ライフサイエンスコーパス: defect

1 sease and 4 studies of persistent epithelial defect.

2 were sensitive to benomyl, indicating a SAC defect.

3 st group) or EMD+ABG (control group) in each defect.

4 d fingerprint regions representative of each defect.

5 ation were performed to identify the genetic defect.

6 eby produce material samples with uniform GB defects.

7 treatment solution for molars with furcation defects.

8 tes with vesicular trafficking and autophagy defects.

9 and promote neovascularisation to repair the defects.

10 arding the potential causes of cardiac birth defects.

11 o-moderate progression of their visual field defects.

12 increased offspring risk of congenital heart defects.

13 d 30S contact sites all show severe assembly defects.

14 ed (hcp) lattices with the least fraction of defects.

15 AC activity, downstream of condensin complex defects.

16 inst protein aggregation-associated cellular defects.

17 s, at least, in those with F1Fo ATP synthase defects.

18 ed stents were used to exclude sinus venosus defects.

19 ch as surface orientation or the presence of defects.

20 eir ability to produce similar morphological defects.

21 cribed to QseBC may originate from cell wall defects.

22 ISC and villus aging and nutrient absorption defects.

23 enitors accelerates healing of cortical bone defects.

24 properties behave in the presence of planar defects.

25 away from the keyhole and become trapped as defects.

26 nthesis as potential causes of complex birth defects.

27 t kinase rescued Smc5 cKO neurodevelopmental defects.

28 ne1(CreERt2)) did not demonstrate conduction defects.

29 ut the detailed dynamical processes of these defects.

30 nism, both hyperplasia and stem cell lineage defects.

31 lacing Tbx5 upstream of Hh-signaling in limb defects.

32 nsitization to antibiotics, and colonization defects.

33 tipsychotic drugs to rescue adult behavioral defects.

34 ce, as has been demonstrated for solid-state defects.

35 ubjects exhibit signs of severe neurological defects.

36 nd family members to characterize any immune defects.

37 r bone measurements of periodontal intrabony defects.

38 patients scheduled for elective LVHR (hernia defects 3 to 10 cm on computed tomography scan) were ran

39 causes of child deaths were congenital birth defects (39 [13%] of 304 deaths), lower respiratory infe

40 For the calculation of the relative mass defect, a new approach incorporating two correction func

41 fied genes whose disruption leads to fitness defects, a critical step in identifying candidate cancer

42 normalities were classified as a major birth defect according to the European Concerted Action on Con

43 h Tetralogy of Fallot, a serious heart valve defect, affects the substrate selectivity of ADAM17 towa

44 e that BALOs recapitulate lung developmental defects after knockdown of a critical regulatory gene, a

45 itis (AD) is characterized by a skin barrier defect aggravated by mechanical injury inflicted by scra

46 e subject to "superluminal boosts," yielding defects analogous to shock waves.

47 s are mild exhibited an improvement in motor defects and a decreased oligomeric alpha-synuclein burde

48 most common infectious cause of infant birth defects and an etiology of significant morbidity and mor

49 HyperD-ALL cells show chromatid cohesion defects and an impaired spindle assembly checkpoint (SAC

50 electron trap states associated with both N-defects and C-OH terminal groups.

51 ection, inflammation, wounds, cardiovascular defects and cancer.

52 Mid stage, congenital defects and neurological lesions in foetuses like haemor

53 e interrelationship between crystallographic defects and redox reactions.

54 honon scattering because of the excess point defects and rich microstructures.

55 onuclease RNAse H1 rescues the DNA synthesis defects and suppresses DNA damage caused by INO80 deplet

56 gests that pathogenesis results from folding defects and the disruption of autoinhibition and activat

57 re segmented for ventilation and ventilation defects and were compared with noble gas MRI scans using

58 oma, severity of glaucoma, visual field mean defect, and retinal nerve fiber layer thickness were not

59 isruption of ttc7a, which develop intestinal defects, and colonoids derived from biopsy samples of pa

60 al structure, scattering from boundaries and defects, and strain.

