ライフサイエンスコーパス: dead

1 o dead, healthy to disabled, and disabled to dead).

2 have impaired kinase activity or are kinase-dead.

3 and others to wonder if cardioprotection is dead.

4 dent on the flagella only when bacteria were dead.

5 rgan donation in patients who are pronounced dead.

6 could not be resuscitated and was pronounced dead.

7 % of patients were functionally dependent or dead.

8 roke patients were functionally dependent or dead 3 months postacute stroke; functional recovery rate

9 lower risks of transitioning from healthy to dead (adjusted HR, 0.58 [95% confidence interval (CI), 0

10 Complete nuclease-dead AdnAB enzyme can sustain recombination in vivo, as

11 le-specific knockout (mKO) of Rac1, a kinase-dead alpha2 AMPK (alpha2KD), and double knockout (KO) of

12 time points after osteotomy, the fate of the dead alveolar bone was followed.

13 oth dead and living trees were sampled (2970 dead and 4224 living trees from 190 sites, including 36

14 low cytometry showed about 70% population of dead and compromised cells after 24 h of exposure of bot

15 e controls (p </= 0.05), while the number of dead and defect sperm cells was 27% (p = 0.07) and 15% (

16 d rats, all drilling tools created a zone of dead and dying osteocytes around the osteotomy.

17 dence, we found that these lesions represent dead and dying tissues due to an aberrant hypersensitive

18 ther a sulfinic/sulfonic acid (catalytically dead and irreversible inactivation) or a stable sulfenam

19 t, the wild type formed large cell clumps of dead and live cells, indicating the attempt to form biof

20 hila mounts differential immune responses to dead and live Gram-negative bacteria using the single pe

21 ee-ring width database from sites where both dead and living trees were sampled (2970 dead and 4224 l

22 ] cycloaddition of diethyl azodicarboxylate (DEAD) and quadricyclane and reported that the addition o

23 ges clustered around enlarged hypertrophied, dead, and dying adipocytes, forming crown-like structure

24 organisms and their genes associated with a dead animal) interactions, such as insect species arriva

25 acatenin using cre recombinase driven by the DEAD (Asp-Glu-Ala-Asp) box protein 4 (Ddx4) gene promote

26 iodistribution of UCNPs@mSiO2, cellular live/dead assay, and histologic analysis of main organs of tr

27 Among three people dead at the time of the follow-up survey, one was deemed

28 res ranging from 0 [fully independent] to 6 [dead]) at 90 days.

29 Expression of kinase-dead ATM (Atm(KD/-)) is more oncogenic than loss of ATM

30 Kinase-dead ATM protein (Atm-KD), but not loss of ATM (Atm-null

31 Indeed, kinase-dead AURKA can effectively transactivate the FOXM1 promo

32 implementation), and reluctance to deliver a dead baby.

33 co-elimination of apoptotic immune cells and dead bacteria but barely influenced bacterial sequestrat

34 ed as the basis of a viability assay to tell dead bacteria cells apart from live ones.

35 omplete denitrification, large proportion of dead bacteria in depth, and low functional diversity.

36 in the affected countries from patients and dead bodies meeting the case definitions for Ebola virus

37 A female chimpanzee sat down at the dead body of a young male, selected a firm stem of grass

38 The DEAD box helicase p72/DDX17 was identified as a factor t

39 eukaryotic initiation factor 4A (eIF4A) is a DEAD box helicase that unwinds RNA structure in the 5' u

40 Herein, we identified the RNA helicase, DEAD box protein 5 (DDX5), as a regulator of SUZ12 stabi

41 s, we identified among multiple proteins the DEAD box RNA helicase CshA (NWMN_1985 or SA1885) by mass

42 DDX3 is a DEAD box RNA helicase with oncogenic properties.

43 DEAD box RNA helicases play central roles in RNP biogene

44 show that in budding yeast, mutations in the DEAD-box ATPase Dhh1 that prevent ATP hydrolysis, or tha

45 highly conserved regulator of RNA-dependent DEAD-box ATPase proteins, with critical roles in both mR

46 th the BS independently of the action of the DEAD-box ATPase Prp5.

