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1 DEN administration caused greater increases in serum int
2 DEN administration increased the levels of malondialdehy
3 DEN exposure promoted production of IL-6 in Kupffer cell
4 DEN treatment also reduced survival of LKO mice compared
5 DEN treatment induced p53-independent PUMA expression, P
6 DEN-1 was subsequently detected by RT-PCR from cell cult
7 DEN-2 genome RNA failed to accumulate in FB 9.1 cells af
8 DEN-induced HCCs with constitutive Notch2 signaling (DEN
9 DEN/PB treatment was associated with specific degradatio
10 e elucidate the role of human deneddylase-1 (DEN-1, also called SENP8) in inflammatory responses in v
13 virus serotypes, i.e., DEN-1 (strain 16007), DEN-2 (16681), DEN-3 (16562), and DEN-4 (1036) viruses b
14 , i.e., DEN-1 (strain 16007), DEN-2 (16681), DEN-3 (16562), and DEN-4 (1036) viruses by over 4 log10,
16 four genotypes) of dengue virus serotype 2 (DEN-2) can induce the development of human-like disease,
20 The live attenuated dengue virus type 4 (DEN-4) vaccine candidate virus rDEN4 Delta 30 was previo
21 eans of weekly oral gavage with 5 mL of 1.5% DEN solution per kilogram of body weight for 3-11 weeks,
23 by alternately passaging a non-mouse-adapted DEN strain between mosquito cells and mice, thereby mimi
25 not develop liver cancer with age and after DEN injections due to failure to activate gankyrin and e
26 ver nuclear extracts of both genotypes after DEN exposure, the complex formed in MTKO mice was predom
27 e, treatment with an IRAK1/4 inhibitor after DEN administration reduced serum IL-6 levels and liver t
29 Apoptosis assays performed monthly after DEN treatment showed no differences between mutant and w
31 mmatory cytokines in LKO liver shortly after DEN exposure indicates predisposition of a pro-tumorigen
33 S exhibited hepatoprotective effects against DEN/CCl4-induced injury by reducing DCLK1 expression and
36 HP potentially can be useful for alleviating DEN infection-associated symptoms by reducing titers of
37 in 16007), DEN-2 (16681), DEN-3 (16562), and DEN-4 (1036) viruses by over 4 log10, in most cases to b
39 so seen in the (D)(V/K) results with DMN and DEN for the minor products resulting from the denitrosat
43 parameters measured for oxidation of DMN and DEN to the aldehydes and for oxidation of the aldehydes
48 rom mosquito-borne flaviviruses (WN-rED3 and DEN-rED3) were similar to each other yet distinct from r
52 Analyses of WA-treated HepG2-xenografts and DEN-induced-HCC tumors showed elevated levels of ERK, RS
54 lly hybridized to labeled sense or antisense DEN-2 RNA derived from the target region of the genome.
56 ocyte-specific deletion of IKKbeta augmented DEN-induced hepatocyte death and cytokine-driven compens
58 matically reduced the LNP's ability to boost DEN-80E specific immune responses, highlighting the cruc
60 to TNF-alpha, whose expression is induced by DEN, and JNK activity is required for normal hepatocyte
62 n be initiated by exposure to the carcinogen DEN, which has been shown to rely upon activation of NF-
63 se FGF21 is induced in response to chemical (DEN treatment) and genetic-induced hepatocarcinogenesis
65 sions produced by the tetravalent ChimeriVax-DEN vaccine were significantly less severe than those ob
66 yellow fever virus-dengue virus (ChimeriVax-DEN) vaccine candidates against dengue virus types 1 to
67 onstruct chimeric YF/DEN viruses (ChimeriVax-DEN), the premembrane (prM) and envelope (E) genes of ye
69 in impairs the liver's ability to counteract DEN-induced oxidative stress and enhances tumorigenesis
70 emonstrating that RIPK1 deficiency decreases DEN-induced liver tumor formation in a TNFR1-dependent m
72 lammatory cytokines induced during a dengue (DEN) virus infection plays a role in either protection o
73 a worst-case recombinant, ChimeriVax-dengue (DEN) 4 virus was chimerized with the WT Asibi yellow fev
76 s of previously described monovalent dengue (DEN) virus vaccine candidates were compared to a tetrava
82 ing HCC in response to a Diethylnitrosamine (DEN)/Phenobarbital (PB) liver tumor-induction protocol.
