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1 ion is increased in human cells treated with interferon alpha.
2 on, a defect that was completely reversed by interferon-alpha.
3 en in patients treated with interleukin-2 or interferon-alpha.
4 n a model using the prototypic SLE cytokine, interferon-alpha.
5 ctably translated and induced high levels of interferon-alpha.
6 so ruled out involvement of BAFF, IL-12, and interferon-alpha.
8 MDM2, both alone and combined with pegylated interferon alpha 2a (Peg-IFNalpha 2a), significantly dec
9 f the NLEM decided to include both pegylated interferon alpha 2a and alpha 2b into the NLEM for treat
10 mparing between the combination of pegylated interferon alpha 2a or alpha 2b and ribavirin with a usu
11 , this research determined whether pegylated interferon alpha 2a or alpha 2b plus ribavirin is more c
14 ort the three-dimensional structure of human interferon alpha-2A (IFN-alpha2A) bound to the Fab fragm
15 of subtenon injections of natural leukocyte interferon alpha-2a (IFNalpha) on best corrected visual
17 ith vaniprevir in combination with pegylated interferon alpha-2a (Peg-IFN-alpha-2a) plus ribavirin (R
19 ducted a short-course (4 weeks) of pegylated interferon alpha-2a (Peg-IFN-alpha2a) plus ribavirin (RB
20 ce-daily (BID) in combination with pegylated interferon alpha-2a (Peg-IFNalpha-2a)/ribavirin (RBV).
22 ties of TG4040 in combination with pegylated interferon alpha-2a and ribavirin (PEG-IFNalpha/RBV) in
23 e safety and efficacy of simeprevir with peg-interferon alpha-2a and ribavirin (PR) in a randomized,
25 factor (EGF) as a cell targeting element and interferon-alpha-2a (IFNalpha-2a) to initiate signal tra
27 800 mg/d) plus amantadine (200 mg/d), or PEG interferon alpha 2b (1.0 microg/kg per week) plus ribavi
28 tive patients were randomized to receive PEG interferon alpha 2b (1.0 microg/kg per week), ribavirin
29 ferent antiviral therapy regimens (pegylated interferon alpha 2b and ribavirin different dosages, and
30 are the cost associated with surgical versus interferon-alpha 2b (IFNalpha2b) treatment for ocular su
31 consecutively with topical MMC (0.4 mg/mL), interferon alpha-2b (1 million units/mL), or both for OS
32 f Escherichia coli-derived recombinant human interferon alpha-2b (rhIFN alpha-2b), generated by postt
34 ficacy and safety of pretransplant pegylated interferon alpha-2b plus ribavirin (Peg-IFN-alpha2b/RBV)
36 ed and constant plasma levels of leuprolide, interferon alpha-2b, letrozole, Y-27632, octreotide, and
38 ither bevacizumab (10 mg/kg every 2 wk) with interferon-alpha (3-9 million IU 3 times/wk) (n = 11) or
40 depression in the context of treatment with interferon-alpha, a widely used model to mimic depressio
41 ll eight cases assayed showed elevated serum interferon alpha activity, and gene expression profiling
43 nd multiple myeloma) and 9 treatment agents (interferon-alpha, alemtuzumab, bendamustine, bortezomib,
44 by proinflammatory cytokines, which include interferon alpha and gamma and interleukin 2, 2R, 6, 7,
46 te HCV treated with 24-48 weeks of pegylated interferon alpha and ribavirin, 15 failed to achieve a s
47 ients under various treatment protocols with interferon alpha and/or nucleoside or nucleotide analogs
48 ular endothelial cells confers an ability of interferon-alpha and a soluble IL-6 receptor/IL-6 (sIL-6
50 phalitis virus NS1s in the blood of infected interferon-alpha and gamma receptor-deficient mice (AG6)
51 g CCR5(+) monocytes/macrophages and enhanced interferon-alpha and interferon-gamma production 2 days
53 Importantly, SOCS1 coexpression inhibited interferon-alpha and interferon-gamma signaling and prot
55 ere capable of secreting effector cytokines, interferon-alpha and interleukin-12, respectively, in re
57 GS-9620 administration induced production of interferon-alpha and other cytokines and chemokines, and
59 laprevir (TVR) in combination with pegylated interferon-alpha and ribavirin (P/R) for the treatment o
60 eavy alcohol use on treatment with pegylated interferon-alpha and ribavirin (P/R) in an insured house
61 HCV infection in combination with pegylated interferon-alpha and ribavirin in Japan, Canada, and USA
62 roven difficult and the regimen of pegylated interferon-alpha and ribavirin is only effective for hal
