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1 hy, Oral-Facial-Digital syndrome Type I (OFD Type I).
2 ppaB signaling, and increases AngII receptor type I a expression, thus potentiating AngII signaling i
7 his plasticity was dependent on the Rutabaga type I adenylyl cyclase, linking cAMP-dependent plastici
8 gnaling pathway that preferentially uses two type I (ALK2 and ALK3) and two type II (ActRIIA and BMPR
11 odes on a low-cost disposable chip; one cell type is allowed to pass through the chip whereas the oth
12 h" and then assigned levels of causality for type I and II autoimmunity in patients with CSU from lev
15 us and tibialis anterior muscles (with mixed type I and II fiber content), while a significant increa
17 lates with SAMHD1 protein up-regulation upon type I and II interferon stimulation in primary human mo
18 r ruxolitinib reduced hyperresponsiveness to type I and II interferons, normalized TH1 and follicular
21 ces PGC1alpha expression and a switch toward type I and IIa fibers in rat muscle and myotubes in vitr
22 Isolated collagens were characterized as type I and maintained their triple-helical structure, co
26 at anti-Ebola virus activity was overlooked, type I and type II IFNs (alpha-2a, alpha-2b, -beta, -gam
27 blocked binding of their cognate ligands to type I and type II TGF-beta receptors, indicating that C
32 ulated by cGMP/cGMP-dependent protein kinase type I, and recent ex vivo studies implicated that incre
36 erentiation by their activation of different type I BMP receptors and distinct modulations of the cel
37 e proportion of densely compact, homogenous (type I) bone versus more trabeculated, cancellous (type
39 asmalemmal-mitochondrial microenvironment in Type I cells and how theories of acute oxygen sensing ar
43 pe I procollagen (PINP) and C-telopeptide of type I collagen (CTX-I) are markers of bone formation an
44 chondral bone were determined by MicroCT and type I collagen alpha1/alpha2 ratio was determined by SD
50 t inactivation of Fam20C in cells expressing type I collagen led to skeletal defects and hypophosphat
51 imperfecta (OI) is a bone disease caused by type I collagen mutations and characterized by bone frag
52 as to investigate the use of self-assembling type I collagen oligomers as an injectable therapeutic d
55 f intron 36 of the Col1a1 gene, encoding the type I collagen, alpha1 chain, was responsible for the p
56 n, metabolism, and pharmacokinetics of a new type I collagen-targeted magnetic resonance (MR) probe,
63 ecause LBH gene variants are associated with type I diabetes mellitus, systemic lupus erythematosus,
64 remains the gold standard for treatment for type I diabetes providing an insulin-independent, normog
65 .c. islet delivery as a treatment option for type I diabetes, the more immediate benefit may be for t
67 class of reactions four pathways (Type I Z, Type I E, Type II Z, Type II E) are possible, leading to
69 genomic regions and of different transcript types (i.e., protein coding, noncoding, and pseudogenes)
70 kine response to IL-1beta in the tested cell types, i.e., neutrophils, macrophages, and fibroblasts,
72 ymer-GNR intraribbon heterostructures have a type-I energy level alignment and strongly localized int
74 s showed that the new method can control the type I error rate and is a bit conservative when compare
79 dispersed, the NB regression shows inflated Type-I error rates but the Classical logistic and Bayes
83 that cortical tissue normally operates as a type I excitable medium but it is locally transformed in
85 at many Tn7-like transposons contain minimal type I-F CRISPR-Cas systems that consist of fused cas8f
86 pe I-F system can be overcome through use of type I-F spacers by a horizontally-acquired type III-B s
87 n 'arms race' in which phage escape from the type I-F system can be overcome through use of type I-F
88 ive immune system in Pseudomonas aeruginosa (type I-F) relies on a 350 kDa CRISPR RNA (crRNA)-guided
92 ps, lipid infusion increased IMTG content in type I fibres (trained: +62%, sedentary: +79%; P < 0.05)
94 n about the allergen molecules causative for type I food allergy in animals, which, like in human pat
95 KEY POINTS: In the synaptic cleft between type I hair cells and calyceal afferents, K(+) ions accu
97 vitro, the afferent nerve calyx surrounding type I hair cells causes unstable intercellular K(+) con
98 nd that in the absence of the calyx, IK,L in type I hair cells exhibited unique biophysical activatio
100 el was established; within a dilute collagen-type I hydrogel, a novel clonal strain of rat cancer-ass
103 disease-exacerbatory role of LRV1 relies on type I IFN (type I IFNs) production by macrophages and s
106 although the inflammation is independent of type I IFN and the nucleic acid sensing TLRs, blocking t
108 FN treatment restricts HRV replication, with type I IFN being more potent than type III IFN, suggesti
109 L-6 production by control keratinocytes, and type I IFN blockade decreased IL-6 secretion by lupus ke
110 , CHOP and spliced XBP1 gene expression, and type I IFN by measuring IFNB1 (IFN-beta) and CXCL10 expr
116 ate that PRDM16 diminishes responsiveness to type I IFN in adipose cells to promote thermogenic and m
120 of chicken IFN-kappa (chIFN-kappa) near the type I IFN locus on the sex-determining Z chromosome.