47 ding of the mRNA-binding protein Yra1 by the DEAD-box ATPase Sub2 as assisted by the hetero-pentameri

48 Members of the DEAD-box family are often multifunctional proteins invol

49 Cellular DEAD-box helicase DEAD-box protein 1 (DDX1) plays a role

50 revious work identified a number of cellular DEAD-box helicases as in vivo binding partners of Rev, a

51 the helicase activity of recruited cellular DEAD-box helicases, which are involved in the production

52 The human DEAD-box protein 1 (DDX1) enhances the RNA export activi

53 Cellular DEAD-box helicase DEAD-box protein 1 (DDX1) plays a role in HIV replicatio

54 ucleus depends on the ATPase activity of the DEAD-box protein Dbp5/DDX19.

55 e subfamily-specific extensions of the human DEAD-box protein DDX3.

56 Here, we establish that the DEAD-box protein Dhh1p is a sensor of codon optimality t

57 (helicase antigen gene), is a member of the DEAD-box protein family.

58 to the pericentriolar material positions the DEAD-box protein regulator to function in localized mRNA

59 DEAD-box proteins (DBPs) are required in gene expression

60 The Ded1/DDX3 subfamily of DEAD-box proteins is of particular interest as members f

61 All DEAD-box proteins share a conserved core that consists o

62 adigm for finely controlling the activity of DEAD-box proteins to optimize their function in RNA-base

63 Two DEAD-box proteins, DDX1 and DDX3, had previously been sh

64 Here we show that the DEAD-box RBP DDX5 inhibits reprogramming by repressing t

65 116 colon carcinoma cells, we identified the DEAD-box RNA helicase DDX41 as a novel regulator of p21

66 DDX3X is a conserved DEAD-box RNA helicase involved in translation initiation

67 DEAD-box RNA helicases (DBRHs) modulate RNA secondary st

68 siRNA) library screen targeting the 58 human DEAD-box RNA helicases in two permissive human cancer ce

69 al activities of human DDX3X are typical for DEAD-box RNA helicases, but diverge quantitatively from

70 ranslation initiation involves two conserved DEAD-box RNA helicases, eIF4A and Ded1p.

71 d positively and negatively by multiple host DEAD-box RNA helicases.

72 eIF4A is a DEAD-box RNA-dependent ATPase thought to unwind RNA seco

73 ication plan of key experiments from "Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor pro

74 tners for measuring the kinetics of nuclease-dead Cas9 (dCas9) interactions.

75 nes using either nuclease-active or nuclease-dead Cas9 (dCas9).

76 e guide RNAs (sgRNAs) for targeting nuclease-dead Cas9-mediated transcriptional repression (CRISPRi)

77 upon the reexpression of wild-type or kinase-dead CDK19.

78 Previously, defects in dead cell clearance were linked to neurodegeneration, bu

79 covered by direct extraction of plasmid from dead cell colonies followed by plasmid transformation in

80 -length AIM in facilitating the clearance of dead cell debris in injured kidney, which is a key respo

81 ME-ECTs displayed the lowest dead cell ratio (p < 0.001) and matured into 0.5 mm diam

82 nner and that controls cross-presentation of dead cell-associated antigens.

83 nase Syk to promote DC cross-presentation of dead cell-associated antigens.

84 thereby activating immune responses against dead-cell antigens.

85 Dead cells accumulated in bone marrow from lupus patient

86 of self-RNA, but not self-DNA, released from dead cells accumulated in GCs drives enhanced GC respons

87 Dead cells accumulating in the tissues may contribute to

88 n mice led to the accumulation of unengulfed dead cells after MI, resulting in exacerbated inflammato

89 hich surveil their surroundings for dying or dead cells and efficiently clear them in a quiescent man

90 Inflammatory reaction clears dead cells and matrix debris, while prolongation or expa

91 Recognition of microbial pathogens and dead cells and their phagocytic uptake by specialized im

92 uired to initiate CD8(+) T cell responses to dead cells and to induce effective antitumor immune resp

93 The responsibility of handling these dead cells falls on phagocytes of the immune system, whi

94 ulation after excluding debris, doublets and dead cells from the analysis.

95 s, we detect and separate a subpopulation of dead cells in an unsupervised manner and, in classifying

96 molecules responsible for the engulfment of dead cells in the infarcted area remain largely unknown.

97 infarction (MI) results in the generation of dead cells in the infarcted area.

