ライフサイエンスコーパス: I

1 I address these issues first by evaluating the extent to

2 I argue that the existing framework for grass infloresce

3 I conclude by proposing ways in which this framework can

4 I found significant variation in niche position, niche b

5 I have been blessed with the selection of my research to

6 I implement this method in an accurate and low-overhead

7 I reviewed 187 existing applications of computer vision

8 I-5 injection improves coordinated locomotion, and this

9 an Joint Committee on Cancer [AJCC] stage 0, I, or II), and 48 (51.6%) were diagnosed with late-stage

10 ssociation with HSIL-CIN2+ (0.65, 0.40-1.06; I(2)=30%).

11 In addition, (123)I-FP-CIT has modest affinity for the serotonin transport

12 -FP-CIT binding to DAT and hypothalamic (123)I-FP-CIT binding to SERT are significantly lower in MSA-

13 Striatal (123)I-FP-CIT binding to DAT and hypothalamic (123)I-FP-CIT b

14 aphy was performed with (125)I-JR11 and (125)I-Tyr(3)-octreotide in cancers from prostate, breast, co

15 was induced by jugular vein infusion of (125)I-fibrin or fluorescein isothiocyanate-fibrin labeled em

16 The biodistribution of (125)I-iodo-DPA-713 was determined under the same conditions,

17 as imaged using a fluorescent analog of (125)I-iodo-DPA-713, DPA-713-IRDye800CW, for correlative hist

18 s were performed 1 h after injection of (125)I-pentixafor (7.5 MBq/kg).

19 einjection of a CXCR4 inhibitor reduced (125)I-pentixafor uptake in atherosclerotic plaques by approx

20 ptor autoradiography was performed with (125)I-JR11 and (125)I-Tyr(3)-octreotide in cancers from pros

21 ies (relative risk, 0.93; 95% CI, 0.77-1.13; I = 0.0%) or observational studies (odds ratio, 0.90; 95

22 dose per unit administered activity of (131)I, after THW and rhTSH, was 232 and 62 (patient 1), 12 a

23 recorded in cultured astrocytes was [Ca(2+)]I dependent.

24 received TC6 plus bevacizumab on NSABP B-46-I/USOR 07132 were not included.

25 tudies (odds ratio, 0.90; 95% CI, 0.54-1.51; I = 76.1%).

26 en with a cysteine protease inhibitor, E-64 (I-1).

27 lted in an HR of 1.52 (95% CI, 1.39 to 1.67; I(2) = 0%) per 0.1 unit.

28 ted odds ratio [aOR] 0.83, 95% CI 0.70-0.99; I(2)=51%, adjusted for CD4 cell count and ART duration),

29 nfected with phytoplasma subgroup16SrXIII-(A/I)I (SbGP/MPV).

30 lure was a relatively infrequent event after I-125 brachytherapy in our series.

31 metallochaperone that transfers Cu(I) and Ag(I) to the CusCBA transporter from the periplasm.

32 The limits of detection for Br and I using the MIC method followed by ICP-MS determination

33 rent amino acid compositions and angiotensin I-converting enzyme (ACE) inhibitory potentials.

34 Angiotensin-I converting enzyme (ACE) is a zinc metalloprotease cons

35 o were in the higher cholesterol efflux/apoA-I presented significantly higher disposition index (beta

36 n, HDL-cholesterol efflux normalised to apoA-I was inversely associated with T2DM development in card

37 transcription, which are found within areas I (bp -2694 to -2561), II (bp -2139 to -1958), III (bp -

38 ession of immunosuppressive factors arginase I and iNOS.

39 rvation of natural hydrothermal pyrites, As(-I) is usually assigned to the occupation of tetrahedral

40 ations of Bemisia tabaci genetic groups Asia-I, Asia-II-1, and Asia-II-7.

