ライフサイエンスコーパス: ID

1 ID + IM without EP resulted in a similar pattern of resp

2 ID prevalence in pregnant females increased significantl

3 ID prevalence varied depending on socioeconomic status a

4 ID promotes production and cleavage of intact fibroblast

5 ID was defined as SF <12 mug/L in the absence of infecti

6 ID/AST performance, the average times to results, and wo

7 uptake in BXPC-3 tumors (peak at 31.5+/-6.0%ID/g at 48h post-injection; n=3), which was significantl

8 negligible for the pancreas (0.07 +/- 0.01 %ID/g).

9 tion in bone (0.07% ID/g +/- 0.02 and 0.010% ID/g +/- 0.004 at 1 and 14 days, respectively).

10 nografts (0.34 +/- 0.08 vs. 0.098 +/- 0.033 %ID/g at 2 h after injection, P = 0.03).

11 om a maximum for the stomach (0.52 +/- 0.04 %ID/g) to almost negligible for the pancreas (0.07 +/- 0.

12 with negligible accumulation in bone (0.07% ID/g +/- 0.02 and 0.010% ID/g +/- 0.004 at 1 and 14 days

13 r the kidneys, where uptake was 1.8 +/- 1.1 %ID/g at 30 min after injection.

14 mpared with 1.25 +/- 0.08 and 2.24 +/- 0.11 %ID/g for controls (P < 0.05 for all regions except stria

15 creatic uptake (19.8 +/- 6.9 vs. 105 +/- 13 %ID/g of tissue at 240 min after injection) with the high

16 ged between 1.74 +/- 0.11 and 2.93 +/- 0.15 %ID/g for EAE mice, compared with 1.25 +/- 0.08 and 2.24

17 ection, the blood levels were 0.44 +/- 0.28 %ID/g.

18 The method used a column with 2mm ID that was tightly packed with silica gel followed by a

19 [%ID/g]) and lowest in Calu-1 (2.3 +/- 0.3 %ID/g) xenografts.

20 5 xenografts (HGF-negative) was 5.0 +/- 1.3 %ID/g and a control of nonspecific human IgG (89)Zr-DFO-I

21 tumor uptake (17.9 +/- 3.3 vs. 11.6 +/- 1.3 %ID/g of tissue at 240 min after injection) and a lower p

22 Zr-DFO-IgG in U87MG tumors was 11.5 +/- 3.3 %ID/g, demonstrating selective uptake in HGF-positive tum

23 The Top 3-ID-DIA strategy proved to be equivalent to the gold-stan

24 The method named Top 3-ID-DIA was benchmarked against ELISA and a gold-standard

25 +/- 0.99 %ID/g for female vs. 1.9 +/- 0.30 %ID/g for male, P = 0.03).

26 and 10-fold lower levels at 14 days (<0.33% ID/g +/- 12) after CM-101 injection with negligible accu

27 nel and exome sequencing) in a cohort of 337 ID subjects as a first-tier test and compared it with a

28 ar to that of (68)Ga-PSMA-11 (4.89 +/- 1.34 %ID/g).

29 01) and in CCR2-deficient mice (mean = 0.39% ID per gram of tissue; P < .001).

30 ea-Lys-HBED-CC-AlexaFluor488 (9.12 +/- 5.47 %ID/g) revealed a tumor uptake similar to that of (68)Ga-

31 which was significantly abrogated (2.3+/-0.5%ID/g at 48h post-injection; n=3) when mice were pre-inje

32 on in the amniotic fluid was 0.028 x 10(-5) %ID/g (percentage injected dose per gram of tissue) 50 da

33 /g), and one juvenile brain (0.095 x 10(-5) %ID/g) and kidney (0.13 x 10(-5) %ID/g) sample.

34 5 x 10(-5) %ID/g) and kidney (0.13 x 10(-5) %ID/g) sample.

