ライフサイエンスコーパス: shine

1 teric control of proteins provides a tool to shine a light on the complex cascades of cellular proces

2 We shine a spotlight on his seminal work describing how the

3 We shine a spotlight on how this work has inspired the deve

4 Here we shine a spotlight on the calcitonin and PACAP (PAC(1)) r

5 e parallel epidemics of obesity and diabetes shine a spotlight on the potential for therapeutic manip

6 ctural reconstruction mechanism in this work shines a light on new materials and structural design th

7 e scale research in marine biology, but also shines a new light on big biology, suggesting new ways t

8 This collaborative review shines a spotlight on technologies that will be crucial

9 A lively musical shines a stylized spotlight on Marie Curie's extraordina

10 A particular focus is placed on shining a light on challenges in glyco-data handling, co

11 compatible with statistical decision theory, shining a new light on the old questions of how such jud

12 The COVID-19 pandemic is shining a spotlight on the field of immunology like neve

13 nano-bioreplicated surfaces were verified by shining a white laser on the decoys in a dark room and p

14 The COVID-19 pandemic has shone a bright light on the weaknesses in US infectious

15 the physical world, recent decoding work has shone a light on how the brain instantiates internally g

16 the southern hemisphere illuminated by Pluto-shine and also images taken during the approach phase th

17 A mechanism proposed by Shine and Dalgarno (SD), focused on the base pairing of

18 riophage T4 gene 25 contains three potential Shine and Dalgarno sequences: SD1, SD2 and SD3.

19 is(p-tolyl)-1,2-dioxin (1g) was suggested by Shine and Zhao as a product in an electron-transfer (ET)

20 tes when the illumination light periodically shines at the junction/interface of materials.

21 th cases the crystals take the form of black shining blades and are indistinguishable by optical micr

22 nous x-ray sources (ULXs) in nearby galaxies shine brighter than any x-ray source in our Galaxy.

23 kable rates and active galactic nuclei (AGN) shone brightly as a result of accretion onto black holes

24 ralis and its specialist brood parasite, the shining bronze-cuckoo Chalcites lucidus in New Caledonia

25 e IYCF and WASH interventions implemented in SHINE caused clinically important improvements in child

26 in MYH6 accounting for approximately 11% of Shone complex, and dominant FLT4 mutations accounting fo

27 These include a Shine Dalgarno (SD)-like sequence, a slippery sequence o

28 Such sequences include the Shine- Dalgarno ribosome-binding site, as well as other

29 erved helix/loop 70 of 23S rRNA and the anti-Shine-Dalgarno (aSD) sequence of 16S rRNA.

30 one AAG) that surround and overlap the trpP Shine-Dalgarno (S-D) sequence and translation start codo

31 leading to extended interaction between the Shine-Dalgarno (SD) and anti-SD sequences compensate for

32 d downstream of the initiation codon, called Shine-Dalgarno (SD) and downstream box (DB) sequences, r

33 tif in the 5' UTR of toxT, with a fourU anti-Shine-Dalgarno (SD) element that base pairs with the SD

34 like 70S ribosome complex containing an 8-bp Shine-Dalgarno (SD) helix was determined at 3.8-A resolu

35 Shine-Dalgarno (SD) motifs are thought to play an import

36 The relationship between this Shine-Dalgarno (SD) region and the binding of ribosomes

37 ndent RNA structure that sequesters the trpE Shine-Dalgarno (SD) sequence (the SD blocking hairpin).

38 not bind mRNA with the wild-type, canonical Shine-Dalgarno (SD) sequence and (iii) minimally interac

39 signals: a slippery sequence (A AAA AAG), a Shine-Dalgarno (SD) sequence and a downstream hairpin.

