1 elomeric oligonucleotide 5'-d[AGGGTTAG(8)G(
9)
GTT AG(14)G(15)GTTAGGGTGT]-3'.
2 ch nondiabetic control subjects were given
a GTT.
3 elective antagonist to WT mice resulted in
a GTT profile that mirrored that of Ucn 2-null mice.
4 > CCA at amino acid 576, and the other was
a GTT deletion at amino acid 560.
5 iedreich ataxia, as well as for ATT, CCT
and GTT repeats.
6 predictor of mortality in both diabetes
and GTT population samples.
7 triplet repeat sequences (GTA.TAC, GAT.
ATC,
GTT.AAC, CAC.GTG, AGG.CCT, TCG.CGA, and AAG.CTT), and th
8 subunit; H156Y-beta (CAT to TAT), V69G-
beta (
GTT to GGT), IVS 9 del[-7:-4], and 1109 ins 8bp (exon 10
9 bi from native blood using the point-of-
care GTT can identify ACS patients at risk of future cardiac
10 d glucose and slowed glucose disposal
during GTTs.
11 d variants were determined to contain
either GTT or TGACTGTT sequence, in lieu of 20,214 or 18,895 bp
12 r sequential or combination chemotherapy
for GTT.
13 No deaths
from GTT have occurred later than 2 years after the end [corr
14 -binding site (MBS) sequence (YG(A/G)C(A/C/
G)
GTT(G/A)).
15 d the Myb-binding site (MBS) [YG(A/G)C(A/C/
G)
GTT(G/A)].
16 a-inhibitory aptamer oligonucleotide, 5'-
GGG GTT GGT TGT GTT GGG TGT TGT GT, as a model system.
17 Oligonucleotide 5'-
GGG GTT GGT TGT GTT GGG TGT TGT GT-RNH2 (oligo I) blocks mul
18 ' splice site mutation in intron 24, GGT --&
gt;
GTT (maternal allele), and a new 3' splice site mutation
19 Epm2b-/- mice also showed no differences
in GTTs and ITTs.
20 by action of ppGaNTase-T1 on MUC5AC (
mainly GTT(GalNAc)PSPVPTTSTT(GalNAc)SAP), additional incorporat
21 Neither TTG
nor GTT start codons, inferred for several genes of other ne
22 increased insulin area under curve (AUC)
on GTT compared with MTPa+/+ littermates.
23 were noted on other clinical parameters (
PD,
GTT, KG, GI, and PI).
24 ast to Pot1pN, tandem trinucleotide
repeats (
GTT) within d(GGTTACGGTTAC) are specifically recognized
25 ly toxic regimen for patients with high-
risk GTT who become refractory to or relapse from EMA/CO chem
26 otal of 272 consecutive women with high-
risk GTT, including 121 previously treated patients, were tre
27 ive and well-tolerated regimen for high-
risk GTT.
28 onths led to similar weight gain and
similar GTT and ITT responses.
29 We used the global thrombosis
test (
GTT) to assess thrombotic and thrombolytic status in 300
30 was evaluated using glucose tolerance
test (
GTT) and insulin tolerance test (ITT).
31 g an intraperitoneal glucose tolerance
test (
GTT).
32 ype 2 diabetes and glucose-tolerance-
tested (
GTT) multiethnic population samples.
33 n sensitivity using glucose tolerance
tests (
GTTs) and hyperinsulinemic-euglycemic clamps in mouse mo
34 d no differences in glucose tolerance
tests (
GTTs) or insulin tolerance tests (ITTs) compared with wi
35 Using glucose-tolerance
tests (
GTTs), insulin-tolerance tests (ITTs), and hyperinsuline
36 aptamer oligonucleotide, 5'-GGG GTT GGT
TGT GTT GGG TGT TGT GT, as a model system.
37 Oligonucleotide 5'-GGG GTT GGT
TGT GTT GGG TGT TGT GT-RNH2 (oligo I) blocks multiple IFN-ga
38 CHCl3@3, and CHCl3@4 complexes, whereas
the GTT conformation was found the most favorable for the CH
39 of synthetic Ucn 2 to mutant mice before
the GTTs and ITTs restored blood glucose to WT levels.
40 obing depth (PD), gingival tissue
thickness (
GTT), and width of keratinized gingiva (KG) were assesse
41 from the same patient (at codon 525; ATT
to GTT, isoleucine to valine).
42 Applying the same protocol
to GTT, NTL9, and protein G suggests that some beta contain
43 herapy for gestational trophoblastic
tumors (
GTT).
44 The survival for patients
with GTT is 30 (88%) out of 34 patients and four (50%) out of