35 one juvenile spleen sample (0.039 x 10(-5) %ID/g), and one juvenile brain (0.095 x 10(-5) %ID/g) and

36 of one juvenile skin sample (0.07 x 10(-5) %ID/g), one juvenile spleen sample (0.039 x 10(-5) %ID/g)

37 3.73 %ID/g), and DyLight800 (15.62 +/- 5.52 %ID/g) resulted in a significantly increased specific tum

38 The maximum tumor accumulation (15.6 %ID g(-1) , 72 h p.i.) and ideal tumor-to-muscle ratio (1

39 onradiolabeled ECL1i in excess (mean = 0.63% ID per gram of tissue; P < .001) and in CCR2-deficient m

40 ke of (89)Zr-DFO-AMG102 ( approximately 4-7 %ID/g), which corresponded with low HGF levels in these t

41 d dose [%ID]/g), IRDye800CW (13.66 +/- 3.73 %ID/g), and DyLight800 (15.62 +/- 5.52 %ID/g) resulted in

42 (18)F-FLT tumor uptake values (4.5 +/- 0.99 %ID/g for female vs. 1.9 +/- 0.30 %ID/g for male, P = 0.0

43 ate Pheno system provides rapid and accurate ID/AST results for most of the organisms found routinely

44 t/hip ratio, and visual and auditory acuity (ID between -2.3 and -5.2 phenotypic SDs for complete inb

45 We report the mTOR activator gene RHEB as an ID gene that is associated with megalencephaly when muta

46 Implementation of an ID team for the early management of SS/SS in the ED impr

47 Patients that received an ID consult were significantly less likely to die in the

48 an adjusted hazard ratio of not receiving an ID consult of 4.1 (95% CI: 2.2, 7.6).

49 ificant improvement in patients receiving an ID consult, targeted antimicrobial therapy, and adherenc

50 These data suggest that an ID consult should be an integral part of clinical care o

51 The patients with an ID consult had a higher fungal burden but a lower 90-day

52 tivariable-adjusted Cox regression analyses, ID associated with increased mortality (81 events; hazar

53 tudy including children with ASD (n=545) and ID (n=181) identified from the California Department of

54 ssociated with cognitive deficits of ASD and ID in humans, and overexpression of small 22q11.2 segmen

55 this genetically defined subtype of ASD and ID, suggesting an individualized therapeutic approach fo

56 re associated with decreased odds of ASD and ID, though not in girls.

57 during pregnancy are associated with ASD and ID.

58 orders, 4th Edition (DSM-IV-TR) criteria and ID (n = 181), as well as general population (GP) control

59 ur WGS dataset with those of several DEE and ID series.

60 d the prevalence of iron deficiency (ID) and ID anemia (IDA) among toddlers, nonpregnant females, and

61 ittle is known regarding B cell and antibody ID despite its importance in immunity to viruses and oth

62 r attaining deeper understanding of antibody ID to viruses and other complex immunogens.

63 nitive and adaptive composite score<70) (ASD+ID, N=184) and those without (composite score70) (ASD-no

64 inction between mothers of children with ASD+ID from mothers of children with ASD-noID or DD suggests

65 Mothers of children with ASD+ID had significantly elevated mid-gestational levels of

66 standard selected reaction monitoring assay (ID-SRM).

67 show that individuals with TRMT1-associated ID are likely to have major perturbations in cellular ho

68 ) or intellectual disability without autism (ID).

69 and intellectual disability without autism (ID).

70 F23 explained 46% of the association between ID and mortality, whereas iFGF23 did not mediate this as

71 mportant mediator of the association between ID and mortality.

72 echanism explaining the relationship between ID and adverse outcome in RTRs.

73 sized that in RTRs, the relationship between ID and mortality is mediated by FGF23.

74 (LD) between causal variants and SNPs biases ID estimates, and we develop an approach to correct this

75 nonpregnant and nonbreastfeeding women.Both ID and elevated iron stores are present in women of repr

76 on status but are not bioindicators of brain ID and brain dysfunction in children.