121 , suggesting that extraepithelial sources of type I IFN may be the critical IFN for limiting enteric
122 alpha in immunosuppression and predicts that type I IFN modulation will be pivotal to cure human chro
123 peared to be independent of the induction of type I IFN or the effects of type II and III IFNs but we
124 se findings suggest that the STING-dependent type I IFN pathway is critical for the GBP-mediated rele
129 the treatment did not reduce the spontaneous type I IFN response and did not ameliorate lethal inflam
135 es have indicated that ZIKV evades the human type I IFN response, suggesting a role for the adaptive
138 ter, without which inflammatory cytokine and type I IFN responses to the double-stranded RNA analogue
140 7A NP-induced protection is mediated through type I IFN signaling and requires monocytes in PBMCs.
141 munomodulatory role by negatively regulating type I IFN signaling and, thus, HEV sensitivity to type
142 that DCIR deficiency impairs STAT1-mediated type I IFN signaling in DCs, leading to increased produc
144 This study highlights the importance of type I IFN signaling in inflammatory monocytes and the i
145 horiomeningitis virus infection, blockade of type I IFN signaling partially restores antiviral respon
157 LgyLRV1(-) ) strain of parasites followed by type I IFN treatment increased lesion size and parasite
159 enic analyses indicate that chIFN-kappa is a type I IFN with conserved genetic features and promoter
160 we tested whether chronic administration of type I IFN, at doses mimicking chronic viral infection,
161 by pretreatment of AMPK-deficient MEFs with type I IFN, illustrating that de novo production of IFN-
163 Moreover, significant associations between type I IFN-alpha/beta protein levels with the DNA methyl
164 induced early during HIV infection and that type I IFN-associated gene signatures persist, even duri
165 ing that hypomethylation and upregulation of type I IFN-associated genes might be critical in systemi
168 These findings identify HgIA as a novel type I IFN-independent model of systemic autoimmunity an
169 r studies define a TRIF-dependent, TLR4- and type I IFN-independent pathway of sterile liver injury i
173 cy also leads to persistently high levels of type I IFN-stimulated gene expression and to increased r
176 e and regulates HEV sensitivity to exogenous type I IFN.IMPORTANCE Hepatitis E virus (HEV) infection
177 ways between Nb and DBP-FITC, but revealed a type-I IFN (IFN-I) signature unique to DCs from Nb-prime
178 ition receptors (TLR9 and TLR3) leading to a type-I IFN mediated innate immune response that is modul
182 ited an alpha-helical fold characteristic of type I IFNs and bound to IFNalpha/beta receptor 1 (IFNAR
183 se studies were limited to a small number of type I IFNs and, during the most recent outbreak of Ebol
187 cerbatory role of LRV1 relies on type I IFN (type I IFNs) production by macrophages and signaling in
188 ive, and antibacterial activities typical of type I IFNs, albeit with 100-1000-fold reduced potency c
191 etal (M) replacement in the framework nodes (type I), (ii) metal node extension (type II), and (iii)
193 pregnant C57BL/6 mice and protects type I or type I/II interferon receptor-deficient mice against let
195 mily that signals through the IL-20 receptor type I (IL-20Ralpha:IL-20Rbeta), is a cytokine whose fun
196 s are differentiated into >220 different emm types, is immunogenic and elicits protective antibodies.