40 A, resulting in the sequestering of the anti-Shine-Dalgarno (SD) sequence and freeing the SD for tran

41 karyotic genomes between the presence of the Shine-Dalgarno (SD) sequence and other gene features, in

42 to many mRNAs through base pairing with the Shine-Dalgarno (SD) sequence and RNA binding by ribosoma

43 rearrangement in the RNA that sequesters the Shine-Dalgarno (SD) sequence by pairing with a complemen

44 structural rearrangement that sequesters the Shine-Dalgarno (SD) sequence by pairing with an anti-SD

45 DNA sequencing uncovered a mutation in the Shine-Dalgarno (SD) sequence for gIIp, a protein involve

46 (5'-GAGGAGG-3') that resemble the consensus Shine-Dalgarno (SD) sequence found at translation initia

47 ventionally leadered lacZ with and without a Shine-Dalgarno (SD) sequence in Escherichia coli and fou

48 RNAs by forming a duplex that sequesters the Shine-Dalgarno (SD) sequence or start codon and prevents

49 regulation originates from occlusion of the Shine-Dalgarno (SD) sequence upon ligand binding; howeve

50 bosome to a translational start site are the Shine-Dalgarno (SD) sequence within the untranslated lea

51 reason for inefficient translation is a weak Shine-Dalgarno (SD) sequence, AGG(G).

52 onstrate that, in the absence of an upstream Shine-Dalgarno (SD) sequence, PoTC breakdown proceeds in

53 t sequesters a sequence complementary to the Shine-Dalgarno (SD) sequence, thus freeing the SD sequen

54 sembled on an mRNA with and without a strong Shine-Dalgarno (SD) sequence-a sequence found just upstr

55 n the RF2 gene (prfB) involves an intragenic Shine-Dalgarno (SD) sequence.

56 upstream of the initiation codon, called the Shine-Dalgarno (SD) sequence.

57 spI, and is located 11 bases upstream of the Shine-Dalgarno (SD) sequence.

58 terial ribosome to the partially overlapping Shine-Dalgarno (SD) sequence.

59 ed by a 4- to 6-mer adenosine/guanosine-rich Shine-Dalgarno (SD) sequence.

60 Members of this phylum naturally lack Shine-Dalgarno (SD) sequences in their mRNA, and yet the

61 uctures with various stabilities and contain Shine-Dalgarno (SD) sequences of different strengths.

62 teractions with the 3' end of 16S rRNA, mRNA Shine-Dalgarno (SD) sequences positioned upstream of ope

63 rial lineages such as the Bacteroidetes lack Shine-Dalgarno (SD) sequences, and yet with few exceptio

64 y RNAs would be predicted to occlude the rot Shine-Dalgarno (SD) site and to block rot translation.

65 ficiency and cis-regulatory features such as Shine-Dalgarno (SD) strength and RNA secondary structure

66 frameshifting in translation of dnaX mRNA: a Shine-Dalgarno (SD)-like sequence, a double-shift site,

67 (stem-loop) and two others mapped just 5' to Shine-Dalgarno (SD)-like sequences located immediately u

68 ound E-site tRNA and the Shine-Dalgarno-anti-Shine-Dalgarno (SD-aSD) interaction on A-site tRNA inter

69 The role of the Shine-Dalgarno blocking hairpin in controlling translati

70 R, including the terminator 5'-stem-loop and Shine-Dalgarno blocking hairpins, demonstrated 5'-tripho

71 NA (mRNA/rRNA elements forming the bacterial Shine-Dalgarno duplex) also resembles elements of the ba

72 und in yeast, calling into question the anti-Shine-Dalgarno effect's role in ribosome pausing.

73 t the espADB leader region contains a strong Shine-Dalgarno element (SD2) and a translatable mini-ORF

74 mRNA translation not only by binding to the Shine-Dalgarno element but also by base pairing anywhere

75 state in which its T-loop base pairs to the Shine-Dalgarno element of the mRNA.

76 mobilities of features interacting with the Shine-Dalgarno helix are decreased in the presence of th

77 ting the proposal that that formation of the Shine-Dalgarno helix during initiation may contribute to

78 The Shine-Dalgarno helix is bound in a large cleft between t

79 o helix are decreased in the presence of the Shine-Dalgarno helix, supporting the proposal that that

80 s an untranslated leader with a conventional Shine-Dalgarno homology.

