting O
changes O
in O
the O
WCXR I-GENE
included O
time O
to O
first O
positive O
culture O
and O
antibody I-GENE
titer O
for O
Pa I-GENE
elastase I-GENE
. O

RESULTS O
: O
The O
parameters O
SF2 I-GENE
and O
plating I-GENE
efficiency O
were O
stable O
throughout O
the O
4 I-GENE
- I-GENE
year O
test O
period O
. O

The O
process O
has O
been O
applied O
to O
the O
river I-GENE
reclamation I-GENE
in O
Yangpu I-GENE
District I-GENE
of O
Shanghai I-GENE
City O
, O
China I-GENE
. O

Multiple O
regression O
analysis O
performed O
between O
these O
long O
- I-GENE
term O
abiotic I-GENE
factors I-GENE
and O
nymphal I-GENE
abundance O
in O
positive O
sites I-GENE
showed O
high O
relationship O
( O
R2 I-GENE
coefficients O
) O
for O
every O
habitat I-GENE
category O
and O
explained O
> O
50 O
% O
of O
the O
variation O
in O
tick I-GENE
abundance O
. O

The O
v I-GENE
- I-GENE
Src I-GENE
SH3 I-GENE
domain I-GENE
facilitates I-GENE
a O
cell O
adhesion I-GENE
- I-GENE
independent O
association O
with O
focal I-GENE
adhesion I-GENE
kinase I-GENE
. O

Of O
the O
six O
cases O
of O
malignant O
polyposis I-GENE
, O
none O
were O
identified O
using O
CT I-GENE
, O
and O
only O
two O
were O
diagnosed O
by O
small I-GENE
bowel O
follow O
- I-GENE
through O
. O

Right I-GENE
LHR I-GENE
( O
R I-GENE
- I-GENE
LHR I-GENE
) O
provided O
the O
best O
interobserver I-GENE
and O
intraobserver I-GENE
reproducibility O
. O

We O
also O
reported O
the O
identification O
of O
three O
corresponding O
alternative O
first O
exons O
and O
an O
intronic I-GENE
promoter I-GENE
in O
the O
human I-GENE
PDE5A I-GENE
gene I-GENE
. O

Of O
major I-GENE
concern I-GENE
to O
food O
processors I-GENE
is O
the O
inadvertent I-GENE
cross O
- I-GENE
contact O
of O
food O
products I-GENE
with O
allergenic I-GENE
residues O
, O
which O
could O
result O
in O
potentially O
life O
- I-GENE
threatening I-GENE
reactions O
in O
those O
with O
a O
food O
allergy O
. O

Diffuse I-GENE
myalgias I-GENE
were O
more O
frequent O
in O
patients O
with O
than O
without O
an O
MMF I-GENE
lesion O
at O
deltoid I-GENE
muscle O
biopsy O
( O
P I-GENE
< O
0 O
. O
0001 O
). O

Functional O
analysis O
of O
various O
PTP I-GENE
- I-GENE
deficient O
DT40 I-GENE
B I-GENE
cell O
lines O
stably O
expressing O
wild I-GENE
- I-GENE
type I-GENE
chimeric I-GENE
Fc I-GENE
gamma I-GENE
RIIB1 I-GENE
- I-GENE
PECAM I-GENE
- I-GENE
1 I-GENE
receptor I-GENE
indicated O
that O
cytoplasmic I-GENE
Src I-GENE
homology I-GENE
2 I-GENE
- I-GENE
domain I-GENE
- I-GENE
containing O
phosphatases I-GENE
, O
SHP I-GENE
- I-GENE
1 I-GENE
and O
SHP I-GENE
- I-GENE
2 I-GENE
, O
were O
both O
necessary O
and O
sufficient O
to O
deliver I-GENE
inhibitory I-GENE
negative O
regulation O
upon O
coligation I-GENE
of O
BCR I-GENE
complex I-GENE
with O
inhibitory I-GENE
receptor I-GENE
. O

Subtraction I-GENE
hybridization O
identified O
melanoma O
differentiation O
associated I-GENE
gene I-GENE
- I-GENE
7 O
( O
mda I-GENE
- I-GENE
7 O
), O
as O
a O
gene I-GENE
induced O
during O
these O
physiological O
changes O
in O
human I-GENE
melanoma O
cells O
. O

A I-GENE
rare O
case O
of O
primary O
group O
A I-GENE
streptococcal I-GENE
peritonitis I-GENE
. O

Among O
individuals O
, O
however O
, O
changes O
were O
strongly O
correlated O
with O
ACR I-GENE
levels O
at O
baseline O
. O

RESULTS O
: O
The O
subjects O
in O
the O
augmented O
feedback I-GENE
group O
significantly O
reduced O
their O
peak O
vertical O
ground I-GENE
reaction O
force O
in O
both O
post O
- I-GENE
test O
conditions O
( O
2 I-GENE
- I-GENE
minute O
post O
- I-GENE
test O
reduction O
, O
0 O
. O
85 O
+/- O
0 O
. O
62 O
; O
1 I-GENE
- I-GENE
week O
post O
- I-GENE
test O
reduction O
, O
0 O
. O
74 O
+/- O
0 O
. O
58 O
) O
as O
compared O
to O
the O
sensory O
, O
control O
I I-GENE
, O
and O
control O
II I-GENE
feedback I-GENE
groups O
. O

The O
blood O
levels O
of O
lactate I-GENE
, O
pyruvate I-GENE
and O
amino O
acids O
were O
not O
elevated O
. O

Histological O
examination O
showed O
lichenoid I-GENE
changes O
, O
acantholytic I-GENE
blister I-GENE
formation O
and O
apoptotic O
keratinocytes I-GENE
. O

Enantiomer I-GENE
separation O
of O
venlafaxine I-GENE
and O
O I-GENE
- I-GENE
desmethylvenlafaxine I-GENE
in O
human I-GENE
plasma I-GENE
. O

Paul I-GENE
Monagle I-GENE
addresses I-GENE
the O
epidemiology I-GENE
of O
neonatal O
thrombosis O
outside O
of O
the O
central O
nervous O
system O
in O
both O
arterial O
and O
venous O
locations O
, O
and O
those O
that O
occur O
in O
utero I-GENE
. O

The O
MSL I-GENE
complex I-GENE
is O
specifically O
localized O
on O
the O
male O
X I-GENE
chromosome O
to O
increase O
its O
expression O
approximately O
2 I-GENE
- I-GENE
fold O
. O

Effects O
of O
a O
booster I-GENE
dose O
of O
tetanus I-GENE
toxoid I-GENE
after O
different O
primary O
courses O
of O
vaccination O
: O
implications O
on O
the O
use O
of O
immune I-GENE
globulin I-GENE
. O

Our O
results O
suggest O
that O
the O
C I-GENE
- I-GENE
terminal I-GENE
region O
of O
Crk I-GENE
contains O
negative O
regulatory I-GENE
elements O
important O
for O
both O
Abl I-GENE
and O
FAK I-GENE
dependent I-GENE
signal I-GENE
pathways O
, O
and O
offers O
a O
paradigm I-GENE
for O
an O
autoinhibitory I-GENE
region O
in O
the O
SH3 I-GENE
linker I-GENE
/ I-GENE
C I-GENE
- I-GENE
terminal I-GENE
SH3 I-GENE
domain I-GENE
. O

The O
distribution O
of O
red I-GENE
rice I-GENE
cultivation I-GENE
in O
Sri I-GENE
Lanka I-GENE
is O
coincident I-GENE
with O
the O
HIDD I-GENE
villages I-GENE
. O

Prophylactic I-GENE
lymph O
node O
dissection O
or O
radiation O
therapy O
to O
the O
nodal O
chain I-GENE
may O
decrease O
local O
recurrence O
but O
does O
not O
consistently O
affect O
overall O
survival O
. O

Secretion I-GENE
of O
interleukin I-GENE
- I-GENE
8 O
, O
RANTES I-GENE
, O
macrophage I-GENE
inflammatory O
protein I-GENE
1alpha I-GENE
, O
and O
10 O
- I-GENE
kappaDa I-GENE
IFN I-GENE
- I-GENE
gamma I-GENE
- I-GENE
inducible I-GENE
protein I-GENE
were O
increased O
in O
differentiating O
keratinocytes I-GENE
by O
E6 I-GENE
. O

CONCLUSIONS O
: O
ChromaFlo I-GENE
- I-GENE
enhanced O
IVUS I-GENE
demonstrates O
colorized I-GENE
blood O
flow O
inside I-GENE
the O
vessel O
lumen I-GENE
, O
which O
is O
helpful O
in O
distinguishing I-GENE
echolucent I-GENE
disease O
from O
luminal O
blood O
flow O
and O
can O
also O
be O
used O
to O
perform O
peripheral O
interventions I-GENE
in O
patients O
with O
renal O
failure O
or O
allergy O
, O
avoiding I-GENE
the O
use O
of O
contrast O
media O
. O

Additional I-GENE
factors I-GENE
such O
as O
advanced O
age O
, O
concomitant O
use O
of O
corticosteroids O
or O
anticoagulants I-GENE
, O
prior O
ulcer O
complications O
and O
co O
- I-GENE
morbid I-GENE
diseases O
may O
further O
increase O
the O
risk O
of O
bleeding O
. O

CONCLUSIONS O
: O
Using O
icodextrin I-GENE
- I-GENE
based O
instead O
of O
glucose O
- I-GENE
based O
PD I-GENE
fluids O
can O
largely O
reduce O
the O
formation O
of O
Amadori I-GENE
albumin I-GENE
and O
AGEs I-GENE
. O

A I-GENE
central O
finding O
is O
the O
identification O
of O
a O
GC I-GENE
- I-GENE
rich O
sequence I-GENE
in O
the O
- I-GENE
99 O
/- O
91 O
Cp I-GENE
region O
that O
is O
essential O
for O
oriPI I-GENE
- I-GENE
EBNA1 I-GENE
- I-GENE
independent O
as O
well O
as O
oriPI I-GENE
- I-GENE
EBNA1 I-GENE
- I-GENE
dependent I-GENE
activity O
of O
the O
promoter I-GENE
. O

Furthermore O
, O
SB203580 I-GENE
inhibited O
LPS I-GENE
- I-GENE
induced O
activation O
of O
Sp1 I-GENE
, O
as O
well O
as O
the O
promoter I-GENE
activity O
in O
cells O
transfected O
with O
a O
plasmid O
containing O
the O
Sp1 I-GENE
consensus I-GENE
sequence I-GENE
. O

A I-GENE
new O
echocardiographic O
technique O
is O
described O
with O
a O
conventional O
M I-GENE
mode O
, O
digitalised I-GENE
2D I-GENE
and O
tissular I-GENE
Doppler O
which O
has O
a O
comparable O
ability O
to O
identify O
the O
anomalous I-GENE
pathways O
of O
electric I-GENE
conduction O
using O
a O
non O
- I-GENE
invasive O
method O
. O