77 Second, brain ID, independently of IDA, is responsible for long-term n

78 Patients seen by ID physicians were more likely to be managed according t

79 rain tissues showed that the novel candidate ID genes formed a network significantly enriched for tra

80 ed ID genes and 30 affecting novel candidate ID genes.

81 Additionally, we identify three candidate ID/DD-associated genes of which two have an established

82 st that recessive mutations in SLC45A1 cause ID and epilepsy.

83 y lipids and other small molecules (e.g. CFM-ID, MetFrag, GNPS, LipidBlast and MS-DIAL), and was foun

84 th in silico spectra prediction programs CFM-ID and MS-FINDER to derive the best candidates.

85 Data regarding the current ID workforce are presented here, along with perspectives

86 Hdac3-deficient iNKT cells have less Cyto-ID staining and lower LC3A/B expression, indicative of r

87 re managed in collaboration with a dedicated ID team performing a bedside patient evaluation within 1

88 f TBI and the prevalence of iron deficiency (ID) and ID anemia (IDA) among toddlers, nonpregnant fema

89 The prevalence of iron deficiency (ID) and iron deficiency anemia (IDA) was 10-32% and 2-5%

90 Iron deficiency (ID) and vitamin D deficiency (VDD) are common among youn

91 Iron deficiency (ID) anemia is a prevalent disease, yet molecular mechani

92 Iron deficiency (ID) before the age of 3 y can lead to long-term neurolog

93 ns are at increased risk of iron deficiency (ID) but also have higher serum ferritin (SF) concentrati

94 nflammation on estimates of iron deficiency (ID) in low- and high-infection-burden settings.

95 Iron deficiency (ID) is an urgent public health problem that has devastat

96 Iron deficiency (ID) is common in young children aged 6-36 mo.

97 Iron deficiency (ID) is independently associated with an increased risk o

98 urrent reports suggest that iron deficiency (ID) prevalence is low.

99 Clinical diagnosis of iron deficiency (ID) through sampling of bone marrow to identify the abse

100 The diagnosis of iron deficiency (ID) through SF concentration, the most commonly used ind

101 containing BRPF1 and SETD5, cause a defined ID syndrome where most of the clinical features are attr

102 intellectual disability/developmental delay (ID/DD).

103 only used to estimate inbreeding depression (ID).

104 bility of standard iron indicators to detect ID-induced brain dysfunction, and evaluate the efficacy

105 commonly deployed indicator for determining ID, and low SF concentrations reflect a state of iron de

106 ended by different expert groups to diagnose ID.

107 solute quantification with isotope dilution (ID).

108 schizophrenia and intellectual disabilities (ID), implicating this atypical process in the trajectory

109 gene, UPF3B, cause intellectual disability (ID) and are strongly associated with autism spectrum dis

110 to confer risk for intellectual disability (ID) and autism spectrum disorder (ASD) and affects an es

111 are associated with intellectual disability (ID) and autism spectrum disorder (ASD).

112 cause of syndromic intellectual disability (ID) and autism spectrum disorder, and somatic mutations

113 cause of heritable intellectual disability (ID) and autism spectrum disorders (ASD), Fragile X syndr

114 he association with intellectual disability (ID) has not been investigated.

115 Intellectual disability (ID) is a clinically and genetically heterogeneous disord

116 Intellectual disability (ID) is a common neurodevelopmental disorder exhibiting e

117 Intellectual disability (ID) is a highly heterogeneous disorder involving at leas

118 Intellectual disability (ID) is a measurable phenotypic consequence of genetic an

119 Intellectual disability (ID) is a prevailing neurodevelopmental condition associa

120 oint mutations from intellectual disability (ID) patients that showed convergent disruptive effects o

121 disorder (ASD) and intellectual disability (ID), and frequently presents with attention deficits.

122 result in epilepsy, intellectual disability (ID), and movement disorder.

123 mental delay (GDD), intellectual disability (ID), severe speech impairment and gait abnormalities.

