ライフサイエンスコーパス: CST

1 CST (-/-)x GalNAc-T (-/-) mice develop normally to postn

2 CST deficiency increases MRE11 binding to stalled forks,

3 CST first aids in duplication of the telomeric dsDNA.

4 CST improved QoL in patients with HF.

5 CST resembles Replication Protein A (RPA) in that the tw

6 CST resulted in greater improvements in QoL compared wit

7 CST was identified as a direct inhibitor of CaMKIIdelta

8 age (standard deviation): 12.87 m (+/-4.5), CST wiring: 9 contralateral, 9 ipsilateral, 6 bilateral)

9 Participants were randomized to either a CST intervention or heart failure education, both delive

10 re-association of individual OB-folds allow CST to mediate loading and unloading of partner proteins

11 structure metrics varied substantially along CST and OR.

12 (OR, 3.59; 95% CI, 2.22-5.80; P < .001) and CST less than 300 microm (OR, 5.30; 95% CI, 2.40-11.67;

13 ommunity state type (CST)-IVA (P = .005) and CST-IVB (P = .018) as well as PTB (P = .049).

14 endent protein kinase IIdelta) activity, and CST reduced CaMKIIdelta-dependent phosphorylation of pho

15 FAZ area and CST did not differ significantly between groups (P > 0.0

16 k 24, the mean changes from week 12 BCVA and CST were +7.0 letters (P = .01) and -108.25 mum (P = .04

17 outcomes were correlations between BCVA and CST, and between BCVA and 4 central subfield EZ grades.

18 from baseline to 24 weeks for both BCVA and CST, Pearson correlation coefficients were: ME from RVO,

19 For baseline BCVA and CST, Pearson correlation coefficients were: ME from RVO,

20 Best-corrected visual acuity (BCVA) and CST were measured at baseline and every 4 weeks.

21 duration of diabetes, HbA1c, BMI, BCVA, and CST had no impact on the ability to achieve >/=2-step im

22 , telomerase-mediated G-strand extension and CST-mediated C-strand fill-in are equally important for

23 naive DMO with VA between 35-54 letters and CST of 400 um or more when aflibercept is used as the co

24 Mean VA at M01 was 63.2 letters, and CST was 299.7 mum.

25 One-year VA and CST outcomes within prespecified subgroups based on both

26 fied subgroups based on both baseline VA and CST thresholds, defined as worse (20/50 or worse) or bet

27 reverted epigenetic changes and antagonized CST.

28 More studies are needed to apply CST on evaluating corneal biomechanics after refractive

29 oned blocks of spinal cord, we also assessed CST-YFP mice for 3D imaging and found that YFP fluoresce

30 Baseline CST and number of injections were not predictive (P >= 0

31 Baseline CST and RVO diagnosis were the only significant predicto

32 utcome measure was mean change from baseline CST at week 12.

33 At week 12, mean change from baseline CST was significantly greater in the combination group (

34 With lower baseline CST, a trend of decreased baseline and 24-week change co

35 eline VA (n = 305), irrespective of baseline CST, aflibercept showed greater improvement than bevaciz

36 ally to loading dose than eyes with baseline CST of 400 um or more (n = 104, p = 0.02), indicating th

37 Patients with baseline CST of less than 400 um (n = 96) responded less well fun

38 .16 letters; P = 0.0005, with baseline BCVA, CST, and age as covariates).

39 rimotor functional connectivity seemed to be CST-dependent rather than specific from all the uCP popu

40 ard deviation): 14.54 (+/-4.8)), and between CST-wiring patterns.

41 and premotor cortices, whereas the bilateral CST group showed higher connectivity between M1 and soma

42 acuity changes beyond what was explained by CST.