Is O
clopidogrel I-GENE
superior O
to O
aspirin I-GENE
in O
secondary O
prevention O
of O
vascular I-GENE
disease O
? O
The O
cornerstone I-GENE
in O
clinical O
evidence O
of O
the O
relative O
efficacy O
of O
thienopyridines I-GENE
( O
clopidogrel I-GENE
, O
ticlopidine I-GENE
) O
versus O
aspirin I-GENE
in O
the O
secondary O
prevention O
of O
vascular I-GENE
disease O
is O
the O
Clopidogrel I-GENE
versus O
Aspirin I-GENE
in O
Patients O
at O
Risk O
of O
Ischaemic I-GENE
Events I-GENE
trial O
. O

The O
role O
of O
the O
Vp1 I-GENE
DBD I-GENE
during O
infection O
was O
investigated O
by O
taking O
advantage O
of O
NLS O
phenotypic I-GENE
complementation O
( O
N I-GENE
. O

The O
probability I-GENE
of O
treatment O
with O
lamotrigine I-GENE
being O
maintained O
for O
six O
months O
was O
86 I-GENE
%, O
for O
twelve I-GENE
months O
61 O
% O
and O
for O
three O
years O
31 O
%. O

Recent O
advances I-GENE
have O
shown O
that O
volatile O
sulfur O
is O
a O
result O
of O
ecological I-GENE
interactions O
and O
transformation O
processes O
through O
planktonic I-GENE
food O
webs I-GENE
. O

OsBBPI I-GENE
was O
found O
to O
be O
rapidly O
induced O
in O
rice I-GENE
seedling I-GENE
leaf O
in O
response O
to O
cut I-GENE
, O
exogenous O
jasmonic I-GENE
acid I-GENE
( O
JA I-GENE
), O
and O
two O
potent O
protein I-GENE
phosphatase I-GENE
2A I-GENE
( O
PP2A I-GENE
) O
inhibitors O
, O
cantharidin I-GENE
( O
CN I-GENE
) O
and O
endothall I-GENE
( O
EN I-GENE
), O
in O
a O
light I-GENE
/ I-GENE
dark O
-, I-GENE
time O
- I-GENE
and O
dose O
- I-GENE
dependent I-GENE
manner O
; O
this O
induction O
was O
completely O
inhibited O
by O
cycloheximide I-GENE
( O
CHX I-GENE
), O
indicating O
a O
requirement O
for O
de O
novo I-GENE
protein I-GENE
synthesis O
in O
its O
induction O
. O

Analysis O
of O
ace2Delta I-GENE
cells O
reveals O
that O
Ace2p I-GENE
is O
required O
for O
cell O
separation O
but O
not O
for O
polarized I-GENE
growth I-GENE
. O

The O
purpose O
of O
this O
investigation O
was O
to O
study O
the O
morphological O
characteristics O
of O
the O
fibrous I-GENE
tissue I-GENE
capsule I-GENE
resulting O
from O
the O
implantation O
of O
aluminum O
calcium O
phosphate I-GENE
( O
ALCAP I-GENE
) O
and O
hydroxyapetite I-GENE
( O
HA I-GENE
) O
bioceramics I-GENE
. O

The O
event O
rate O
in O
patients O
with O
chronic O
Irr I-GENE
- I-GENE
rMFP I-GENE
or O
Un I-GENE
- I-GENE
nrMFP I-GENE
was O
markedly O
higher O
than O
it O
was O
in O
those O
with O
Rev I-GENE
- I-GENE
rMFP I-GENE
or O
Sta I-GENE
- I-GENE
nrMFP I-GENE
. O

In O
summary O
, O
we O
conclude O
that O
the O
adenoviral I-GENE
oncoprotein I-GENE
E1A I-GENE
activates O
transcription I-GENE
from O
the O
endogenous I-GENE
AP I-GENE
- I-GENE
2alpha I-GENE
gene I-GENE
, O
an O
effect O
that O
involves O
transcriptional O
derepression O
of O
the O
AP I-GENE
- I-GENE
2alpha I-GENE
promoter I-GENE
by O
interaction O
of O
E1A I-GENE
with O
the O
AP I-GENE
- I-GENE
2rep I-GENE
corepressor I-GENE
CtBP1 I-GENE
. O

Unusual I-GENE
two O
- I-GENE
domain I-GENE
arginine I-GENE
kinases I-GENE
( O
AKs I-GENE
) O
arose I-GENE
independently O
at O
least O
two O
times O
during O
molecular O
evolution O
of O
phosphagen I-GENE
kinases I-GENE
: O
AKs I-GENE
from O
the O
primitive I-GENE
sea O
anemone I-GENE
Anthopleurura I-GENE
japonicus I-GENE
and O
from O
the O
clam I-GENE
Pseudocardium I-GENE
sachalinensis I-GENE
. O

Mutagenesis I-GENE
of O
SNT1 I-GENE
( O
IRS I-GENE
) O
CX I-GENE
identified O
three O
classes O
of O
effector O
motifs O
within O
SNT I-GENE
critical O
for O
both O
sustained O
ERK I-GENE
activation O
and O
neuronal O
differentiation O
: O
1 I-GENE
) O
four O
phosphotyrosine I-GENE
motifs O
that O
mediate O
recruitment O
of O
Grb2 I-GENE
, O
2 I-GENE
) O
two O
phosphotyrosine I-GENE
motifs O
that O
mediate O
recruitment O
of O
Shp2 I-GENE
, O
and O
3 I-GENE
) O
a O
C I-GENE
- I-GENE
terminal I-GENE
motif I-GENE
that O
functions O
by O
helping I-GENE
to O
recruit O
Sos I-GENE
. O

CONCLUSIONS O
: O
Our O
meta I-GENE
- I-GENE
analysis O
of O
randomized O
controlled O
trials O
of O
HRT I-GENE
noted O
a O
statistically O
significant O
reduction O
in O
nonvertebral I-GENE
fractures I-GENE
. O

However O
, O
C4B I-GENE
proteins I-GENE
encoded I-GENE
by O
monomodular I-GENE
short O
genes I-GENE
may O
have O
relatively O
higher O
concentrations O
than O
those O
from O
long O
C4A I-GENE
genes I-GENE
. O

CSR I-GENE
is O
directed O
to O
specific I-GENE
heavy I-GENE
chain I-GENE
isotypes I-GENE
by O
cytokines O
and O
B I-GENE
cell O
activators I-GENE
that O
induce O
transcription I-GENE
from O
the O
unrearranged I-GENE
, O
or O
germline I-GENE
( O
GL I-GENE
), O
C I-GENE
( O
H I-GENE
) O
region O
genes I-GENE
. O

The O
patterns O
of O
early I-GENE
mRNA I-GENE
and O
protein I-GENE
expression O
in O
these O
seven O
mutants I-GENE
were O
examined O
, O
and O
it O
was O
found O
that O
mutation I-GENE
of O
the O
T I-GENE
'( I-GENE
135 O
) O
acceptor O
site I-GENE
resulted O
in O
the O
utilization O
of O
cryptic I-GENE
splice O
sites I-GENE
and O
the O
generation O
of O
new O
T I-GENE
' O
species O
. O

Mutational O
analysis O
showed O
that O
the O
U O
- I-GENE
box I-GENE
, O
like I-GENE
the O
RING I-GENE
finger I-GENE
in O
other O
proteins I-GENE
, O
forms O
the O
physical O
basis O
for O
the O
interaction O
with O
E2 I-GENE
enzymes O
. O

GafChromic I-GENE
( O
MD I-GENE
- I-GENE
55 O
- I-GENE
2 I-GENE
) O
radiochromic I-GENE
film I-GENE
has O
become O
increasingly I-GENE
popular I-GENE
for O
medical O
applications O
and O
has O
proven O
to O
be O
useful O
for O
brachytherapy I-GENE
dosimetry I-GENE
. O

The O
438 I-GENE
bp O
EcoRI I-GENE
fragment I-GENE
, O
which O
was O
detected O
by O
Southern O
hybridization O
, O
reveals O
an O
open O
reading O
frame O
which O
encodes O
a O
protein I-GENE
of O
103 I-GENE
amino O
acids O
. O

Furthermore O
, O
hormonal O
regulation O
of O
G I-GENE
( O
1 I-GENE
) O
gene I-GENE
transcription I-GENE
can O
occur O
even O
without O
additional O
activation O
of O
the O
Mek I-GENE
- I-GENE
Erk1 I-GENE
/ I-GENE
2 I-GENE
pathway O
by O
estrogen I-GENE
receptors I-GENE
. O

In O
mammalian I-GENE
tissue I-GENE
culture O
cells O
, O
overexpression O
of O
any O
of O
the O
four O
mouse I-GENE
deltex I-GENE
homologs I-GENE
suppressed O
the O
transcriptional O
activity O
of O
E47 I-GENE
, O
a O
basic I-GENE
helix I-GENE
- I-GENE
loop I-GENE
- I-GENE
helix I-GENE
( O
bHLH I-GENE
) O
protein I-GENE
, O
in O
a O
manner O
similar O
to O
suppression O
by O
an O
activated I-GENE
form O
of O
human I-GENE
Notch1 I-GENE
or O
human I-GENE
DTX1 I-GENE
. O

The O
authors O
undertook I-GENE
a O
retrospective O
analysis O
of O
pathology O
with O
quantification I-GENE
of O
the O
percentage O
of O
papillary I-GENE
serous I-GENE
component O
(% I-GENE
PSC I-GENE
) O
and O
p53 I-GENE
expression O
. O

This O
function O
requires O
not O
only O
the O
kinase I-GENE
domain I-GENE
of O
Csk I-GENE
, O
but O
also O
its O
Src I-GENE
homology I-GENE
3 I-GENE
( O
SH3 I-GENE
) O
and O
SH2 I-GENE
regions O
. O

Nucleotide O
sequence I-GENE
, O
transcription I-GENE
map O
, O
and O
mutation I-GENE
analysis O
of O
the O
13q14 I-GENE
chromosomal I-GENE
region O
deleted O
in O
B I-GENE
- I-GENE
cell O
chronic O
lymphocytic I-GENE
leukemia I-GENE
. O

In O
conclusion O
, O
primary O
chemotherapy O
based O
on O
high O
dose O
MTX I-GENE
and O
ara I-GENE
- I-GENE
C I-GENE
is O
highly O
efficient O
in O
PCNSL I-GENE
. O

NGF I-GENE
, O
but O
not O
EGF I-GENE
, O
enhances O
the O
upper O
bands O
, O
corresponding O
to O
phosphorylated O
Fra I-GENE
- I-GENE
2 I-GENE
. O