81 less stringent in the RF2 context, as if the Shine-Dalgarno interaction can help stabilize a quasi-st

82 Increasing the strength of the Shine-Dalgarno interaction with 16S rRNA at the gene VII

83 540 and 1541 (E. coli numbering) in the anti-Shine-Dalgarno mRNA binding sequence.

84 ons because they terminate either within the Shine-Dalgarno or coding sequence of the next gene on th

85 signal extracted by computer analysis was a Shine-Dalgarno pattern matching the complementary sequen

86 nd formed 70S ribosomes, to release the anti-Shine-Dalgarno region and prevent translation.

87 epA on ARD is related to the sequence of the Shine-Dalgarno region.

88 nscript lacking a 5'-untranslated region and Shine-Dalgarno ribosome binding site.

89 site shows little homology to the canonical Shine-Dalgarno ribosome recognition sequence, but the re

90 Archaeal genomes feature a strong Shine-Dalgarno ribosome-binding motif more pronounced in

91 nism to compensate for the lack of a classic Shine-Dalgarno rRNA interaction in the translation of so

92 ely), followed by stop codon context and the Shine-Dalgarno sequence (3.7-5.1% and 1.9-3.8%, respecti

93 tiary KL interaction directly sequesters the Shine-Dalgarno sequence (i.e., the ribosome binding site

94 preQ(1)-binding pocket through the adjoining Shine-Dalgarno sequence (SDS) and include A-minor motifs

95 Conversely, the Shine-Dalgarno sequence (SDS) in the S2 helix of each st

96 sequence in the 3' end of the 16S rRNA (anti-Shine-Dalgarno sequence [aSD]).

97 nce element upstream of the start codon (the Shine-Dalgarno sequence [SD]) and a complementary sequen

98 ion by CsrA involves binding directly to the Shine-Dalgarno sequence and blocking ribosome binding.

99 ture is achieved in the presence of both the Shine-Dalgarno sequence and DB.

100 ations in CsrA binding sites overlapping the Shine-Dalgarno sequence and initiation codon partially r

101 that this translation initiates from a weak Shine-Dalgarno sequence and is facilitated by a putative

102 ocessing occurs just upstream of a consensus Shine-Dalgarno sequence and results in the removal of 54

103 a stem-loop structure upstream of the CC3461 Shine-Dalgarno sequence and stabilizes the transcript.

104 d charged-tRNA(Trp) deficiency to expose the Shine-Dalgarno sequence and start codon for the AT prote

105 d two dipeptide coding minigenes between the Shine-Dalgarno sequence and start codon of ycbK.

106 and stimulates translation by releasing the Shine-Dalgarno sequence and start site from a stable sec

107 d CsrA prevents ribosome binding to the glgC Shine-Dalgarno sequence and that this reduces GlgC synth

108 omes were identified, the "AGGA" core of the Shine-Dalgarno sequence and the "A-rich" sequence locate

109 tain fragmented operator sites such that the Shine-Dalgarno sequence and the initiation codon of the

110 inding to a 19 nt RNA hairpin containing the Shine-Dalgarno sequence and the initiation codon of the

111 sumptive TRAP binding site overlaps the yhaG Shine-Dalgarno sequence and translation initiation regio

112 d a hairpin structure that can sequester the Shine-Dalgarno sequence are necessary for cobalamin-depe

113 age site in C ACCU maps just before the anti-Shine-Dalgarno sequence at the 3' end of 16S rRNA.

114 the leader nucleotides just upstream of the Shine-Dalgarno sequence but is conflicted on the questio

115 epended also on ribosome binding to a nearby Shine-Dalgarno sequence but was independent of downstrea

116 get site of glgC that lies upstream from the Shine-Dalgarno sequence did not affect regulation by HD-

117 anslation as independent elements, e.g., the Shine-Dalgarno sequence in prokaryotes, the rRNA-binding

118 ort that three-base substitutions around the Shine-Dalgarno sequence in the 159-base 5'-untranslated

119 ed expression in the absence of a leader and Shine-Dalgarno sequence indicated that stimulation by CA

120 target (translational operator), but that a Shine-Dalgarno sequence is not required for specificity.