43 Stratification by CST SD demonstrated a 10-letter difference in 12-month V

44 HF and whether the CgA fragment catestatin (CST) may directly influence cardiomyocyte function.

45 st was used to determine the change in CDVA, CST, intraocular pressure, and hard exudate area over ti

46 In cells, CST is recruited to telomeric and non-telomeric chromati

47 To clarify CST mechanism, we examined the capacity of CST to bind a

48 (crym-GFP), comprehensive and near complete CST labeling is achieved throughout the spinal cord.

49 ome reveals how the telomere capping complex CST maintains linear but not circular chromosomes.

50 otoneuronal connections from fast conducting CST fibers are indeed made exclusively from new M1 and i

51 onal connections over more slowly conducting CST axons, as well as exert disynaptic effects on motone

52 n the dominant hemisphere, the contralateral CST group showed increased connectivity between M1 and p

53 xcitatory transmission in the contralesional CST.

54 gaging the intrinsic mechanisms that control CST regrowth, it remains to be tested whether such metho

55 and epigenetic factors integrate to control CST and paves the way for the development of novel antim

56 dorsal hemisection in the midthoracic cord, CST axons did not significantly regenerate in ngr1(+/+)

57 Despite these correlations, CST and EZ integrity, as graded herein, account for the

58 eighbour along-strike faults where coseismic CST is greatest.

59 ult system is >+/-50 bars, whereas coseismic CST is <+/-2 bars, so the latter will rarely overwhelm t

60 of 15 or more, change from baseline in CST, CST less than 300 microm, and resolution of ME.

61 rate that Coulomb pre-stress (the cumulative CST from multiple earthquakes and interseismic loading o

62 s studies have evaluated caregiver-delivered CST.

63 We derive CSTs from multivariate canopy structure data, illustrati

64 This newly developed CST can detect five typical periodontal pathogens with a

65 High-diversity CSTs and specific bacterial phyla (Gardnerella vaginalis

66 Within the non-Lactobacillus-dominant CST IV, GBS positive status was significantly more preva

67 Severity of macular thickening (i.e., CST) was associated significantly with macular leakage i

68 ups (controls vs. uCP; and controls vs. each CST-wiring group).

69 ellen measurements, amount of retinal edema (CST) did: increased CST correlated with increased variab

70 c variables such as extent of retinal edema (CST) may have a meaningful impact on the anticipated var

71 s, most YFP-labeled axons beyond established CST locations do not undergo Wallerian degeneration foll

72 For CST, 2 clinical trials for each disorder were analyzed.

73 x structures, thus providing a mechanism for CST to facilitate replication through telomeres and othe

74 rall, our findings indicate a novel role for CST in maintaining genome integrity through resolution o

75 f human CTC1 and demonstrate that functional CST is essential for telomere length maintenance due to

76 an be used as a standardized tool for future CST spinal cord injury studies.

77 ractions between sulfatide and gangliosides, CST (-/-) and GalNAc-T (-/-) genotypes were interbred.

78 llen equivalent, 20/44]; P = 0.001), greater CST (523.8+/-32 mum vs. 345.9+/-11.8 mum; P < 0.001), we

79 tical early transcriptomic responses in host CST neurons.

80 associated with the change in VALS; however, CST was a more important predictor.

81 Human CST (CTC1-STN1-TEN1) is a ssDNA-binding complex that hel

82 Human CST (CTC1-STN1-TEN1) is an RPA-like complex that associa

83 cryo-electron microscopy structure of human CST bound to telomeric single-stranded DNA (ssDNA), whic

84 Here, we report that human CST (CTC1-STN1-TEN1) proteins, which form a single-stran

85 All treatment groups demonstrated improved CST during follow-up.

86 gain of 15 or more, change from baseline in CST, CST less than 300 microm, and resolution of ME.

