ライフサイエンスコーパス: TTC

1 TTC documents dating from 1989 to 2004/5 were retrieved

2 TTC influenced survival outcomes in the overall study co

3 TTC stain was used to mark infarct areas, which were siz

4 (TTC)n repeat in both expansions and contractions drastic

5 TTC-derived infarct volumes were not significantly diffe

6 TTCs did not, however, make SLT investments until 2002,

7 TTCs were detected in 51% (n = 136) of bottled water sam

8 TTCs' efforts to undermine the FCTC were comprehensive,

9 les were from 11-100, 101-1,000, and > 1,000 TTC/100 mL, respectively compared to < 1 TTC/100 mL.

10 000 TTC/100 mL, respectively compared to < 1 TTC/100 mL.

11 effectively bound and internalized the IGF-1-TTC in vitro.

12 Similarly, IGF-1-TTC injected into skeletal muscles was taken up and retr

13 Three monthly IGF-1-TTC injections into muscles of ageing mice did not incre

14 IGF-1-TTC retains IGF-1 activity as indicated by [(3)H]thymidi

15 complex in muscle fibres injected with IGF-1-TTC, compared to the other groups, suggesting preservati

16 IGF-1:TTC exhibited IGF-1 and TTC activity in vitro; it increa

17 ular- or intrathecal administration of IGF-1:TTC had no significant effect on disease progression or

18 tein resulted in substantial levels of IGF-1:TTC in spinal cord tissue extracts.

19 IGF-1:TTC may prove to be neuroprotective in other animal mode

20 Like rhIGF-1, infusion of IGF-1:TTC reduced levels of IGF-1 receptor immunoreactivity in

21 mbar spinal cords of mice infused with IGF-1:TTC were estimated to be approximately 500-fold higher t

22 tanus toxin fragment C fusion protein (IGF-1:TTC) as a secreted product from insect cells.

23 diarrhea with contamination levels below 11 TTC/100 mL, either in adults or children.

24 that HCN3(+) cells coexpress T-type Ca(2+) (TTC) channels and that TTC channel inhibition with R(-)e

25 rved for the destabilization of the (GAA)2T4(TTC)2T4(CTT)2 triplex to the corresponding Watson-Crick

26 (3-)) or 5,10,15-tris(4-tolyl)corrolate (H(3)TTC(3-))) leads to NO labilization.

27 ropean mutational spectrum, 5'-TCC-3' --> 5'-TTC-3' is known to be the most common somatic mutation p

28 enriched for the transition 5'-TCC-3' --> 5'-TTC-3'.

29 d recognises the symmetrical sequence GAAN(7)TTC.

30 This bioactivity was produced in a TTC-dose dependent manner.

31 Our results demonstrate that ShcV is a TTC for the HopPtoV effector.

32 All TTCs have now invested in snus (and recently in pure nic

33 IGF-1:TTC exhibited IGF-1 and TTC activity in vitro; it increased levels of immunoreac

34 ermeability of the BBB to Evans blue dye and TTC as detected by augmented concentrations of these sub

35 eks the extent of extracellular enhanced and TTC regions were smaller (13.2 +/- 1.4% and 12.0 +/- 1.5

36 iplexes that could be assembled with GAA and TTC strands; the two hybrid duplexes [r(GAA):d(TTC) and

37 rct size determined by (99m)Tc-glucarate and TTC staining (r = 0.96; slope = 0.87).

38 icity in 2 distinct muscle types, as HCN and TTC channels also mediate cardiac pacemaker activity.

39 R imaging (6.6% +/- 0.5 of the LV mass), and TTC staining (7.0% +/- 0.6 of the LV mass).

40 Hemodynamic values were recorded, and TTC staining was used to assess necrosis.

41 istochemistry demonstrated that both TTC and TTC-SOD-1 were distributed in a punctate perineuronal an

42 entrality of evidence to debates over SP and TTCs' history of denying harms and manufacturing uncerta

43 7-Anthraquinone stabilizes (TC)n (CCT)n and (TTC)n, although it has the greatest effect on the latter

44 t analyses with anti-SMN, anti-DTx, and anti-TTC antibodies.