121 A operator sites, including one in which the Shine-Dalgarno sequence is positioned 4 nt outside the c

122 otes refolding of the RNA such that the trpE Shine-Dalgarno sequence is sequestered in a hairpin, thu

123 proximal to regulatory features such as the Shine-Dalgarno sequence is sufficient to enable regulati

124 t abolish the structure without altering the Shine-Dalgarno sequence itself.

125 d TUP resulting from a G-->A mutation in the Shine-Dalgarno sequence of gene II.

126 otential CsrA binding site that overlaps the Shine-Dalgarno sequence of hfq, a gene that encodes an R

127 o analyzed the 350-bp region upstream of the Shine-Dalgarno sequence of norA by gel mobility shift ex

128 of 3-methyl-3-buten-1-ol by engineering the Shine-Dalgarno sequence of nudB, which increased protein

129 pseudoknot, occur to sequester the putative Shine-Dalgarno sequence of the RNA only after metabolite

130 tion regulates the accessibility of the secA Shine-Dalgarno sequence on secM secA mRNA.

131 bstantial number of genes overlap either the Shine-Dalgarno sequence or the coding sequence of the ne

132 By mutating either the Shine-Dalgarno sequence or the start codon, we find that

133 The trpG Shine-Dalgarno sequence overlaps the stop codon of the u

134 ether with the contribution of 16S rRNA anti-Shine-Dalgarno sequence pairing with GAG, facilitates pe

135 , different segments of the single consensus Shine-Dalgarno sequence serve the two translational star

136 -terminal region immediately upstream of the Shine-Dalgarno sequence that contributes to formation of

137 Addition of an untranslated lac leader and Shine-Dalgarno sequence to cI increased expression but s

138 Addition of an untranslated leader and Shine-Dalgarno sequence to the cat coding sequence incre

139 tends to be compensated by mutations in the Shine-Dalgarno sequence towards a stronger translation i

140 mRNA) contained the frameshifting signals: a Shine-Dalgarno sequence, a slippery sequence, and a down

141 ted region of the psbA mRNA that disrupt the Shine-Dalgarno sequence, acting as a ribosome binding si

142 inding sites, one of which overlaps the cstA Shine-Dalgarno sequence, as predicted.

143 modimer to the 5'UTR of an mRNA occludes the Shine-Dalgarno sequence, blocking ribosome access for tr

144 e found either in or upstream of the gene II Shine-Dalgarno sequence, but still within the mRNA trans

145 des of the mRNA, immediately upstream of the Shine-Dalgarno sequence, explains the protein's role in

146 close to the AUG, including over a potential Shine-Dalgarno sequence, have little effect on Fis prote

147 n RNA hairpin at a distance of 9 nt from the Shine-Dalgarno sequence, implying that a discrete region

148 its stop codon, it blocks the adjacent rtpA Shine-Dalgarno sequence, inhibiting AT synthesis.

149 ryotes, whereas the CCUCC, known as the anti-Shine-Dalgarno sequence, is conserved in noneukaryotes o

150 otes refolding of the RNA such that the trpE Shine-Dalgarno sequence, located more than 100 nucleotid

151 re resistant to viomycin indicating that the Shine-Dalgarno sequence, or other features contained wit

152 Because the recJ gene lacks a canonical Shine-Dalgarno sequence, other unknown features of the m

153 This stalling exposes the rtpA Shine-Dalgarno sequence, permitting AT synthesis.

154 econdary stem-loop structure that blocks the Shine-Dalgarno sequence, preventing ribosome access and

155 in the absence of an untranslated leader and Shine-Dalgarno sequence, the streptomycete cat mRNA is t

156 by binding to a site that overlaps the trpG Shine-Dalgarno sequence, thereby blocking ribosome bindi

157 airing with a short sequence overlapping the Shine-Dalgarno sequence, thereby blocking ribosome bindi

158 One of these sites overlaps the glgC Shine-Dalgarno sequence, whereas the other CsrA target i

159 erlaps with that of the messenger RNA (mRNA) Shine-Dalgarno sequence, which prevents the interaction

160 not formation and, in turn, sequestering the Shine-Dalgarno sequence.

