gene_test.p2.out

Third O
, O
consistent O
with O
these O
data O
, O
N O
- O
acetylcysteine O
reduced O
the O
stimulatory O
effect O
of O
HGF I-GENE
on O
stress I-GENE
kinase I-GENE
activities O
, O
while O
p42 O
/ O
44 O
mitogen I-GENE
activated I-GENE
kinase I-GENE
( I-GENE
MAPK I-GENE
) O
was O
unmodified O
, 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
( I-GENE
JNK I-GENE
) I-GENE
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
( I-GENE
Sry I-GENE
like I-GENE
HMG I-GENE
box I-GENE
gene I-GENE
) O
is O
characterised O
by O
a O
conserved O
DNA O
sequence O
encoding O
a O
domain O
of O
approximately O
80 O
amino O
acids O
which O
is O
responsible O
for O
sequence O
specific O
DNA O
binding O
. O

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

This O
slow O
progression O
through O
the O
early O
G1 O
- O
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 O
phase O
transition O
. O

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

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

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

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

CHAP O
and O
the O
Department O
of O
Veterans O
Affairs O
. O

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

As O
an O
oral O
, O
nontoxic O
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 O
SCH66336 O
shows O
promise O
for O
the O
treatment O
of O
BCR I-GENE
/ I-GENE
ABL I-GENE
- I-GENE
induced O
leukemia O
. O

Recruitment O
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 O
in O
CREB I-GENE
, O
independently O
of O
CREB I-GENE
phosphorylation O
. O

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

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

At O
the O
end O
of O
each O
day O
of O
migration O
the O
pulmonary O
hemolymph O
PO2 O
decreased O
by O
1 O
- O
2 O
. O
5 O
kPa O
, O
but O
the O
hemocyanin O
remained O
saturated O
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 O
mmol O
x O
l O
(- O
1 O
)). O

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

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

TaqMan O
analysis O
of O
gene O
expression O
following O
chronic O
FA O
treatment O
showed O
neither O
a O
decrease O
in O
the O
amount O
of O
leptin I-GENE
receptor I-GENE
( I-GENE
Ob I-GENE
- I-GENE
R I-GENE
) I-GENE
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 O
( O
suppressors O
of O
cytokine O
signalling O
) O
or O
cytokine O
inducible O
sequence O
( O
CIS O
). O

Nine O
animals O
served O
as O
control O
animals O
, O
whereas O
20 O
animals O
received O
a O
focal O
arachnoid O
scar O
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 O
comparison O
of O
the O
duplicated O
Vkappa O
genes O
suggests O
positive O
selection O
on O
the O
complementarity O
- O
determining O
regions O
of O
the O
duplicated O
genes O
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 O
. O
contrast O
material O
. O

The O
presence O
of O
AS O
- O
oligo O
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 O
- O
mediated O
activation O
. O

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

Additional O
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 O
associated O
with O
G1 O
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 O
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 O
isoenzymes O
as O
statins O
. O

Regulation O
of O
laminin I-GENE
beta2 I-GENE
chain I-GENE
gene I-GENE
expression O
in O
human O
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 O
promoter O
prevents O
its O
induction O
by O
TNF I-GENE
- I-GENE
alpha I-GENE
. O

Effect O
of O
heat O
treatments O
on O
the O
meltability O
of O
cheeses O
. O

In O
vitro O
binding O
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 O
/ O
exportin1 O
and O
that O
eIF I-GENE
- I-GENE
5A I-GENE
interacts O
with O
the O
nucleoporins O
CAN O
/ O
nup214 O
, O
nup153 O
, O
nup98 O
, O
and O
nup62 O
. O

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

Copyright O
2001 O
Academic O
Press O
. O

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

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

E47 O
protein O
levels O
remain O
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 O
upon O
transition O
to O
the O
single O
positive O
stage O
. O

By O
Caveman O
. 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 O
away O
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 O
, O
T255A O
, O
lost O
the O
ability O
to O
bind O
E4orf6 O
, O
but O
unexpectedly O
, O
viral O
late O
- O
gene O
expression O
was O
not O
affected O
. O

However O
, O
the O
N63S O
mutation O
in O
the O
wild O
- O
type O
VP5 O
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 O
of O
9 O
relative O
to O
when O
the O
PR7 O
mutation O
was O
present O
. O

Here O
we O
report O
the O
isolation O
and O
characterization O
of O
the O
forkhead O
homologue O
in O
rhabdomyosarcoma O
( O
FKHR O
), 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
( I-GENE
NR I-GENE
) I-GENE
intermediary I-GENE
protein I-GENE
. O

Unlike O
other O
progenitor O
cells O
of O
the O
brain O
, O
SVZa O
progenitor O
cells O
have O
the O
capacity O
to O
divide O
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 O
/ O
G1 O
phase O
to O
S O
and O
G2 O
/ O
M O
phases O
in O
human O
T O
- O
cell O
line O
Kit O
225 O
cells O
. O

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

In O
Exp O
. O

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

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

We O
used O
a O
rev I-GENE
- I-GENE
and O
RRE I-GENE
- I-GENE
defective I-GENE
HIV I-GENE
type I-GENE
1 I-GENE
( I-GENE
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 O
elements O
from O
the O
mammalian O
genome O
by O
selecting O
for O
rescue O
of O
virus O
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 O
of O
the O
diaphragm O
with O
and O
without O
spermicide O
. O

DESIGN O
: O
Retrospective O
study O
. O

Considering O
that O
the O
reactor O
is O
thoroughly O
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 O
. O
coli O
concentrations O
in O
the O
range O
of O
2 O
x O
10 O
( O
3 O
) O
< O
or O
= O
E O
coli O
/ O
cfu O
mL O
(- O
1 O
) O
< O
or O
= O
3 O
x O
10 O
( O
6 O
), O
we O
ascribe O
the O
nonexponential O
Pn O
decay O
of O
single O
- O
strain O
E O
. O
coli O
colonies O
to O
a O
shielding O
phenomenon O
where O
inactive O
cells O
protect O
the O
successively O
smaller O
numbers O
of O
viable O
cells O
in O
the O
EHD O
. O

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

Body O
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 O
at O
chromosome O
ends O
, O
is O
usually O
inactive O
in O
most O
primary O
somatic O
human O
cells O
, O
but O
is O
specifically O
activated O
with O
in O
vitro O
immortalization O
and O
during O
tumorigenesis O
. O

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

SELECTION O
CRITERIA O
: O
All O
randomised O
controlled O
trials O
comparing O
IUSs O
with O
other O
forms O
of O
reversible O
contraceptives O
and O
reporting O
on O
pre O
- O
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 O
and O
in O
Cherry O
Hill O
( O
Acer O
, O
r O
( O
p O
) O
= O
0 O
. O
987 O
, O
Quercus O
, O
r O
( O
p O
) O
= O
0 O
. O
645 O
, O
Betula O
, O
r O
( O
p O
) O
= O
0 O
. O
896 O
, O
Pinus O
, O
r O
( O
p O
) O
= O
0 O
. O
732 O
, O
Cupressaceae O
, O
r O
( O
p O
) O
= O
0 O
. O
695 O
, O
Poaceae O
, O
r O
( O
p O
) O
= O
0 O
. O
950 O
, O
Ambrosia O
, O
r O
( O
p O
) O
= O
0 O
. O
903 O
, O
and O
Rumex O
, O
r O
( O
p O
) O
= O
0 O
. O
572 O
, O
P O
< O
0 O
. O
001 O
). O