64 levels at baseline of therapy with pegylated interferon-alpha and ribavirin or before biopsy were cor
65 b infection and a null response to pegylated interferon-alpha and ribavirin who developed decompensat
67 erapy relies upon a combination of pegylated interferon-alpha and ribavirin, a poorly tolerated regim
69 hibitors, used in combination with pegylated interferon-alpha and ribavirin; however, this is just th
70 meth inhibited the expression of endogenous interferon-alpha and signal transducer and activator of
71 e response involving the induction of type I interferons (alpha and beta interferons [IFN-alpha and -
73 etroviral therapy, 11 received consolidation interferon-alpha, and 6 received consolidation high-dose
76 ron-beta, 2',5'-oligoadenylate synthetase 1, interferon-alpha, and interferon-alpha-inducible protein
77 an be constitutively expressed or induced by interferon-alpha, and it consists of protein-based tethe
78 rmore, we show that HCV clearance induced by interferon-alpha based antiviral normalized the ER-stres
79 The long-term consequences of unsuccessful interferon-alpha based hepatitis C treatment on liver di
80 d findings suggest that patients who receive interferon-alpha based therapies but fail to clear the h
82 erwent liver biopsy during consideration for interferon-alpha based treatment between 1992 and 2007.
88 virus (MHV) induced the expression of type I interferon (alpha/beta interferon [IFN-alpha/beta]) in m
90 ing Ebola virus (EBOV) infection, the type I interferon alpha/beta (IFN-alpha/beta) innate immune res
92 signaling cascade resulting in production of interferon alpha/beta (IFN-alpha/beta), which promotes i
93 cently developed in AG129 mice (deficient in interferon alpha/beta and interferon gamma receptor sign
94 t positive correlation between host SOD1 and interferon alpha/beta messenger RNA (mRNA) levels, as we
97 -regulation and lysosomal degradation of the interferon alpha/beta receptor chain 1 (IFNAR1) of the r
98 on and disease progression in CCHFV-infected interferon alpha/beta receptor knockout (IFNAR(-/-)) mic
99 red virus replication and spread in infected interferon alpha/beta receptor knockout mice via biolumi
100 action of IFN-beta with its receptor IFNAR1 (interferon alpha/beta receptor subunit 1) is vital for h
101 macrophages (BMMs) and partially restored in interferon alpha/beta receptor-deficient (IFNAR(-/-)) BM
104 ) triple knockout mice, which produce little interferon alpha/beta, and mice lacking the interferon r
105 ro-treated NSCLC cell lines, we elucidate an interferon alpha/beta-based transcriptional program with
106 cells and considered the main source of the interferon-alpha/beta (IFN-alpha/beta), have been found
108 tor 3 activation to induce the expression of interferon-alpha/beta and antiviral/interferon-stimulate
109 ), interferon regulatory factor 3 (IRF3), or Interferon-alpha/beta receptor (IFNAR) by in vivo immort
111 phosphorylation-dependent degradation of the interferon-alpha/beta receptor 1 chain of the type I int
114 nt studies have revealed the existence of an interferon-alpha/beta-independent, innate antiviral resp
116 major host antiviral response by binding the interferon-alpha/beta-induced, ubiquitin-like ISG15 prot
119 ed alphaviruses differentially induce type I interferons (alpha/beta interferon [IFN-alpha/beta]) in
122 lasmacytoid DCs can be stimulated to produce interferon-alpha by Cramp/DNA complexes, and we further
124 rmal and stimulated conditions using chicken interferon-alpha (chIFN-alpha) and the attenuated infect
130 age disease (IIB-IV) and include bexarotene, interferon alpha, extracorporeal photopheresis, histone
131 y of plasmacytoid dendritic cells to produce interferon alpha following stimulation of Toll-like rece
132 s and the subsequent production of unopposed interferon-alpha, following a triggering event in predis
134 ata, hydroxyurea, somatostatin analogues and interferon-alpha have been modestly successful in patien
135 endritic cells (pDCs) produce high levels of interferon alpha (IFN-alpha) and express the apoptotic l
137 ion has been treated with the combination of interferon alpha (IFN-alpha) and ribavirin (RBV) for ove
139 he activation of NFkappaB, the expression of interferon alpha (IFN-alpha) and the induction of interf