197 a humanized mouse model and demonstrate that type I interferon (IFN) is induced early during HIV infe
199 d that the brain parenchyma has a functional type I interferon (IFN) response that can limit VSV spre
201 ost karyopherin alpha (KPNA) proteins blocks type I interferon (IFN) signaling, which is a central co
202 r T-bet acts as a selective repressor of the type I interferon (IFN) transcriptional program in respo
204 tive CD11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct
205 rica serovar Typhimurium exploits the host's type I interferon (IFN-I) response to induce receptor-in
207 antiretroviral therapy (cART), low levels of type I interferon (IFN-I) signaling persist in some indi
208 sly and induces the subsequent expression of type I interferon and other proinflammatory cytokines.
209 he authors show that the chronic presence of type I interferon in aged mouse brain impedes cognitive
212 cal roles in coordinating both virus-induced type I interferon production and apoptosis; however, the
213 e, a synthetic analogue of histamine reduces type I interferon production in a mouse model of influen
214 e the neuropathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 (-/-)
215 NAR(fl/fl) C57BL/6 (H-2(b)) mice lacking the type I interferon receptor in a subset of myeloid cells.
217 onstrated impaired viral clearance, a slower type I interferon response and delayed production of vir
222 n of host responses, including inhibition of type I interferon responses, suppression of dendritic ce
223 stimulation with anti-CD3/CD28 antibodies or type I interferon resulted in upregulation of distinct s
227 ol, preventing accumulation and a subsequent type I interferon-associated inflammatory response.
228 in conjunction with a global suppression of type I interferon-signalling pathway and an aberrant exp
230 ce with polyethylene glycolyated (PEGylated) type-I interferon-alpha2b reduces the expression of many
234 ion of toll-like receptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from plasmacytoid de
236 be a driving force in immune exhaustion, and type I interferons (IFN-I) are emerging as critical comp
239 ctivates the adaptor protein STING to induce type I interferons (IFNs) and other immune modulatory mo
243 ta support a model wherein the production of type I interferons driven by an autoimmune risk variant
244 387 of U-STAT2 might enhance the efficacy of type I interferons in many different clinical settings.
245 d that the proinflammatory cytokines TNF and type I interferons induced transcriptional cascades that
248 To evaluate the safety of concurrent Boston type I keratoprosthesis (KPro) and glaucoma drainage dev
252 hangiogenesis (in melanomas and other tumour types) is limited by the paucity of mouse models for liv
253 s around 125 K, leading to the presence of a type-I multiferroic phase with huge electric polarizatio
254 Fitzpatrick skin phototype (for type IV vs. type I, multivariable-adjusted RR = 0.99, 95% CI: 0.92,
259 f ZIKV in pregnant C57BL/6 mice and protects type I or type I/II interferon receptor-deficient mice a
260 tially fatal condition caused by deficiency (type I) or dysfunction (type II) of the C1 inhibitor pro
261 We recently reported 1a (skepinone-L) as a type I p38alpha MAP kinase inhibitor with high potency a
262 I crystal lattice in contrast to the typical type I packing seen from membrane protein structures cry
263 ed levels of plasminogen activator inhibitor type I (PAI-1) have been shown to promote fibrosis in mu
265 duced aquaporin-2 phosphorylation within the type I PDZ-ligand motif disrupted the interaction, in as
270 eveals two distinct tumor types: the mutator type is positively associated with potential response to
274 approximately 60% of all PV-IR synapses, and Type I PV-IR synapses from putative thalamocortical term
277 ral motif essential for binding the TGF-beta type I receptor (TbetaRI) but dispensable for binding th
279 ungus Blastocladiella emersonii, combining a type I rhodopsin domain with a guanylyl cyclase domain.
280 netobacter species produce both a functional type I secretion system (T1SS) and a contact-dependent i
282 end not only on TLR9, but also on interferon type I signaling, and both mechanisms can be inhibited b
286 a partial agonist at AMPARs associated with Type I TARPs, evoked whole-cell currents in lamina II ne
289 hat used by the previous study, wherein case Types I to IV defined increasing severity of periodontal
290 mbining the historical nomenclature for penA types I to XXXVIII with novel nucleotide sequence design
291 ive infantile paralysis and premature death (type I) to limited motor neuron loss and normal life exp
294 ort three distinct types of ependymal cilia, type-I, type-II and type-III classified based upon their
297 caSR is similar to the adenovirus-associated type I (VAI) RNA in terms of both nucleotide sequence an
298 To test the hypothesis that muscles rich in type I vs. type II muscle fibers would exhibit similar c
299 emia is categorized into two main subgroups: type I, which is seen exclusively in clonal hematologic
300 For this class of reactions four pathways (Type I Z, Type I E, Type II Z, Type II E) are possible,
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