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

2 O
: O
The O
dynamic O
moduli O
of O
microcrystalline O
cellulose O
. O

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

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

Our O
results O
suggest O
that O
WASP O
activates O
transcription O
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 O
/ O
3 O
- O
directed O
actin I-GENE
polymerization I-GENE
. O

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

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

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

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

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

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

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

Rind O
et O
al O
.' O
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 O
Available O

Lactate O
accumulation O
peak O
was O
unaffected O
by O
supplementation O
( O
HMB O
, O
8 O
. O
1 O
+/- O
1 O
. O
1 O
mM O
; O
LEU O
, O
6 O
. O
2 O
+/- O
0 O
. O
8 O
mM O
; O
CON O
, O
7 O
. O
5 O
+/- O
1 O
. O
3 O
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 O
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 O
antibodies O
against O
the O
N O
- O
terminal O
part O
( O
amino O
acids O
12 O
- O
363 O
) O
and O
the O
C O
- O
terminal O
part O
( O
amino O
acids O
330 O
- O
730 O
) O
of O
rainbow I-GENE
trout I-GENE
HIF I-GENE
- I-GENE
1alpha I-GENE
protein I-GENE
recognized I-GENE
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 O
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 O
is O
a O
modular O
protein O
, 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 O
terminus O
. O

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

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

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

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

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

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

Three O
patients O
received O
additional O
cycles O
of O
5 O
- O
fluorouracil O
+/- O
leucovorin O
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
- O
acquired O
responding O
for O
heroin O
under O
CRF O
at O
rates O
similar O
to O
their O
pre O
- O
lesion O
performance O
. O

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

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

Utility O
of O
OAE O
screener O
( O
GSI O
70 O
) O
for O
the O
evaluation O
of O
distortion O
product O
otoacoustic O
emissions O
] 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 O
screener O
GSI O
70 O
to O
evaluate O
of O
cochlea O
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 O
artery O
- O
alone O
ALT O
graft O
showed O
almost O
normal O
structure O
histologically O
at O
1 O
month O
after O
grafting O
, O
with O
bile O
secretion O
preserved O
. O

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

We O
show O
here O
that O
the O
in O
vitro O
transcription O
extract O
contains O
a O
binding O
activity O
that O
is O
specific O
for O
the O
initiator O
element O
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 O
function O
is O
based O
on O
the O
search O
for O
a O
global O
optimum O
[ O
D O
= O
f O
( O
Y1 O
, O
Y2 O
, O
..., O
Yn O
)] O
by O
the O
transformation O
of O
the O
measured O
property O
to O
a O
dimensionless O
scale O
for O
each O
criterion O
. O

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

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

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

The O
child O
left O
behind O
. O

Using O
the O
two O
- O
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 O
to O
the O
predominant O
role O
of O
protein O
- O
isoprene O
interaction O
in O
complex O
formation O
. O

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

The O
region O
containing O
both O
serines O
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 O
clinical O
factor O
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 O
order O
fracture O
rate O
, O
and O
manufacturing O
period O
as O
risk O
factors O
for O
OSF O
. O

A O
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 O
1 O
is O
normally O
expressed O
in O
brain O
, O
spleen O
, O
stom O
ach O
, O
and O
liver O
. O

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

As O
a O
complement O
to O
genome O
- O
wide O
mapping O
and O
sequencing O
efforts O
, O
it O
is O
often O
important O
to O
generate O
detailed O
maps O
and O
sequence O
data O
for O
specific O
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
- O
low O
- O
density O
lipoprotein O
secretion O
due O
to O
decreased O
expression O
of O
genes I-GENE
encoding I-GENE
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 O
cholesterol O
uptake O
due O
to O
increased O
expression O
of O
the O
major O
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 O
uptake O
to O
the O
liver O
due O
to O
down O
- O
regulation O
of O
the O
major O
basolateral O
bile O
acid O
transporters I-GENE
sodium I-GENE
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 I-GENE
jet I-GENE
fuel I-GENE
on O
the O
functional O
observational O
battery O
, O
and O
learning O
and O
memory O
in O
the O
rat O
. O

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

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

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

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

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

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

Copyright O
2001 O
Academic O
Press O
. O

CONCLUSIONS O
: O
Although O
the O
levels O
of O
oxLDL O
antibodies O
might O
be O
modified O
in O
early O
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 O
genetics O
, O
we O
introduced O
one O
nucleotide O
change O
( O
UCU O
to O
ACU O
) O
to O
immediate O
downstream O
of O
the O
RNA O
- O
editing O
site O
of O
the O
V O
gene O
in O
the O
full O
- O
length O
hPIV2 O
cDNA O
and O
were O
able O
to O
obtain O
infectious O
viruses O
[ O
rPIV2V O
(-)] O
from O
the O
cDNA O
. O

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

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

Tumor I-GENE
- I-GENE
like I-GENE
accumulation O
on O
Tl O
- O
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 O
structures O
including O
tetraplex O
and O
triplex O
DNA O
, O
and O
Holliday O
junctions O
. O

The O
increase O
in O
number O
of O
terminal O
hairs O
, O
which O
are O
defined O
as O
hairs O
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 O
cm O
square O
= O
0 O
. O
25 O
cm2 O
area O
) O
of O
the O
procyanidin O
B O
- O
2 O
group O
subjects O
after O
the O
6 O
- O
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 O
B O
- O
2 O
, O
1 O
. O
99 O
+/- O
2 O
. O
58 O
( O
mean O
+/- O
SD O
)/ O
0 O
. O
25 O
cm2 O
; O
placebo O
, O
- O
0 O
. O
82 O
+/- O
3 O
. O
40 O
( O
mean O
+/- O
SD O
)/ O
0 O
. O
25 O
cm2 O
; O
P O
< O
0 O
. O
02 O
, O
two O
- O
sample O
t O
test O
). O

SKP1 I-GENE
- I-GENE
SnRK I-GENE
protein I-GENE
kinase I-GENE
interactions O
mediate O
proteasomal O
binding O
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 O
, O
we O
compared O
the O
amino O
acid O
sequence O
of O
C O
/ O
EBPalpha O
from O
different O
species O
( O
frog O
to O
human O
) O
and O
identified O
four O
highly O
conserved O
regions O
( O
CR1 O
- O
CR4 O
) O
within O
the O
transactivation O
domain O
. O