161 faster rate than phage bearing the wild-type Shine-Dalgarno sequence.

162 d segment of nhaR, one of which overlaps the Shine-Dalgarno sequence.

163 nitiation codon, one of which overlapped its Shine-Dalgarno sequence.

164 tes, with one of these sites overlapping the Shine-Dalgarno sequence.

165 er transcript, one of which overlaps the hag Shine-Dalgarno sequence.

166 ranslational enhancer (TE) located 5' to the Shine-Dalgarno sequence.

167 egion located immediately preceding the rtpA Shine-Dalgarno sequence.

168 thereby blocking ribosome access to the glgC Shine-Dalgarno sequence.

169 contained an exact match that overlapped its Shine-Dalgarno sequence.

170 at is facilitated by ribosome binding to the Shine-Dalgarno sequence.

171 acent RNA to the 3' side, which contains the Shine-Dalgarno sequence.

172 tential RNA secondary structure overlaps the Shine-Dalgarno sequence.

173 , the latter of which would occlude the secA Shine-Dalgarno sequence.

174 of >50 codons or the presence of an upstream Shine-Dalgarno sequence.

175 oded by 25t and the first adenine within the Shine-Dalgarno sequence.

176 zing stem-loop structures that sequester the Shine-Dalgarno sequence.

177 Shine-Dalgarno sequences (SD) in prokaryotic mRNA facili

178 rocessed equally by RegB; those found at the Shine-Dalgarno sequences and in intercistronic regions a

179 utation of 27 rare codons and five secondary Shine-Dalgarno sequences in the cDNA.

180 Loss of good Shine-Dalgarno sequences might then have fixed the fusio

181 SgrS binding sites overlapping the Shine-Dalgarno sequences of adiY and folE mRNAs suggest

182 and targets mostly (but not exclusively) the Shine-Dalgarno sequences of early genes.

183 ferential translation of specific mRNAs, the Shine-Dalgarno sequences of which do not play a critical

184 hia coli mRNAs, particularly those with weak Shine-Dalgarno sequences or structured 5' UTRs, in addit

185 e 3' end of the 16S ribosomal rRNA (internal Shine-Dalgarno sequences), there is an increased probabi

186 s with structured standby sites, upstream of Shine-Dalgarno sequences, and show that these interactio

187 t the deep learning models learn to identify Shine-Dalgarno sequences, deprioritize the wobble positi

188 We describe in detail programs for finding Shine-Dalgarno sequences, resources used for confident i

189 ferent translational stages: (i) initiation, Shine-Dalgarno sequences, start codon identity, and star

190 ing profiling on ribosomes with altered anti-Shine-Dalgarno sequences, we reveal a genome-wide correl

191 with structured 5'-ends, or with no or weak Shine-Dalgarno sequences.

192 mitochondrial mRNAs, which lack typical anti-Shine-Dalgarno sequences.

193 genes are positively correlated with strong Shine-Dalgarno signal sequences.

194 secondary structure: a loop with projecting Shine-Dalgarno site and well-defined stem that interacts

195 y of a hairpin stem comprising the coat gene Shine-Dalgarno site was incrementally increased, there w

196 /G-any nucleotide) often associated with the Shine-Dalgarno translation initiation sequence in mRNAs.

197 e pair with the 3'end of 16 S rRNA (the anti-Shine-Dalgarno) to enhance frameshifting.