124 nce of epilepsy and intellectual disability (ID), typically with developmental plateauing or regressi

125 st 1 offspring with intellectual disability (ID).

126 h in the context of intellectual disability (ID).

127 autosomal-recessive intellectual disability (ID).

128 Discordant ID and mecA results were resolved by rpoB gene sequencin

129 An infectious disease (ID) consultation is often obtained to treat patients wit

130 n patient survival of an infectious disease (ID) team dedicated to the early management of severe sep

131 Infectious diseases (ID) consultation and antimicrobial stewardship intervent

132 ine in applications for infectious diseases (ID) fellowships has been an area of active introspection

133 While a career in infectious diseases (ID) has always been challenging and exciting, recognitio

134 amples of management of infectious diseases (IDs) at the University Hospital Institute Mediterranee I

135 exception to the rule of intrinsic disorder (ID), believed to require a unique structure for catalysi

136 Intrinsically disordered (ID) regions of the transcription factor proteins have mu

137 tual disability and developmental disorders (ID/DD) and successfully identify 15 genes with clusterin

138 ontrol group (mean = 4.43% of injected dose [ID] per gram of tissue vs 0.99% of injected dose per gra

139 G521R ER xenografts (percent injected dose [ID] per gram, 0.49 +/- 0.042), which was similar to the

140 ium levels at 24 hours (<3.9% injected dose [ID]/g +/- 0.6) and 10-fold lower levels at 14 days (<0.3

141 vs. 1.6 +/- 0.14 percentage injected dose [%ID]/g at 2 h after injection, P = 0.006) and the CWR22 p

142 e (10.86 +/- 0.94 percentage injected dose [%ID]/g), IRDye800CW (13.66 +/- 3.73 %ID/g), and DyLight80

143 tion (9.2 +/- 2.0 percentage injected dose [%ID]/g).

144 vs. 3.33 +/- 0.20 percentage injected dose [%ID]/g, P < 0.05).

145 synthesis in vivo in erythroid cells during ID.

146 nd to reduce oxidative stress in vivo during ID.

147 unization combining IM injection with either ID or TC administration.

148 o SAB quality-of-care measures and encourage ID consultation.

149 es that did not differentiate these factors, ID prevalence was 4-18%.

150 Without regard to these factors, ID was reported in 3-48% of children aged >/=12 mo acros

151 133 [51.5%] male and 86 874 [48.5%] female), ID was diagnosed in 37 children (0.9%) exposed to antide

152 ere either known or are novel candidates for ID.

153 Various definitions for ID and IDA were applied across studies.

154 d affordability, screening and diagnosis for ID is often limited to proxy hemoglobin measurements alo

155 ams is occurring at a time when the need for ID providers has never been greater and the excitement a

156 atterns overall and by sex were observed for ID.

157 provides additional future opportunities for ID physicians.

158 or associations with ASD, and separately for ID, compared with GP controls, by quartiles of analyte c

159 It is easy to use, reduces hands on time for ID/AST of common blood pathogens, and enables clinically

160 concentration is an indicator of functional ID that is not an acute-phase reactant, but challenges i

161 al Center for Biotechnology Information Gene ID 1854), affecting both the mitochondrial (DUT-M p.Y142

162 olecule metabolic process, cell adhesion (GO IDs: 0030198, 0044281, 0007155) and pathways in cancer,

163 +/- 3.3 percentage injected dose per gram (%ID/g) of tissue, respectively, at 120 min after injectio

164 ositive (percentage injected dose per gram [%ID/g] = 2.56 +/- 0.33) and -negative (%ID/g = 0.32 +/- 0

165 +/- 1.1 percentage injected dose per gram [%ID/g]) and lowest in Calu-1 (2.3 +/- 0.3 %ID/g) xenograf

166 +/- 7.8 percentage injected dose per gram [%ID/g]), whereas uptake in MKN45 xenografts (HGF-negative

167 multiple children (107 families [70.4%]) had ID; additional features were present in 140 of the famil

168 serology (TB&S) and the kmer identification (ID) derived from the WGS data.