61 Topological defects are a consequence of broken symmetry in ordered

62 es to diagnose and target epithelial barrier defects are currently being developed.

63 While bulk defects are detrimental for the device performance by ma

64 dels for the tri-exponential decay involving defects are discussed.

65 Oxygen defects are essential building blocks for designing func

66 Buried under the SEI, these early-stage defects are inaccessible by most surface-probing techniq

67 mice treated at 12 months of age when motor defects are mild exhibited an improvement in motor defec

68 the cellular mechanisms that underlie these defects are not understood.

69 ne loss when severe mitochondrial functional defects are present.

70 Particularly, it is unclear which defects are responsible for the emergent magnetic interf

71 efects is deterministic even when individual defects are stochastic.

72 Furthermore, Sspo defects are sufficient to induce oxidative stress and ne

73 A2 VUS, those causing partial/leaky splicing defects are the most challenging to classify because the

74 The difference in the change in EZ defect area from baseline to month 24 between the 2 trea

75 ed that oocytes undergo a variety of transit defects as they enter and exit the spermatheca during ov

76 which have been implicated in communication defects associated with cardiac injury, namely arrhythmo

77 and increasing sensitivity to somitogenesis defects associated with congenital scoliosis in amniotes

78 The impact of topological defects associated with grain boundaries (GB defects) on

79 early gene expression, suggesting a possible defect at the level of viral replication or later in the

80 erity of skin condition, specific hair shaft defects, atopy, and recurrent infections.

81 a good option for the treatment of infrabony defects because it can improve both tooth retention rate

82 , gingival recession [GR]) and radiographic (defect Bone level [(DBL)] parameters for the different t

83 b single mutant females showed minor chorion defects, but chorions from eggs laid by larp6a;larp6b do

84 Crystal defects called <c> loops, routinely seen no smaller than

85 m in which the microscopic dynamics of these defects can be studied in real time using video microsco

86 less of the initial distribution of defects, defects can coalesce into grain boundaries via the mobil

87 For instance, defects can lead to an enhanced photoconduction, a compl

88 mechanistic insight into neurodevelopmental defects caused by maternal n-3 PUFAs dietary deficiency.

89 during pregnancy related to congenital heart defects (CHD) in Shaanxi province, Northwestern China.

90 In this review we focus on an area of ceria defect chemistry which has received comparatively little

91 , maternal adverse effects, congenital birth defects, childhood cancer.

92 These defects coincided with altered synapse protein organizat

93 causes roughening and synaptic transmission defect, common findings in neurodegenerative and mitocho

94 exception of a residual T cell developmental defect, completely rescued in irradiated wild-type recip

95 d store analogue states using the bulk point defect concentration, yielding predictable switching bec

96 FG, indicating that FG has among the lowest defect concentrations reported so far for graphene, and

97 ependent transport behaviour(8-10) and lower defect concentrations(11,12).

98 at encompasses insulin resistance, lysosomal defects, decreased survival factors, increased reactive

99 s, regardless of the initial distribution of defects, defects can coalesce into grain boundaries via

100 Complex multiscale microstructures including defects, domains, and new phases, can be induced by mech

101 iogenesis of most miRNAs and leads to severe defects during mouse embryonic development and skin morp

102 n environments and understanding fundamental defect dynamics in layered oxides.

103 Defect engineering can enhance key properties of metal-o

104 tching and open a new direction in precision defect engineering, down to a single defect, towards ach

105 toward realizing strongly interacting atomic defect ensembles with applications to quantum informatio

106 e atom that diffuses into the N-doped carbon defect forming Fe(1)(II)-N(4) above 600 degrees C.

107 : (1) measure the rate of failure to provide defect-free postoperative venous thromboembolism (VTE) c

108 (2) identify reasons for failure to provide defect-free VTE chemoprophylaxis, and (3) examine patien

109 stress likely contributes to the late-onset defects, given that hira-1 mutants display mitochondrial

110 Surface defects have been a key constraint for perovskite photov

111 Recently, birth defects have been observed in patients with variants in

112 It is found that macroscopic defects have effects that are confined to their localize

113 s of patients with severe spine segmentation defects have implicated several human orthologues of cyc

114 isms by which METH causes neurodevelopmental defects have remained elusive.