87 re was minimal correlation between change in CST and change in VA at 4 months (r = - 0.27), suggestin

88 At 12 months, the mean change in CST and MV were -133.9 (+/- 160.12) mum (P = .0001) and

89 measures included determining the change in CST, median number of injections, proportion gaining 15

90 Corresponding changes in CST were -46.8 vs. +2.6 mum (P = 0.0683) in the overall

91 virally expressed Channelrhodopsin (ChR2) in CST cell bodies and in axon terminals in cervical spinal

92 urden, yet experienced a greater decrease in CST (-197.8+/-45.3 mum vs. -51.7+/-14.7 mum; P = 0.005).

93 roups revealed no significant differences in CST (359.9 +/- 108.3 mum and 335.4+/-94.6 mum, respectiv

94 D imaging and found that YFP fluorescence in CST-YFP mice is faint for clearing-based 3D imaging in c

95 Greater improvement in CST was seen in the active versus control group (ITT pop

96 -3-methanol, promotes further improvement in CST-dependent behavioral tasks.

97 trength training; there were no increases in CST responses.

98 e status was significantly more prevalent in CST IV-A than CST IV-B.

99 Mean reductions in CST from baseline were 153 mum versus 18 mum (P < 0.001)

100 roup had clinically meaningful reductions in CST relative to baseline (PropBL: 0.77, 0.61, and 0.54,

101 .87% CI, 0.56-0.86) had larger reductions in CST than PTA (P < 0.0001).

102 mab resulted in dose-dependent reductions in CST, improvements in DRSS score, and longer time to re-t

103 roperty were derived from the values seen in CSTs, and a flagging system is proposed to identify nonc

104 ry and exploratory outcome measures included CST, Diabetic Retinopathy Severity Scale (DRSS) score, a

105 amount of retinal edema (CST) did: increased CST correlated with increased variability.

106 dicators included increasing age, increasing CST, the presence of intraretinal fluid, pigment epithel

107 In line with CaMKIIdelta inhibition, CST reduced Ca(2+) spark and wave frequency, reduced Ca(

108 re the cumulative coseismic and interseismic CST is positive, although there are notable examples whe

109 The potential to classify ecosystems into CSTs based on suites of structural traits represents an

110 connectivity of the sensorimotor network is CST-wiring-dependent, although the impact on upper limb

111 ions beyond those with anterogradely labeled CST axons, most YFP-labeled axons beyond established CST

112 d thicker maculae at baseline, showed larger CST reductions after 12 months of treatment.

113 d in the PC (-11.98%, p = 0.006) and lateral CST (-12.96%, p = 0.014).

114 unctional independence and FA in the lateral CST (z score 3.68, p = 0.020).

115 Mean CST at week 12 and percentage of eyes with resolved edem

116 Mean CST decreased from baseline to 5 years by 154 mum (95% C

117 ants to have a substantial reduction in mean CST between 1 and 2 years were those with a baseline VA

118 The mean VA, mean CST, and mean MV at baseline were 54.4 (+/- 15.26) lette

119 m of minimum angle of resolution, and median CST improved from 397 to 236 mum.

120 8 logMAR; P = .015) and insignificant median CST change (from 223.34 +/- 21.1 mum to 249.12 +/- 19.24

121 Vaginal microbiota CST and alpha-diversity are not related to GBS status.

122 /=400 microm) or thinner (250 to 399 microm) CST.

123 Mean baseline and 12-month CST were 488.6 +/- 165.0 mum and 334.3 +/- 131.9 mum (ch

124 dition to sulfatide-dependent loss of NF155, CST (-/-) x GalNAc-T (-/-) mice exhibited a major reduct

125 diate zone and motor nuclei for RST, but not CST, stimulation.

126 fundus photographs have no DME based on OCT CST, while many eyes diagnosed as not having DME or CSME

127 photography, while treatment of DME uses OCT CST.

128 VA, OCT CST, and macular volume (MV) were recorded at baseline a

129 spinal fibers but spared approximately 3% of CST fibers that project via the dorsolateral funiculus.

130 ion in vitro, and the DNA-binding ability of CST is required for blocking MRE11-mediated nascent-stra

131 nses resulted from optogenetic activation of CST terminals, demonstrating the ability of Sox11-stimul

132 de novo, reveals the overall architecture of CST and the DNA-binding anchor site.