98 These dead cells persist in the brain throughout the lifespan

99 microfluidic technique to separate live and dead cells that exploits differences in cellular stiffne

100 actors that can stimulate the replacement of dead cells to the promotion of tissue repair or tissue r

101 The contribution of both living and dead cells to water storage can be derived from rehydrat

102 The ratio of live/dead cells varied in different size-fractions, and the p

103 Binding of dead cells via receptors present on the macrophage surfa

104 cannot differentiate between the viable and dead cells which may overestimate the risk of infections

105 Mtb grew as a clump in dead cells, and macrophages which internalized dead infe

106 ronic smoke exposure increased the number of dead cells, lactate dehydrogenase release, and interleuk

107 Considering a recent finding that, in dead cells, nucleoli were targeted by C1q and two nucleo

108 responsible for the elimination of microbes, dead cells, redundant synapses, protein aggregates, and

109 cellular matrix proteins, efficiently engulf dead cells.

110 es for efficient recycling of molecules from dead cells.

111 stortion products were found in live but not dead chickens.

112 total number of alive children and number of dead children among the three sampled groups.

113 rated as a result of aging or injury contain dead chondrocytes and damaged cartilage.

114 ounted for both erosion and fragmentation of dead colonies.

115 s and 76% of the 416 morphospecies (live and dead combined) in our samples.

116 Nuclease-dead CRISPR-dCas9 transcriptional regulators, while offe

117 group demonstrated less cytotoxic from Live/Dead cytotoxic assay and displayed higher cell attachmen

118 beling DNA in living cells based on nuclease-dead (d) Cas9 combined with engineered single guide RNA

119 ed binding interaction between DDX protein's DEAD domain and Rev was identified, with Rev's nuclear d

120 CD4+ cells in the HIV-negative (HIV-) brain-dead donor (BDD) is not known.

121 mes using advanced age brain-dead or cardiac-dead donor kidneys are similar.

122 donor liver transplantation (LDLT) or brain-dead donor liver transplantation (BDLT) across 5 French

123 Living and brain-dead donor strategies are not mutually exclusive and, in

124 A brain-dead donor strategy is more acceptable from an ethical v

125 Compared with a brain-dead donor strategy, a living donor strategy offers grea

126 ros and cons of using living donors or brain-dead donors in uterus transplantation programs, 2 years

127 report 2 transplants with kidneys from brain dead donors with known DIC.

128 ter circulatory death [DCD] and 3 from brain-dead donors), median Donor Risk Index 2.15, were subject

129 formed at outside institutions, all on brain-dead donors.

130 s" to assess the production and clearance of dead, dying and activated cells, i.e. pivotal events for

131 They also transitioned from disabled to dead earlier (adjusted HR, 1.26 [95% CI, 0.99-1.60] for

132 alling elongation complexes at catalytically dead EcoRIE111Q roadblocks.

133 , are significant drawbacks of conventional 'dead end' filtration.

134 asexuality is supposed to be an evolutionary dead end, morphological, cytogenetic, and genomic data s

135 y breaking or reversed as the cell reaches a dead end.

136 ation of nanos1 after fertilization requires Dead-end 1 (Dnd1), a vertebrate-specific germline RNA-bi

137 a means to control the colloid transport in dead-end channels by introducing a solute gradient.

138 Transport of colloids in dead-end channels is involved in widespread applications

139 ects of ppGpp to drive formation of inactive dead-end complexes formed by RNA polymerase at the ArgX

140 ecies transmission episodes can be singular, dead-end events or can result in viral replication and s

141 We present an automated dead-end filling (DEF) approach, which is derived from t

142 al agent, as demonstrated by both short-term dead-end filtration and long-term cross-flow filtration

143 Long-term dead-end filtration experiments for 1 week reveal a high

144 By operation in dead-end filtration mode using the model virus MS2 (diam

145 Dead-end filtration was carried out using 10(7) and 10(8

146 diffusive zones adjacent to flow paths or in dead-end fractures.

147 alvin-Benson-Bassham cycle in higher plants, dead-end inhibited complexes of Rubisco must constantly

148 ansported intracellularly and reduced to the dead-end metabolite xylitol.

149 ing reactions that are indirectly related to dead-end metabolites but of biological importance to the

150 iJR904 model, for instance, about 42% of the dead-end metabolites were fixed by our proposed method.

151 The non-swapped oligomers likely represent a dead-end offshoot of the amyloid pathway and must dissoc

152 tribution of carbonate minerals that form in dead-end one-dimensional diffusion-limited zones that ar

153 g that this is a true intermediate and not a dead-end product.

154 dentified as both intermediates and apparent dead-end products.