198 iple sources, sequence motifs (promoters and Shine-Dalgarno), microarray data, multi-genome alignment

199 s appear not to use a ribosome-binding site (Shine-Dalgarno)-based mechanism for translation initiati

200 Instead, Shine-Dalgarno-(SD)-like features within coding sequence

201 sed on the role of bound E-site tRNA and the Shine-Dalgarno-anti-Shine-Dalgarno (SD-aSD) interaction

202 The RNA exit tunnel of RNAP aligns with the Shine-Dalgarno-binding site of the 30S subunit.

203 y programmed into the coding sequence, where Shine-Dalgarno-like elements trigger elongation pauses a

204 It is suggested that the Shine-Dalgarno-like interaction elevates frameshifting s

205 In this issue of Neuron, Shine et al. (2016) describe a possible mechanism respon

206 In the 1970s China was a shining example of health development, but no longer.

207 n the premature aging disorder Progeria is a shining example of the impact that studies of rare disea

208 ote with admiration how she leaves us with a shining example to emulate.

209 As a result, the nanoparticle shines >30 times brighter than state-of-the-art organic

210 SHINE has the potential to be used outside of hospitals

211 d integrated longitudinal intervention for a SHINE household as it expects (during pregnancy) and the

212 The WASH interventions implemented in SHINE (improved pit latrine, hand-washing stations, liqu

213 connection between the points of light that shine in the night sky and the diffuse and abundant cell

214 ve fragment ion series, UniSpec particularly shines in generating more complex MS2 spectra with diver

215 Information visualization shines in this type of exploratory analysis, motivating

216 We hypothesize that the impact of SHINE interventions on child stunting and anemia will be

217 will increase understanding of the impact of SHINE interventions, and the generalizability of our fin

218 SHINE is a proof-of-concept, 2 x 2 factorial, cluster-ra

219 SHINE is a randomized trial evaluating shorter treatment

220 Medical Research Council and others; SHINE ISRCTN number, ISRCTN63579542.).

221 By shining laser light through a nanomechanical beam, we me

222 s approaches that we and others have used to shine light into these previously dark corners of the hu

223 Herein, we shine light on CPs and MOFs as optical media for state-o

224 e studies of the Btbd9 mutant mice will help shine light on its role in the pathophysiology of RLS.

225 functional genomic technology have begun to shine light on such gene network problems at both transc

226 NEXAFS measurements shine light on the action of the functional groups and e

227 ll-defined heparan sulfate structures helped shine light on the fine substrate specificities of biosy

228 iglio et al. and Gruber et al. have begun to shine light on the immune drivers of this enigmatic dise

229 ization of chromosome fragmentation may also shine light on the mechanism of chromosomal pulverizatio

230 Our data may thus shine light on the pathophysiological mechanisms underly

231 the existence of secondary binding sites and shine light on the preference for intramolecular rather

232 Our findings shine light on the robustness of single-mode operation a

233 udied substrate binding by these two CBMs to shine light on their functional variation and determined

234 second crystallography (SFX) can potentially shine light on these conformational changes.

235 In this issue of JCI, Rokavec and colleagues shine light on this murky aspect of tumor biology by foc

236 A new study shines light on an already well-known and mutually benef

237 This study also shines light on the motility of flagellated bacteria in

238 The study of photon-induced materials growth shines light on the rational design of complex nanostruc

239 This remarkable observation shines light onto the preferred binding mode of auristat

240 However, doing so requires shining light into the black box that is the trained neu

241 solution microscopy for neuroscience lies in shining light on the nanoscale structures and biochemica

242 Shining light on Zeise: In a study of Zeise's anion, [Pt

243 peech and audio, whereas recurrent nets have shone light on sequential data such as text and speech.

244 ) antineutrinos radiate to space from Earth, shining like a faint antineutrino star.