Colorectal O
cancer O
was O
shown O
to O
disproportionately O
overburden O
Ashkenazi O
Jews O
, 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
- O
Hodgkin O
' O
s O
lymphoma O
. O

Percentages O
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 O
, O
NHEJ O
deficiency O
leads O
to O
genomic O
rearrangements O
, O
in O
agreement O
with O
chromosomal O
studies O
. O

Copyright O
2001 O
S O
. O

After O
nerve O
injury O
, O
the O
nociceptive O
responses O
through O
type O
I O
neurons O
, O
which O
are O
polymodal O
C O
- O
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 O
II O
ones O
, O
which O
are O
polymodal O
C O
- O
fibers O
and O
drive O
NMDA I-GENE
receptor I-GENE
- I-GENE
mechanisms O
, O
while O
type O
III O
ones O
, O
which O
are O
capsaicin O
- O
insensitive O
( O
possibly O
A O
- O
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 O
has O
a O
33 O
- O
amino O
acid O
insert O
in O
the O
S1 I-GENE
transmembrane I-GENE
domain I-GENE
that O
does O
not O
alter O
S1 O
overall O
hydrophobicity O
, O
but O
makes O
the O
S0 I-GENE
- I-GENE
S1 I-GENE
linker I-GENE
longer O
. O

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

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

Our O
results O
indicate O
that O
D O
( O
4 O
) O
and O
D O
( O
2L O
) O
receptors O
activate O
the O
ERK I-GENE
kinase I-GENE
cascade O
by O
first O
mobilizing O
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 O
with O
this O
receptor I-GENE
tyrosine I-GENE
kinase I-GENE
. O

Raes O
, O
P O
. 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 O
. O

C I-GENE
/ I-GENE
EBPbeta I-GENE
LIP I-GENE
overexpressing O
HC11 O
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 O
hormones O
. O

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

Subacute O
diencephalic O
angioencephalopathy O
( O
SDAE O
) 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 O
bilaterally O
. O

NGF O
elicits O
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 O
levels O
, O
oxygen O
- O
radical O
absorbing O
capacity O
assay O
and O
AFR O
release O
assessed O
by O
electron O
paramagnetic O
resonance O
( O
EPR O
) 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 O
vein O
varix O
in O
association O
with O
bilateral O
pulmonary O
vein O
stenosis O
. O

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

The O
images O
showed O
rapid O
, O
predominantly O
urinary O
excretion O
of O
99mTc O
ciprofloxacin O
, 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 O
- O
2 O
may O
contribute O
to O
the O
establishment O
of O
a O
chronic O
or O
latent O
infection O
. O

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

Two O
remotely O
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 O
' O
end O
and O
proximal O
ORF O
under O
the O
control O
of O
a O
bidirectional O
promoter O
. O

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

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

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

NB O
- O
506 O
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 O
splicing O
factor O
2 O
/ O
alternative O
splicing O
factor O
( O
SF2 O
/ O
ASF O
). O

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

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

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

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

Autoregulation O
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
( I-GENE
C I-GENE
/ I-GENE
EBP I-GENE
beta I-GENE
) I-GENE
transcription I-GENE
. O

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

In O
strains O
lacking O
tup11 O
and O
tup12 O
, O
the O
atf1 O
- O
pcr1 O
transcriptional O
activator O
continues O
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 O
is O
no O
longer O
essential O
for O
its O
activation O
. O

Single O
amino O
acid O
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 I-GENE
[ I-GENE
C I-GENE
] I-GENE
palmitoyl I-GENE
- I-GENE
CoA I-GENE
binding I-GENE
of O
ACBP2 O
, 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 O
repeats O
. O

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

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

It O
was O
found O
that O
intrathecal O
administration O
( O
i O
. O
t O
.) 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 O
increased O
pain O
threshold O
and O
had O
a O
potentiating O
effect O
on O
AA O
. O

Interactions O
between O
the O
checkpoint O
abrogator O
UCN O
- O
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
( I-GENE
MAPK I-GENE
) I-GENE
kinase I-GENE
( I-GENE
MEK I-GENE
)/ I-GENE
MAPK I-GENE
pathway O
have O
been O
examined O
in O
a O
variety O
of O
human O
leukemia O
cell O
lines O
. O

Analysis O
of O
regulatory O
regions O
in O
the O
promoter O
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 O
- O
signaling O
element O
( O
CuSE O
), 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
- O
deficient O
virus O
expressing O
the O
ASF O
/ O
SF2 O
splicing O
factor O
from O
a O
progesterone O
antagonist O
- I-GENE
inducible I-GENE
gene I-GENE
cassette I-GENE
, O
we O
discovered O
that O
ASF O
/ O
SF2 O
was O
expressed O
at O
a O
significant O
level O
in O
the O
293 O
producer O
cell O
line O
, O
even O
in O
the O
absence O
of O
inducer O
. O

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

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

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

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

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

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

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

Identical O
effects O
were O
obtained O
when O
inhibitors O
and O
dominant O
negative O
mutants O
were O
tested O
on O
the O
- O
29 O
to O
+ O
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 O
dephosphorylating O
enzymes O
, O
the O
protein I-GENE
- I-GENE
tyrosine I-GENE
phosphatases I-GENE
( O
PTPs O
), O
are O
studied O
which O
can O
be O
grouped O
into O
two O
subfamilies O
, O
the O
soluble O
PTPs O
and O
the O
receptor O
PTPs O
( O
RPTPs O
). O

Coexposure O
to O
FP O
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 I-GENE
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 O
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 O
to O
1970 O
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 O
- O
and O
clarithromycin O
- O
resistant O
strains O
were O
eradicated O
at O
an O
equal O
rate O
by O
each O
of O
the O
three O
regimens O
. O

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

Thus O
, O
MKK7 O
is O
an O
essential O
and O
specific O
regulator O
of O
stress O
- O
induced O
SAPK I-GENE
/ I-GENE
JNK I-GENE
activation O
in O
mast O
cells O
and O
MKK7 O
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 O
cells O
. O

The O
N O
- O
terminal O
portion O
of O
Notch I-GENE
( I-GENE
IC I-GENE
) I-GENE
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 O
pulsation O
in O
children O
creating O
motion O
artifact O
, O
changes O
in O
arterial O
oxygen O
concentration O
intrinsic O
to O
propofol O
or O
related O
to O
the O
supplemental O
oxygen O
normally O
administered O
, O
or O
changes O
in O
CSF I-GENE
protein I-GENE
levels O
related O
to O
propofol O
binding O
to O
proteins O
for O
uptake O
into O
CSF I-GENE
. O

Molecular O
cloning O
and O
characterization O
of O
OsPSK O
, O
a O
gene O
encoding O
a O
precursor O
for O
phytosulfokine I-GENE
- I-GENE
alpha I-GENE
, O
required O
for O
rice O
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 O
, O
combining O
trickling O
filter O
( O
TF O
) O
and O
activated O
sludge O
process O
( O
ASP O
), O
to O
treat O
wastewater O
containing O
trichloroethylene O
( O
TCE O
) O
at O
ambient O
temperature O
at O
different O
hydraulic O
retention O
time O
( O
HRT O
). O