METHODS O
AND O
RESULTS O
: O
Palmaz I-GENE
- I-GENE
Schatz I-GENE
stents I-GENE
were O
dip I-GENE
- I-GENE
coated I-GENE
with O
paclitaxel I-GENE
( O
0 O
, O
0 O
. O
2 I-GENE
, O
15 O
, O
or O
187 I-GENE
microgram O
/ I-GENE
stent I-GENE
) O
by O
immersion O
in O
ethanolic I-GENE
paclitaxel I-GENE
and O
evaporation I-GENE
of O
the O
solvent O
. O

Currently I-GENE
, O
the O
clinical O
use O
of O
5 I-GENE
- I-GENE
aminolaevulinic I-GENE
acid I-GENE
( O
ALA I-GENE
) O
induced O
protoporphyrin I-GENE
IX I-GENE
( O
PPIX I-GENE
) O
for O
photodynamic I-GENE
therapy O
( O
PDT I-GENE
) O
is O
limited O
by O
the O
maximum O
tolerated O
oral O
ALA I-GENE
dose O
( O
60 O
mg O
/ I-GENE
kg O
). O

A I-GENE
twelfth I-GENE
insertion O
disrupts I-GENE
two O
genes I-GENE
, O
Nrk I-GENE
, O
a O
" O
neurospecific I-GENE
" O
receptor I-GENE
tyrosine I-GENE
kinase I-GENE
, O
and O
Tpp I-GENE
, O
which O
encodes O
a O
neuropeptidase I-GENE
. O

These O
results O
indicate O
that O
ATF4 I-GENE
regulates O
basal O
and O
CdCl I-GENE
( O
2 I-GENE
)- I-GENE
induced O
expression O
of O
the O
ho I-GENE
- I-GENE
1 I-GENE
gene I-GENE
in O
a O
cell O
- I-GENE
specific I-GENE
manner O
and O
possibly O
in O
a O
complex I-GENE
with O
Nrf2 I-GENE
. O

Adjuvant I-GENE
and O
neoadjuvant I-GENE
treatment O
of O
breast O
cancer O
. O

The O
% O
SVend I-GENE
of O
HCM I-GENE
- I-GENE
I I-GENE
was O
significantly O
lower O
than O
the O
respective O
values O
of O
the O
HCM I-GENE
- I-GENE
II I-GENE
and O
Control O
groups O
. O

Inhibition O
of O
the O
Raf I-GENE
- I-GENE
1 I-GENE
target O
ERK I-GENE
kinase I-GENE
( O
MEK I-GENE
) O
either O
attenuated O
or O
abolished O
Rp I-GENE
- I-GENE
cAMPS I-GENE
- I-GENE
and O
PKI I-GENE
- I-GENE
induced O
ERK I-GENE
activation O
, O
caldesmon I-GENE
phosphorylation O
, O
and O
stress O
fiber O
formation O
. O

In O
the O
TVD I-GENE
- I-GENE
patients O
decreases O
in O
skin O
blood O
flow O
were O
similar O
compared O
with O
the O
healthy O
controls O
. O

Analysis O
of O
mCTR I-GENE
mRNAs I-GENE
has O
revealed O
that O
the O
three O
alternative O
promoters I-GENE
give O
rise O
to O
at O
least O
seven O
mCTR I-GENE
isoforms I-GENE
in O
the O
5 I-GENE
' O
region O
of O
the O
gene I-GENE
and O
generate O
5 I-GENE
'- O
untranslated O
regions O
of O
very O
different O
lengths O
. O

The O
regulation O
of O
PGHS I-GENE
- I-GENE
2 I-GENE
mRNA I-GENE
and O
protein I-GENE
was O
studied O
in O
primary O
cultures O
of O
bovine I-GENE
uterine O
stromal I-GENE
cells O
stimulated O
with O
phorbol O
12 O
- I-GENE
myristate O
13 O
- I-GENE
acetate O
( O
PMA O
; O
100 O
nM O
). O

There O
was O
no O
evidence O
of O
linkage O
disequilibrium I-GENE
between O
the O
polymorphic O
site I-GENE
in O
the O
B I-GENE
cell O
specific I-GENE
promoter I-GENE
and O
those O
in O
the O
3 I-GENE
' O
UTR I-GENE
. O

Several O
dozen I-GENE
HIF I-GENE
- I-GENE
1 I-GENE
targets O
are O
known O
, O
including O
the O
gene I-GENE
encoding O
vascular I-GENE
endothelial I-GENE
growth I-GENE
factor I-GENE
( O
VEGF I-GENE
). O

In O
Klinefelter I-GENE
' O
s O
syndrome O
( O
47XXY I-GENE
), O
serum I-GENE
testosterone O
levels O
are O
at O
the O
lower O
end O
of O
the O
normal O
range O
and O
dihydrotestosterone I-GENE
levels O
are O
low O
. O

The O
protein I-GENE
is O
composed O
of O
two O
major I-GENE
domains I-GENE
separated O
by O
a O
hydrophobic O
linker I-GENE
region O
of O
20 O
amino O
acid I-GENE
residues O
. O

When O
mixed O
with O
aqueous O
solutions O
of O
TMT I-GENE
- I-GENE
55 O
, O
aqueous O
solutions O
of O
either O
reagent I-GENE
- I-GENE
grade O
zinc I-GENE
, O
cadmium O
, O
or O
lead O
salts I-GENE
precipitate I-GENE
crystalline O
" O
Zn I-GENE
- I-GENE
TMT I-GENE
", I-GENE
amorphous I-GENE
or O
crystalline O
" O
Cd O
- I-GENE
TMT I-GENE
" O
or O
amorphous I-GENE
" O
Pb I-GENE
- I-GENE
TMT I-GENE
" O
( O
M3 I-GENE
[ O
S3C3N3 I-GENE
] O
2 I-GENE
. O
nH2O I-GENE
, O
where O
M I-GENE
= O
Cd2 I-GENE
+, I-GENE
Pb2 I-GENE
+, I-GENE
and O
Zn2 I-GENE
+ I-GENE
and O
n O
> O
or O
= O
0 O
) O
that O
may O
eventually I-GENE
crystallize I-GENE
if O
stored O
in O
air O
. O

Online I-GENE
teaching I-GENE
: O
design O
and O
techniques O
. O

This O
interaction O
is O
reciprocal O
, O
since O
C I-GENE
/ I-GENE
EBP I-GENE
dimer O
binding I-GENE
to O
a O
strong O
C I-GENE
/ I-GENE
EBP I-GENE
site I-GENE
leads O
to O
enhanced O
CREB I-GENE
- I-GENE
1 I-GENE
recruitment O
to O
ATF I-GENE
/ I-GENE
CREB I-GENE
sites I-GENE
that O
are O
weakly O
bound O
by O
CREB I-GENE
. O

The O
absorbed O
dose O
was O
measured O
by O
combination O
of O
two O
integrating I-GENE
detectors I-GENE
: O
thermo I-GENE
- I-GENE
luminescent I-GENE
dosemeter I-GENE
of O
Mg2SiO4 I-GENE
: O
Tb I-GENE
( O
TDMS I-GENE
) O
and O
plastic I-GENE
nuclear I-GENE
track I-GENE
detector O
( O
PNTD I-GENE
). O

To O
determine O
the O
genomic O
complexity O
of O
the O
deleted O
region O
shared O
among O
tumors O
, O
we O
assembled O
a O
physical O
map O
of O
the O
I I-GENE
Mbp I-GENE
SRO I-GENE
consisting O
predominantly O
of O
bacteriophage I-GENE
P1 I-GENE
- I-GENE
derived O
artificial O
chromosome O
( O
PAC I-GENE
) O
clones O
. O

Thus O
, O
Xlim I-GENE
- I-GENE
1 I-GENE
not O
only O
contains O
a O
unique O
tyrosine I-GENE
- I-GENE
rich O
activation O
domain I-GENE
but O
also O
contains O
a O
negative O
regulatory I-GENE
domain I-GENE
in O
CT239 I-GENE
- I-GENE
403 I-GENE
, O
suggesting O
a O
complex I-GENE
regulatory I-GENE
mechanism O
underlying O
the O
transcriptional O
activity O
of O
Xlim I-GENE
- I-GENE
1 I-GENE
in O
the O
organizer I-GENE
. O

Low O
- I-GENE
selenium O
diet O
has O
a O
human I-GENE
unfavourable I-GENE
impact O
. O

In O
the O
next O
week O
, O
the O
beta I-GENE
- I-GENE
adrenergic I-GENE
antagonist O
atenolol I-GENE
was O
added O
at O
an O
initial O
dose O
of O
25 O
mg O
/ I-GENE
day O
and O
titrated I-GENE
to O
50 O
mg O
/ I-GENE
day O
within O
1 I-GENE
week O
. O

To O
assess O
more O
specific I-GENE
PKA I-GENE
- I-GENE
dependent I-GENE
mediation I-GENE
of O
LH I-GENE
' O
s O
contribution O
to O
combined O
hormonal O
drive O
, O
the O
LDL I-GENE
receptor I-GENE
(- O
1076 I-GENE
to O
+ I-GENE
11 O
bp O
) O
reporter I-GENE
plasmid O
was O
cotransfected O
with O
a O
full I-GENE
- I-GENE
sequence I-GENE
rabbit I-GENE
muscle O
protein I-GENE
kinase I-GENE
inhibitor I-GENE
( O
PKI I-GENE
) O
minigene I-GENE
driven O
constitutively O
by O
a O
Rous I-GENE
sarcoma I-GENE
virus I-GENE
promoter I-GENE
. O

In O
SN I-GENE
- I-GENE
48 O
neuronal O
cells O
that O
express O
MR O
, O
GR I-GENE
, O
and O
5 I-GENE
- I-GENE
HT1A I-GENE
receptors I-GENE
, O
deletion O
or O
inactivation O
of O
the O
nGRE I-GENE
( O
negative O
GRE I-GENE
) O
eliminated I-GENE
negative O
regulation O
of O
the O
rat I-GENE
5 I-GENE
- I-GENE
HT1A I-GENE
or O
heterologous O
promoters I-GENE
by O
corticosteroids O
, O
whereas O
its O
inclusion O
conferred O
corticosteroid I-GENE
- I-GENE
induced O
inhibition O
to O
a O
heterologous O
promoter I-GENE
. O

Transition I-GENE
between O
P I-GENE
- I-GENE
and O
H I-GENE
- I-GENE
BPPV I-GENE
was O
found O
in O
6 I-GENE
cases O
. O