245 We show that shining mid-infrared circularly polarized light on 1T-Ti

246 atory systems, with a promising potential to shine new light on environmental microbial and chemical

247 alence of renal biopsy in various regions to shine new light on the pathogenesis of various renal dis

248 These results shine new light onto stereoselective molecular recogniti

249 perties of these membraneless organelles and shines new light on neurodegenerative diseases, which ma

250 This work shines new light on studies of thermal conductivity in f

251 neoformans glucosylceramide (GlcCer) mutant shines new light on the initiation of cryptococcal infec

252 This work shines new light onto this powerful C-H oxidation method

253 g and in deciphering the 'tubulin code' have shone new light on this cytoskeletal network and its rol

254 anslucent protective shell ensures the vivid shine of the blue stripes, which can be perceived under

255 We validate SHINE on 50 nasopharyngeal patient samples, demonstratin

256 n has often been analogized to a 'spotlight' shining on the item of relevance.

257 When light from above is shone on a dye-doped LCE sample floating on water, the L

258 Then the spotlight is shone on the sophisticated fabrication methods that have

259 In this article, we present the SHINE PIP including definitions and measurements of key

260 Stroke Hyperglycemia Insulin Network Effort (SHINE) randomized clinical trial included adult patients

261 photosensitizer (PS) with the photoCORM and shining red light, energy transfer occurs from triplet e

262 SHINE's results can be visualized with an in-tube fluore

263 l (hazard ratio 4.76, 95% CI 1.59 to 14.30), Shone's syndrome (hazard ratio 3.68, 95% CI 1.14 to 11.8

264 Jude prosthesis and more likely to have Shone's syndrome.

265 (Arabidopsis thaliana) transcription factor, SHINE (SHN), in rice (Oryza sativa), a model for the gra

266 s and ribosomes in functional binding states shine some light on this fundamental life-sustaining pro

267 Here, we develop SHINE (Streamlined Highlighting of Infections to Navigat

268 Whereas most of the literature on this topic shines the spotlight toward melanocytes, the focus of th

269 SHINE therefore provides an opportunity to longitudinall

270 Let the light shine through: A transparent film of copper nanowires wa

271 The shine-through activity could reach 46% of the reconstruc

272 The ratio between the activity of the shine-through and the activity reconstructed in the orig

273 For the radioactive paper, shine-through artifacts appeared in the location of the

274 etic field, the axial resolution worsens and shine-through artifacts may appear.

275 n air, was scanned, and the magnitude of the shine-through was quantified from the PET images for var

276 g gratings with a larger number of elements (shine-through).

277 ch is better than the constraints from Light-Shining-through-a-Wall experiments while not exceeding t

278 Application of SHINE to the analysis of subtype-specific breast cancer

279 In a secondary analysis of the SHINE trial in rural Zimbabwe we explored biological pat

280 The SHINE trial infant feeding intervention led to significa

281 In the SHINE trial, high-risk patients had poor outcomes despit

282 n, and our approach to evaluating EED in the SHINE trial.

283 iratory samples from Ugandan children in the SHINE trial.

284 a constrained randomization technique in the SHINE trial.

285 ationale, design, and methods underlying the SHINE trial.

286 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial in rural Zimbabwe.

287 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial in rural Zimbabwe.

288 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial in Zimbabwe is evaluating the independent a

289 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial is designed to measure the independent and

290 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial is motivated by the premise that environmen

291 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial, we utilize the concept of maternal capabil

292 ation Hygiene and Infant Nutrition Efficacy (SHINE) Trial, we utilize the program impact pathway (PIP

293 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial.

294 rowth was detected by fluorescence caused by shining UV light (lambda = 365 nm) onto the indicator on

295 We demonstrate that by shining UV light for an hour on a frozen pure endogenous

296 so, the single crystal shows photocurrent on shining visible light at no external bias, exhibiting an

297 aser diode with a digital micromirror device shining visible light onto silicon acts as the spatial T

298 SHINE was a cluster-randomized community-based 2x2 facto

299 Within SHINE we will measure 2 causal pathways.

300 t twenty-three known satellite galaxies that shine with luminosities ranging from about a thousand to