45 t was similar to that of infarcted tissue at TTC staining (mean, 13.6% +/- 6.0; range, 7.8%-30.9%).

46 ATC/TTC haplotype cells significantly increased transmigrati

47 When stimulated with Poly I:C, ATC/TTC haplotype, cells significantly up-regulated the IL-8

48 a provides evidence that carriage of the ATC/TTC haplotype in itself may increase the influx of neutr

49 To test whether ATC/TTC haplotype is functional, we used a trans-well assay

50 We evaluated the association between TTC and survival according to breast cancer subtype and

51 We investigated the association between TTC in drinking water and diarrhea using data from seven

52 patible with NusG bridging and NusA binding (TTC-A, previously termed "expressome").

53 patible with NusG bridging and NusA binding (TTC-B) and reveal how NusG bridges and NusA binds.

54 intramuscular injection, and exhibited both TTC- and IGF-1 activity in the CNS following intrathecal

55 Immunohistochemistry demonstrated that both TTC and TTC-SOD-1 were distributed in a punctate perineu

56 +/-1.8% of LV mass by MRI and 27.5+/-1.7% by TTC (P=NS).

57 nd correlated with infarct volume defined by TTC staining at 24 h after MCAO.

58 ld exist naturally if Phe-508 was encoded by TTC, has wild type-like mRNA structure, and enhanced exp

59 Cerebral infarction was visualized by TTC staining on day 3 post-surgery.

60 or neurone loss, a tetanus toxin fragment-C (TTC) fusion protein was created to target IGF-1 to motor

61 of tetanus toxin (tetanus toxin fragment C, TTC) has been used as a vector to enhance delivery of po

62 exogenous protein (tetanus toxin fragment C; TTC), and a viral vector (recombinant adeno-associated v

63 alleles of HLA-C and CDSN (HLA-Cw6 and CDSN*TTC) were genotyped in 678 families with early-onset pso

64 aplotypes retaining HLA-Cw6 but lacking CDSN*TTC were significantly associated with psoriasis, wherea

65 oriasis, whereas recombinants retaining CDSN*TTC but lacking HLA-Cw6 were not associated, despite goo

66 531 (TCG-->TTG or TTC), and 526 (CAC-->CGC, TTC, AAC, or CAA) demonstrated an association with highe

67 tion next to a candidate type III chaperone (TTC) gene, shcV, and within a pathogenicity island in th

68 cessory proteins called type III chaperones (TTCs) to be secreted via the TTSS.

69 time to initiation of adjuvant chemotherapy (TTC) after definitive surgery is unknown.

70 on via 2,3,5-triphenyl tetrazolium chloride (TTC) staining.

71 he indicator triphenyl tetrazolium chloride (TTC).

72 assessed with triphenyltetrazolium chloride (TTC) staining and a transmission electron microscope (TE

73 with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining for stroke volume measurement.

74 Triphenyltetrazolium chloride (TTC) staining indicated that pretreatment with MANF sign

75 determined by triphenyltetrazolium chloride (TTC) staining versus (99m)Tc-glucarate imaging ex vivo.

76 ized by 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (H&E) staining, the ter

77 ents by 2,3,5-triphenyltetrazolium chloride (TTC) staining.

78 staining with triphenyltetrazolium chloride (TTC) was used to confirm and quantify heterogeneous micr

79 Triphenyltetrazolium chloride (TTC) was used to delineate infarctions at postmortem.

80 lood flow and triphenyltetrazolium chloride (TTC)-stained tissue samples for infarct assessment by us

81 with 2, 3, 5-triphenyltetrazolium chloride (TTC).

82 arly as measured by thermotolerant coliform (TTC) bacteria, a WHO-approved indicator of drinking wate

83 scherichia coli or thermotolerant coliforms (TTC) were included provided they associated results with

84 er was assayed for thermotolerant coliforms (TTC), an indicator of faecal contamination.

85 t log reduction in thermotolerant coliforms (TTCs) ( - 0.66 log10 TTC most probable number/100 mL), f

86 isease-free survival, and time to colostomy (TTC) with pretreatment and treatment variables.