155 , to fill gaps by finding the most efficient dead-end utilization paths in a constructed quasi-endosy

156 lly unstable, the reactions proceeded via a "dead-end" polymerization mechanism, and only low to mode

157 This method is capable of finding indirectly dead-end-related reactions with biological importance fo

158 The recalls of reactions and dead ends of DEF reach around 73% and 86%, respectively.

159 ity benefits the bacteria because males are "dead ends" regarding bacterial transmission, and their a

160 ent proteins: an endonuclease (R.CglI) and a DEAD-family helicase-like ATPase (H.CglI).

161 Active ERK1 phosphorylated kinase dead FLAG-MLK3 in vitro, whereas ERK1 phosphorylation of

162 itro, whereas ERK1 phosphorylation of kinase dead FLAG-MLK3-S705A-S758A was reduced.

163 e in the hospital discharge status (alive or dead) for only 0.47% of all linked records (kappa = 1.00

164 rate and quantify live coral colonies versus dead framework.

165 ed N2 was formed in the presence of live and dead fungi and in the absence of fungi, while N2O steadi

166 report near total rescue of this ostensibly dead general base mutant by a synthetic substrate, 3beta

167 Acetylation-dead H4 mutations cause mis-localization of the CENP-A-H

168 RK2 wild type or LRRK2 D1994A mutant (kinase dead) had no effect on mtDNA damage in either midbrain o

169 s (HRs) for 3 health transitions (healthy to dead, healthy to disabled, and disabled to dead).

170 undancy with UTY, a Y-chromosome demethylase-dead homolog.

171 We find that kinase-dead Ikkalpha knockin mice develop APECED-like phenotype

172 All 3 patients were found dead in circumstances typical of SUDEP.

173 Of dead index attempters, 72.9% used guns, yielding an odds

174 ad cells, and macrophages which internalized dead infected cells were very likely to die themselves,

175 ls expressing wild-type, but not phosphatase dead, inositol polyphosphate 4-phosphatase show impaired

176 pression of wild-type, but not 5-phosphatase-dead, INPP5E restored TZ molecular organization and Smoo

177 Homozygous MLL4 enzyme-dead KI (Mll4(KI/KI)) mice are embryonic lethal and die

178 tratracheally inoculated with either live or dead Klebsiella pneumoniae to induce either lung infecti

179 ss this issue, we have generated MLL4 enzyme-dead knock-in (KI) embryonic stem (ES) cells and mice, w

180 A "redox-dead" knock-in mouse containing a C43S mutation exhibits

181 ndings are substantiated through demethylase-dead knockin mutation of UTX, which supports appropriate

182 ce expressing LRRK2-G2019S or D2017A (kinase-dead) knockin mutations.

183 microglia depletion impaired the removal of dead labeled retinal ganglion cells after optic nerve cr

184 y in STO and the existence of the dielectric dead layer at the interfaces of STO with metallic films.

185 sponse to apoptotic immune cells and live or dead Listeria monocytogenes scavenger receptor BI (SR-BI

186 Reexpression of wild-type Met, kinase-dead Met, or integrin alpha3 was sufficient to rescue de

187 Here we show that heterozygous Vps34 kinase-dead mice are healthy and display a robustly enhanced in

188 ring mesoderm development akin to FAK kinase-dead mice.

189 Interestingly, enzyme-dead MLL4 protein in ES cells is highly unstable.

190 ressing either one or two copies of a kinase-dead mTOR mutant (KD-mTOR) transgene exclusively in beta

191 wild-type (WT) Pak2 but not by a Pak2-kinase dead mutant (KD).

192 ampal CA3-CA1 pathway, but the catalytically-dead mutant did not affect LTD induction.

193 Complementation with a catalytically dead mutant highlights that nick sealing activity is imp

194 her GSK2656157 or overexpression of a kinase-dead mutant of PERK (PERK-K618A) rescues BDNF and PSD95

195 ith either wild-type PTEN or a catalytically dead mutant stabilizes IP3R3 and induces persistent Ca(2

196 Furthermore, the catalytically dead mutant TRAF6 C70A abolished the TRAF6-mediated poly

197 pression of SIRT2, but not its catalytically dead mutant, increased intracellular levels of reactive

198 series of phosphomimetic and phosphorylation-dead mutants by mutating known conserved regulatory seri

199 On the contrary, the kinase-dead mutants, ZAK-alpha K45M and ZAK-beta K45M, were not

200 A kinase-dead mutation of Snf1 lowered iron resistance as did del

201 ils and macrophages to facilitate removal of dead myocytes as well as turnover of the extracellular m

202 pared with kidneys from neurologically brain dead (NBD) donors, DCD kidneys had a higher adjusted odd

203 ceptor leads to a pronounced accumulation of dead neurons in the brain of the fruit fly Drosophila me

204 ous estimates of the volumetric flow rate of dead oil from the emission source.