140 rential induction of key cytokines including interferon alpha (IFN-alpha) and tumor necrosis factor a
142 atment and may be associated with the use of interferon alpha (IFN-alpha) but also with the primary p
143 n, the two accepted treatment modalities are interferon alpha (IFN-alpha) given subcutaneously for a
148 pression is one of the major side effects of interferon alpha (IFN-alpha) treatment, but the molecula
150 dendritic cells (pDCs), a primary source of interferon alpha (IFN-alpha), provide a first line of in
155 s from healthy donors after stimulation with interferon-alpha (IFN-alpha) and anti-immunoglobulin (Ig
156 We report here that although the cytokines interferon-alpha (IFN-alpha) and IFN-beta prevented the
157 proved treatment, a combination of pegylated interferon-alpha (IFN-alpha) and ribavirin, is frequentl
160 e efficacy and safety of corticosteroids and interferon-alpha (IFN-alpha) in adults with such conditi
161 DCs derived from women produce markedly more interferon-alpha (IFN-alpha) in response to HIV-1-encode
163 ifferent viruses and can act in synergy with interferon-alpha (IFN-alpha) on hepatitis C virus (HCV)
164 whether the elevated levels of HIV-1-induced interferon-alpha (IFN-alpha) production observed in fema
165 kappaB; however, thymocytes deficient in the interferon-alpha (IFN-alpha) receptor IFN-alphaR showed
168 develop depression within a short timeframe, interferon-alpha (IFN-alpha) treatment for chronic hepat
169 Currently, around 30% of patients receiving interferon-alpha (IFN-alpha) treatment for HCV experienc
170 h risk for recurrence of malignant melanoma, interferon-alpha (IFN-alpha), a stimulator of innate imm
171 ally euthymic patients during treatment with interferon-alpha (IFN-alpha), assessing serum BDNF and r
172 replication during long-term treatment using interferon-alpha (IFN-alpha), IFN-lambda, and ribavirin
179 e deduced that AGM HSCs show lower levels of interferon-alpha (IFN-alpha)/Jak-Stat1-associated gene e
180 ulate the expression of antiviral cytokines (interferon alpha [IFN-alpha] and IFN-beta) but induced c
181 ity of intranasal treatment with human alpha interferon (alpha-IFN) to reduce lung and nasal wash tit
188 erapeutic options are available, among which interferon alpha (IFNalpha) presents interesting propert
189 ic cells (pDCs) with excessive production of interferon alpha (IFNalpha) represents one of the hallma
190 t tumor necrosis factor alpha (TNFalpha) and interferon alpha (IFNalpha) stimulate PML expression whi
192 to show that HIV infection of the thymus and interferon alpha (IFNalpha) treatment alone result in MH
193 into hepatoma cells and inhibit signaling by interferon alpha (IFNalpha), but have no effect on HCV-R
195 have demonstrated that high levels of serum interferon-alpha (IFNalpha) activity are a heritable ris
196 vels, lupus-associated autoantibodies, serum interferon-alpha (IFNalpha) activity, 25-hydroxyvitamin
197 production of inflammatory cytokines such as interferon-alpha (IFNalpha) and tumour necrosis factor (
210 TLR) agonists and proteasome inhibitors, and interferon-alpha (IFNalpha) levels were measured by ELIS
211 ary monocyte-derived cells were treated with interferon-alpha (IFNalpha) or IFNalpha-inducing toll-li
212 rosine phosphatases (PTPs) in the absence of interferon-alpha (IFNalpha) response associated with ins
214 ring antiviral therapy, specific delivery of interferon-alpha (IFNalpha) to infected cells may increa
215 pression of genes suggesting the presence of interferon-alpha (IFNalpha), despite the apparent absenc
216 ps of hematopoiesis as well as the effect of interferon-alpha (IFNalpha), which may target the JAK2(V
217 s unknown, the antiosteoclastogenic cytokine interferon-alpha (IFNalpha), whose transcriptome is pres
221 associated with a reduced ability to induce interferon-alpha in primary human plasmacytoid dendritic
222 dendritic cells (pDCs) produce markedly less interferon-alpha in response to SIV and other Toll-like
224 ists identify patients at risk of developing interferon-alpha-induced depression, and monitor those r
226 the (NZB x NZW)F(1) (NZB/NZW) mouse model of interferon-alpha-induced lupus nephritis and treated mic
227 owards, the identification and monitoring of interferon-alpha-induced-depression and the decision-mak