These O
included O
HNF I-GENE
- I-GENE
3 I-GENE
beta I-GENE
, O
HFH I-GENE
- I-GENE
1 I-GENE
, O
HFH I-GENE
- I-GENE
2 I-GENE
, O
HFH I-GENE
- I-GENE
3 I-GENE
, O
C I-GENE
/ I-GENE
EBP I-GENE
, O
and O
C I-GENE
/ I-GENE
EBP I-GENE
beta I-GENE
, O
all O
of O
which O
are O
consistent O
with O
the O
tissue I-GENE
- I-GENE
specific I-GENE
expression O
profiles O
of O
the O
gene I-GENE
. O

RESULTS O
: O
Of O
the O
24 O
patients O
, O
6 I-GENE
had O
Grade I-GENE
1 I-GENE
pneumonitis I-GENE
, O
and O
13 O
had O
Grade I-GENE
2 I-GENE
pneumonitis I-GENE
. O

METHODS O
: O
The O
passive O
and O
active O
transport O
of O
fluorescein I-GENE
through O
the O
BRB I-GENE
was O
quantitated I-GENE
by O
vitreous O
fluorometry I-GENE
. O

Sixteen I-GENE
out O
of O
52 O
seropositive O
MS O
patients O
( O
30 O
. O
8 O
%) O
showed O
intrathecal I-GENE
synthesis O
of O
C I-GENE
. O
pneumoniae I-GENE
- I-GENE
specific I-GENE
IgG I-GENE
but O
only O
one O
of O
43 I-GENE
seropositive O
controls O
( O
2 I-GENE
. O
3 I-GENE
%). O

Consistent O
with O
the O
specificity O
observed O
for O
the O
interaction O
of O
DmCKIIalpha I-GENE
with O
these O
bHLH I-GENE
proteins I-GENE
, O
sequence I-GENE
alignment O
suggests O
that O
only O
m5 I-GENE
, O
m7 I-GENE
, O
and O
m8 I-GENE
contain O
a O
consensus I-GENE
site I-GENE
for O
phosphorylation O
by O
CKII I-GENE
within O
a O
subdomain I-GENE
unique O
to O
these O
three O
proteins I-GENE
. O

Deletion O
of O
the O
potential O
initiator O
element I-GENE
does O
not O
affect O
repression O
of O
the O
p21 I-GENE
promoter I-GENE
by O
c I-GENE
- I-GENE
Myc I-GENE
. O

PATIENTS O
AND O
METHODS O
: O
Between I-GENE
June I-GENE
1991 O
and O
December I-GENE
1996 O
, O
we O
administered O
the O
nucleoside I-GENE
analog O
2 I-GENE
- I-GENE
chlorodeoxyadenosine I-GENE
( O
2 I-GENE
- I-GENE
CDA I-GENE
) O
to O
73 O
children O
with O
primary O
AML I-GENE
and O
20 O
children O
with O
secondary O
AML I-GENE
or O
myelodysplastic I-GENE
syndrome O
( O
MDS I-GENE
). O

Drosophila I-GENE
Menin1 I-GENE
gene I-GENE
transcripts I-GENE
use O
alternative O
polyadenylation O
sites I-GENE
resulting O
in O
4 I-GENE
. O
3 I-GENE
and O
5 I-GENE
- I-GENE
kb O
messages I-GENE
. O

Mice I-GENE
homozygous O
for O
the O
dlg I-GENE
mutation I-GENE
exhibit O
growth I-GENE
retardation O
in O
utero I-GENE
, O
have O
hypoplasia I-GENE
of O
the O
premaxilla I-GENE
and O
mandible I-GENE
, O
have O
a O
cleft I-GENE
secondary O
palate I-GENE
, O
and O
die I-GENE
perinatally I-GENE
. O

In O
contrast O
, O
we O
did O
not O
detect O
a O
significant O
correlation O
between O
plasma I-GENE
TNFalpha I-GENE
and O
radiation O
pneumonitis I-GENE
. O

Its O
transcription I-GENE
in O
vitro O
by O
pol I-GENE
III I-GENE
requires O
the O
same O
factors I-GENE
as O
the O
U6 I-GENE
gene I-GENE
with O
the O
major I-GENE
exception O
that O
the O
modified O
TATA I-GENE
- I-GENE
box I-GENE
of O
this O
construct I-GENE
only O
interacts O
with O
a O
TATA I-GENE
- I-GENE
binding I-GENE
protein I-GENE
( O
TBP I-GENE
) O
mutant I-GENE
( O
TBP I-GENE
- I-GENE
DR2 I-GENE
) O
but O
not O
with O
TBP I-GENE
wild I-GENE
- I-GENE
type I-GENE
( O
TBPwt I-GENE
). O

Expression O
of O
the O
src I-GENE
homology I-GENE
3 I-GENE
( O
SH3 I-GENE
)- I-GENE
encoding O
, O
expressed O
in O
tumorigenic O
astrocytes I-GENE
( O
SETA I-GENE
) O
gene I-GENE
is O
associated I-GENE
with O
astrocyte I-GENE
transformation O
in O
culture O
and O
tumors O
in O
the O
adult O
brain O
. O

In O
such O
conditions O
, O
the O
following O
kinetic O
reactions O
have O
been O
studied O
: O
N2 O
( O
A I-GENE
) O
+ I-GENE
N2 O
( O
A I-GENE
) O
--> I-GENE
N2 O
( O
C I-GENE
, O
B I-GENE
, O
V I-GENE
') I-GENE
+ I-GENE
N2 O
( O
X I-GENE
), O
N2 O
( O
A I-GENE
) O
+ I-GENE
N2 O
( O
X I-GENE
, O
V I-GENE
> O
5 I-GENE
) O
--> I-GENE
N2 O
( O
X I-GENE
) O
+ I-GENE
N2 O
( O
B I-GENE
, O
V I-GENE
') I-GENE
in O
pure O
N2 O
post O
- I-GENE
discharges I-GENE
and O
N2 O
( O
A I-GENE
) O
+ I-GENE
CH4 I-GENE
--> I-GENE
products I-GENE
, O
C I-GENE
+ I-GENE
N I-GENE
+ I-GENE
M2 I-GENE
--> I-GENE
CN I-GENE
( O
B I-GENE
, O
V I-GENE
') I-GENE
+ I-GENE
M2 I-GENE
, O
N2 O
( O
X I-GENE
, O
V I-GENE
> O
4 I-GENE
) O
+ I-GENE
CN I-GENE
--> I-GENE
N2 O
( O
X I-GENE
) O
+ I-GENE
CN I-GENE
( O
B I-GENE
, O
A I-GENE
, O
V I-GENE
'), I-GENE
in O
N2 O
- I-GENE
1 I-GENE
% O
CH4 I-GENE
post O
- I-GENE
discharges I-GENE
. O

BACKGROUND O
/ I-GENE
AIMS I-GENE
: O
Hepatitis I-GENE
C I-GENE
and O
nonalcoholic I-GENE
fatty I-GENE
liver O
disease O
( O
NAFL I-GENE
) O
are O
the O
two O
most O
common O
forms O
of O
liver O
disease O
in O
the O
United O
States I-GENE
. O

These O
results O
suggested O
a O
critical O
role O
for O
tyrosine I-GENE
residue O
1229 I-GENE
in O
the O
regulation O
of O
L1 I-GENE
endocytosis I-GENE
. O

The O
androgen O
receptor I-GENE
( O
AR I-GENE
) O
amino O
- I-GENE
terminus O
imposes I-GENE
androgen O
- I-GENE
specific I-GENE
regulation O
of O
AR I-GENE
gene I-GENE
expression O
via O
an O
exonic I-GENE
enhancer I-GENE
. O

Can I-GENE
survival O
be O
prolonged O
for O
patients O
with O
hormone I-GENE
- I-GENE
resistant O
prostate O
cancer O
? O

In O
conclusion O
, O
NF I-GENE
- I-GENE
Y I-GENE
and O
Sp1 I-GENE
binding I-GENE
sites I-GENE
play O
a O
decisive I-GENE
role O
in O
the O
basal O
expression O
of O
the O
rat I-GENE
mrp2 I-GENE
gene I-GENE
, O
while O
the O
human I-GENE
MRP2 I-GENE
gene I-GENE
is O
regulated O
differently O
. O

Intact I-GENE
Flag I-GENE
- I-GENE
tagged O
protein I-GENE
products I-GENE
from O
all O
six O
were O
produced O
from O
genomic O
expression O
vectors O
, O
although O
the O
ORF40 I-GENE
/ I-GENE
41 O
transcript I-GENE
encoding O
a O
primase I-GENE
- I-GENE
helicase I-GENE
component O
proved O
to O
be O
spliced O
with O
a O
127 I-GENE
- I-GENE
bp O
intron O
. O

Hypomorphic I-GENE
dSLBP I-GENE
alleles I-GENE
support O
zygotic I-GENE
development O
but O
cause O
female O
sterility I-GENE
. O

In O
hypertensive O
nephrosclerosis I-GENE
, O
therapy O
containing O
an O
ACEI I-GENE
alone O
or O
in O
combination O
significantly O
reduces O
the O
incidence O
of O
renal O
events O
. O

We O
confirmed O
the O
interaction O
between O
TLS I-GENE
and O
p65 I-GENE
by O
the O
pull I-GENE
- I-GENE
down O
assay O
in O
vitro O
and O
by O
a O
coimmunoprecipitation I-GENE
experiment O
followed O
by O
Western O
blot O
of O
the O
cultured O
cell O
in O
vivo O
. O

In O
addition O
, O
we O
did O
not O
detect O
significant O
differences O
in O
CDR3 I-GENE
sequences I-GENE
of O
endogenous I-GENE
Ig I-GENE
lambdaL I-GENE
and O
kappaL I-GENE
chain I-GENE
gene I-GENE
loci I-GENE
cloned O
from O
peripheral O
blood O
lymphocytes O
of O
an O
NBS I-GENE
patient O
and O
of O
healthy O
individuals O
. O

The O
diet O
of O
migrants I-GENE
showed O
both O
positive O
( O
macronutrients I-GENE
) O
and O
negative O
( O
micronutrients I-GENE
) O
differences O
with O
the O
general O
Dutch I-GENE
diet O
. O

Copyright O
2001 I-GENE
Academic O
Press O
. O

Experimental O
study O
of O
ta I-GENE
chengchi I-GENE
tang I-GENE
decoction I-GENE
for O
relieving I-GENE
lung O
injury O
during O
acute O
necrotizing I-GENE
pancreatitis O
] O
The O
objectives I-GENE
of O
the O
study O
were O
to O
investigate O
the O
changes O
of O
leukocyte I-GENE
adhesiveness I-GENE
and O
tumor I-GENE
necrosis I-GENE
factor I-GENE
( O
TNF I-GENE
) O
in O
the O
early I-GENE
stage O
of O
acute O
necrotizing I-GENE
pancreatitis O
( O
ANP I-GENE
), O
to O
go I-GENE
further O
into O
the O
relation O
of O
those O
changes O
to O
lung O
injury O
of O
ANP I-GENE
, O
and O
to O
evaluate O
the O
prohibitive I-GENE
effect O
of O
ta I-GENE
chengchi I-GENE
tang I-GENE
Decoction I-GENE
on O
leukocyte I-GENE
adhesion I-GENE
and O
TNF I-GENE
secretion O
. O