205 It was found that normally slaughtered and dead on arrival chicken can be differentiated based on t

206 d liver tissue from normally slaughtered and dead on arrival chickens.

207 ic and able to differentiate live cells from dead ones.

208 Outcomes using advanced age brain-dead or cardiac-dead donor kidneys are similar.

209 tials, VPs can be measured beyond regions of dead or chemically treated tissue that block signal gene

210 ted with food are present (although possibly dead or dormant) in the caterpillar gut, but host-specif

211 troduce efferocytosis - the process by which dead or dying cells are engulfed and digested by phagocy

212 allele present but mutating it to be kinase-dead or have PI4P 5-kinase activity, we show that all of

213 ion, half of older ICD recipients are either dead or in hospice.

214 ne therapy may serve to replace or resurrect dead or injured retinal neurons.

215 Yet, 125/167 (74.9%) were dead or institutionalised after the event.

216 Conditioning the brain-dead organ donor by altering metabolism could be a novel

217 intestines) sites from a population of brain-dead organ donors (2 months-93 years; n = 291) across ei

218 Upper limbs were procured from brain-dead organ donors.

219 Live biomass and dead organic carbon residence times exhibit contrasting

220 iven by the production and standing stock of dead organic material and soil development.

221 e lacking due to insufficient information on dead organic matter (DOM).

222 iods of 1984-1988 to 2004-2008, the national dead organic matter carbon stock has increased by 6.7 +/

223 ects of climate and stand characteristics on dead organic matter distribution.Reliable estimates of t

224 by enhancing the processing and turnover of dead organic matter in soils of arid regions), reduce hu

225 s, that is, C fluxes from live vegetation to dead organic matter pools.

226 of available information on carbon stocks in dead organic matter, including woody debris and litter,

227 ists, the p38 inhibitor SB202190, and kinase-dead [p38(KD)] and dominant-negative [p38(DN)] forms of

228 in functional complex with its catalytically dead paralogous partner, prozyme.

229 y exceeded, resulting in the accumulation of dead parasites in the circulation, that parasite clearan

230 of PARN or exogenous expression of an enzyme-dead PARN mutant (D28A) accumulated 18S-E in both the cy

231 2.21; p < 0.001), care of relatives of brain-dead patients as complex (odds ratio, 1.59; 95% CI, 1.32

232 ng the study period, there were 22,270 brain-dead patients diagnosed in France, of whom 161 with extr

233 Brain-dead patients with ongoing extracorporeal membrane oxyge

234 Brain-dead patients with ongoing extracorporeal membrane oxyge

235 However, expression of kinase-dead PI3Kgamma resulted in rescue of insulin-stimulated

236 Furthermore, either kinase-dead PKCzeta expression (KD-PKCzeta) or disruption of PK

237 thout efficient decomposition and recycling, dead plant biomass would quickly accumulate and become i

238 re are connected carbon release pathways for dead plant material: slower litter decomposition leads t

239 Using a dominant-negative, deacetylase-dead point mutant virus (AAV-HDAC3(Y298H)-v5), we found

240 Ska1 fusion to catalytically dead PP1 mutant does not rescue and shows dominant negat

241 isoforms or overexpression of a phosphatase-dead PP1c-1 mutant attenuates infection, demonstrating t

242 led that expression of wild-type but not GEF-dead PREX1 resulted in the formation of larger tumors th

243 tored by expression of wild-type but not GEF-dead-PREX1.

244 an N-terminal truncated and a catalytically dead RAG1.

245 antioxidative processes in kidneys of brain-dead rats after fast and slow BD induction.

246 Healthy non-brain-dead rats served as reference values.

247 Brain-dead rats were monitored for 0.5, 1, 2, or 4 hours, afte

248 We also find that DEAD reacts with itself to form a variety of hydrazine c

249 requency hearing loss, including people with dead regions (DRs) in the cochlea.