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

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

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

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

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

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

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

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

Compared O
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 O
and O
a O
longer O
isovolumic O
relaxation O
time O
. O

The O
corresponding O
orifice O
voltages O
for O
the O
three O
instruments O
were O
20 O
/ O
50 O
/ O
80 O
V O
( O
API O
365 O
), O
30 O
/ O
90 O
/ O
130 O
V O
( O
API O
2000 O
) O
and O
40 O
/ O
80 O
/ O
120 O
V O
( O
API O
3000 O
). 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 O
Genomic O
Scanning O
for O
Methylation O
( O
RLGS O
- O
M O
) O
and O
identified O
several O
loci O
/ O
spots O
that O
appeared O
to O
be O
methylated O
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
( I-GENE
II I-GENE
) O
140 O
, O
containing O
an O
HFD O
and O
a O
plant O
homeodomain I-GENE
( O
PHD O
) O
finger O
, O
which O
we O
demonstrated O
by O
immunoprecipitation O
to O
be O
a O
mammalian I-GENE
TFIID I-GENE
component I-GENE
. O

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

A O
proposal O
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 O
indicators O
, O
water O
and O
service O
quality O
indicators O
, O
personnel O
indicators O
and O
economic O
indicators O
. O

These O
analyses O
re O
- O
open O
the O
question O
whether O
all O
the O
CesA O
genes O
encode O
cellulose O
synthases O
or O
whether O
some O
of O
the O
sub O
- O
class O
members O
may O
encode O
other O
non O
- I-GENE
cellulosic I-GENE
( I-GENE
1 I-GENE
--> I-GENE
4 I-GENE
) I-GENE
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 O
V O
Leiden O
mutation O
or O
the O
deletion O
- O
deletion O
polymorphism O
of O
the O
angiotensin I-GENE
converting I-GENE
enzyme I-GENE
to O
postoperative O
thromboembolic O
events O
following O
total O
joint O
arthroplasty O
. O

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

Against O
gram O
- O
positive O
organisms O
, O
E O
- O
4767 O
and O
E O
- O
5065 O
were O
, O
in O
general O
, O
eight O
- O
and O
fourfold O
more O
active O
than O
tosufloxacin O
, 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 O
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 O
transcription O
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 O
, O
the O
authors O
estimate O
that O
nearly O
13 O
, O
000 O
Asian O
and O
Pacific O
Islander O
children O
living O
in O
the O
United O
States O
today O
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 O
structured O
interview O
was O
undertaken O
at O
the O
time O
of O
initial O
consultation O
and O
at O
subsequent O
1 O
- O
year O
intervals O
regarding O
type O
of O
BHS O
, O
frequency O
of O
spells O
, O
associated O
phenomenon O
, O
sequelae O
, O
family O
history O
, O
and O
age O
at O
termination O
of O
spells O
. O

Cell O
. O

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

These O
mutations O
, O
when O
placed O
in O
a O
wild O
- O
type O
fliF O
background O
, O
had O
no O
mutant O
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 O
negative O
mutant I-GENE
JNK1 I-GENE
or O
by O
treatment O
with O
a O
selective O
chemical O
inhibitor O
of O
ERK I-GENE
( O
PD098059 O
) O
substantially O
abrogates O
the O
UV O
induction O
of O
the O
GADD45 O
promoter O
. O

At O
termination O
( O
gd O
20 O
), O
confirmed O
- O
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 O
were O
examined O
for O
external O
, O
visceral O
, O
and O
skeletal O
malformations O
. O

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

Intravenous O
L O
- O
carnitine O
treatment O
increased O
plasma O
carnitine O
concentrations O
, O
improved O
patient O
- O
assessed O
fatigue O
, 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 O
der O
Hoeve O
' O
s O
syndrome O
lesions O
as O
poorly O
mineralized O
, O
with O
low O
calcium O
salt O
and O
apparent O
increase O
of O
phosphates O
. O

A O
computerized O
method O
of O
determining O
the O
focal O
point O
of O
electrical O
activity O
in O
the O
pallidum O
of O
parkinsonian O
patients O
was O
developed O
using O
on O
- O
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 O
processing O
in O
normal O
participants O
. O

We O
interpret O
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 O
function O
of O
the O
C1 O
domain O
in O
yeast O
. O

This O
effect O
was O
observed O
in O
the O
absence O
of O
de O
novo O
protein O
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 O
- O
responsive O
sequences O
as O
the O
stress O
- O
response O
elements O
( O
StREs O
). O

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

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

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

Deterministic O
effects O
. O

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

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

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

Cloning O
and O
characterization O
of O
the O
murine I-GENE
beta I-GENE
( I-GENE
3 I-GENE
) I-GENE
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 O
binding O
assays O
confirmed O
the O
interference O
of O
p30 O
( O
II O
) 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
- O
bp O
repeat O
oligonucleotides O
in O
vitro O
. O

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

In O
conclusion O
, O
tube O
size O
estimated O
by O
Cole O
' O
s O
formula O
tends O
to O
be O
smaller O
than O
practically O
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 O
breast O
carcinoma O
cells O
, O
IL I-GENE
- I-GENE
6 I-GENE
acts O
in O
synergy O
with O
EGF I-GENE
receptor I-GENE
autocrine O
activity O
to O
signal O
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 O
) O
and O
retinoic O
acid O
( O
RA O
) O
exert O
important O
actions O
on O
PC12 O
cells O
. O

HexA71 O
negatively O
affects O
RpoS O
, 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 O
- O
mutant O
than O
in O
the O
HexA O
+ O
strain O
. O

Moreover O
, O
elderly O
men O
with O
bioavailable O
estradiol O
levels O
below O
the O
median O
[ O
40 O
pmol O
/ O
liter O
( O
11 O
pg O
/ O
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 O
estradiol O
levels O
above O
40 O
pmol O
/ O
liter O
. O

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

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

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

Managing O
HIV O
. O

BACKGROUND O
: O
There O
is O
increasing O
interest O
on O
the O
part O
of O
investigators O
and O
the O
public O
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 O
mentally O
ill O
without O
exposing O
such O
individuals O
to O
unnecessary O
risks O
. O

Multidrug O
resistance O
in O
Saccharomyces O
cerevisiae O
mainly O
results O
from O
the O
overexpression O
of O
genes O
coding O
for O
the O
membrane O
efflux O
pumps O
, O
the O
major O
facilitators O
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 O
regulators O
encoded O
by O
the O
PDR1 O
and O
PDR3 O
genes O
. O

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

Bandshift O
experiments O
demonstrate O
that O
BmHR3A O
binds O
specifically O
to O
RORE O
( 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 O
in O
the O
promoters O
of O
both O
genes O
, O
thus O
suggesting O
a O
direct O
role O
for O
BmHR3A O
in O
regulating O
the O
expression O
of O
BmGATAbeta O
and O
ESP O
genes O
during O
vitellogenesis O
. O