41 ophos and 3x for cypermethrin among the Asia-I, while, they were 7x for cypermethrin, 6x for deltamet

42 ithelial cells, primarily alveolar type (AT) I cells, die and slough off, resulting in enhanced perme

43 S technique was used to separate isomeric Au(I) metallopeptide ions that were formed by Zn(II) displa

44 The catalytic power of Au(I) in BC stems from a combination of two sources: stereo

45 at compared activation in patients with axis I disorders and matched healthy control participants dur

46 date and putamen of 16 RC BD-I, 34 non-RC BD-I and 44 healthy controls were assessed.

47 s (P<0.005) and in ACC compared to non-RC BD-I patients (P<0.05).

48 levels in ACC, putamen and caudate of RC BD-I patients compared to healthy controls (P<0.005) and in

49 ortex (ACC), caudate and putamen of 16 RC BD-I, 34 non-RC BD-I and 44 healthy controls were assessed.

50 ) or at an interstimulus interval in-between I-waves (3.5 ms; control protocol) on separate days in a

51 kers (midkine, adiponectin, apolipoprotein C-I, and kidney injury molecule-1).

52 Ag(110) surfaces leads to the scission of C-I bonds followed by the formation of organometallic zigz

53 est status areas lost 0.13% yr(-1) (IUCN Cat I).

54 on causes a reduction in the CENP-T and CENP-I CCAN components at the centromere and leads to lagging

55 an additional chromosome, such as chromosome I.

56 Class I KNOTTED-LIKE HOMEOBOX (KNOX) proteins regulate develop

57 tibodies alone, 4% Class II, and 14.4% class I and class II at mean fluorescent intensity greater tha

58 Current guidelines give a class I recommendation to use of embolic protection devices (E

59 e eliminates surface expression of all class I molecules, but leaves the cells vulnerable to lysis by

60 nsgenic FVB mice that express the D(b) class I molecule.

61 30% of subjects had circulating class I antibodies alone, 4% Class II, and 14.4% class I and c

62 ptide-major histocompatibility complex class I (p-MHC I) proteins displayed by antigen-presenting cel

63 Major histocompatibility complex class I molecules (MHC I) help protect jawed vertebrates by bi

64 on of major histocompatibility complex class I molecules to brain atrophy in Theiler's murine encepha

65 intermediate filaments, SH3-containing class I myosins, the dual-GEF Trio, and other adaptors and sig

66 To achieve this, we predicted HLA class I- and class II-restricted peptides from rDEN2Delta30 an

67 ry miRNA signature associated with HLA class I-DSA could improve our understanding of ABMR and be use

68 Accordingly, like class I, DP(84Gly) constitutively presents endogenous peptides

69 nal transfer of immunity can cross MHC class I barriers and that Th1 immunity can be imparted to Th2-

70 s presented on the cell surface by MHC class I molecules.

71 city depends on the recognition of MHC class I-epitope complexes at the cell surface.

72 accine vectors expressing a single MHC class I-restricted high-avidity epitope provided strong, T cel

73 cell corpse-associated antigens to MHC class I-restricted T cells, a property that was associated wit

74 Forty patients presenting Miller Class I and II GRs were previously treated by CTG (control gro

75 S family, including the monofunctional class I diTPS PxaTPS8, which converts geranylgeranyl diphospha

76 NRG3 class I was increased in bipolar and major depressive disorder

77 with a significant higher frequency of class I, a higher frequency and a higher mean fluorescence int

78 -binding region contains both putative Class I (-(592)SAV-) and Class II (-(595)CLDM-) PDZ-binding mo

79 is in its infancy as compared to their class I counterparts.

80 Silencing of the HLA class-I APM is due to histone deacetylation as inhibition of h

81 In contrast to re-induction of HLA class-I by interferons, HDAC inhibitors did not interfere with

82 Indeed, a reduced HLA class-I expression was observed in MCC tumor tissues and MCC c

83 Thus, HDAC inhibition restored HLA class-I surface expression in vitro and in a mouse xenotranspl

84 Depletion of TANGO1 in HSCs blocked collagen I secretion without affecting other matrix proteins.

85 mutation carriers, showed decreased complex I activity and altered mitochondrial network morphology.