84 eed oil extracts against diethylnitrosamine (DEN) and phenobarbital (PB) induced hepatic injury in ra
86 f c-Fos protects against diethylnitrosamine (DEN)-induced HCCs, whereas liver-specific c-Fos expressi
88 (NO) in spontaneous and diethylnitrosamine (DEN)-initiated and/or phenobarbital (Pb)-promoted HCC de
89 arcinogenesis induced by diethylnitrosamine (DEN) produced large carcinomas in all AhR-/- mice but mo
92 to the liver carcinogen diethylnitrosamine (DEN) and fed diets with well-defined sugar and fat conte
97 y the genotoxic chemical diethylnitrosamine (DEN), a hepatic carcinogen that is not an AHR ligand.
98 njection of 10 micro g/g diethylnitrosamine (DEN) and continued administration of phenobarbital (PB)
102 ation of liver cancer in diethylnitrosamine (DEN)-treated CUGBP1-S302A mice showed these mice develop
103 hout the tumor initiator diethylnitrosamine (DEN) at 5 weeks of age and then orally inoculated with H
104 itrosamine (DMN) and N,N-diethylnitrosamine (DEN), to alkyl diazohydroxides (which are DNA-alkylating
105 nitrosodiethylamine [N,N-diethylnitrosamine (DEN)], the intrinsic KIE was slightly lower and was not
106 ed with a combination of diethylnitrosamine (DEN) and CCl4, along with either LPS or E. coli infectio
107 raperitoneal delivery of diethylnitrosamine (DEN), a known carcinogen, induced HCC at 6 months in TG
108 , low-dose injections of diethylnitrosamine (DEN), a mouse model induced by carbon tetrachloride (CCl
109 er a single injection of diethylnitrosamine (DEN), SV1 hepatocyte transgenic mice developed more hist
112 peritoneal injections of diethylnitrosamine (DEN); 2 weeks later, some mice also received left and me
113 Using the procarcinogen diethylnitrosamine (DEN) to initiate tumorigenesis in mice, we discovered th
118 WT) mice were exposed to diethylnitrosamine (DEN) and induction of HCC was monitored at 23 and 33 wee
119 much more susceptible to diethylnitrosamine (DEN)-induced acute liver injury and liver carcinogenesis
122 Cre; Rosa(YFP) mice with diethylnitrosamine (DEN), followed by multiple injections of carbon tetrachl
126 iters of all four DEN virus serotypes, i.e., DEN-1 (strain 16007), DEN-2 (16681), DEN-3 (16562), and
127 -derived dendritic cell cultures with either DEN or Sindbis virus, another positive-strand RNA virus,
129 RB deletion in the mouse liver enhances DEN-induced tumorigenesis, associated with increased hep
131 satory proliferation and prevented excessive DEN-induced carcinogenesis in Ikkbeta(Deltahep) mice.
137 mutagenic O6-ethyldeoxyguanosines following DEN challenge in livers of GSNOR-deficient (GSNOR(-/-))
138 otably, short-term iNOS inhibition following DEN treatment had little effect on carcinogenesis in wil
139 osis and compensatory regeneration following DEN treatment, and does not require the HBV X protein.