169 parison II, time to organism identification (ID) and antimicrobial susceptibility (AST) reports were

170 r the rapid and simultaneous identification (ID) of Staphylococcus aureus, Staphylococcus lugdunensis

171 sis to provide rapid species identification (ID) and antimicrobial susceptibility testing (AST) resul

172 Immunodominance (ID) defines the hierarchical immune response to competin

173 requently recurrent than those identified in ID series.

174 CLIP1), thus supporting their involvement in ID pathogenesis.

175 CB138/158 was also associated with increased ID (AOR = 2.41; 95% CI: 1.18, 4.91), though no trend was

176 issues via transcutaneous (TC), intradermal (ID) and intramuscular (IM) injection has the potential t

177 Mismatches between the TB&S and kmer ID results were explained by the close phylogenetic rela

178 s Shigella flexneri or S. boydii by the kmer ID, and 8 were S. flexneri isolates misidentified by TB&

179 analyzing 101 mMTOR-related genes in a large ID patient cohort and two independent population cohorts

180 to assign mapping results to the most-likely IDs, (iii) comprehensive ribosomal RNA filtering for acc

181 n in healthy European children aged 6-36 mo, ID is still common.

182 -loop GTPase and the first discovered native ID enzyme, involved in the maturation of the nickel-cont

183 ram [%ID/g] = 2.56 +/- 0.33) and -negative (%ID/g = 0.32 +/- 0.05) tumors (P = 0.0006).

184 Furthermore, pre- or nonanemic ID alters neurobehavioral function and is 3 times more c

185 Wild-type GRASP1, but not ID mutants, rescued spine loss in hippocampal CA1 neuron

186 Notably, ID-causing TRMT1 variants are unable to catalyze the for

187 In addition, proteins encoded by 12 novel ID genes directly interact with previously reported ID p

188 s that were primarily ascertained because of ID.

189 ed mutations in PPM1D as a possible cause of ID.

190 Although research into the genetic causes of ID has recently gained momentum, identification of patho

191 stimated relative risks (RRs) and 95% CIs of ID in children exposed during pregnancy to any antidepre

192 logical deficits despite prompt diagnosis of ID anemia (IDA) by screening of hemoglobin concentration

193 of TRMT1 to uncover the cellular effects of ID-causing TRMT1 mutations.

194 protein (AGP) concentrations on estimates of ID according to serum ferritin (SF) (used generically to

195 s of TBI and produce prevalence estimates of ID and IDA for each target population.

196 appears to substantially change estimates of ID prevalence in low- and high-infection-burden countrie

197 models that unveil the molecular etiology of ID, and outline the direction in which this field is mov

198 We find unique evidence of ID for handgrip strength, waist/hip ratio, and visual an

199 s have been implicated in Mendelian forms of ID.

200 The incidence of ID consult improved significantly by almost 20% in the i

201 Third, most currently used indexes of ID are population statistical cutoffs for either hematol

202 ular mechanisms and the transcriptome map of ID.

203 fancy are critical to the pathophysiology of ID.

204 he excitement and variety in the practice of ID has never been higher.

205 o determine the prevalence and predictors of ID (SF concentration </=15 mug/L) and elevated iron stor

206 Racial disparities in the prevalence of ID among both nonpregnant and pregnant females exist, wi

207 Given the global prevalence of ID and the enormous societal cost of developmental disab

208 rrection changed the estimated prevalence of ID in PSC by a median of +25 percentage points (pps) whe

209 en TBI was used; the estimated prevalence of ID in WRA changed by a median of +8 pps when SF concentr

210 ations increased the estimated prevalence of ID when SF concentrations were used by 3 pps in PSC and

211 tus in Europe, we describe the prevalence of ID, IDA, iron repletion, and excess stores with the use

212 plements displayed increasing prevalences of ID and IDA during pregnancy, which peaked in the middle

213 trations were 6-21 mug/L, and prevalences of ID and IDA were 28-85% and 21-35%, respectively.