87 opposed by transnational tobacco companies (TTCs) whose responses to the UK government's public cons

88 r examines transnational tobacco companies' (TTCs') efforts to influence policy there, paying particu

89 ms to explore transnational tobacco company (TTC) interests in SLT and pure nicotine in Europe from t

90 ia coli transcription-translation complexes (TTCs) containing different-length mRNA spacers between R

91 h EFSA's toxicological threshold of concern (TTC) and sum of oligomers approaches were applied.

92 sing the threshold of toxicological concern (TTC) approach.

93 rm daily threshold of toxicological concern (TTC) of 1.5 mug/g and the potential for quantitative ana

94 s (SML) and threshold toxicological concern (TTC) recommended values according to the Cramer classifi

95 Targeted (227)Th conjugates (TTCs) represent a new class of therapeutic radiopharmace

96 iated by transnational tobacco corporations (TTCs) to try to undermine the proposed convention.

97 inbred lines (RILs) and a triple test cross (TTC), the latter produced by crossing the RILs to Col, L

98 n repeat expansion during replication of a d(TTC)n repeat template.

99 In the collapsed R-loops, antiparallel d(TTC+).d(GAA):r(UUC) is unstable, while parallel d(GAA).r

100 is unstable, while parallel d(GAA).r(GAA):d(TTC) and d(GA+A).r(GAA):d(TTC) are stable.

101 C strands; the two hybrid duplexes [r(GAA):d(TTC) and d(GAA):r(UUC)] in an R-loop; and three hybrid t

102 el d(GAA).r(GAA):d(TTC) and d(GA+A).r(GAA):d(TTC) are stable.

103 and antiparallel protonated d(GA+A).d(GAA):d(TTC) triplexes are stable.

104 Delayed TTC was particularly detrimental among patients with tri

105 the first dose of chemotherapy, and delayed TTC was defined as 91 or more days from surgery to the f

106 FS) estimates were similar for the different TTC categories.

107 C linked to the enzyme superoxide dismutase (TTC-SOD-1).

108 HopO1-1 secretion and translocation and each TTC was able to bind the other's cognate effectors in ye

109 highly profitable) cigarettes while ensuring TTCs' long-term future should cigarette sales decline fu

110 e tumor diameter independently predicted for TTC (P = .008).

111 bilize the (TTC)6.(GAA)6 composite function (TTC)6 triplex.

112 analyses of (TTC)6.(GAA)6 composite function(TTC)6 triplex detected ions due to both triplex and sing

113 and formation of triplex DNA at expanded GAA TTC repeats have been shown to regulate the FXN gene sil

114 of heterochromatin at the long expanded GAA TTC repeats, which is enriched in hypoacetylated histone

115 to the pUC control DNA) and that the GAA GAA TTC triplex further lowers the nucleosome assembly effic

116 ylation on the GAA TTC duplex or the GAA GAA TTC triplex has been measured in vitro.

117 ments for the GAA TTC duplex and the GAA GAA TTC triplex, and on the effect of histone acetylation, t

118 ved from the human FXN gene, and the GAA GAA TTC triplex, were examined for their ability to assemble

119 ng the formation of nucleosome arrays on GAA TTC-containing plasmids, the triplex structure was shown

120 In this study, GAA TTC repeating DNAs derived from the human FXN gene, and

121 irst direct binding measurements for the GAA TTC duplex and the GAA GAA TTC triplex, and on the effec

122 onstitution assays demonstrated that the GAA TTC duplex excludes nucleosomes (53% decrease compared t

123 the effect of histone acetylation on the GAA TTC duplex or the GAA GAA TTC triplex has been measured

124 Expansion of a GAA . TTC repeat in the first intron of the frataxin (FXN) gen

125 molecular model of FRDA by inserting 560 GAA*TTC repeats into an intron of a GFP reporter minigene.

126 s and number of tracts (one or two) of a GAA*TTC repeat in Escherichia coli to evaluate the in vivo r

127 of FRDA mutations involve expansion of a GAA*TTC-repeat tract in intron 1, which leads to an FXN mRNA

128 eletions as observed for the CTG*CAG and GAA*TTC repeats.