115 Other defects, however, such as periods of hyperactivity and a

116 EMD) with ABG in the management of intrabony defects (IBDs).

117 roquine, indicating that Rab27b KD induces a defect in autophagic flux.

118 14 RNA splicing factors leads to a specific defect in centriole duplication, but the cause of this d

119 ivates autophagy, but it does not rescue the defect in cystine loading.

120 the developmental phenotypes arising from a defect in cytokinin signaling.

121 negatively charged nitrogen-vacancy (NV(-)) defect in diamond is attracting particular current inter

122 In conclusion, a defect in folate metabolism can lead to prenatal aqueduc

123 signatures of HR deficiency had a functional defect in HR, assessed by impaired RAD51 foci formation

124 in the plasma insulin response to offset the defect in insulin action to maintain normal glucose tole

125 severe depletion of insulin SG content and a defect in insulin secretion.

126 ckdown of Cep85l causes a neuronal migration defect in mice.

127 eolus upon activation of Hog1 is linked to a defect in ribosomal DNA (rDNA) and telomere segregation,

128 enal proximal tubule cell AT(2)R natriuretic defect in SHR that may contribute to the development of

129 e photoresponse induced by oxidation-related defects in 2D black phosphorus (BP) is exploited to achi

130 We attribute loss of function to defects in a chemical interaction network that links eff

131 l synaptogenesis, and causes horizontal cell defects in a potentially cell-autonomous fashion.

132 h MDSCs, are implanted into corpus cavernosa defects in a rabbit model to show good histocompatibilit

133 Sixty intrabony defects in AgP and CP patients associated with >= 6 mm r

134 eview, we present current evidence on immune defects in AML, discuss the challenges with selective ta

135 sphate (PIP2), resulting in VEGF-exacerbated defects in angiogenesis and angiogenic signaling.

136 tes associated with treatment resistance and defects in antigen presentation.

137 onse and widespread auxin-related phenotypic defects in Arabidopsis (Arabidopsis thaliana).

138 Here we show that defects in both cell division and cell expansion underli

139 used poor nucleosome positioning also led to defects in both heterochromatin stability and the abilit

140 ting autophagy and exacerbating proteostasis defects in C9-ALS/FTD.

141 on channel subunits partially rescue sensory defects in Caenorhabditis elegans osm-9 and tax-4 knock-

142 cus on chromosome 6 (pi6) produce sperm with defects in capacitation and egg fertilization.

143 ent trios, and case-control cohorts revealed defects in cardiomyopathy-associated genes in patients w

144 abling temporary aggregations of topological defects in cell packing.

145 Defects in cell polarity are associated with neurologic

146 quantitation of these chromosome segregation defects in cells undergoing mitosis.

147 phenotypes of FUT8 null mice, which display defects in cellular signaling, development, and subseque

148 Furthermore, we identify analogous genetic defects in children causing a previously uncharacterized

149 ferent IBMFSs are variable and can relate to defects in diverse biological processes, including DNA d

150 dysfunction-induced foci (TIFs), indicating defects in DNA damage checkpoint signaling.

151 is acquired more frequently in isolates with defects in DNA mismatch repair that confer an elevated m

152 deficiency plays a causative role in visual defects in early DR.

153 iocapillaris vascular perfusion showed focal defects in every layer.

154 21 loss-of-function mutants displayed severe defects in Fe homeostasis that could be reverted by exog

155 entify compounds that can reverse microglial defects in Grn-deficient mouse microglia, we performed a

156 lone, and the virus progeny was analyzed for defects in growth and in competition with the parental v

157 For example, defects in homologous recombination (HR) repair arise in

158 itical window of development results in limb defects in humans and non-human primates while mice and

159 ndrome (HOS), which is characterized by limb defects in humans, but the underlying mechanistic basis

160 biology field focused on how to correct the defects in insulin exocytosis.