133 y CST mechanism, we examined the capacity of CST to bind and resolve DNA structures found at sites of

134 caused by mutations in the CTC1 component of CST, which promotes polymerase alpha (polalpha)/primase-

135 ways to engineer target-specific control of CST connections to promote recovery.

136 deprive the left side of the spinal cord of CST input, and the right CST was treated with adeno-asso

137 treatment caused robust midline crossing of CST axons into previously denervated left spinal cord.

138 Mapping of the distribution of CST-evoked spinal activity revealed overall similarity b

139 r, the overall architecture and functions of CST and RPA are distinct.

140 brain neurons leading to genetic labeling of CST axons in the spinal cord, and it was suggested that

141 The detection limit of CST revealed 1.2 x 10(4) for Treponema denticola (T.d.)

142 king sites, allowing allosteric mediation of CST decamer assembly.

143 wed reductions of 299.6 mum and 355.2 mum of CST on SD OCT.

144 The similarities in NoR phenotype of CST (-/-), GalNAc-T (-/-), and axo-glial protein-deficie

145 osis were the only significant predictors of CST SD (CRVO vs. BRVO: +34.64 mum/100 mum [95% CI, 29.33

146 s to robust CST regrowth and the recovery of CST-dependent behavioral performance after both T10 late

147 Here we examine the remodeling of CST axons directed by sensory fibers.

148 tion enables prediction of the remodeling of CST connections and spinal circuits after injury and inf

149 ts with acute HF, and the functional role of CST was explored in experimental models.

150 and resolve DNA structures found at sites of CST activity.

151 CST-YFP mice would be useful for studies of CST regeneration.

152 -/-) phenotype was fully restored to that of CST (-/-) mice by neuron-specific expression of complex

153 h Network eligibility criteria thresholds of CST for trials evaluating anti-vascular endothelial grow

154 tors 53BP1, RIF1, REV7-Shieldin (SHLD1-3) or CST-DNA polymerase alpha (Pol-alpha) in BRCA1-deficient

155 ide (cerebroside sulfotransferase knock-out, CST (-/-)) or complex gangliosides (beta-1,4-N-acetylega

156 ropose that CP is caused by a defect in POT1/CST-dependent telomere fill-in.

157 luid (OR, 2.15; 95% CI, 1.06-4.40) predicted CST <=250 mum.

158 baseline subretinal fluid modestly predicted CST <=250 mum (OR, 1.08; 95% CI, 1.00-1.16).

159 ubjects older than 40 years, and progressive CST FA reductions can be identified on 18-month follow-u

160 In addition, purified CST complex binds to 5' DNA overhangs and directly block

161 rently, NPC-treated mice displayed a reduced CST degeneration, increased axonal rewiring, and augment

162 50 or worse at baseline, bevacizumab reduced CST less than the other agents at 1 year, but at 2 years

163 y neuron activity reveals that the regrowing CST axons select their postsynaptic partners in a compet

164 x largely distinct and functionally relevant CSTs.

165 the spinal cord of CST input, and the right CST was treated with adeno-associated virus (AAV)-Sox11

166 n (OPN), in cortical neurons leads to robust CST regrowth and the recovery of CST-dependent behaviora

167 gion of the reorganizing dorsal horn; (2) S1 CST and primary afferent inputs connect in different way

168 Our findings show that the affected S1 CST sprouts well beyond its normal range in response to

169 ary sprouting of the primary afferent and S1 CST populations into an overlapping region of the reorga

170 r tracer injection placement to determine S1 CST termination patterns within the cord.

171 aptogenesis was also assessed for labeled S1 CST terminals within the dorsal horn.

172 ration; and (3) there is a loss of larger S1 CST terminal boutons in the affected dorsal horn, but no

173 model spinal cord injury, we asked if the S1 CST response is conserved in rodents.