129 prior work demonstrated that CTG*CAG and GAA*TTC triplet repeats (responsible for DM1 and Friedreich'

130 We previously showed that cloned (GAA*TTC)n sequences replicated in Escherichia coli are more

131 The expanded GAA*TTC repeat sequence associated with Friedreich's ataxia

132 Most FRDA patients have expanded GAA*TTC repeats (up to 1700 triplets), which inhibit the tra

133 We examined instability of the expanded (GAA*TTC)(n) sequence in mammalian cells by analyzing individ

134 ion in Friedreich ataxia is an expanded (GAA*TTC)n sequence, which is highly unstable in human somati

135 edreich ataxia is caused by an expanded (GAA*TTC)n sequence, which is unstable during intergeneration

136 The GFP_(GAA*TTC)(560) minigene recapitulates the molecular hallmarks

137 ion, increase the expression of the GFP_(GAA*TTC)(560) reporter.

138 quence unaffected and (iii) heterozygous GAA*TTC expansion carriers with approximately 50% decrease o

139 plasmids by the association of two long GAA*TTC tracts at lengths that are found in the sequence of

140 ia (FRDA) is caused by hyperexpansion of GAA*TTC repeats located in the first intron of the FXN gene,

141 Replication of (GAA*TTC)n sequences (9-105 triplets) in plasmids propagated

142 othesized that genetic stability of the (GAA*TTC)n sequence may require efficient RecA-dependent reco

143 eplication is known to occur within the (GAA*TTC)n sequence when GAA is the lagging strand template,

144 ect of DSB repair on instability of the (GAA*TTC)n sequence.

145 echanism for genetic instability of the (GAA*TTC)n sequence.

146 echanism for genetic instability of the (GAA*TTC)n sequence.

147 Based on the knowledge that a GAA.TTC repeat expansion in the first intron of FXN induces

148 ents is the unstable hyperexpansion of a GAA.TTC triplet repeat in the first intron of the frataxin g

149 as evaluated following replication of a (GAA.TTC)115 sequence in transfected COS1 cells under the con

150 eating tracts of CTG.CAG, CCTG.CAGG, and GAA.TTC are integral to the etiology of myotonic dystrophy t

151 The capacity of (CTG.CAG)n and (GAA.TTC)n repeat tracts in plasmids to induce mutations in D

152 linked pyrrole-imidazole polyamides bind GAA.TTC tracts with high affinity and disrupt the intramolec

153 diseases caused by expansion of CTG.CAG, GAA.TTC, or CGG.CCG repeat tracts.

154 Expanded GAA.TTC repeats result in decreased transcription and reduce

155 edreich ataxia is caused by an expanded (GAA.TTC)n sequence in intron 1 of the FXN gene.

156 yeast and reporter construct models for GAA.TTC triplet-repeat expansion have been reported, studies

157 These studies suggest that in FRDA, GAA.TTC triplet-repeat instability occurs in embryonic cells

158 locus-specific differences for genomic (GAA.TTC)n sequences.

159 However, GAA.TTC triplet repeats were stable in FRDA fibroblasts and

160 shRNA silencing of MSH2 and MSH6 impeded GAA.TTC triplet-repeat expansion.

161 er characterized the role of MutSbeta in GAA.TTC expansion using a functional assay in primary FRDA p

162 Thus, despite its essential role in GAA.TTC expansion, MSH2 is not an attractive therapeutic tar

163 RNA.DNA hybrids have a potential role in GAA.TTC tract instability and in the mechanism underlying re

164 opic expression of MSH2 and MSH3 induced GAA.TTC repeat expansion in the native FXN gene.

165 d ataxia caused primarily by an intronic GAA.TTC triplet repeat expansion in the frataxin (FXN) gene.

166 During propagation of the iPSCs, GAA.TTC triplet repeats expanded at a rate of about two GAA.

167 DNA conformation of genes harboring long GAA.TTC repeats or by chromatin opening.

168 e sticky-DNA conformation formed by long GAA.TTC repeats.