161 ion of defined mutations in vitro identified defects in intracellular survival and protection against

162 namic movements are not well understood, but defects in intraflagellar transport components, includin

163 t cells lack Rab7 activation and show severe defects in late endosome morphology and endosomal LDL tr

164 Mice lacking PCBP1 in hepatocytes exhibited defects in liver iron homeostasis with low levels of liv

165 Defects in mammal and algal homologues of this gene coin

166 SAF-A-RNA complexes on mitotic chromosomes, defects in metaphase chromosome alignment, and elevated

167 young mice, but not older adult mice, causes defects in muscle function, consistent with a prolonged

168 Using Xenopus, we identified defects in neural crest cells (NCCs) upon emc1 depletion

169 he patients' phenotype with early lethality, defects in neurogenesis and cardiac dilation.

170 compromised spindle disassembly, and led to defects in nuclear integrity and DNA damage.

171 though cell transplantation can rescue motor defects in Parkinson's disease (PD) models, whether and

172 tion (VCA) has appeared for replacing tissue defects in patients for whom no other satisfactory recon

173 The Deltagpi7 mutant showed significant defects in penetration and invasive growth.

174 sed attention recently due to the maturation defects in pluripotent stem cell-derived cardiomyocyte,

175 In vitro, VE-cadDEE mutant cells displayed defects in polarization and cell migration that were res

176 nd that the double knockout cells have major defects in proliferation.

177 s well as amelioration of K153Del-associated defects in PRPH2/ROM1 oligomerization.

178 L2 secretion is not responsible for skeletal defects in PTRPLS patients.

179 ly, inhibition of mTOR, or Rheb, rescues HSC defects in Sel1L knockout mice.

180 e the feasibility of regenerating large bone defects in sheep using 3D-printed customized calcium pho

181 elated with improvements in several splicing defects in skeletal and cardiac muscles.

182 len might be more tolerant to CWC15-mediated defects in splicing than either embryo or female gametop

183 rons, and further exacerbates SV trafficking defects in Synj1+/- midbrain neurons.

184 ary metabolism rather than respiratory chain defects in the bioenergetic impacts of tafazzin deficien

185 the 10-2 test revealed additional undetected defects in the central visual field.

186 sent at and above 400 nm are ascribed to the defects in the crystalline structure in the form of oxyg

187 library of viable yeast deletion mutants for defects in the degradation of cortical ER following trea

188 rus (ZIKV) infects human placentas, inducing defects in the developing fetus.

189 oscopy of HIPK4-null male germ cells reveals defects in the filamentous actin (F-actin)-scaffolded ac

190 tological analysis also showed developmental defects in the formation of the fore-, mid- and hindbrai

191 ologists Workshop 'Understanding Human Birth Defects in the Genomic Age' held in the UK in November 2

192 Many behavioral defects in the grin1 double-mutant larvae, including abn

193 Any defects in the maintenance of Fe homeostasis will alter

194 due to the random kinetic motion of discrete defects in the nanometer-sized filament.

195 reasons, this led to the generation of four defects in the resulting hexosome structure.

196 Finally, by visualizing the topological defects in these N(r, E) density waves at 2Q, we find th

197 The finding that circadian period defects in two classically derived Neurospora clock muta

198 rus mutants lacking E1B55K or E4orf6 display defects in viral RNA processing and protein production,

199 Optically active defects in wide band gap materials, for instance, are cr

200 sider information on the risk of neural tube defects in women taking dolutegravir at time of concepti

201 ecific overexpression of YAP rescues cardiac defects in Xinbeta knock-out mice-indicating a functiona

202 WBP11 depletion causes centriole duplication defects, in part by causing a rapid decline in the level

203 ndrome, characterized by multiple congenital defects including congenital heart disease (CHD).

204 es of the three ion pairs formed by the V(O) defect, including Cu(1+) -Ti(4+) , Ti(3+) -Ti(4+) and Ti

205 f the disease caused directly by the genetic defect, including other primary immune deficiencies and

206 le exogenous dNTPs rescues the proliferation defect induced by lincNMR depletion.

207 as received comparatively little attention - defect-induced local distortions and short-range associa

208 -level crumpled excitons with some traces of defect-induced trap state emission.