86 he elusive "energy-coupling" site in complex I at which energy generated by the redox reaction is use

87 odynamically drive proton pumping in complex I.

88 mTOR complex I (mTORC1) is a central growth regulator that senses ami

89 Energy-transducing respiratory complex I (NADH:ubiquinone oxidoreductase) is one of the largest

90 alescence of the 5 and 3 sites in a complex (I, initial), but if this cannot form the components show

91 posed to increase the reactivity of compound I with respect to C-H bond activation.

92 la embryos, we dissect the role of condensin I in the maintenance of mitotic chromosome structure wit

93 process has been incredibly time-consuming, I have become quite familiar with every paper that we pu

94 ene is insertion of the alkene into a copper(I) hydride formed by reversible dissociation of HBpin fr

95 between arylazides N3 Ar with a bulky copper(I) beta-diketiminate.

96 macrocycle cavity are able to chelate copper(I) endotopically.

97 of eukaryotic cells contain a labile copper(I) pool localized in the matrix where also the mitochond

98 one involving intermediates with only copper(I).

99 d alkyne, has been established by the copper(I)-catalyzed cross-coupling of 1,1-dibromoenamides with

100 odal tDCS increased activation in right Crus I/II during semantic prediction and enhanced resting-sta

101 m hydrogen gas by selective adsorption at Cu(I) sites in a metal-organic framework.

102 ace in the full CusB protein upon binding Cu(I).

103 A copper complex, [Cu(I)(tmpa)(MeCN)](+), effectively reductively couples NO(g

104 tion, the nature and stability of the GSH-Cu(I) complexes formed under biologically relevant conditio

105 CusF is a metallochaperone that transfers Cu(I) and Ag(I) to the CusCBA transporter from the periplas

106 er via an out-of-cage mechanism in which [Cu(I)(carb)2](-) and [Cu(II)(carb)3](-) (carb = carbazolide

107 -Cys(IV) and Cys(II)-Cys(III)), or bead (Cys(I)-Cys(II) and Cys(III)-Cys(IV)).

108 ible disulfide connectivities: globular (Cys(I)-Cys(III) and Cys(II)-Cys(IV)), ribbon (Cys(I)-Cys(IV)

109 )-Cys(III) and Cys(II)-Cys(IV)), ribbon (Cys(I)-Cys(IV) and Cys(II)-Cys(III)), or bead (Cys(I)-Cys(II

110 egatively correlated with LLD, such as DNase I hypersensitivity sites (DHSs).

111 dentified based on hypersensitivity to DNase I digestion and association with H3K4me3-modified nucleo

112 Enrichment of SNPs associated with DNase I-hypersensitive sites was also found in many tissue typ

113 ed with plasmid DNA encoding perlecan domain I and VEGF189 and analyzed in vivo for their ability to

114 mid DNA encoding VEGF189 and perlecan domain I have the potential to induce angiogenesis and wound he

115 (also known as Esp1) contains four domains (I-IV), and a substrate-binding domain immediately preced

116 Importantly, neurobehavioral deficits, E/I imbalance, and histological damage are all ameliorated

117 creased ratio of excitatory to inhibitory (E/I) neurotransmission.

118 provide a framework for the development of E/I balance at the cellular level.

119 a model of Fragile-X Syndrome, to test the E/I imbalance theory.

120 P robabilistic A lgorithm for S omatic Tr ee I nference (PASTRI), a new algorithm for bulk-tumor sequ

121 reveal evidence of heterogeneity of effect (I(2)=0.0, p=0.56).

122 the Syrian conflict and the Ebola epidemic, I recommend four sets of actions that would make the hum

123 Fol strains that evade I-2 recognition carry point mutations in Avr2 (e.g. Avr2

124 decay-accelerating activity (DAA) and factor I cofactor activity (CA).