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

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

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

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

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

We O
observed O
NP O
/ O
NMP4 O
/ O
CIZ O
expression O
in O
osteocytes O
, O
osteoblasts O
, O
and O
chondrocytes O
in O
rat O
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 O
surgery O
with O
free O
gingival O
grafts O
for O
treatment O
of O
insufficient O
attached O
gingiva O
. O

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

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

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

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

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

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

The O
cyclins O
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 O
to O
progress O
from O
the O
G1 O
to O
S O
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 O
creatinine O
level O
did O
not O
change O
during O
the O
first O
6 O
months O
after O
withdrawal O
of O
MMF O
. O

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

Patients O
with O
antibody O
peaks O
, O
defined O
as O
fivefold O
or O
higher O
increase O
in O
antibody O
titer O
compared O
to O
the O
lowest O
antibody O
titer O
over O
the O
course O
of O
GBS O
, O
had O
higher O
disability O
scores O
during O
the O
first O
two O
weeks O
of O
GBS O
and O
a O
worse O
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 O
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 O
titers O
. O

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

TE O
- O
671 O
cells O
that O
were O
transfected O
with O
cAMP O
response O
element O
mutant O
constructs O
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 O
score O
( O
group O
A O
0 O
. O
3 I-GENE
- I-GENE
1 I-GENE
- I-GENE
1 I-GENE
. O
3 O
point O
, O
group O
B O
2 O
. O
2 O
- O
2 O
. O
9 O
- O
2 O
. O
6 O
point O
, O
group O
C O
7 O
. O
4 O
- O
8 O
. O
3 O
- O
7 O
. O
7 O
point O
) O
and O
APACHE O
II O
score O
( O
group O
A O
3 O
. O
7 O
- O
7 O
. O
6 O
- O
8 O
. O
1 O
point O
, O
group O
B O
8 O
. O
6 O
- O
11 O
. O
1 O
- O
10 O
. O
5 O
point O
, O
group O
C O
16 O
. O
3 O
- O
15 O
. O
2 O
- O
14 O
. O
3 O
point O
). O

A O
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 O
. O

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

Structure O
of O
the O
EMAPII O
domain O
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 O
. O

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

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

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

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

In O
Ka13 O
cells O
, O
CoCl O
( O
2 O
) 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
- O
kilobase O
pair O
mouse I-GENE
ho I-GENE
- I-GENE
1 I-GENE
promoter I-GENE
( I-GENE
pHO15luc I-GENE
). O

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

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

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

We O
investigated O
the O
production O
of O
hyaluronan O
( O
HA O
) 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 O
supplementation O
of O
L O
- O
arginine O
significantly O
increased O
plasma O
L O
- O
citrulline O
, O
which O
indicated O
enhancement O
of O
NO O
production O
. O

We O
can O
classify O
antibiotics O
into O
two O
groups O
based O
on O
initial O
bactericidal O
activity O
against O
P O
. O
aeruginosa O
; O
one O
class O
is O
antibiotics O
having O
rapid O
initial O
killing O
such O
as O
AMK O
, O
IPM O
and O
PAPM O
, O
the O
other O
is O
CAZ O
, O
MEPM O
showing O
slow O
initial O
killing O
. 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 O
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 O
products O
, 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 O
of O
Rab6A O
- O
GTP O
was O
also O
observed O
( O
K O
( O
d O
) O
= O
16 O
microm O
), O
whereas O
Rab1B O
, O
- O
5 O
, O
- O
7 O
, O
- O
8 O
, O
or O
- O
11A O
did O
not O
bind O
. O

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

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

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

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

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

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

No O
ISREs O
could O
be O
identified O
in O
the O
mouse O
promoter O
. O

GABA O
( O
B O
) O
R1g O
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
( I-GENE
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 O
mechanisms O
against O
infection O
by O
different O
microbes O
. O

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

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

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

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

Multiple O
regression O
analysis O
performed O
between O
these O
long O
- O
term O
abiotic O
factors O
and O
nymphal O
abundance O
in O
positive O
sites O
showed O
high O
relationship O
( O
R2 O
coefficients O
) O
for O
every O
habitat O
category O
and O
explained O
> O
50 O
% O
of O
the O
variation O
in O
tick O
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 O
- O
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 O
, O
none O
were O
identified O
using O
CT O
, O
and O
only O
two O
were O
diagnosed O
by O
small O
bowel O
follow O
- O
through O
. O

Right I-GENE
LHR I-GENE
( I-GENE
R I-GENE
- I-GENE
LHR I-GENE
) O
provided O
the O
best O
interobserver O
and O
intraobserver O
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 O
promoter O
in O
the O
human I-GENE
PDE5A I-GENE
gene I-GENE
. O

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

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

Functional O
analysis O
of O
various O
PTP I-GENE
- I-GENE
deficient O
DT40 O
B O
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 O
Src I-GENE
homology I-GENE
2 I-GENE
- I-GENE
domain I-GENE
- I-GENE
containing I-GENE
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 O
inhibitory O
negative O
regulation O
upon O
coligation O
of O
BCR I-GENE
complex I-GENE
with O
inhibitory I-GENE
receptor I-GENE
. O

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

A O
rare O
case O
of O
primary O
group O
A O
streptococcal O
peritonitis O
. O

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

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

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

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

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

Paul O
Monagle O
addresses O
the O
epidemiology O
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 O
. O

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

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

Our O
results O
suggest O
that O
the O
C O
- O
terminal O
region O
of O
Crk I-GENE
contains O
negative O
regulatory O
elements O
important O
for O
both O
Abl I-GENE
and O
FAK I-GENE
dependent I-GENE
signal O
pathways O
, O
and O
offers O
a O
paradigm O
for O
an O
autoinhibitory O
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 O
rice O
cultivation O
in O
Sri O
Lanka O
is O
coincident O
with O
the O
HIDD O
villages O
. O

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

Secretion O
of O
interleukin I-GENE
- I-GENE
8 I-GENE
, 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 O
by O
E6 I-GENE
. O

CONCLUSIONS O
: O
ChromaFlo O
- O
enhanced O
IVUS O
demonstrates O
colorized O
blood O
flow O
inside O
the O
vessel O
lumen O
, O
which O
is O
helpful O
in O
distinguishing O
echolucent O
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 O
in O
patients O
with O
renal O
failure O
or O
allergy O
, O
avoiding O
the O
use O
of O
contrast O
media O
. O

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

CONCLUSIONS O
: O
Using O
icodextrin O
- O
based O
instead O
of O
glucose O
- O
based O
PD O
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 O
central O
finding O
is O
the O
identification O
of O
a O
GC O
- O
rich O
sequence O
in O
the O
- O
99 O
/- O
91 O
Cp I-GENE
region O
that O
is O
essential O
for O
oriPI O
- O
EBNA1 O
- O
independent O
as O
well O
as O
oriPI O
- O
EBNA1 O
- O
dependent O
activity O
of O
the O
promoter O
. O