214 higher iron status and lower prevalences of ID and IDA, which were dependent on the dose of iron and

215 The probability of ID (OR 0.42; 95% CI:0.18, 0.95; P = 0.036) and VDD (OR 0

216 mproves both detection and quantification of ID using SNP data.

217 on birth outcomes among women at low risk of ID and the potential mechanisms for adverse effects of h

218 endently associated with a decreased risk of ID in nonpregnant and nonbreastfeeding women and in preg

219 1) were associated with an increased risk of ID in nonpregnant and nonbreastfeeding women.

220 on-Hispanic black females at greater risk of ID than non-Hispanic white females.

221 s, whereas nonmonotonic increases in risk of ID were found with p,p -DDE.

222 ustment for potential confounders, the RR of ID after antidepressant exposure was estimated at 1.33 (

223 The unadjusted RR of ID was increased in offspring born to mothers treated wi

224 , the model did not indicate the severity of ID and produced categorical estimates.

225 brain dysfunction in the preanemic stage of ID, assess the ability of standard iron indicators to de

226 linical Affairs Committee-sponsored study of ID physicians' positive impact on patient outcomes shows

227 onal proliferation/differentiation switch of ID-bHLH factors.

228 scape of DEE might be different from that of ID without epilepsy.

229 protocols feeding standardized management of IDs.

230 n repletion and excess stores, as well as on ID and IDA, is needed.

231 F MS significantly improved TAT for organism ID.

232 MALDI significantly improved TAT to organism ID compared to CONV (21.3 to 18 h).

233 , TLA significantly improved TAT to organism ID, AST report, and preliminary negative results.

234 s, median pre- and post-TLA TATs to organism IDs (18.5 to 16.9 h), AST results (41.8 to 40.8 h), and

235 encing in 121 large consanguineous Pakistani ID families.

236 gnaling pathway, metabolic pathways (pathway IDs: 5200, 4151, 1100) were significantly enriched.

237 Users can submit either a PDB ID or PDB file for pocket detection to our NVIDIA GPU-eq

238 the ATP binding site of EGFR-TK domain (PDB ID:1M17) to elucidate vital structural residues necessar

239 dered structure of the truncated peptide PDB ID 1GNB.

240 ATTT]2 with compound 1 solved at 1.25 A (PDB-ID: 5LIT) shows that the drug covers the minor groove of

241 .20) and nonspecific muscle uptake (percent ID per gram, 0.41 +/- 0.0095; P = .06).

242 ative control MDA-MB-231 xenografts (percent ID per gram, 0.42 +/- 0.051; P = .20) and nonspecific mu

243 ith a sensitivity of over 90% for predicting ID (ferritin<15.0microg/L) via the ironPhone, demonstrat

244 treatment strategies do not reliably prevent ID-induced neurological deficits.

245 ficacy of early iron treatment in preventing ID-induced brain dysfunction.

246 We developed an assay using Primer ID-tagged deep sequencing to quantify HIV-1 splicing.

247 p-sequencing technology combined with Primer ID-tagged cDNA primers to efficiently quantify HIV-1 spl

248 versity Institutional Review Board, Protocol ID# AAAO3003.

249 ing LDMS, and confirmed previously published ID for 4 traits.

250 We quantified ID in 25 traits measured in [Formula: see text] particip

251 nic mutations that cause autosomal recessive ID (ARID) has lagged behind, predominantly due to non-av

252 ants in a single gene, 30 affecting reported ID genes and 30 affecting novel candidate ID genes.

253 s directly interact with previously reported ID proteins in six known pathways essential for cognitiv

254 from inbred mice demonstrate a reproducible ID hierarchy to the five major antigenic sites in the in

255 Dietary iron repletion completely reversed ID anemia and ineffective erythropoiesis of Hri(-/-) , e

256 ning of vaccinators for campaign and routine ID fIPV administration should focus on generating an 8-

257 oblematic SNPs, including SNPs with wrong RS ID and SNPs with mismatched probe sequences.