We O
suggest O
that O
ventriculopleural I-GENE
shunting I-GENE
should O
be O
considered O
as O
the O
preferred O
alternative O
to O
peritoneal O
drainage O
in O
children O
with O
intra O
- I-GENE
abdominal O
adhesions O
or O
with O
a O
history O
of O
recent O
peritoneal O
infection O
. O

Positive I-GENE
and O
significant O
correlations O
were O
found O
between O
the O
weeks O
of O
pregnancy O
and O
Se I-GENE
levels O
in O
kidney O
( O
r O
= O
0 O
. O
433 I-GENE
, O
P I-GENE
= O
0 O
. O
023 I-GENE
) O
and O
heart O
( O
r O
= O
0 O
. O
313 I-GENE
, O
P I-GENE
= O
0 O
. O
030 I-GENE
). O

Doxorubicin I-GENE
( O
DOX I-GENE
) O
is O
commonly O
used O
for O
the O
treatment O
of O
hematological I-GENE
and O
solid O
tumors O
. O

There O
was O
no O
significant O
difference O
in O
developmental O
scores O
at O
9 O
or O
18 O
months O
, O
although O
PDF I-GENE
infants O
had O
a O
2 I-GENE
. O
8 O
(- O
1 I-GENE
. O
3 I-GENE
- I-GENE
6 I-GENE
. O
8 O
) O
point O
advantage O
in O
Bayley I-GENE
motor O
score O
scales I-GENE
. O

Immunofixation I-GENE
experiments O
of O
C4A I-GENE
and O
C4B I-GENE
demonstrate O
> O
41 O
allotypes I-GENE
in O
the O
two O
classes O
of O
proteins I-GENE
. O

These O
effects O
were O
not O
seen O
with O
SHIP2 I-GENE
possessing I-GENE
a O
mutation I-GENE
in O
the O
SH2 I-GENE
domain I-GENE
( O
R47G I-GENE
). O

Myasthenia I-GENE
gravis I-GENE
is O
an O
autoimmune I-GENE
disease O
resulting O
from O
the O
production O
of O
antibodies I-GENE
against O
the O
ACh I-GENE
receptors I-GENE
of O
the O
neuromuscular O
synapse I-GENE
. O

Human I-GENE
homologue I-GENE
of O
yeast I-GENE
Rad23 I-GENE
protein I-GENE
A I-GENE
interacts O
with O
p300 I-GENE
/ I-GENE
cyclic I-GENE
AMP I-GENE
- I-GENE
responsive I-GENE
element I-GENE
binding I-GENE
( O
CREB I-GENE
)- I-GENE
binding I-GENE
protein I-GENE
to O
down O
- I-GENE
regulate O
transcriptional O
activity O
of O
p53 I-GENE
. O

METHODS O
: O
Sixteen I-GENE
pigs O
were O
assigned O
randomly O
to O
control O
and O
shock I-GENE
groups O
. O

RESULTS O
: O
There O
is O
a O
considerable O
amount O
of O
variation O
between O
the O
results O
of O
TRA1 I-GENE
and O
TRA2 I-GENE
and O
between O
the O
results O
of O
both O
TRA I-GENE
' O
s O
and O
the O
door I-GENE
- I-GENE
to O
- I-GENE
door I-GENE
survey O
. O

Thus O
, O
our O
studies O
define O
Rac I-GENE
/ I-GENE
Cdc42 I-GENE
/ I-GENE
Pak I-GENE
as O
a O
module I-GENE
upstream O
of O
Raf I-GENE
- I-GENE
1 I-GENE
during O
its O
activation O
by O
microtubule I-GENE
disruption O
. O

Zhu I-GENE
, O
V I-GENE
. O

However O
, O
plasmids O
carrying O
the O
yeast I-GENE
TyrRS I-GENE
gene I-GENE
could O
not O
be O
stably O
maintained O
in O
E I-GENE
. O
coli I-GENE
. O

This O
supports O
previous O
arguments I-GENE
for O
the O
improbability I-GENE
of O
biological O
effects O
at O
UHF I-GENE
frequencies O
unless O
a O
mechanism O
can O
be O
found O
for O
accumulating I-GENE
energy O
over O
time O
and O
space O
and O
focussing I-GENE
it O
. O

The O
students O
who O
had O
abnormal O
urine O
screening O
results O
at O
the O
first O
time O
received O
a O
second O
urine O
analysis O
10 O
to O
15 O
days O
later O
to O
confirm O
the O
abnormal O
urine O
analysis O
. O

Cells I-GENE
containing O
alpha I-GENE
subunits I-GENE
that O
lacked O
a O
distal O
domain I-GENE
( O
term O
- I-GENE
3 I-GENE
) O
or O
had O
the O
alternatively O
spliced O
alpha I-GENE
- I-GENE
2 I-GENE
distal O
domain I-GENE
showed O
markedly O
decreased O
ability O
to O
support O
tyrosine I-GENE
phosphorylation O
of O
Jak I-GENE
- I-GENE
2 I-GENE
and O
its O
substrates O
or O
to O
up O
- I-GENE
regulate O
CD86 I-GENE
. O

Despite O
abundant O
expression O
of O
NtmybAS I-GENE
transcripts I-GENE
in O
mature O
pollen O
, O
gPAL1 I-GENE
transcripts I-GENE
were O
not O
detectable O
in O
pollen O
. O

Finally O
, O
profiling I-GENE
of O
a O
gcn4Delta I-GENE
mutant I-GENE
uncovered I-GENE
an O
alternative O
induction O
pathway O
operating O
at O
many O
Gcn4p I-GENE
target O
genes I-GENE
in O
histidine O
- I-GENE
starved I-GENE
cells O
. O

The O
R2 I-GENE
between O
MFI I-GENE
of O
fresh O
and O
frozen I-GENE
muscle O
was O
0 O
. O
94 O
and O
0 O
. O
92 O
for O
lamb I-GENE
and O
pork I-GENE
longissimus I-GENE
, O
respectively O
. O

To O
this O
end O
, O
an O
expression O
cassette I-GENE
consisting O
of O
the O
gene I-GENE
for O
a O
green I-GENE
fluorescent O
protein I-GENE
( O
GFP I-GENE
) O
flanked O
at O
its O
3 I-GENE
' O
end O
by O
EAV I-GENE
- I-GENE
specific I-GENE
transcription I-GENE
- I-GENE
regulating O
sequences I-GENE
was O
constructed O
. O

Significantly O
higher O
lung O
function O
parameters O
were O
obtained O
in O
extubated I-GENE
recipients O
of O
LPD I-GENE
preserved I-GENE
grafts O
2 I-GENE
weeks O
after O
TX I-GENE
. O

Lack I-GENE
of O
association O
between O
Kawasaki I-GENE
syndrome O
and O
infection O
with O
Rickettsia I-GENE
conorii I-GENE
, O
Rickettsia I-GENE
typhi I-GENE
, O
Coxiella I-GENE
burnetii I-GENE
or O
Ehrlichia I-GENE
phagocytophila I-GENE
group O
. O

These O
utilisation I-GENE
data O
imply O
annual O
drug O
costs O
in O
the O
range O
of O
$ I-GENE
US O
480 I-GENE
, O
000 O
to O
$ I-GENE
US O
3 I-GENE
, O
600 O
, O
000 O
for O
TNF I-GENE
antagonists O
for O
RA O
per O
1 I-GENE
million O
population O
. O

Alignment I-GENE
of O
different O
cDNAs I-GENE
of O
the O
NR5A2 I-GENE
( O
hB1F I-GENE
) O
gene I-GENE
with O
the O
genomic O
sequence I-GENE
facilitated O
the O
delineation I-GENE
of O
its O
structural O
organization O
, O
which O
spans O
over O
150 O
kb O
and O
consists O
of O
eight O
exons O
interrupted O
by O
seven O
introns O
. O

CONCLUSIONS O
: O
Ketamine I-GENE
- I-GENE
induced O
dissociative I-GENE
anesthesia O
produces O
persistently I-GENE
elevated O
BIS I-GENE
index O
which O
is O
different O
from O
thiamylal I-GENE
and O
those O
reported O
with O
other O
conventional O
anesthetic I-GENE
agents O
. O

In O
the O
remaining O
case O
, O
the O
aneurysm I-GENE
originated I-GENE
from O
the O
proximal I-GENE
end O
of O
the O
associated I-GENE
A1 I-GENE
fenestration I-GENE
. O

This O
domain I-GENE
without O
the O
canonical O
anticodon I-GENE
loop I-GENE
or O
the O
tyrosine I-GENE
anticodon I-GENE
acts O
as O
an O
anchor I-GENE
for O
TyrRS I-GENE
interaction O
leading O
to O
a O
better O
efficiency O
of O
tyrosylation I-GENE
. O

Temperature I-GENE
measurement O
in O
microfluidic I-GENE
systems O
using O
a O
temperature O
- I-GENE
dependent I-GENE
fluorescent O
dye O
. O

The O
first O
exon O
( O
exon O
1A I-GENE
) O
that O
corresponded O
to O
the O
5 I-GENE
'- O
untranslated O
region O
of O
the O
GHR I-GENE
1A I-GENE
mRNA I-GENE
was O
15 O
, O
250 O
bp O
upstream O
from O
exon O
2 I-GENE
in O
the O
GHR I-GENE
gene I-GENE
. O

The O
NAUSICAA I-GENE
system O
gives O
a O
good O
knowledge O
of O
LET I-GENE
spectra O
for O
the O
first O
time O
in O
space O
dosimetry I-GENE
. O

The O
MABP I-GENE
and O
MCBFV I-GENE
signals O
were O
bandpass I-GENE
filtered I-GENE
in O
the O
very O
low O
- I-GENE
frequency O
range O
( O
VLF I-GENE
, O
0 O
. O
015 I-GENE
- I-GENE
0 O
. O
07 O
Hz O
), O
low O
- I-GENE
frequency O
range O
( O
LF I-GENE
, O
0 O
. O
07 O
- I-GENE
0 O
. O
15 O
Hz O
) O
and O
high O
- I-GENE
frequency O
range O
( O
HF I-GENE
, O
0 O
. O
15 O
- I-GENE
0 O
. O
40 I-GENE
Hz O
) O
before O
applying O
CCF I-GENE
for O
the O
purpose O
of O
studying O
the O
effect O
of O
different O
bandwidths I-GENE
on O
the O
resulting O
mean O
CCFs I-GENE
. O