125 Inhibition of the insulin-like growth factor I receptor (IGF-IR) is a new therapeutic strategy to att

126 glucose, insulin, insulin-like growth factor I, triglycerides, cholesterol, cortisol, and leptin, wer

127 d a 2.55% (95% CI, 0.93, 4.21) increase in G/I ratio.

128 g of IAV RNA by retinoic acid inducible gene I (RIG-I) initiates ZBP1-mediated cell death via the RIG

129 /- SD recruitment age: 2.8 +/- 0.9 y; GMFCS: I, 48%; II, 11%; III, 15%; IV, 11%; and V, 15%).

130 Finally, the intercalating dye SYBR Green I (SG) was inserted into the dsDNA, generating enhanced

131 wer FFM-for-height than those in GMFCS group I.

132 with movement execution, EAAC1 limits group I metabotropic glutamate receptor (mGluRI) activation, f

133 right eyes of 14 rats (low dose; study group I, high dose; study group II).

134 = 153) failed to show noninferiority of GSH-I (adjusted effect, 1.47; 95% CI, -0.01 to 2.91; P = .05

135 nd activation product [1-F-2-IMe -C6 H4 ](+) I(-) (3).

136 Here, I review current progress in the pursuit of an evolution

137 Here, I review the evidence of whether mito-nuclear interactio

138 Here, I review these accounts and discuss their implications f

139 Here, I summarize key features of current knowledge of genomic

140 Herein I summarize the considerable progress made and remaining

141 ent (Egger P = .51); heterogeneity was high (I(2) = 92%, P < .001).

142 Maximal heterozygosity at HLA-I loci ("A," "B," and "C") improved overall survival aft

143 e presence of conformational variants of HLA-I on SAB, assessment of which would increase the concord

144 silences protective mucosal interferon (IFN)-I and III production associated with enhanced rhinovirus

145 WNV) infection by regulating type I IFN (IFN-I) response.

146 th elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct link between reduced CD

147 Type I interferons (IFN-I) are critical in antimicrobial and antitumor defense.

148 Under these conditions, the IGF-I receptor signals through an alternate scaffold protein

149 functional intrathymic negative selection in I-A(12%) mice, transfer of I-A(12%) CD25(-)CD4(+) T cell

150 nd mice with various ribonucleases including I, A, S7 and T1, characterized their cutting preferences

151 the rhythmicity of descending late indirect (I) waves in corticospinal neurons (4.3 ms; I-wave protoc

152 to reveal the heterogeneity in IL-4-induced I transcription.

153 red by flow cytometry on day 28 of induction I.

154 ell line) with the BET bromodomain inhibitor I-BET151 resulted in selective growth inhibition, wherea

155 itors (such as ruxolitinib and JAK inhibitor I) strongly stimulate VSV replication and oncolysis in a

156 uropean Leukemia Net (ELN) 2010 intermediate I prognostic risk AML (EFS, 26% +/- 4 vs 40% +/- 5 at 4

157 er, whether CD6 plays any role in intestinal I/R-induced injury and, if so, the underlying mechanisms

158 s afferent synapses onto immature rat lamina I spino-parabrachial neurons, which serve as a major sou

159 ccumulation of p62 and downregulation of LC3-I/II conversion as well as reduced Tfeb expression.

160 creased LC3B-II level and conversion of LC3B-I to LC3B-II, decreased autophagosome formation, and inc

161 was limited given the preponderance of level I studies.

162 hiff base deprotonation at the lumirhodopsin I intermediate stage.

163 ailed to segregate accurately during meiosis I.

164 eductional chromosome segregation of meiosis I, which also results in chromosomal exchanges.

165 identified scavenger receptor class A member I (SR-AI) as a receptor for coagulation factor X (FX), m

166 glutamated substrates, which activate mGluR I.

167 associated Ags into peptide displayed by MHC I is however defective in hepatocytes lacking collectrin

168 compatibility complex class I molecules (MHC I) help protect jawed vertebrates by binding and present

169 or histocompatibility complex class I (p-MHC I) proteins displayed by antigen-presenting cells.