229 denylate synthetase 1, interferon-alpha, and interferon-alpha-inducible protein 27 messenger RNAs of
230 in-12 and interleukin-18), but was bereft of interferon-alpha inducing properties, confirming its hig
231 mary reporter gene assays were paralleled by interferon-alpha induction activities in whole human blo
233 proved that autoantibodies directed against interferon-alpha, interferon-beta, interleukin-1alpha (I
236 kinase 2 (JAK2) inhibitors, or low doses of interferon-alpha led to the generation of greater number
237 numbers correlated positively with IL-10 and interferon alpha levels and fewer CD4(+) and CD8(+) T ce
238 Here, we show that monocytes activated by interferon alpha, lipopolysaccharide or a combination of
240 suggested that these genes were involved in interferon alpha, nuclear factor-kappa B (NFkB), extrace
242 ne of HCV RNA was typically slower than with interferon-alpha or protease inhibitors, and 12 patients
246 activation (patients with HCV-infection and interferon-alpha, patients with major depression, and he
247 ials investigating the efficacy of pegylated interferon alpha (PEG-IFNa) showed HDV RNA negativity ra
248 (MDM2) antagonist (RG7112) and the pegylated interferon alpha (Peg-IFNalpha 2a) to target JAK2V617F h
251 d difficult to treat in the era of pegylated interferon-alpha (Peg-IFN-alpha) and ribavirin regimens.
255 e studied the antiviral potency of pegylated interferon-alpha (pegIFNalpha) against HEV infections in
256 response (SVR) in CHC patients on pegylated interferon alpha plus ribavirin (pegIFNalpha/ribavirin)
259 roxyurea, mainly used in older patients, and interferon alpha, primarily given to younger patients.
263 not result in significantly higher levels of interferon-alpha production than the levels in mock-infe
264 cytes had impaired STAT1 phosphorylation and interferon-alpha production to CpG stimulation and a den
265 s R892W carrier responded normally to CpG by interferon-alpha production, carrier B cells showed impa
268 this question, we introduced a deficiency of interferon alpha receptor 1 (Ifnar1) into B6.Aec1Aec2 mi
269 P also plays an important inhibitory role in interferon-alpha receptor (IFNAR) signaling in mice.
270 1 transcription factor signaling through the interferon-alpha receptor (Ifnar1), resulting in the ant
273 Aim of this study was to compare ETR to Interferon alpha (recombinant Interferon) & Ribavirin in
274 f direct acting antivirals (DAAs), pegylated interferon-alpha remains the backbone of HCV therapy.
276 he haplotype (rs12979860) also affects other interferon-alpha responsive chronic viral illnesses, nam
277 on the surface of primary macrophages in an interferon-alpha-responsive manner, captures murine leuk
278 cells with TKI alone, or in combination with interferon-alpha, results in the preferential survival o
279 ort of 876 naive CHC patients, who completed Interferon alpha & Ribavirin for 24 weeks, was studied f
280 ilable therapy for HCV infection is based on interferon-alpha, ribavirin and the new direct-acting an
281 ponsiveness in treatment-naive and pegylated interferon alpha-ribavirin (P/R)-experienced subjects an
283 nd safety of standard-therapy with pegylated-interferon-alpha/ribavirin (Peg-IFN-alpha/RBV (48 weeks)
285 led us to prospectively evaluate recombinant interferon-alpha (rIFNalpha) in "early" PM patients with
286 rculating mononuclear cells revealed reduced interferon-alpha secretion in response to herpes simplex
291 nistration of inflammatory cytokines such as interferon-alpha to otherwise non-depressed controls inc
292 rongly determines the outcome of natural and interferon-alpha treated hepatitis C virus (HCV) infecti
294 d directly in the care of patients receiving interferon-alpha treatment and had at least one year exp
295 oreover, the specific activation of pDCs and interferon-alpha treatment promoted plaque growth, assoc
296 gated via this method include interleukin-2, interferon-alpha, ubiquitin, antibodies and several sing
299 signaling and leading to rapid secretion of interferon-alpha, which was essential for the innate ant
300 survival compared with the regimen combining interferon-alpha with 5-fluorouracil-based chemoradiatio
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