At O
cross O
purposes I-GENE
. O

For O
these O
patients O
the O
introduction O
of O
a O
separate O
category O
" O
extended O
oligoarthritis I-GENE
at O
onset O
" O
should O
be O
considered O
to O
establish O
comparable O
patient O
groups O
. O

The O
susceptibility I-GENE
of O
Aspergillus I-GENE
fumigatus I-GENE
to O
mulundocandin I-GENE
, O
an O
echinocandin I-GENE
- I-GENE
like I-GENE
compound O
, O
and O
other O
antifungal I-GENE
agents O
was O
assessed O
by O
the O
National O
Committee O
for O
Clinical O
Laboratory O
Standards I-GENE
( O
NCCLS I-GENE
) O
M38 I-GENE
- I-GENE
P I-GENE
method O
, O
a O
2 I-GENE
, O
3 I-GENE
- I-GENE
bis I-GENE
( O
2 I-GENE
- I-GENE
methoxy I-GENE
- I-GENE
4 I-GENE
- I-GENE
nitro I-GENE
- I-GENE
5 I-GENE
- I-GENE
sulfophenyl I-GENE
)- I-GENE
5 I-GENE
-[( I-GENE
phenyl I-GENE
- I-GENE
amino O
) O
carbonyl I-GENE
]- I-GENE
2H I-GENE
- I-GENE
tetrazolium I-GENE
hydroxide I-GENE
( O
XTT I-GENE
)- I-GENE
based O
colorimetric I-GENE
assay O
, O
and O
determination O
of O
morphologic O
alterations O
by O
microscopy O
. O

The O
most O
important O
risk O
factors I-GENE
are O
: O
1 I-GENE
) O
genetic O
; O
2 I-GENE
) O
Epstein I-GENE
- I-GENE
Barr I-GENE
virus I-GENE
( O
infectious O
mononucleosis I-GENE
); O
3 I-GENE
) O
congenital O
and O
acquired O
immunodeficiency I-GENE
; O
4 I-GENE
) O
occupational I-GENE
exposure O
( O
the O
wood I-GENE
industry I-GENE
). O

Members O
of O
the O
AP I-GENE
- I-GENE
1 I-GENE
superfamily I-GENE
of O
basic I-GENE
- I-GENE
leucine I-GENE
zipper I-GENE
factors I-GENE
bind O
to O
the O
StRE I-GENE
. O

DNA I-GENE
recognition I-GENE
by O
F I-GENE
factor I-GENE
TraI36 I-GENE
: O
highly O
sequence I-GENE
- I-GENE
specific I-GENE
binding I-GENE
of O
single O
- I-GENE
stranded I-GENE
DNA I-GENE
. O

Overexpression O
of O
RORgamma I-GENE
has O
been O
shown O
to O
inhibit O
T I-GENE
cell O
receptor I-GENE
- I-GENE
mediated O
apoptosis O
in O
T I-GENE
cell O
hybridomas I-GENE
and O
to O
repress O
the O
induction O
of O
Fas I-GENE
- I-GENE
ligand O
and O
interleukin I-GENE
2 I-GENE
. O

Although O
metabolized I-GENE
by O
the O
cytochrome I-GENE
P I-GENE
- I-GENE
450 I-GENE
( O
CYP I-GENE
) O
system O
, O
venlafaxine I-GENE
inhibits O
CYP I-GENE
2D6 I-GENE
and O
3A4 I-GENE
to O
a O
far O
lesser O
extent O
than O
do O
the O
SSRIs I-GENE
. O

SAPK I-GENE
/ I-GENE
JNK I-GENE
activation O
was O
completely O
abolished O
in O
the O
absence O
of O
MKK7 I-GENE
, O
even O
though O
expression O
of O
MKK4 I-GENE
was O
strongly O
upregulated I-GENE
in O
mkk7 I-GENE
(-/-) I-GENE
mast I-GENE
cell O
lines O
, O
and O
phosphorylation O
of O
MKK4 I-GENE
occurred O
normally O
in O
response O
to O
multiple O
stress O
stimuli O
. O

However O
these O
search O
engines I-GENE
respond O
with O
such O
cumbersome I-GENE
results O
that O
domain I-GENE
specific I-GENE
experts I-GENE
can O
not O
tolerate I-GENE
. O

The O
titer O
of O
TSH I-GENE
binding I-GENE
inhibitor I-GENE
immunoglobulin I-GENE
( O
TBII I-GENE
), O
which O
had O
been O
8 O
. O
6 I-GENE
% O
at O
initial O
presentation O
, O
rose O
to O
14 O
. O
9 O
% O
in O
2 I-GENE
weeks O
. O

The O
extraordinary I-GENE
stability O
of O
peptide I-GENE
-- O
gp96 I-GENE
complexes I-GENE
and O
the O
plasticity I-GENE
of O
the O
peptide I-GENE
- I-GENE
binding I-GENE
pocket O
support O
the O
proposed O
relay I-GENE
of O
diverse O
peptides I-GENE
to O
MHC I-GENE
and O
/ I-GENE
or O
other O
molecules I-GENE
via O
molecular O
recognition I-GENE
. O

Elevated I-GENE
expression O
of O
full I-GENE
- I-GENE
length I-GENE
UhpB I-GENE
or O
of O
a O
soluble I-GENE
hybrid O
protein I-GENE
, O
GST I-GENE
- I-GENE
Bc I-GENE
, O
which O
is O
glutathione I-GENE
S I-GENE
- I-GENE
transferase I-GENE
( O
GST I-GENE
) O
fused O
to O
the O
cytoplasmic I-GENE
C I-GENE
- I-GENE
terminal I-GENE
portion O
of O
UhpB I-GENE
, O
results O
in O
complete O
blockage I-GENE
of O
uhpT I-GENE
expression O
in O
a O
uhp I-GENE
(+) I-GENE
strain O
. O

Physical I-GENE
principles I-GENE
in O
therapeutic O
apheresis I-GENE
. O

Evidence O
from O
a O
Northern O
hybridization O
indicated O
that O
jadM I-GENE
expression O
is O
correlated O
with O
jadomycin I-GENE
B I-GENE
synthesis O
. O

Multiple O
copies O
of O
rsmB I-GENE
+ I-GENE
DNA I-GENE
, O
on O
the O
other O
hand O
, O
stimulate O
exoenzyme I-GENE
production O
by O
relieving I-GENE
the O
negative O
effects O
of O
a O
chromosomal I-GENE
copy O
of O
hexA I-GENE
+. I-GENE

Systematic I-GENE
review O
of O
diagnostic O
tests O
for O
vaginal O
trichomoniasis I-GENE
. O

Anecdotal I-GENE
observations O
scattered I-GENE
throughout O
the O
literature O
have O
often O
provided O
clues I-GENE
to O
underlying O
variations O
in O
humans O
' O
ability O
to O
handle I-GENE
dietary O
chemicals I-GENE
. O

Here O
we O
show O
that O
phosphorylation O
- I-GENE
induced O
loss O
of O
the O
protein I-GENE
kinase I-GENE
activity O
of O
DNA I-GENE
- I-GENE
PK I-GENE
is O
restored O
by O
the O
addition O
of O
the O
purified O
catalytic O
subunit I-GENE
of O
either O
protein I-GENE
phosphatase I-GENE
1 I-GENE
or O
protein I-GENE
phosphatase I-GENE
2A I-GENE
( O
PP2A I-GENE
) O
and O
that O
this O
reactivation I-GENE
is O
blocked O
by O
the O
potent O
protein I-GENE
phosphatase I-GENE
inhibitor I-GENE
, O
microcystin I-GENE
. O

Herein I-GENE
PPARgamma I-GENE
, O
liganded I-GENE
by O
either O
natural O
( O
15d I-GENE
- I-GENE
PGJ I-GENE
( O
2 I-GENE
) O
and O
PGD I-GENE
( O
2 I-GENE
)) O
or O
synthetic O
ligands O
( O
BRL49653 I-GENE
and O
troglitazone I-GENE
), O
selectively O
inhibited O
expression O
of O
the O
cyclin I-GENE
D1 I-GENE
gene I-GENE
. O

An O
integrated O
RTC I-GENE
algorithm O
for O
the O
urban I-GENE
wastewater I-GENE
system O
is O
formulated I-GENE
, O
the O
parameters O
of O
which O
are O
optimized I-GENE
using O
various O
global O
optimization I-GENE
routines I-GENE
. O

Recently O
, O
we O
discovered O
that O
alanine I-GENE
substitutions O
of O
the O
active O
center I-GENE
cleft I-GENE
residues O
significantly O
impair I-GENE
the O
depurinating I-GENE
and O
ribosome I-GENE
inhibitory I-GENE
activity O
of O
PAP I-GENE
. O

This O
partial O
transection I-GENE
could O
permit O
vasopressin I-GENE
to O
be O
secreted O
in O
response O
to O
a O
larger O
rise O
in O
plasma I-GENE
sodium O
concentration O
. O

Reciprocally I-GENE
, O
HMGI I-GENE
- I-GENE
C I-GENE
expression O
also O
coordinately I-GENE
enhances O
PIAS3 I-GENE
- I-GENE
mediated O
repression O
of O
STAT3 I-GENE
- I-GENE
dependent I-GENE
transactivation O
. O

The O
genomic O
structure O
of O
the O
human I-GENE
SPEC1 I-GENE
gene I-GENE
reveals O
complex I-GENE
splicing O
and O
close O
promoter I-GENE
proximity I-GENE
to O
the O
AF1q I-GENE
translocation O
gene I-GENE
. O

Here O
, O
the O
PEX5 I-GENE
- I-GENE
TPR O
domains I-GENE
from O
human I-GENE
, O
tobacco I-GENE
, O
and O
nematode O
were O
inserted O
into O
a O
TPR O
- I-GENE
less O
yeast I-GENE
Pex5p I-GENE
construct I-GENE
to O
generate O
Pex5p I-GENE
chimaeras I-GENE
. O

This O
study O
demonstrates O
that O
inducible I-GENE
expression O
in O
response O
to O
either O
PMA O
or O
TPO I-GENE
is O
mediated O
through O
the O
Ets I-GENE
site I-GENE
in O
the O
proximal I-GENE
promoter I-GENE
of O
GPIX I-GENE
and O
is O
dependent I-GENE
upon O
the O
upstream O
activation O
of O
MAPK I-GENE
/ I-GENE
extracellular I-GENE
signal I-GENE
- I-GENE
regulated O
kinase I-GENE
. O

Molecular O
identification O
of O
smg I-GENE
- I-GENE
4 I-GENE
, O
required O
for O
mRNA I-GENE
surveillance I-GENE
in O
C I-GENE
. O
elegans I-GENE
. O