170 development, precedes the expression of MHC-I-specific inhibitory receptors, and is modulated in an

171 levels when fed a diet supplying the minimum I(-) requirement for rodents.

172 -dimesityl-2,2'-bipyridine ligand in [fac-Mn(I)(mes2bpy)(CO)3(CH3CN)](OTf), which prevents Mn(0)-Mn(0

173 s study explores a potential therapy for MPS-I at a very early stage in life and represents a novel m

174 (I) waves in corticospinal neurons (4.3 ms; I-wave protocol) or at an interstimulus interval in-betw

175 The isotropic and nematic (I + N) coexistence for rod-like colloids is a signature

176 Characterization of the Ni(I)-CO species through spectroscopic and computational te

177 The recessive and functionally null I/LnJ H2-Ob allele supported the production of virus-neu

178 tive selection in I-A(12%) mice, transfer of I-A(12%) CD25(-)CD4(+) T cells into RAG-knockout hosts r

179 MDS-UPDRS Part I total mean (SD) scores increased from baseline 5.6 (4.

180 parasite-specific transcription factor PfAP2-I, belonging to the Apicomplexan AP2 (ApiAP2) family, th

181 luminescent up-converting phosphor anti-PGL-I test [UCP-LFA].

182 We conducted a phase I, randomized, double-blind, placebo-controlled, dose-es

183 de-based therapies have been tested in phase I clinical trials, a quarter of which have reached phase

184 AC-C) showed limited immunogenicity in phase I clinical trials.

185 Patients and Methods This phase I study tested durvalumab doublets in parallel 3 + 3 dos

186 Patients and Methods This phase I study tested the combination of M6620 and topotecan in

187 one and donor-side limitation of photosystem I (PSI).

188 This demonstrates the essentiality of a Pol I-transcribed ES, as well as conserved VSG 3'UTR 16-mer

189 e to sequential challenges with LPS and Poly I:C, a TLR3 ligand, which was physiologically associated

190 upregulated for LTA, LPS, Poly(dT), and Poly(I:C), and 12, 142, 249, and 16 genes were downregulated

191 wnregulated for LTA, LPS, Poly(dT), and Poly(I:C), respectively, with at least a 1-fold change relati

192 II) chelated PyED outcompetes DNA polymerase I to successfully inhibit template strand extension.

193 s of established prognostic factors: PRETEXT I/II, PRETEXT III, PRETEXT IV, metastatic disease, and A

194 Process I is seen at temperatures below the bulk solvent Tg, has

195 of characterizing most biological processes, I propose that the progression and outcome of disease-ca

196 In meiotic prophase I, homologous chromosome pairing is promoted through chr

197 icient SC destruction at the end of prophase I to ensure faithful inheritance of the genome.

198 9m)Tc-MAS3-y-nal-k(Sub-KuE) and (99m)Tc-PSMA-I&S in consistently high radiochemical yield and purity

199 The pharmacokinetics of (99m)Tc-PSMA-I&S in humans were investigated in a patient with advanc

200 perative SPECT/CT showed a high (99m)Tc-PSMA-I&S uptake in all suspect lesions identified in previous

201 xamined in mouse focal ischemia/reperfusion (I/R) model.

202 In this focused review, I examine recent paradigm shifts that have transformed o

203 In this review, I summarize the current knowledge on the mode of activat

204 and a Cu(II) oxidant to styrene using the Rh(I) catalyst ((Fl)DAB)Rh(TFA)(eta(2)-C2H4) [(Fl)DAB = N,N

205 ote mitochondrial localization to actin-rich I-bands in body wall muscle.

206 tion on the promoters of IRF1, IRF7, and RIG-I, producing their enhanced expression by transcriptiona

207 cell different complexes formed between RIG-I, TRIM25, and MAVS, in the presence or absence of two v

208 we directly monitor RNA proof-reading by RIG-I and we show that it is controlled by a set of conserve

209 V RNA by retinoic acid inducible gene I (RIG-I) initiates ZBP1-mediated cell death via the RIG-I-MAVS

210 and that the proteasome plays a role in RIG-I degradation.