209 Populations with severe TM defects initially adapted via mutations in the TM, but T

210 rve end synapsis in real-time show that this defect is due to a failure to closely align DNA ends.

211 We conclude that the partition defect is due to altered nsDNA binding kinetics and affi

212 The HSC self-renewal defect is rescued after cell transplantation into a norm

213 A potential mechanism for this defect is the uncontrolled initiation of the unfolded pr

214 nge interactions between multiple dopants or defects is challenging(13,14).

215 tistical ensemble behavior of oxygen vacancy defects is deterministic even when individual defects ar

216 sient spectroscopy to characterize the ionic defect landscape in methylammonium lead triiodide (MAPbI

217 extracellular glutamate levels, indicating a defect linked with decreased extracellular glutamate ava

218 silicon, with no or only a few coordination defects (<=1%), a narrow bond-angle distribution of widt

219 , indicating that pre-translational splicing defects may be a critical component of the disease mecha

220 re)combination of the elementary topological defects, merons and antimerons, into a plethora of compo

221 Likewise, defect morphology (P = 0.02), PD (P = 0.003), and MBL (P

222 However, these defects move merely to comply with the mechanical forces

223 We directly image defect nanodomains in the MOF UiO-66(Hf) over an area of

224 protein eventually resulted in muscle fiber defects, neuromuscular junction abnormalities, compromis

225 Cre) and Mekk2(-/-) each displaying skeletal defects, Nf1(fl/fl);Mekk2(-/-);Dmp1-Cre mice show an ame

226 Neural tube defects (NTDs) are a group of severe congenital malforma

227 ural tube (NT) closure result in neural tube defects (NTDs).

228 mkk1/2/3RNAi/mkk7/9) phenocopied pollination defects observed in the mpk4RNAi/mpk3 double mutant.

229 ial resin adhesives ingeniously overcome the defect of the present materials and hold great promise f

230 lamp examination showed no transillumination defects of either iris.

231 n of Pfn1 successfully rescued the migration defects of HuR-deleted neurons.

232 Overexpression of Ago2 rescues some of the defects of miR-451 processing.

233 We found that the defects of the bon mutants in osmotic stress responses w

234 to the nervous system, or stems from broader defects of the motor unit, arguing for systemic SMN repl

235 Despite this, migration defects of WNK1-deficient thymocytes do not account for

236 Although point defects often induce only shallow electronic states in t

237 f Aurora B in interphase leads to cell cycle defects often linked to aberrant chromosomal condensatio

238 In patients without regional perfusion defects on clinical read and no known macrovascular coro

239 tions, provides a way to study the effect of defects on DNA supercoiling and the dynamics of supercoi

240 or PE because of either worsened ventilation defects on ventilation-perfusion scanning (VQ) or increa

241 defects associated with grain boundaries (GB defects) on the electrical, optical, magnetic, mechanica

242 atients with NK with a persistent epithelial defect or corneal ulcer, treated with topical rhNGF, and

243 aling and aberrant HH signaling causes birth defects or cancers.

244 on or overexpression can cause developmental defects or embryonic lethality.

245 diagnosis, to search novel causative genetic defects or investigate environmental factors or co-morbi

246 ss of dental enamel, caused by developmental defects or tooth decay (caries), affect health and quali

247 rea (before treatment), myocardial perfusion defect over time (infarct size), and global longitudinal

248 measures included the size of the epithelial defect overlying the Intacs body, the intended implantat

249 this septation, phenocopying the human heart defect persistent truncus arteriosus (PTA), which trunk

250 Peri-implant marginal mucosa defects (PMMDs) are alterations of the peri-implant soft

251 The arising metastable point defect population explains a common root cause of perfor

252 s-of-function variants leads to craniofacial defects possibly akin to the dysmorphic facial features

253 12 (4%; 2-6) were adjudicated as major birth defects potentially related to DOAC exposure.

254 ed, which results in detrimental pleiotropic defects, questioning the purpose of the miR159-GAMYB pat

255 articipants with relative afferent pupillary defects (RAPDs) confirmed using the swinging flashlight

256 conditions and is the leading cause of birth defects related to infectious disease.