174 The S1 CST sprouting response is particularly dramatic, indicat

175 subcomponent of the corticospinal tract (S1 CST), and is critically important in modulating sensory

176 l column lesion (DRL/DCL), both motor and S1 CSTs sprout well beyond their normal terminal range.

177 uential recruitment of RIF1 and the shieldin-CST-POLalpha complex(2).

178 antagonists of the 53BP1/RIF1/REV7/Shieldin/CST pathway.

179 s opposed to FTD) also exhibited significant CST FA reduction at baseline.

180 ty afforded by crym-GFP revealed significant CST regeneration in NgR1 knock-out mice.

181 The summary score of Corvis ST (CST) after SMILE was comparable to FS-LASIK/LASIK with t

182 r Response Analyzer (ORA) and the Corvis ST (CST) measured the corneal biomechanical changes before a

183 s, to assess the ability of Sox11-stimulated CST axons to functionally integrate in the circuitry of

184 n of functional synapses by Sox11-stimulated CST axons without significant behavioral benefit, sugges

185 r telomerase has extended the G-rich strand, CST facilitates fill-in synthesis of the complementary C

186 However, the impact of such CST-wiring on functional connectivity remains unknown.

187 he neurite density in the bilateral superior CST.

188 The CTC1-STN1-TEN1 (CST) complex is essential for telomere maintenance and r

189 STN1, a member of the human CTC1-STN1-TEN1 (CST) complex, thus linking this gene for the first time

190 a newly developed chairside bacterial test (CST) for the most relevant periodontal pathogens.

191 ignificantly more prevalent in CST IV-A than CST IV-B.

192 Here, we demonstrate that CST binds and unfolds G4 with similar efficiency to RPA.

193 Finally, smFRET analysis indicates that CST binding to ssDNA is dynamic with CST complexes under

194 d synaptogenesis post-lesion, indicates that CST terminal sprouting following a central sensory lesio

195 We show that CST binds preferentially to ss-dsDNA junctions, an activ

196 We also show that CST unfolds G-quadruplex structures, thus providing a me

197 We previously showed that CST binds and disrupts G-quadruplex (G4) DNA in vitro, s

198 Our results suggest that CST inhibits MRE11 binding to reversed forks, thus antag

199 uadruplex (G4) DNA in vitro, suggesting that CST may prevent in vivo blocks to replication by resolvi

200 The decameric structure suggests that CST can organize ssDNA analogously to the nucleosome's o

201 Finally, we uncover that CST complex inactivation exacerbates genome instability

202 The CST (-/-) x GalNAc-T (-/-) phenotype was fully restored

203 The CST (CTC1-STN1-TEN1) complex mediates critical functions

204 t difference in the IOP with the ORA and the CST pre and postoperatively in either group.

205 In human cells, the CST complex (CTC1-STN1-TEN1) also functions in telomere

206 In each case, we contextualize the CST distribution against a snapshot of the human antibod

207 In regard to the clinical diagnosis, the CST assay and the qPCR method reached a sensitivity of 8

208 e appears to be little contribution from the CST.SIGNIFICANCE STATEMENT We provide the first report o

209 Collectively, our findings identify the CST complex as an important fork protector that preserve

210 on and ATM regulation, two components of the CST (CTC1-STN1-TEN1) complex involved in preventing telo

211 , we quantified tissue microstructure of the CST and OR with the neurite orientation dispersion and d

212 A conserved biochemical function of the CST complex is its primase-Pol alpha (PP) stimulatory ac

213 to an embryonic transcriptional state of the CST neuron.

214 was reduced in the extensive regions of the CST, the corpus callosum and the right PCG.

215 ce, resulting in abnormal decussation of the CST.