258 tionally active ordered conformation in GR's ID AF1 domain.

259 n the human glucocorticoid receptor's (GR's) ID AF1 domain.

260 population, mainly due to multiple sequence ID assignment caused by short read length.

261 dentified 14 individuals with mild to severe ID and/or developmental delay and de novo truncating PPM

262 s multiplex families with moderate to severe ID, epilepsy, and variable neuropsychiatric features.

263 %-40% of individuals with moderate to severe ID.

264 yield was higher in individuals with severe ID (35 of 77 [45.5%]), in multiplex families (42 of 107

265 nductively coupled plasma mass spectrometry (ID-ICP-MS).

266 proved to be equivalent to the gold-standard ID-SRM in terms of sensitivity (1-10 ppm), accuracy, and

267 alysis, the overall ratios of Portrait Staph ID/R BCP positive percent agreement and negative percent

268 The Portrait Staph ID/R BCP results were compared with results from convent

269 We evaluated the Portrait Staph ID/R blood culture panel (BCP) multiplex PCR assay (Grea

270 greement were 99.4%/99.9% for Staphylococcus ID and 99.7%/99.2% for mecA detection.

271 nt or breastfeeding at the time of the study.ID was present in 12.5% of 20,080 nonpregnant and nonbre

272 e last and penultimate exons cause syndromic ID, which provides additional insight into the role of c

273 an autosomal-dominant form of mild syndromic ID with ptosis, growth retardation, and hypotonia, and w

274 and that FEVR can be a part of the syndromic ID phenotype, further establishing the role that beta-ca

275 We discuss data showing that ID physicians improve clinical outcomes, positively impa

276 nationally representative data suggest that ID and IDA remain a concern in the United States.

277 and exciting, recognition of the value that ID physicians provide to the healthcare system as a whol

278 The ID consult group was more likely to receive an indicated

279 ers were higher in the ASD group than in the ID and GP groups.

280 C (7.5 vs 1 days, p<0.001) was longer in the ID consult group.

281 of transcription factors are located in the ID N-terminal domain that contains a powerful activation

282 on for brain development (i.e., brain tissue ID) before dysfunction occurs and to monitor its amelior

283 5% +/- 0.04% injected dose per gram tissue [%ID/g]), it was still higher than in all other organs exc

284 Ironically, the decline in applications to ID programs is occurring at a time when the need for ID

285 curate within a factor of 2 when compared to ID-SRM.

286 TLA further improved overall TAT to ID (18 to 16.5 h) and AST (42.3 to 40.7 h) results compa

287 duce both mortality and morbidity related to IDs.

288 er cellular and molecular defects underlying ID and neurodevelopmental disorders.

289 However, the molecular pathology underlying ID-associated TRMT1 mutations is unknown, since the biol

290 doses of the inactivated poliovirus vaccine (ID fIPV) is positively correlated with the size of the i

291 r data demonstrate a mechanism through which ID domain of the steroid receptors and other similar tra

292 r careers in public health and describes why ID physicians are so well suited to them.

293 sex (including 99 females with ASD, 77 with ID, and 73 with GP), estimates were consistent with over

294 lators have been genetically associated with ID disorders (IDDs).

295 o histone acetyltransferases associated with ID: KAT6A (also known as MOZ or MYST3) and KAT6B (MORF o

296 ressant medication use during pregnancy with ID in offspring and investigate the importance of parent

297 RTRs with ID had median (interquartile range) cFGF23 concentration

298 0-day mortality compared to patients without ID involvement (27% vs 45%, p<0.001), with an adjusted h

299 entrations higher than those of RTRs without ID (223 [131-361] versus 124 [88-180] RU/ml; P<0.001), w

300 accuracy and workflow of bacterial and yeast ID and bacterial AST using the Accelerate Pheno system i