Cytosolic I-GENE
acetyl I-GENE
- I-GENE
CoA I-GENE
synthetase I-GENE
( O
AceCS1 I-GENE
) O
activates O
acetate O
to O
supply O
the O
cells O
with O
acetyl I-GENE
- I-GENE
CoA I-GENE
for O
lipid O
synthesis O
. O

There O
was O
an O
increase O
in O
protein I-GENE
binding I-GENE
onto O
this O
element I-GENE
only O
after O
peptide I-GENE
treatment O
. O

While O
these O
results O
are O
consistent O
with O
previously O
reported O
effects O
of O
the O
C I-GENE
- I-GENE
terminal I-GENE
domain I-GENE
on O
nucleotide I-GENE
binding I-GENE
, O
they O
also O
demonstrate O
that O
interactions O
with O
the O
N I-GENE
- I-GENE
terminal I-GENE
domains I-GENE
are O
necessary O
to O
inhibit O
proton I-GENE
transport O
. O

These O
findings O
suggest O
that O
an O
intracellular O
WT I-GENE
- I-GENE
1 I-GENE
/ I-GENE
HSAL2 I-GENE
pathway O
may O
play O
a O
role O
in O
development O
and O
hematopoiesis I-GENE
. O

The O
radial I-GENE
forearm I-GENE
flap O
is O
used O
most O
commonly O
, O
however O
the O
lateral O
arm O
flap O
may O
be O
the O
flap O
of O
choice O
in O
certain O
situations O
. O

The O
procedure O
is O
less O
aggressive O
and O
painful I-GENE
than O
sternotomy I-GENE
. O

In O
addition O
, O
we O
have O
isolated O
a O
genomic O
fragment I-GENE
containing O
the O
most O
distal O
5 I-GENE
' O
sequences I-GENE
of O
the O
major I-GENE
GGT I-GENE
mRNA I-GENE
in O
HepG2 O
cells O
. O

Further O
, O
the O
osteo I-GENE
- I-GENE
retentive I-GENE
ability O
of O
the O
hydroxyapatite I-GENE
in O
the O
sockets I-GENE
was O
seen O
to O
be O
close O
to O
significance O
( O
after O
six O
months O
width I-GENE
differences O
, O
in O
the O
canine O
region O
: O
P I-GENE
= O
0 O
. O
059 I-GENE
, O
LHS I-GENE
, O
and O
P I-GENE
= O
0 O
. O
065 I-GENE
, O
RHS I-GENE
). O

These O
findings O
suggest O
a O
novel O
ankyrin I-GENE
- I-GENE
independent O
role O
for O
LAD O
- I-GENE
1 I-GENE
related I-GENE
to O
FGFR I-GENE
signaling O
. O

Managing I-GENE
vertigo I-GENE
and O
vertigo I-GENE
syndromes O
in O
the O
elderly O

A I-GENE
single O
base O
change O
( O
A8G I-GENE
) O
in O
either O
sequence I-GENE
reduces O
hnRNP I-GENE
A2 I-GENE
binding I-GENE
and O
, O
in O
the O
case O
of O
A2RE I-GENE
- I-GENE
2 I-GENE
, O
inhibits O
RNA I-GENE
transport O
. O

A I-GENE
method O
of O
three O
- I-GENE
station I-GENE
three O
- I-GENE
dimensional O
magnetic O
resonance O
( O
MR O
) O
angiography O
of O
the O
lower O
extremities I-GENE
with O
segmented I-GENE
volume O
acquisition O
is O
presented O
. O

Treatment O
of O
N18TG I-GENE
- I-GENE
2 I-GENE
cells O
with O
a O
demethylating I-GENE
agent O
, O
5 I-GENE
- I-GENE
aza I-GENE
- I-GENE
deoxycytidine I-GENE
, O
resulted O
in O
an O
expression O
of O
mlt I-GENE
1 I-GENE
, O
indicating O
that O
the O
repression O
of O
mlt I-GENE
1 I-GENE
is O
attributable I-GENE
to O
methylation O
Thus O
, O
mlt I-GENE
1 I-GENE
is O
a O
novel O
target O
gene I-GENE
that O
is O
silenced I-GENE
by O
methylation O
during O
liver O
tumorigenesis O
initiated O
by O
SV40 I-GENE
T I-GENE
antigen I-GENE
. O

We O
found O
in O
the O
control O
subjects O
rCBF O
increases O
in O
regions O
associated I-GENE
with O
the O
meso I-GENE
- I-GENE
striatal I-GENE
and O
meso I-GENE
- I-GENE
corticolimbic I-GENE
circuits I-GENE
in O
response O
to O
both O
monetary I-GENE
reward I-GENE
and O
nonmonetary I-GENE
reinforcement I-GENE
. O

Reverse I-GENE
transcriptase I-GENE
- I-GENE
polymerase I-GENE
chain I-GENE
reaction O
assays O
showed O
that O
PKRDeltaE7 I-GENE
is O
expressed O
in O
a O
broad O
range O
of O
human I-GENE
tissues O
at O
variable O
levels O
. O

For O
this O
purpose O
, O
the O
immediate I-GENE
and O
the O
final O
( O
after O
swelling O
) O
fixation O
strengths O
of O
two O
variations O
of O
the O
swellable I-GENE
bone O
anchor I-GENE
designs I-GENE
( O
a O
smooth I-GENE
anchor I-GENE
and O
a O
screw I-GENE
anchor I-GENE
) O
were O
measured O
in O
two O
different O
foams I-GENE
( O
used O
to O
simulate I-GENE
bone O
) O
with O
different O
densities I-GENE
. O

CYP2C19 I-GENE
genotype I-GENE
was O
determined O
by O
the O
polymerase I-GENE
chain I-GENE
reaction O
- I-GENE
restriction I-GENE
fragment I-GENE
length I-GENE
polymorphism O
method O
. O

It O
is O
useful O
as O
an O
adjunct I-GENE
to O
mammography I-GENE
in O
those O
patients O
with O
radiographically I-GENE
dense I-GENE
breasts I-GENE
for O
the O
characterization O
of O
palpable I-GENE
masses O
. O

Activation O
of O
transcription I-GENE
through O
the O
AP I-GENE
- I-GENE
1 I-GENE
site I-GENE
in O
Jurkat O
cells O
by O
JunD I-GENE
and O
/ I-GENE
or O
Fra I-GENE
- I-GENE
2 I-GENE
was O
weak O
. O
c I-GENE
- I-GENE
Jun I-GENE
, O
JunB I-GENE
, O
and O
c I-GENE
- I-GENE
Fos I-GENE
activation O
was O
greater O
, O
although O
the O
level O
was O
still O
less O
than O
that O
with O
Tax I-GENE
. O

Thus O
, O
the O
screen O
for O
toxic O
p53 I-GENE
mutants I-GENE
in O
yeast I-GENE
can O
identify O
novel O
p53 I-GENE
variants I-GENE
that O
may O
be O
useful O
in O
dissecting I-GENE
p53 I-GENE
regulated O
cellular O
responses O
and O
in O
developing O
p53 I-GENE
- I-GENE
based O
cancer O
therapies I-GENE
. O

Local I-GENE
control O
rates O
were O
91 O
% O
for O
metastatic O
lung O
cancer O
, O
89 I-GENE
% O
for O
primary O
lung O
cancer O
and O
85 O
% O
for O
T1 O
, O
2N0M0 I-GENE
cases O
. O

The O
results O
show O
that O
cognitive O
stimulation O
enhanced O
performance O
on O
the O
Boston I-GENE
Naming I-GENE
Test O
and O
a O
Word I-GENE
List I-GENE
Recognition I-GENE
Task I-GENE
; O
physical O
intervention O
, O
however O
, O
did O
not O
reach O
statistical O
significance O
. O

Gimpl I-GENE
, O
F I-GENE
. O

The O
actA I-GENE
gene I-GENE
is O
present O
as O
a O
single O
copy O
in O
the O
genome O
of O
A I-GENE
. O
chrysogenum I-GENE
; O
and O
its O
expression O
level O
, O
opposite O
to O
pcbC I-GENE
and O
cefEF I-GENE
cephalosporin I-GENE
biosynthetic O
genes I-GENE
, O
was O
steady O
during O
cephalosporin I-GENE
fermentation I-GENE
, O
showing O
a O
single O
1 I-GENE
. O
4 I-GENE
- I-GENE
kb O
transcript I-GENE
. O

Maternal I-GENE
p O
, O
p O
' O
DDE I-GENE
and O
beta I-GENE
- I-GENE
HCH I-GENE
levels O
were O
also O
associated I-GENE
with O
newborn O
levels O
, O
but O
levels O
of O
PCBs I-GENE
were O
not O
. O

The O
patients O
and O
their O
families O
were O
closely O
questioned I-GENE
, O
and O
full I-GENE
clinical O
examination O
included O
a O
test O
for O
orthostasia I-GENE
. O

The O
expression O
of O
alpha I-GENE
- I-GENE
amylase I-GENE
can O
be O
transactivated O
by O
the O
transcription I-GENE
factor I-GENE
GAMyb I-GENE
, O
which O
is O
itself O
induced O
by O
GA I-GENE
. O

Cardiac I-GENE
output O
at O
anaerobic O
threshold O
( O
COAT I-GENE
) O
< O
or O
= O
7 O
. O
3 I-GENE
L I-GENE
/ I-GENE
min O
was O
the O
best O
cutoff O
value O
for O
identifying O
multivessel I-GENE
coronary O
artery O
disease O
( O
relative O
risk O
, O
3 I-GENE
. O
1 I-GENE
). O

Tolerance I-GENE
to O
ADAL I-GENE
- I-GENE
2 I-GENE
was O
similar O
to O
that O
of O
Vicryl I-GENE
suture I-GENE
and O
tolerance O
to O
ADAL I-GENE
- I-GENE
2 I-GENE
was O
superior O
to O
that O
to O
Tisuacryl I-GENE
. O

In O
the O
base O
- I-GENE
case O
analysis O
, O
total O
direct O
costs O
per O
patient O
were O
$ I-GENE
728 I-GENE
for O
zoledronic I-GENE
acid I-GENE
and O
$ I-GENE
776 I-GENE
for O
pamidronate I-GENE
. O

METHODS O
: O
We O
retrospectively I-GENE
selected O
13 O
TFCD I-GENE
patients O
who O
underwent O
surgery O
for O
intractable I-GENE
epilepsy O
with O
the O
aim O
of O
removing O
the O
magnetic O
resonance O
( O
MR O
)- I-GENE
detectable O
lesion O
and O
/ I-GENE
or O
the O
epileptogenic I-GENE
zone O
defined O
by O
stereoelectroencephalographic I-GENE
recordings O
. O

To O
gain O
an O
understanding O
of O
the O
mGSTM2 I-GENE
regulation O
, O
we O
have O
also O
cloned O
and O
analyzed O
its O
promoter I-GENE
region O
. O