216 As with primates, the CST in rats originates from multiple (albeit fewer) cort

217 Using crym-GFP, we reevaluated the CST in mice lacking nogo receptor 1 (NgR1), a protein im

218 We found that the CST projection is regulated dynamically in maturity by t

219 aseline and month 12 (P = 0.79), whereas the CST significantly decreased at month 12 compared with ba

220 tural changes associated with ALS within the CST and precentral gyrus (PCG) 'in vivo'.

221 DDI demonstrates that axonal loss within the CST is a core feature of degeneration in ALS.

222 hase-I clinical-stage antibody therapeutics (CSTs) and calculate in silico metrics to estimate their

223 Cognitive stimulation therapy (CST) is a well-established group psychosocial interventi

224 spinal cord, and it was suggested that these CST-YFP mice would be useful for studies of CST regenera

225 haviors: 1) the continuous shear-thickening (CST) and discontinuous shear-thickening (DST) behavior o

226 , in the subgroup with better VA and thicker CST at baseline (31-43 eyes), there was a suggestion of

227 for eyes with better initial VA and thicker CST, some VA outcomes may be worse in the bevacizumab gr

228 -treated patients with worse BCVA or thicker CST experienced >/=2-step DRSS score improvement compare

229 offs for VA and central sub-field thickness (CST).

230 letters, central subfield macular thickness (CST) >/=350 mum on Topcon 3D OCT 2000, initiated on a lo

231 oup of eyes with central subfield thickness (CST) >=300 mum at baseline (12.2 [n = 13] vs. 2.1 [n = 7

232 Central subfield thickness (CST) analysis was done.

233 aseline (PropBL) central subfield thickness (CST) at 8 weeks (CST at 8 weeks/CST at baseline) assesse

234 from baseline in central subfield thickness (CST) at week 24.

235 as difference in central subfield thickness (CST) between the control group and the treatment lapse g

236 tomography (OCT) central subfield thickness (CST) can yield different prevalence rates for DME.

237 om baseline mean central subfield thickness (CST) in the 2.0-mg versus 0.5-mg group (396.1 vs. 253.5

238 generation using central subfield thickness (CST) measurements and then correlate these findings with

239 owed a change in central subfield thickness (CST) of -504.1 mum and -552.3 mum, respectively.

240 h 6-month VA and central subfield thickness (CST) outcomes in participants in the Study of Comparativ

241 in VA change and central subfield thickness (CST) reduction were, respectively, +1 letter (1.4 letter

242 included if the central subfield thickness (CST) was >300 mum and corrected distance visual acuity (

243 cuity (BCVA) and central subfield thickness (CST) were prospectively recorded in 40 eyes of 39 CRVO p

244 nd the change in central subfield thickness (CST) were significantly associated with the change in VA

245 ve and change in central subfield thickness (CST) within subgroups based on whether an eye received l

246 l acuity (BCVA), central subfield thickness (CST), and DRSS score.

247 l acuity (BCVA), central subfield thickness (CST), and ellipsoid zone (EZ) integrity in macular edema

248 absence of DME, central subfield thickness (CST), and subretinal fluid.

249 Central subfield thickness (CST), cube volume (CV), and cube average thickness (CAT)

250 zone (FAZ) area, central subfield thickness (CST), macular ganglion cell-inner plexiform layer (GC-IP

251 nth 24 (M24) for central subfield thickness (CST), subretinal fluid, intraretinal fluid, vitreoretina

252 assessed for (1) central subfield thickness (CST); (2) presence of vitreomacular adhesion, vitreomacu

253 ge from baseline central subfield thickness (CST, mum) at week 12 in Group 1 vs 2 was -100.8 vs -63.9

254 omic parameters (central subfield thickness [CST], intraretinal fluid [IRF], or subretinal fluid [SRF

255 In the subgroup with better VA and thinner CST at baseline (61-73 eyes across 3 treatment groups),

256 pared with those with better BCVA or thinner CST, respectively, but these associations were not stati

257 average of 162 of the 6000 labeled thoracic CST axons (2.68%) regenerated >100 mum past the lesion s