211 signaling pathway involves inhibition of RIG-I K63-linked polyubiquitination and that the proteasome

212 sted that NS1-mediated inhibition of the RIG-I-like receptor (RLR) signaling pathway involves inhibit

213 itiates ZBP1-mediated cell death via the RIG-I-MAVS-IFN-beta signaling axis.

214 RNA pseudogene 141 (RNA5SP141), bound to RIG-I during infection with herpes simplex virus 1 (HSV-1).

215 de chain of the neomycin or paromomycin ring I, as part of the dioxabicyclooctane ring, into either t

216 assigned to the occupation of tetrahedral S(-I) sites, with the same oxidation state as in arsenopyri

217 , from the perspective of a young scientist, I naively ask: Is the great diversity of questions in ne

218 he gastroesophageal junction tumors (Siewert I), were randomized between open and MI esophagectomy wi

219 derived aminophosphine ligand for the silver(I) salt and the 2-bis(aryl)methylpyrrolidine catalyst wh

220 on, further substantiating a role for ST6Gal-I in cell survival.

221 richment of clonal variants with high ST6Gal-I expression, further substantiating a role for ST6Gal-I

222 for CCA versus control, 0.905 for CCA stage I-II versus control, 0.789 for PSC versus control, 0.806

223 .796 for CCA versus PSC, 0.956 for CCA stage I-II versus PSC, 0.904 for HCC versus control, and 0.894

224 o identify veterans having surgery for stage I-III colorectal cancer from 1999 to 2010.

225 .2) kg/m(2), respectively, and 82% had stage I or II breast cancer.

226 tified women diagnosed with unilateral stage I to III breast cancer between 1998 and 2012 within the

227 ority of patients (80%) presented with stage I disease.

228 A total of 122 patients with stage I to III colon cancer were included.

229 Patients and Methods Early-stage (I-III) AABCS were randomly assigned to a 6-month interve

230 Complete resection (stages I and II) was achieved in 32 patients, and 28 patients h

231 Women with stages I to III breast cancer who received all or part of their

232 Unexpectedly, the switch I mutations had only modest effects on GTP binding and o

233 I originally enrolled 1230 patients in TENOR I.

234 Furthermore our microCT data showed that I-PTH treatment led to an increased bone volume fraction

235 The I-TASSER-MR algorithm was tested in large-scale benchmar

236 ndividuals with spinal cord injury after the I-wave protocol.

237 ed in cancer cells, involving release of the I(-) ligand in the presence of glutathione (GSH).

238 Thus, I personally select papers (both original investigations

239 s, as well as for adenosine to inosine (A to I) RNA editing of Ctn RNA in muscle cells.

240 ersion both spontaneously and in response to I-SceI-induced DSBs.

241 own of ATF6 in cardiac myocytes subjected to I/R increased reactive oxygen species and necrotic cell

242 Tens of thousands of A-to-I editing events are defined in the mouse, yet the funct

243 tanding of the biological importance of A-to-I editing.

244 ly increased carnitine palmitoyl transferase I in normal rodent hearts has been shown to recapitulate

245 type natriuretic peptide (BNP), and troponin I (TnI) concentrations and electrocardiographic, echocar

246 measuring high-sensitivity cardiac troponin I concentrations in patients with suspected acute corona

247 assay for the detection of cardiac troponin I using electrical double layer gated high field AlGaN/G

248 o Ser200 in mouse) of cTnI (cardiac troponin I) is significantly hyperphosphorylated, and in vitro st

249 Type I IFN-mediated neutrophil activation and NET formation m

250 Type I interferon (IFN) signaling engenders an antiviral stat

251 Type I interferons (IFN-I) are critical in antimicrobial and

252 Type I interferons (IFNalpha/beta) are critical mediators of

253 Type I interferons (IFNs) are essential mediators of antivira

254 e responses through the initiation of a type I IFN-dependent DDR.