257 novel PET MPI agent with superior image and defect resolution.

258 -(guanylhydrazone) (MGBG), but the molecular defects responsible for these cellular characteristics r

259 These defects resulted in bistable populations of cells occupy

260 congenital and acquired K(v)11.1 trafficking defects, resulting in functional K(v)11.1 current.

261 most common infectious cause of infant birth defects, resulting in permanent neurological disability

262 on functions to obtain correct relative mass defect results also for large hydrocarbons, and a multit

263 l nickel nanoclusters (~1.5 nm) deposited on defect-rich boron nitride (BN) nanosheet (Ni/BN) catalys

264 equires a Cu catalyst with a high density of defect sites that promote adsorption of carbon intermedi

265 1% p = 0.04) despite overall larger baseline defect size (32.7 +/- 19.5 mm(2) vs 21.5 +/- 10.7 mm(2),

266 ldren with asthma who had a higher number of defects/slice had a higher rate of health care utilizati

267 g GATA6 variants cause cardiac outflow tract defects, sometimes with pancreatic and diaphragmic malfo

268 ound manipulating the chemical compositions, defects, stability, and passivation of the various inter

269 , water siting information and water-induced defect structure as a response to water loading were obt

270 ially depend on their ionic constitution and defect structure: ionic charges contribute to charge tra

271 ns, into a plethora of composite topological defects such as the fourfold junctions, the bimeron and

272 Herein, crystallographic defects, such as geometrically necessary dislocations, a

273 Lanthanide-based point defects, such as trivalent ytterbium ions (Yb(3+) ), hav

274 perior optic nerve thinning with inferior VF defects, suggest PVL.

275 plish this, we synthesized fluorescent sp(3)-defect tailored (6,5) carbon nanotubes which, when excit

276 , the 24-2C grid identified more clusters of defects than the 24-2 grid, but this was not statistical

277 Genetic defects that accumulate in haematopoietic stem cells (HS

278 in the vertebrate model X. tropicalis induce defects that are concordant with the human phenotype.

279 tient cell lines displayed DNA damage repair defects that were comparable to previously observed RNAi

280 For both defects, the Az values were higher in off MAR condition.

281 ation in Tbx5 heterozygotes rescued the limb defects, thus placing Tbx5 upstream of Hh-signaling in l

282 y cues, yet Wnt mutants display variable PCP defects; thus, how Wnts regulate PCP remains unresolved.

283 nterior mesoderm populations, culminating in defects to anterior embryonic structures, including the

284 ecision defect engineering, down to a single defect, towards achieving the smallest memristor for app

285 minate eyes with repeatable glaucomatous SAP defects vs eyes with normal fields.

286 trafficking, suggesting that the trafficking defect was due to reduced TRAPPC4 levels.

287 increased risk of offspring congenital heart defects was observed.

288 fy that the point mutation caused a splicing defect, we tested wild-type and mutant mRNA substrates,

289 These defects were a consequence of impaired IP3R function in

290 and AB regeneration, mandibular fenestration defects were created in Ank knockout (Ank KO), Enpp1 mut

291 Monocular peripheral VF defects were measured and defined with a head-mounted di

292 Both epiboly and microtubule defects were partially restored by pregnenolone treatmen

293 ad triiodide (MAPbI(3)) perovskites in which defects were purposely introduced by fractionally changi

294 biting at least one unfavorable intraosseous defect, were treated by L-PRF associated with ABG (22 pa

295 port on quasi-periodic arrangements of crack defects which evolve due to thermal stress under cooling

296 roblasts and discovered a number of cellular defects, which are reversed upon expression of ELMOD2-my

297 ifferences in size, lattice distortions, and defects, which can only be understood by structural char

298 tic and receptor mutants have similar growth defects, which initially led to the assumption that the

299 branching patterns are directed by the seed defects, with the emergence of branches from the seed fa

300 rmed at the interface between the Pt NPs and defect Zr nodes via formate species attached to the Zr n