Furthermore O
, O
SB203580 O
inhibited O
LPS O
- O
induced O
activation O
of O
Sp1 I-GENE
, O
as O
well O
as O
the O
promoter O
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 O
new O
echocardiographic O
technique O
is O
described O
with O
a O
conventional O
M O
mode O
, O
digitalised O
2D O
and O
tissular O
Doppler O
which O
has O
a O
comparable O
ability O
to O
identify O
the O
anomalous O
pathways O
of O
electric O
conduction O
using O
a O
non O
- O
invasive O
method O
. O

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

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

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

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

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

Analysis O
of O
ace2Delta O
cells O
reveals O
that O
Ace2p O
is O
required O
for O
cell O
separation O
but O
not O
for O
polarized O
growth O
. 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 O
tissue O
capsule O
resulting O
from O
the O
implantation O
of O
aluminum O
calcium O
phosphate O
( O
ALCAP O
) O
and O
hydroxyapetite O
( O
HA O
) O
bioceramics O
. O

The O
event O
rate O
in O
patients O
with O
chronic O
Irr O
- O
rMFP O
or O
Un O
- O
nrMFP O
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 O
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 O
two O
- I-GENE
domain I-GENE
arginine I-GENE
kinases I-GENE
( O
AKs O
) O
arose O
independently O
at O
least O
two O
times O
during O
molecular O
evolution O
of O
phosphagen O
kinases O
: O
AKs O
from O
the O
primitive O
sea O
anemone O
Anthopleurura O
japonicus O
and O
from O
the O
clam O
Pseudocardium O
sachalinensis O
. O

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

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

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

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

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

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

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

The O
438 O
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 O
of O
103 O
amino O
acids O
. O

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

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

The O
authors O
undertook O
a O
retrospective O
analysis O
of O
pathology O
with O
quantification O
of O
the O
percentage O
of O
papillary O
serous O
component O
(% O
PSC O
) 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
( I-GENE
SH3 I-GENE
) I-GENE
and O
SH2 I-GENE
regions I-GENE
. O

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

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

NGF O
, 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 O
- O
2 O
. O

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

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

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

These O
results O
indicate O
that O
ATF4 O
regulates O
basal O
and O
CdCl O
( O
2 O
)- O
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
- O
specific O
manner O
and O
possibly O
in O
a O
complex O
with O
Nrf2 O
. O

Adjuvant O
and O
neoadjuvant O
treatment O
of O
breast O
cancer O
. O

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

Inhibition O
of O
the O
Raf I-GENE
- I-GENE
1 I-GENE
target I-GENE
ERK I-GENE
kinase I-GENE
( I-GENE
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 O
phosphorylation O
, O
and O
stress O
fiber O
formation O
. O

In O
the O
TVD O
- O
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 O
mRNAs O
has O
revealed O
that O
the O
three O
alternative O
promoters O
give O
rise O
to O
at O
least O
seven O
mCTR O
isoforms O
in O
the O
5 O
' O
region O
of O
the O
gene O
and O
generate O
5 O
'- 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 O
was O
studied O
in O
primary O
cultures O
of O
bovine O
uterine O
stromal O
cells O
stimulated O
with O
phorbol O
12 O
- O
myristate O
13 O
- O
acetate O
( O
PMA O
; O
100 O
nM O
). O

There O
was O
no O
evidence O
of O
linkage O
disequilibrium O
between O
the O
polymorphic O
site O
in O
the O
B O
cell O
specific O
promoter O
and O
those O
in O
the O
3 O
' O
UTR O
. 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 I-GENE
vascular I-GENE
endothelial I-GENE
growth I-GENE
factor I-GENE
( I-GENE
VEGF I-GENE
). O

In O
Klinefelter O
' O
s O
syndrome O
( O
47XXY O
), O
serum O
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 O
levels O
are O
low O
. O

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

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

Online O
teaching O
: 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 O
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 O
detectors O
: O
thermo O
- O
luminescent O
dosemeter O
of O
Mg2SiO4 O
: O
Tb O
( O
TDMS O
) O
and O
plastic O
nuclear O
track O
detector O
( O
PNTD O
). 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 O
Mbp O
SRO O
consisting O
predominantly O
of O
bacteriophage O
P1 O
- O
derived O
artificial O
chromosome O
( O
PAC O
) O
clones O
. O

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

Low O
- O
selenium O
diet O
has O
a O
human O
unfavourable O
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 O
was O
added O
at O
an O
initial O
dose O
of O
25 O
mg O
/ O
day O
and O
titrated O
to O
50 O
mg O
/ O
day O
within O
1 O
week O
. O

To O
assess O
more O
specific O
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 O
to O
+ O
11 O
bp O
) O
reporter O
plasmid O
was O
cotransfected O
with O
a O
full I-GENE
- I-GENE
sequence I-GENE
rabbit I-GENE
muscle I-GENE
protein I-GENE
kinase I-GENE
inhibitor I-GENE
( O
PKI O
) O
minigene O
driven O
constitutively O
by O
a O
Rous I-GENE
sarcoma I-GENE
virus I-GENE
promoter I-GENE
. O

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

Transition O
between O
P O
- O
and O
H O
- O
BPPV O
was O
found O
in O
6 O
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 O
- O
specific O
expression O
profiles O
of O
the O
gene O
. O

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

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

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

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

Deletion O
of O
the O
potential O
initiator O
element O
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 O
June O
1991 O
and O
December O
1996 O
, O
we O
administered O
the O
nucleoside O
analog O
2 O
- O
chlorodeoxyadenosine O
( O
2 O
- O
CDA O
) O
to O
73 O
children O
with O
primary O
AML O
and O
20 O
children O
with O
secondary O
AML O
or O
myelodysplastic O
syndrome O
( O
MDS O
). O

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

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

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

Its O
transcription O
in O
vitro O
by O
pol I-GENE
III I-GENE
requires O
the O
same O
factors O
as O
the O
U6 I-GENE
gene I-GENE
with O
the O
major O
exception O
that O
the O
modified O
TATA O
- O
box O
of O
this O
construct O
only O
interacts O
with O
a O
TATA I-GENE
- I-GENE
binding I-GENE
protein I-GENE
( I-GENE
TBP I-GENE
) I-GENE
mutant I-GENE
( I-GENE
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
( I-GENE
TBPwt I-GENE
). O