Cyclins I-GENE
are O
one O
of O
the O
pivotal O
determinants I-GENE
regulating O
cell O
cycle O
progression O
. O

Architecture I-GENE
and O
anatomy I-GENE
of O
the O
genomic O
locus I-GENE
encoding O
the O
human I-GENE
leukemia I-GENE
- I-GENE
associated I-GENE
transcription I-GENE
factor I-GENE
RUNX1 I-GENE
/ I-GENE
AML1 I-GENE
. O

Three O
of O
the O
proteins I-GENE
involved O
in O
checkpoint I-GENE
signaling O
, O
Rad1 I-GENE
, O
Hus1 I-GENE
, O
and O
Rad9 I-GENE
, O
have O
been O
shown O
to O
interact O
by O
immunoprecipitation O
and O
yeast I-GENE
two O
- I-GENE
hybrid O
studies O
. O

Together O
these O
data O
imply O
that O
the O
HFV I-GENE
R I-GENE
region O
acts O
in O
the O
nucleus O
to O
modify O
the O
cytoplasmic I-GENE
fate O
of O
target O
HFV I-GENE
mRNA I-GENE
. O

However O
, O
patients O
with O
isolated O
office I-GENE
hypertension O
had O
fewer O
previous O
cardiovascular O
complications O
. O

Through I-GENE
deletion O
mutagenesis O
, O
we O
identify O
amino O
acids O
2003 I-GENE
to O
2212 I-GENE
of O
CBP I-GENE
, O
which O
we O
call I-GENE
carboxy I-GENE
- I-GENE
terminal I-GENE
region O
2 I-GENE
( O
CR2 I-GENE
), O
as O
the O
minimal I-GENE
region O
for O
Tax I-GENE
interaction O
. O

Fetal I-GENE
lung O
volume O
: O
estimation O
at O
MR O
imaging O
- I-GENE
initial O
results O
. O

Plane I-GENE
wave O
geometry I-GENE
is O
impractical I-GENE
for O
clinical O
use O
but O
the O
results O
of O
this O
work O
encouraged I-GENE
us O
to O
further O
develop O
the O
P3 I-GENE
approximation I-GENE
for O
a O
spherical I-GENE
geometry I-GENE
, O
described O
in O
this O
paper O
. O

For O
the O
sample O
of O
systematic O
reviews I-GENE
drawn I-GENE
from O
ACP I-GENE
Journal I-GENE
Club I-GENE
( O
n O
= O
103 I-GENE
), O
the O
PubMed I-GENE
strategy O
achieved O
a O
sensitivity O
of O
97 O
% O
( O
CI O
, O
91 O
% O
to O
99 O
%). O

In O
addition O
to O
that O
, O
she I-GENE
received O
hepatic I-GENE
intra O
- I-GENE
arterial O
infusion O
of O
levoforinate I-GENE
( O
l O
- I-GENE
LV O
) O
250 O
mg O
and O
5 I-GENE
- I-GENE
fluorouracil O
( O
5 I-GENE
- I-GENE
FU O
) O
500 O
mg O
for O
combined O
multiple O
hepatic I-GENE
metastases O
starting O
on O
postoperative O
day O
14 O
, O
and O
these O
medications I-GENE
were O
administered O
over O
48 O
hours O
once O
weekly O
by O
infuser I-GENE
pump I-GENE
. O

Because O
of O
differences O
in O
patient O
characteristics O
, O
control O
measurements O
were O
obtained O
from O
normal O
muscle O
in O
all O
patients O
. O

Two O
families O
with O
concordant I-GENE
inheritance I-GENE
of O
DNAH9 I-GENE
alleles I-GENE
in O
affected O
individuals O
were O
observed O
. O

NIRS I-GENE
was O
used O
for O
the O
quantitative O
measurement O
of O
muscle O
O I-GENE
( O
2 I-GENE
) O
consumption O
( O
mV I-GENE
. O
O I-GENE
( O
2 I-GENE
)) O
and O
forearm I-GENE
blood O
flow O
( O
FBF I-GENE
) O
in O
78 O
healthy O
subjects O
. O

Many O
factors I-GENE
do O
influence O
the O
educational I-GENE
outcome O
in O
students O
and O
large O
statistical O
power O
( O
such O
as O
meta I-GENE
analysis O
) O
should O
be O
helpful O
to O
eliminate I-GENE
many O
sources O
of O
error O
. O

B I-GENE
- I-GENE
myb I-GENE
is O
essential O
for O
G1 I-GENE
/ I-GENE
S I-GENE
transition O
and O
has O
been O
shown O
to O
be O
phosphorylated O
by O
the O
cyclin I-GENE
A2 I-GENE
/ I-GENE
cdk2 I-GENE
complex I-GENE
. O

Like O
the O
consensus I-GENE
mammalian I-GENE
LHbeta I-GENE
gene I-GENE
, O
the O
5 I-GENE
'- O
flanking O
region O
of O
the O
gpLH I-GENE
/ I-GENE
CGbeta I-GENE
gene I-GENE
contains O
a O
single O
TATA I-GENE
sequence I-GENE
37 O
bp O
upstream O
of O
the O
translation I-GENE
start O
codon O
. O

HTLV I-GENE
- I-GENE
1 I-GENE
decreases O
Th2 I-GENE
type I-GENE
of O
immune I-GENE
response O
in O
patients O
with O
strongyloidiasis I-GENE
. O

Indeed O
, O
mutation I-GENE
of O
two O
of O
these O
motifs O
, O
known O
to O
be O
important O
to O
regulation O
of O
sid1 I-GENE
, O
altered O
the O
differential O
regulation O
of O
sid2 I-GENE
by O
iron O
. O

Nutritional I-GENE
status O
in O
adults O
on O
an O
alternative O
or O
traditional I-GENE
diet O
] O
BACKGROUND O
: O
Plant I-GENE
food O
lacks O
vitamin O
B12 I-GENE
, O
vitamin O
D I-GENE
and O
higher O
n O
- I-GENE
3 I-GENE
polyunsaturated I-GENE
fatty I-GENE
acids O
. O

On O
the O
other O
hand O
, O
forced I-GENE
overexpression O
of O
the O
wild I-GENE
type I-GENE
, O
but O
not O
the O
kinase I-GENE
- I-GENE
inactivated O
mutant I-GENE
of O
nm23H1 I-GENE
, O
converted O
the O
GDP I-GENE
- I-GENE
bound O
forms O
of O
Rac1 I-GENE
, O
Cdc42 I-GENE
, O
and O
RhoA I-GENE
to O
their O
GTP I-GENE
- I-GENE
bound O
forms O
in O
vitro O
by O
its O
nucleoside I-GENE
diphosphate I-GENE
kinase I-GENE
activity O
, O
but O
nm23H1 I-GENE
alone O
apparently O
did O
not O
produce O
the O
GTP I-GENE
- I-GENE
bound O
form O
of O
these O
GTPases I-GENE
in O
vivo O
. O

Novel I-GENE
intronic I-GENE
promoter I-GENE
in O
the O
rat I-GENE
ER I-GENE
alpha I-GENE
gene I-GENE
responsible O
for O
the O
transient O
transcription I-GENE
of O
a O
variant I-GENE
receptor I-GENE
. O

RESULTS O
: O
Coronary O
mortality O
during O
the O
median O
follow O
- I-GENE
up O
time O
of O
17 O
months O
was O
6 I-GENE
- I-GENE
fold O
higher O
in O
the O
highest O
tertile I-GENE
for O
CRP I-GENE
and O
IL I-GENE
- I-GENE
6 I-GENE
and O
3 I-GENE
. O
5 I-GENE
- I-GENE
fold O
higher O
in O
the O
highest O
tertile I-GENE
for O
fibrinogen I-GENE
and O
TNF I-GENE
- I-GENE
alpha I-GENE
than O
in O
the O
respective O
combined O
lower O
tertiles I-GENE
. O

HIV I-GENE
- I-GENE
1 I-GENE
and O
hepatitis I-GENE
B I-GENE
virus I-GENE
infections O
in O
adolescents I-GENE
lodged I-GENE
in O
security I-GENE
institutes I-GENE
of O
Buenos I-GENE
Aires I-GENE
. O

However O
, O
the O
promoter I-GENE
region O
contains O
several O
potential O
cis O
- I-GENE
regulatory I-GENE
elements O
such O
as O
Sp1 I-GENE
, O
early I-GENE
growth I-GENE
response O
- I-GENE
1 I-GENE
, O
activator I-GENE
protein I-GENE
- I-GENE
2 I-GENE
, O
MyoD I-GENE
, O
p300 I-GENE
, O
nuclear I-GENE
factor I-GENE
- I-GENE
kappaB I-GENE
, O
myeloid O
zinc I-GENE
finger I-GENE
protein I-GENE
- I-GENE
1 I-GENE
, O
caudal I-GENE
- I-GENE
related I-GENE
homeobox I-GENE
( O
Cdx I-GENE
) O
gene I-GENE
A I-GENE
, O
and O
Cdx I-GENE
protein I-GENE
- I-GENE
2 I-GENE
binding I-GENE
sites I-GENE
. O

RPM I-GENE
/ I-GENE
RGL3 I-GENE
resembled I-GENE
AF I-GENE
- I-GENE
6 I-GENE
and O
Nore1 I-GENE
in O
interacting I-GENE
strongly O
with O
constitutively O
active O
M I-GENE
- I-GENE
Ras I-GENE
and O
p21 I-GENE
Ras I-GENE
. O

METHODS O
: O
93 O
female O
and O
43 I-GENE
male O
patients O
undergoing O
thyroid I-GENE
surgery O
were O
stratified I-GENE
according O
to O
gender O
and O
then O
randomised O
to O
receive O
double O
- I-GENE
blind O
one O
of O
four O
antiemetic I-GENE
regimes I-GENE
: O
50 O
mg O
dolasetron I-GENE
given O
orally O
45 O
minutes O
prior O
to O
induction O
of O
anaesthesia O
( O
group O
I I-GENE
), O
12 O
. O
5 I-GENE
mg O
dolasetron I-GENE
given O
intravenously O
during O
induction O
of O
anaesthesia O
( O
group O
II I-GENE
), O
1 I-GENE
. O
25 O
mg O
DHB I-GENE
given O
intravenously O
during O
induction O
of O
anaesthesia O
( O
group O
III I-GENE
) O
or O
placebo O
( O
group O
IV I-GENE
). O

Transcriptional O
regulation O
of O
the O
estrogen I-GENE
- I-GENE
inducible I-GENE
pS2 I-GENE
breast O
cancer O
marker O
gene I-GENE
by O
the O
ERR I-GENE
family I-GENE
of O
orphan I-GENE
nuclear I-GENE
receptors I-GENE
. O