169 c property of transcription through long GAA.TTC tracts.

170 ity on the genetic instabilities of long GAA.TTC, CGG.CCG, and CTG.CAG repeat sequences was studied i

171 In this model, GAA.TTC repeats expand incrementally and continuously.

172 rapeutic target to slow the expansion of GAA.TTC repeats in the future.

173 ard cross-linking studies on a family of GAA.TTC-containing plasmids showed the presence of sticky DN

174 es extensive RNA.DNA hybrid formation on GAA.TTC templates in bacteria as well as in defined transcri

175 mall pool PCR analysis showed that pure (GAA.TTC)44+ sequences at the FXN locus are unstable in somat

176 fied three other genomic loci with pure (GAA.TTC)44+ sequences.

177 DNAs containing a pair of direct repeat GAA.TTC sequences.

178 expansion of the triplet-repeat sequence GAA.TTC within the first intron of the FXN gene.

179 pansions of the triplet-repeat sequence (GAA.TTC) cause transcriptional repression of the Frataxin ge

180 n smaller, so-called 'pre-mutation' size GAA.TTC repeats, that do not cause disease, but are prone to

181 knockdown of either MSH2 or MSH3 slowed GAA.TTC expansion in our system.

182 ic pyrrole-imidazole polyamide targeting GAA.TTC triplet-repeat DNA partially blocked repeat expansio

183 AG.CTG repeat expansion, its role in the GAA.TTC expansion of Friedreich ataxia (FRDA) is less clear.

184 sis is that structures formed within the GAA.TTC repeat during transcription attract DNA repair enzym

185 he gene expression signatures due to the GAA.TTC repeat expansion in FRDA neuronal cells and the effe

186 ated the expansions and deletions of the GAA.TTC repeats.

187 es that differ only in the length of the GAA.TTC repeats.

188 rrests in the promoter distal end of the GAA.TTC tract and an extensive RNA.DNA hybrid is tightly lin

189 tudy the mechanism of instability of the GAA.TTC triplet repeats in the human genome.

190 essentially inert, as observed for the (GAA.TTC)176-containing plasmid.

191 tion of the SV40 origin relative to the (GAA.TTC)n sequence, we noted either no instability, predomin

192 repeats expanded at a rate of about two GAA.TTC triplet repeats/replication.

193 Expansion of an unstable GAA.TTC repeat in the first intron of the FXN gene causes Fr

194 ee of frataxin reduction correlates with GAA.TTC tract length, but the mechanism of reduction remains

195 The formation of a GAA/TTC DNA triplex has been implicated in Friedreich's atax

196 the discovery of agents that destabilize GAA/TTC triplexes and as general methods for the characteriz

197 del system, we demonstrate that expanded GAA/TTC repeats represent a threat to eukaryotic genome inte

198 Expansion of triplex-forming GAA/TTC repeats in the first intron of FXN gene results in F

199 Triplex structure-forming GAA/TTC repeats pose a dual threat to the eukaryotic genome

200 In model systems, long GAA/TTC tracts also act as chromosomal fragile sites that ca

201 The destabilization of GAA/TTC DNA triplexes either by pH or by binding to appropri

202 chanisms that regulate the metabolism of GAA/TTC repeats are poorly understood.

203 ms can mediate detrimental metabolism of GAA/TTC tracts in human cells.

204 We suggest that the mechanism of GAA/TTC-induced chromosomal aberrations defined in yeast can

205 there are a number of other polymorphic GAA/TTC loci in the human genome where the size variations t

206 Expansion of the GAA/TTC repeats in the first intron of the FXN gene causes F

207 Like GDNF, addition of GDNF:TTC to culture media of neuroblastoma cells expressing G

208 intramuscular injection, mice receiving GDNF:TTC revealed intense GDNF immunostaining associated with

209 esent in the purified conjugate sample, GDNF:TTC, had a molecular weight of approximately 80 kDa as d

210 That GDNF:TTC provided neuroprotection of axotomized motor neurons

211 xamination of one signal, an increased TCC-->TTC mutation rate in Europeans, indicates a burst of mut

212 ctively, these data demonstrate that HCN3(+)/TTC(+) cells are the pacemakers that set the origin and

213 C3000; these operons encode three homologous TTCs, ShcO1, ShcS1, and ShcS2.

214 ion provides insights into the nature of how TTCs function.