Expression O
of O
the O
src I-GENE
homology I-GENE
3 I-GENE
( I-GENE
SH3 I-GENE
)- I-GENE
encoding O
, O
expressed O
in O
tumorigenic O
astrocytes O
( O
SETA O
) O
gene O
is O
associated O
with O
astrocyte O
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 O
) O
+ O
N2 O
( O
A O
) O
--> O
N2 O
( O
C O
, O
B O
, O
V O
') O
+ O
N2 O
( O
X O
), O
N2 O
( O
A O
) O
+ O
N2 O
( O
X O
, O
V O
> O
5 O
) O
--> O
N2 O
( O
X O
) O
+ O
N2 O
( O
B O
, O
V O
') O
in O
pure O
N2 O
post O
- O
discharges O
and O
N2 O
( O
A O
) O
+ O
CH4 O
--> O
products O
, O
C O
+ O
N O
+ O
M2 O
--> O
CN O
( O
B O
, O
V O
') O
+ O
M2 O
, O
N2 O
( O
X O
, O
V O
> O
4 O
) O
+ O
CN O
--> O
N2 O
( O
X O
) O
+ O
CN O
( O
B O
, O
A O
, O
V O
'), O
in O
N2 O
- O
1 O
% O
CH4 O
post O
- O
discharges O
. O

BACKGROUND O
/ O
AIMS O
: O
Hepatitis O
C O
and O
nonalcoholic O
fatty O
liver O
disease O
( O
NAFL O
) 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 O
. O

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

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

Can O
survival O
be O
prolonged O
for O
patients O
with O
hormone O
- O
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 O
role O
in O
the O
basal O
expression O
of O
the O
rat O
mrp2 O
gene O
, O
while O
the O
human I-GENE
MRP2 I-GENE
gene I-GENE
is O
regulated O
differently O
. O

Intact O
Flag O
- O
tagged O
protein O
products O
from O
all O
six O
were O
produced O
from O
genomic O
expression O
vectors O
, O
although O
the O
ORF40 O
/ O
41 O
transcript O
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 O
- O
bp O
intron O
. O

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

In O
hypertensive O
nephrosclerosis O
, O
therapy O
containing O
an O
ACEI O
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 O
and O
p65 I-GENE
by O
the O
pull O
- O
down O
assay O
in O
vitro O
and O
by O
a O
coimmunoprecipitation O
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 O
sequences O
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 O
patient O
and O
of O
healthy O
individuals O
. O

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

Copyright O
2001 O
Academic O
Press O
. O

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

We O
suggest O
that O
ventriculopleural O
shunting O
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
- O
abdominal O
adhesions O
or O
with O
a O
history O
of O
recent O
peritoneal O
infection O
. O

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

Doxorubicin O
( O
DOX O
) O
is O
commonly O
used O
for O
the O
treatment O
of O
hematological O
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 O
infants O
had O
a O
2 O
. O
8 O
(- O
1 O
. O
3 O
- O
6 O
. O
8 O
) O
point O
advantage O
in O
Bayley O
motor O
score O
scales O
. O

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

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

Myasthenia O
gravis O
is O
an O
autoimmune O
disease O
resulting O
from O
the O
production O
of O
antibodies O
against O
the O
ACh O
receptors O
of O
the O
neuromuscular O
synapse O
. 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
( I-GENE
CREB I-GENE
)- I-GENE
binding I-GENE
protein I-GENE
to O
down O
- O
regulate O
transcriptional O
activity O
of O
p53 I-GENE
. O

METHODS O
: O
Sixteen O
pigs O
were O
assigned O
randomly O
to O
control O
and O
shock O
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 O
and O
TRA2 O
and O
between O
the O
results O
of O
both O
TRA O
' O
s O
and O
the O
door O
- O
to O
- O
door O
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 O
upstream O
of O
Raf I-GENE
- I-GENE
1 I-GENE
during O
its O
activation O
by O
microtubule O
disruption O
. O

Zhu O
, O
V O
. O

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

This O
supports O
previous O
arguments O
for O
the O
improbability O
of O
biological O
effects O
at O
UHF O
frequencies O
unless O
a O
mechanism O
can O
be O
found O
for O
accumulating O
energy O
over O
time O
and O
space O
and O
focussing O
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 O
containing O
alpha O
subunits O
that O
lacked O
a O
distal O
domain O
( O
term O
- O
3 O
) O
or O
had O
the O
alternatively O
spliced O
alpha I-GENE
- I-GENE
2 I-GENE
distal O
domain O
showed O
markedly O
decreased O
ability O
to O
support O
tyrosine O
phosphorylation O
of O
Jak I-GENE
- I-GENE
2 I-GENE
and O
its O
substrates O
or O
to O
up O
- O
regulate O
CD86 O
. O

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

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

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

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

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

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

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

Alignment O
of O
different O
cDNAs O
of O
the O
NR5A2 O
( O
hB1F O
) O
gene O
with O
the O
genomic O
sequence O
facilitated O
the O
delineation O
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 O
- O
induced O
dissociative O
anesthesia O
produces O
persistently O
elevated O
BIS O
index O
which O
is O
different O
from O
thiamylal O
and O
those O
reported O
with O
other O
conventional O
anesthetic O
agents O
. O

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

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

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

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

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

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

At O
cross O
purposes O
. O

For O
these O
patients O
the O
introduction O
of O
a O
separate O
category O
" O
extended O
oligoarthritis O
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 O
of O
Aspergillus O
fumigatus O
to O
mulundocandin O
, O
an O
echinocandin O
- O
like O
compound O
, O
and O
other O
antifungal O
agents O
was O
assessed O
by O
the O
National O
Committee O
for O
Clinical O
Laboratory O
Standards O
( O
NCCLS O
) O
M38 O
- O
P O
method O
, O
a O
2 O
, O
3 I-GENE
- I-GENE
bis I-GENE
( I-GENE
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 I-GENE
) I-GENE
carbonyl I-GENE
]- I-GENE
2H I-GENE
- I-GENE
tetrazolium I-GENE
hydroxide I-GENE
( O
XTT O
)- O
based O
colorimetric O
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 O
are O
: O
1 O
) O
genetic O
; O
2 O
) O
Epstein I-GENE
- I-GENE
Barr I-GENE
virus I-GENE
( O
infectious O
mononucleosis O
); O
3 O
) O
congenital O
and O
acquired O
immunodeficiency O
; O
4 O
) O
occupational O
exposure O
( O
the O
wood O
industry O
). 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 O
. O

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

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

Although O
metabolized O
by O
the O
cytochrome I-GENE
P I-GENE
- I-GENE
450 I-GENE
( O
CYP O
) O
system O
, O
venlafaxine O
inhibits O
CYP O
2D6 O
and O
3A4 O
to O
a O
far O
lesser O
extent O
than O
do O
the O
SSRIs O
. 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 O
, O
even O
though O
expression O
of O
MKK4 O
was O
strongly O
upregulated O
in O
mkk7 O
(-/-) O
mast O
cell O
lines O
, O
and O
phosphorylation O
of O
MKK4 O
occurred O
normally O
in O
response O
to O
multiple O
stress O
stimuli O
. O

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

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

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

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

Physical O
principles O
in O
therapeutic O
apheresis O
. O

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

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

Systematic O
review O
of O
diagnostic O
tests O
for O
vaginal O
trichomoniasis O
. O