250 e of both sexes bearing a GFP-tagged phospho-dead S193A allele on a null background (Atoh1(S193A/lacZ

251 at a cave in the Judean Desert close to the Dead Sea.

252 tains sequential periderms interspersed with dead secondary phloem (rhytidome), the cork oak outer ba

253 The volume and surface area of dead skeletons decreased by 52% and 47%, respectively, c

254 physiological concepts, we demonstrate that dead space and static compliance determine the effect of

255 apulmonary shunt, whereas increased alveolar dead space explains the alteration of CO2 clearance.

256 acity at rest was a significant predictor of dead space ventilation at maximal exercise (r = -0.524,

257 acity in heart failure is indicative of high dead space ventilation during exercise, leading to exces

258 is include reductions in ventilation circuit dead space, increases in respiratory rate, higher positi

259 lues from -0.80 to -0.84; P < 0.001) but not dead space/tidal volume ratio.

260 ates that geometrical constraints, including dead-space microdomains, contribute to the hindrance to

261 th wider local expansions that may represent dead-spaces.

262 on and display disrupted spindles, producing dead spores or even failing to form spores.

263 ents the formation of electrically inactive "dead spots" in the anode structure and enables the effec

264 The live/dead staining, cell proliferation assay and immunohistoc

265 ues from annual bone growth layer rings from dead-stranded animals, and then combined the bone and re

266 own custom DNA-binding modules, the nuclease-dead Streptococcus pyogenes Cas9 (dCas9) protein, which

267 , herein we propose a strategy to reactivate dead sulfide species by reacting them with sulfur powder

268 n the surface of carbon and lithium (called "dead" sulfide species) leads to continuous capacity degr

269 A kinase-dead tel1 mutation similarly increases Spo11-oligonucleo

270 , including 'live' (Rose Bengal stained) and dead tests, in 5 cores (0-1 cm layer, >150-mum fraction)

271 One patient became brain dead; the condition of two patients subsequently improve

272 longest detectable event (i.e., instrument "dead time") when fitting to PDFs.

273 Sensitivity, dead time, propagation delay, dispersion, background sen

274 mum tubings and show the complex relation of dead time, retention time, efficiency, and optimum veloc

275 ommended injected activity/body weight, peak dead-time correction factor, counting rates, and residua

276 ed MBq/kg values are respected to limit peak dead-time losses during the bolus first-pass transit.

277 less than 10% bias, from which corresponding dead-time, counting rates, and/or injected activity limi

278 p with host trees is colonization of freshly dead tissues, but there are also parasites of living tre

279 ormable ones are capable of circumnavigating dead (trapped) cells ahead of them by choosing a serpent

280 agnitude, typically from tens to hundreds of dead trees per km(2) , rising dramatically during the fo

281 ed expression of a dominant negative, kinase-dead TrkB mutant.

282 Ligase-dead UBE3A did not stimulate Wnt pathway activation.

283 via hypoxia-induced expression of the kinase-dead unc-51-like autophagy-activating kinase (ULK1) muta

284 ffect was antagonized by PknA-K42N, a kinase-dead variant.

285 lculating the killing depth detected by live/dead viability staining.

286 OCT was validated against the standard LIVE/DEAD Viability/Cytotoxicity Assay in small tumor spheroi

287 ffect of design variations such as change in dead volume and pillar size within the lateral channels

288 This LC-ESII/MS approach has little dead volume and thus provides excellent chromatographic

289 0 microl of sample consumption, inclusive of dead volume in the reservoirs.

290 In both categories (live and dead) we distinguished between complete and fragmented s

291 Most of the dead were adult males (68%), but the highest case fatali

292 ptk7 encodes a trunk-expressed kinase-dead Wnt co-receptor, wntP-2 encodes a posterior-express

293 ed using three example separations: live and dead yeast; human cancer cells/red blood cells; and rode

294 Reduced expression of the Indy ("I am Not Dead, Yet") gene in lower organisms promotes longevity i

295 While the dead zone was 0 mm for 89% of transducers, it was 3 mm f

296 he phantom, including: depth of penetration, dead zone, distance measurement accuracy, resolution, un

297 bbean coast of Panama and assess the risk of dead zones to coral reefs worldwide.

298 ed with more than half of the known tropical dead zones worldwide, with >10% of all coral reefs at el

299 ined by the existence of randomly occurring "dead zones" that can significantly delay fixation on net

300 t, leading to what are often referred to as "dead zones," are known primarily from temperate regions.