215 Factors associated with delays in TTC included low socioeconomic status, breast reconstruc

216 iarrhea increased for each log10 increase in TTC/100 mL by 18% (95% CI: 11, 26%) for children < 5 yea

217 re also inhibited by Bacillus sp. strains in TTC presence, to a lesser extent.

218 ave failed, and little evidence was found in TTCs' corporate materials that snus is central to their

219 gs with contemporary documentation including TTC investor presentations.

220 uorescence microscopy revealed that injected TTC was not retained solely in a restricted deposit alon

221 (sum of areas with lacking and intermediate TTC staining) was similar among all six groups.

222 distribution was confirmed using HRP-labeled TTC with electron microscopy along with localization wit

223 ntitative fluorimetry, we found that labeled TTC showed vastly superior retention within brain tissue

224 Neurological evaluation and ischemic lesion (TTC stain) were assessed at 24 hours of reperfusion.

225 ermotolerant coliforms (TTCs) ( - 0.66 log10 TTC most probable number/100 mL), followed by boiling wi

226 bgroup analysis according to subtype, longer TTC caused patients with triple-negative breast cancer t

227 Maximum TTC and TBC were up to 25.5 and 16.6 mug/g (fresh weight

228 ion households than controls (geometric mean TTC count of 50 [95% CI 44-57] per 100 ml compared to 12

229 a from available field studies that measured TTC levels in household-drinking water and reported prev

230 orts the evaluation of the mesothelin (MSLN)-TTC conjugate (BAY 2287411) in combination with several

231 ther, in vivo antitumor efficacy of the MSLN-TTC in combination with ATRi or PARPi was investigated i

232 evaluated the antitumor efficacy of the MSLN-TTC in combination with DDR inhibitors in human ovarian

233 anism-based rationale for combining the MSLN-TTC with DDR inhibitors as new treatment strategies in M

234 d on cancer cell lines by combining the MSLN-TTC with inhibitors of ataxia telangiectasia mutated, at

235 n by the suffix "i") when combined with MSLN-TTC.

236 in the Friedreich ataxia-associated (GAA)n*(TTC)n repeats from the FRDA gene that were cloned with f

237 To follow the effects of (GAA)n*(TTC)n repeats on gene expression, we have chosen E. coli

238 (GAA)n*(TTC)n repeats were cloned into bacterial plasmids in bot

239 sm seems less likely for the AT-rich (GAA)n*(TTC)n repeats.

240 , and were decreased by cholesterol; neutral TTC partitioned into membranes more strongly than the pr

241 by investing in snus, and recently nicotine, TTCs have eliminated competition between cigarettes and

242 Instead, a 3-nucleotide (TTC) deletion in the MLH1 3'-UTR was found in the patien

243 nd tax structures are an important aspect of TTC competitiveness.

244 of a recombinant fusion protein comprised of TTC linked to the enzyme superoxide dismutase (TTC-SOD-1

245 pport for health-based targets for levels of TTC in drinking water and for interventions to improve d

246 d risk of diarrhea with increasing levels of TTC in drinking water.

247 resulted in a substantial overestimation of TTC-defined infarct volume and a lower inter-observer re

248 nodal status and sex were not predictive of TTC.

249 ty against pathogens only in the presence of TTC, suggesting a biotransformation of nitrogenous compo

250 ettles was associated with a reduced risk of TTC contamination [risk ratio (RR) = 0.25, p < 0.001] an

251 ch to examine the conceptual significance of TTC critiques.