258 lyses showed that participants randomized to CST experienced a reduction in the composite end point o

259 der anesthesia mapped potential responses to CST and RST stimulation in the cervical enlargement of t

260 CgA-to-CST conversion in HF is impaired because of hyperglycosy

261 Low CgA-to-CST conversion was also associated with increased mortal

262 d microstructure of the corticospinal tract (CST) and the optic radiation (OR), the primary motor out

263 ally ablated the dorsal corticospinal tract (CST) containing approximately 96% of corticospinal fiber

264 Corticospinal tract (CST) degeneration and cortical atrophy are consistent fe

265 ompanied by significant corticospinal tract (CST) fractional anisotropy (FA) reductions.

266 that the anatomy of the corticospinal tract (CST) is abnormal in patients with NTN1-mutant CMM.

267 The corticospinal tract (CST) is the major descending pathway controlling volunta

268 The corticospinal tract (CST) is the most important motor system in humans, yet r

269 ofiling specifically of corticospinal tract (CST) motor neurons in mice, to identify their 'regenerat

270 ncreases axon growth by corticospinal tract (CST) neurons after spinal injury.

271 nections come only from corticospinal tract (CST) neurons in the subdivision of primary motor cortex

272 limited rewiring of the corticospinal tract (CST) only partially compensates the lost functions after

273 wth of the axons in the corticospinal tract (CST) that originate in the motor cortex and innervate th

274 within the ipsilesional corticospinal tract (CST), and an enhanced NMDA-mediated excitatory transmiss

275 mary motor cortex (M1), corticospinal tract (CST), and reticulospinal tract (RST).

276 y for motor skills, the corticospinal tract (CST), sprout after brain or spinal cord injury.

277 iption maintain nascent corticospinal tract (CST)-relay neuron contacts.

278 rebral palsy (uCP), the corticospinal tract (CST)-wiring patterns may differ (contralateral, ipsilate

279 rpus callosum (CC), and corticospinal tract (CST).

280 f brain injury (smaller corticospinal tract [CST] injury), cortical function (greater ipsilesional mo

281 rity of PC and lateral corticospinal tracts (CST).

282 of a telephone-based coping skills training (CST) intervention.

283 explain with simple Coulomb stress transfer (CST) because it is common for seismicity to circumvent n

284 or cells and promoted cell state transition (CST).

285 d with diverse vaginal community state type (CST)-IVA (P = .005) and CST-IVB (P = .018) as well as PT

286 all vaginal microbiota community state type (CST).

287 of Lactobacillus spp. (community state type-CST IV) with increasing disease severity, irrespective o

288 raits, characterise canopy structural types (CST) and evaluate drivers and functional consequences of

289 ants were composed of community state types (CSTs) showing diversity (20/51; 39%) or predominated by

290 vely, in four and two community state types (CSTs), where most profiles were dominated by Lactobacill

291 Currently, the mechanism underlying CST action at diverse replication issues remains unclear

292 Using CST, the deformation amplitude and HC peak distances inc

293 ree well with the numerical simulation using CST's Microwave Studio(R).

294 central subfield thickness (CST) at 8 weeks (CST at 8 weeks/CST at baseline) assessed with OCT by mas

295 d thickness (CST) at 8 weeks (CST at 8 weeks/CST at baseline) assessed with OCT by masked readers.

296 ange, -154.3 +/- 210.2 mum; P < 0.001), with CST SD of 114.1 +/- 77.0 mum.

297 Samples were analyzed with CST and results (positive signals for every pathogen/con

298 es that CST binding to ssDNA is dynamic with CST complexes undergoing concentration-dependent self-di

299 = 104, p = 0.02), indicating that eyes with CST >= 400 um is another inclusion criteria.

300 um (P = 0.1317) in the subgroup of eyes with CST >=300 mum at baseline, respectively.

301 rtical dendritic changes occur together with CST axonal damage.