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

Here O
we O
show O
that O
phosphorylation O
- O
induced O
loss O
of O
the O
protein I-GENE
kinase I-GENE
activity O
of O
DNA O
- O
PK O
is O
restored O
by O
the O
addition O
of O
the O
purified O
catalytic O
subunit O
of O
either O
protein I-GENE
phosphatase I-GENE
1 I-GENE
or O
protein I-GENE
phosphatase I-GENE
2A I-GENE
( I-GENE
PP2A I-GENE
) O
and O
that O
this O
reactivation O
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 O
by O
either O
natural O
( O
15d O
- O
PGJ O
( O
2 O
) O
and O
PGD O
( O
2 O
)) O
or O
synthetic O
ligands O
( O
BRL49653 O
and O
troglitazone O
), 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 O
algorithm O
for O
the O
urban O
wastewater O
system O
is O
formulated O
, O
the O
parameters O
of O
which O
are O
optimized O
using O
various O
global O
optimization O
routines O
. O

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

This O
partial O
transection O
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 O
sodium O
concentration O
. O

Reciprocally O
, O
HMGI O
- O
C O
expression O
also O
coordinately O
enhances O
PIAS3 O
- O
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 O
splicing O
and O
close O
promoter O
proximity O
to O
the O
AF1q O
translocation O
gene O
. O

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

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

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

Cytosolic I-GENE
acetyl I-GENE
- I-GENE
CoA I-GENE
synthetase I-GENE
( O
AceCS1 O
) 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 O
binding O
onto O
this O
element O
only O
after O
peptide O
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 O
- O
terminal O
domain O
on O
nucleotide O
binding O
, O
they O
also O
demonstrate O
that O
interactions O
with O
the O
N O
- O
terminal O
domains O
are O
necessary O
to O
inhibit O
proton O
transport O
. O

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

The O
radial O
forearm O
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 O
than O
sternotomy O
. O

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

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

These O
findings O
suggest O
a O
novel O
ankyrin O
- O
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 O
vertigo O
and O
vertigo O
syndromes O
in O
the O
elderly O

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

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

Treatment O
of O
N18TG O
- O
2 O
cells O
with O
a O
demethylating O
agent O
, O
5 O
- O
aza O
- O
deoxycytidine O
, O
resulted O
in O
an O
expression O
of O
mlt O
1 O
, O
indicating O
that O
the O
repression O
of O
mlt O
1 O
is O
attributable O
to O
methylation O
Thus O
, O
mlt O
1 O
is O
a O
novel O
target O
gene O
that O
is O
silenced O
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 O
with O
the O
meso O
- O
striatal O
and O
meso O
- O
corticolimbic O
circuits O
in O
response O
to O
both O
monetary O
reward O
and O
nonmonetary O
reinforcement O
. O

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

For O
this O
purpose O
, O
the O
immediate O
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 O
bone O
anchor O
designs O
( O
a O
smooth O
anchor O
and O
a O
screw O
anchor O
) O
were O
measured O
in O
two O
different O
foams O
( O
used O
to O
simulate O
bone O
) O
with O
different O
densities O
. O

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

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

Activation O
of O
transcription O
through O
the O
AP I-GENE
- I-GENE
1 I-GENE
site I-GENE
in O
Jurkat O
cells O
by O
JunD O
and O
/ O
or O
Fra O
- O
2 O
was O
weak O
. O
c I-GENE
- I-GENE
Jun I-GENE
, O
JunB O
, 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 O
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 O
. O

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

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

Gimpl O
, O
F O
. O

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

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

The O
patients O
and O
their O
families O
were O
closely O
questioned O
, O
and O
full O
clinical O
examination O
included O
a O
test O
for O
orthostasia O
. 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 O
factor O
GAMyb O
, O
which O
is O
itself O
induced O
by O
GA O
. O

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

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

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

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

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

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

Architecture O
and O
anatomy O
of O
the O
genomic O
locus O
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 O
involved O
in O
checkpoint O
signaling O
, O
Rad1 O
, O
Hus1 O
, O
and O
Rad9 O
, O
have O
been O
shown O
to O
interact O
by O
immunoprecipitation O
and O
yeast O
two O
- O
hybrid O
studies O
. O

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

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

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

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

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

For O
the O
sample O
of O
systematic O
reviews O
drawn O
from O
ACP O
Journal O
Club O
( O
n O
= O
103 O
), O
the O
PubMed O
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 O
received O
hepatic O
intra O
- O
arterial O
infusion O
of O
levoforinate O
( O
l O
- O
LV O
) O
250 O
mg O
and O
5 O
- O
fluorouracil O
( O
5 O
- O
FU O
) O
500 O
mg O
for O
combined O
multiple O
hepatic O
metastases O
starting O
on O
postoperative O
day O
14 O
, O
and O
these O
medications O
were O
administered O
over O
48 O
hours O
once O
weekly O
by O
infuser O
pump O
. 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 O
inheritance O
of O
DNAH9 O
alleles O
in O
affected O
individuals O
were O
observed O
. O

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

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

B I-GENE
- I-GENE
myb I-GENE
is O
essential O
for O
G1 O
/ O
S O
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 O
mammalian O
LHbeta O
gene O
, O
the O
5 O
'- O
flanking O
region O
of O
the O
gpLH O
/ O
CGbeta O
gene O
contains O
a O
single O
TATA O
sequence O
37 O
bp O
upstream O
of O
the O
translation O
start O
codon O
. O

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

Indeed O
, O
mutation O
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 O
, O
altered O
the O
differential O
regulation O
of O
sid2 O
by O
iron O
. O

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

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

Novel O
intronic O
promoter O
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 O
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
- O
up O
time O
of O
17 O
months O
was O
6 O
- O
fold O
higher O
in O
the O
highest O
tertile O
for O
CRP I-GENE
and O
IL I-GENE
- I-GENE
6 I-GENE
and O
3 O
. O
5 O
- O
fold O
higher O
in O
the O
highest O
tertile O
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 O
. O

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

However O
, O
the O
promoter O
region O
contains O
several O
potential O
cis O
- O
regulatory O
elements O
such O
as O
Sp1 I-GENE
, O
early I-GENE
growth I-GENE
response I-GENE
- 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 I-GENE
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
( I-GENE
Cdx I-GENE
) I-GENE
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 O
/ O
RGL3 O
resembled O
AF O
- O
6 O
and O
Nore1 O
in O
interacting O
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 O
male O
patients O
undergoing O
thyroid O
surgery O
were O
stratified O
according O
to O
gender O
and O
then O
randomised O
to O
receive O
double O
- O
blind O
one O
of O
four O
antiemetic O
regimes O
: O
50 O
mg O
dolasetron O
given O
orally O
45 O
minutes O
prior O
to O
induction O
of O
anaesthesia O
( O
group O
I O
), O
12 O
. O
5 O
mg O
dolasetron O
given O
intravenously O
during O
induction O
of O
anaesthesia O
( O
group O
II O
), O
1 O
. O
25 O
mg O
DHB O
given O
intravenously O
during O
induction O
of O
anaesthesia O
( O
group O
III O
) O
or O
placebo O
( O
group O
IV O
). O

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