252 The existence of TTCs that can bind to dissimilar effectors and that can

253 Structures of TTCs containing longer spacers reveal a new state compat

254 Structures of TTCs containing short spacers show a state incompatible

255 The mass spectrometric analyses of (TTC)6.(GAA)6 composite function(TTC)6 triplex detected i

256 Volumetric calculation based on TTC-derived infarct also correlated significantly strong

257 nfarct size of the left ventricle (% IAR) on TTC staining was smaller in IR30 (49.2 +/- 4.3) than in

258 There is clear evidence of past and ongoing TTC influence over tobacco advertising and excise policy

259 ged controls injected with saline, IGF-1, or TTC.

260 tetanus toxin (tetanus toxin fragment C, or TTC).

261 in codons 523 (GGG-->GCG), 531 (TCG-->TTG or TTC), and 526 (CAC-->CGC, TTC, AAC, or CAA) demonstrated

262 A Phe377 (TTC(1130-1132)) deletion in exon 9 of the pyrophosphate

263 ependent pretreatment variable that predicts TTC and 5-year colostomy rate in patients with anal carc

264 two spectrally distinct isomers, presumably TTC and TTT cis-trans isomers, for the open-ring merocya

265 We hypothesized that prolonged TTC would be associated with adverse outcomes.

266 Estetrol and ShERPA TTC-352 are being evaluated in clinical trials.

267 ly, positioning of normal- and carrier-size (TTC)n repeats into the sense strand for transcription le

268 from short priming sequences such as 3'-TCC, TTC, and TTT, and the consensus sequence is 3'-Pu(Py)2-3

269 ence intensity of membrane-bound tetracaine (TTC) on solution pH.

270 he complexation of Fe(II) with tetracycline (TTC), oxytetracycline (OTC), or chlorotetracycline (CTC)

271 xpress T-type Ca(2+) (TTC) channels and that TTC channel inhibition with R(-)efonidipine or NNC55-039

272 We conclude that TTC may be a useful vector to enhance neuronal delivery

273 These results indicate that TTC can serve as a non-viral vehicle to substantially im

274 We propose that TTC-B mediates NusG- and NusA-dependent transcription-tr

275 came more affordable post-accession and that TTCs have taken advantage of low excise duties by raisin

276 Interview data suggest that TTCs enjoy high-level political support and continue to

277 ating the global application of tactics that TTCs have previously been found to have employed nationa

278 in edible organs at concentrations above the TTC value should be categorized as contaminants of emerg

279 The majority of oligomers were below the TTC (90 ug/person/day), but the limit value of 50 ug/kg

280 Our data show that the TTC value of lamotrigine can be reached for a child at a

281 The TTCs' claim that SP will not lead to public health benef

282 ting ligand acridine orange destabilize the (TTC)6.(GAA)6 composite function (TTC)6 triplex.

283 Third, TTCs engaged in 'evidential landscaping', promoting a pa

284 mes were estimated and compared according to TTC and by BC subtype.

285 e categorized into three groups according to TTC: </= 30, 31 to 60, and >/= 61 days.

286 A single point mutation (TCC to TTC; Ser to Phe) was identified in Lec23 Gcs1 cDNA and g

287 A repair, thereby increasing the response to TTCs.

288 cent to areas of 2,3,5-triphenyltetrazolium (TTC)-negative tissue, normally associated with infarcted

289 24 hour 2,3,5-triphenyltetrazoliumchloride (TTC)-derived infarct volumes.

290 We purposively selected and analysed two TTC submissions using a verification-oriented cross-docu

291 cted for infarct size (IS) measurement using TTC staining.

292 rm the haplotype-I (Hap-I), whereas variants TTC constitute Hap-II.

293 ge at diagnosis was 53 years, and median was TTC was 46 days.

294 Analogous to the case with TTC, intrathecal infusion of the fusion protein resulted

295 ately assess infarct size when compared with TTC staining.

296 ution produced an excellent correlation with TTC-defined infarct volume and inter-observer reliabilit

297 ions showed similar robust correlations with TTC-defined infarct volumes for both groups using previo

298 vidence of adverse outcomes among those with TTC of 31 to 60 or 60 to 90 days.

299 he 1970s to the present, comparing them with TTCs' public claims of support for harm reduction.

300 The expansion of the GAA x TTC tract in intron 1 to as many as 1700 repeats elicits