255 ice or wild-type mice treated with anti-type I IFNR alone.

256 While induction of antiviral type I interferons (IFNs) is the major outcome of STING activ

257 How can neural tissue exhibit both type I and type II excitability?

258 rofiling was conducted to confirm a CDG type I defect.

259 h modified standard errors have correct type I error under the null.

260 iation by their activation of different type I BMP receptors and distinct modulations of the cell cyc

261 ctivation of Fam20C in cells expressing type I collagen led to skeletal defects and hypophosphatemia.

262 For type I and II CRISPR-Cas systems, single-nucleotide mutations

263 acter species produce both a functional type I secretion system (T1SS) and a contact-dependent inhibi

264 Both genes play significant roles in type I interferon (IFN) production and signalling.

265 est the hypothesis that muscles rich in type I vs. type II muscle fibers would exhibit similar change

266 This SAM vaccine-induced type I IFN response has the potential to provide an adjuvant

267 oles in coordinating both virus-induced type I interferon production and apoptosis; however, the regu

268 a fall in oxygen levels might initiate Type I cell activation.

269 ot only on TLR9, but also on interferon type I signaling, and both mechanisms can be inhibited by adm

270 y important roles in the ISG15-mediated type I IFN sensitivity of HEV.

271 The characteristic feature of type I hair cells is the expression of a low-voltage-activate

272 so leads to persistently high levels of type I IFN-stimulated gene expression and to increased resist

273 an alpha-helical fold characteristic of type I IFNs and bound to IFNalpha/beta receptor 1 (IFNAR1) an

274 and antibacterial activities typical of type I IFNs, albeit with 100-1000-fold reduced potency compar

275 n years ago, predating the evolution of type I IFNs.

276 CD11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct link

277 pathies) characterized by expression of type I interferon in the brain.

278 host responses, including inhibition of type I interferon responses, suppression of dendritic cell ma

279 ctional importance in the regulation of type I interferon signaling.

280 onjunction with a global suppression of type I interferon-signalling pathway and an aberrant expressi

281 pport a model wherein the production of type I interferons driven by an autoimmune risk variant and t

282 To control the overall type I error rate at 0.05, a hierarchical testing strategy wa

283 chronic infections display a persistent type I IFN signature.

284 that signals through the IL-20 receptor type I (IL-20Ralpha:IL-20Rbeta), is a cytokine whose function

285 ile virus (WNV) infection by regulating type I IFN (IFN-I) response.

286 reatment did not reduce the spontaneous type I IFN response and did not ameliorate lethal inflammatio

287 reventing accumulation and a subsequent type I interferon-associated inflammatory response.

288 One system (type I-F) targets DNA.

289 in immunosuppression and predicts that type I IFN modulation will be pivotal to cure human chronic i

290 hicken IFN-kappa (chIFN-kappa) near the type I IFN locus on the sex-determining Z chromosome.

291 However, when the type I IFN response of mice was suppressed, then the adaptive

292 unity highlighting key paradigms of the type I IFN response.

293 Using siRNAs to type I and II BMP receptors and the signaling intermediaries

294 ked binding of their cognate ligands to type I and type II TGF-beta receptors, indicating that Cripto

295 patrick skin phototype (for type IV vs. type I, multivariable-adjusted RR = 0.99, 95% CI: 0.92, 1.05)

296 e LBH gene variants are associated with type I diabetes mellitus, systemic lupus erythematosus, RA, a

297 es in the metabolic profile among uninfected I. scapularis nymphal ticks, B. burgdorferi-infected nym

298 hous, with slightly different C-X...NR3 (X = I, Br) distances and packing interactions.

299 calculation allows us to determine that zone I displays an orthorhombic-like monoclinic structure wit

300 erapy for some cases (such as eyes with zone I disease or aggressive posterior ROP), the disadvantage