140 precursors improves cell survival following DEN treatment to a level indistinguishable from ACC-defi
143 0 microM 3'CS reduced the titers of all four DEN virus serotypes, i.e., DEN-1 (strain 16007), DEN-2 (
145 with TV-1 and TV-3 seroconverted to the four DEN components by day 28 with neutralization titers rang
153 tes are the cell of origin of HCA and HCC in DEN/carbon tetrachloride and DEN/TCPOBOP induced liver t
154 iated compensatory proliferation observed in DEN-injured ERRalpha-null livers is concomitant with inc
156 Despite the oncogenic function of STAT3 in DEN-induced liver tumor, hepatocyte-specific STAT3 knock
157 umors and surrounding normal liver tissue in DEN-treated HNF4alpha knockout mice showed significant i
159 gamma and TNF-alpha responses to inactivated DEN Ags were detected in up to 0.54 and 1.17% of total c
161 also suppressed diethylnitrosamine-induced (DEN-induced) hepatocarcinogenesis, as an increased numbe
162 1 showed reduced diethylnitrosamine-induced (DEN-induced) liver tumorigenesis that correlated with in
163 ack of RIPK1 kinase activity did not inhibit DEN-induced liver tumor formation, showing that kinase-i
164 eriments showed that 5'SL and 3'CS inhibited DEN-2 virus replication in a dose-dependent and sequence
165 beta receptor-mediated action limits initial DEN replication in extraneural sites and controls subseq
167 controls were given a single intraperitoneal DEN injection and followed for 6-12 months for hepatic t
168 an isolate, which can be used to investigate DEN pathogenesis and to evaluate candidate vaccines and
169 s in which translation factors are limiting, DEN can alternate between canonical cap-dependent transl
173 tudy, the use of a dopant enriched nitrogen (DEN)-gas combined with sheathless capillary electrophore
179 el that is more relevant to DHF/DSS, a novel DEN strain, D2S10, was generated by alternately passagin
181 g the steady state promoted rapid binding of DEN to the E, followed by subsequent clearance from the
182 crucial for both early and late clearance of DEN infection in mice, and (iii) the IFN system plays a
185 expression contributes to the development of DEN-mediated carcinogenesis by promoting the proliferati
189 ction relationships in the E glycoprotein of DEN virus and provide the first direct evidence that dom
191 ished by continuous steady state infusion of DEN, injection of HP during the steady state promoted ra
192 In mice given a single i.p. injection of DEN, AHR antagonized liver tumor formation and growth by
196 tion after PH, as well as the progression of DEN-induced tumors, providing evidence for a functional
197 ed hepatocyte proliferation and promotion of DEN-induced hepatic tumors secondary to aberrant c-Myc a
198 Although hepatocytes in nontumor regions of DEN-exposed livers were quiescent regardless of RB statu
199 for their ability to inhibit replication of DEN virus serotype 2 (DEN-2 virus) in mammalian cell cul
200 and characterized the cytokine responses of DEN virus-specific memory CD4+ T cells in PBMC of six vo
203 ted responses seem to act at later stages of DEN disease by restricting viral replication in the peri
204 -PMO showed relatively little suppression of DEN-2 virus titer (0.1 and 0.9 log10, respectively).
205 tration of an antioxidant around the time of DEN exposure blocked prolonged JNK activation and compen
207 he enhanced repeatability fosters the use of DEN-gas sheathless CE-ESI-MS in protein glycosylation an
209 ogenesis and hepatocarcinogenesis in mice on DEN challenge by up-regulating several genes involved in
210 ed the influence of cellular growth state on DEN type 2 (DEN2) replication in mosquito and human cell
213 effect was observed for RNAs with globin or DEN 5' sequences, indicating no codependency between vir
214 In contrast, mice infected with the parental DEN strain developed paralysis at late times after infec
215 ce infected with D2S10, but not the parental DEN strain, significant levels of serum tumor necrosis f
216 mice with diethylnitrosamine/phenobarbital (DEN/PB), which induces formation of liver cancer, actual
217 l and seed oil extracts pre, during and post DEN administration improved liver functions, decreased t
221 trate that IFNR-dependent control of primary DEN infection involves both STAT1-dependent and STAT1-in
224 1-independent responses in mice with primary DEN infection included the early activation of B and NK
229 t to demonstrate the safety of a recombinant DEN virus tetravalent vaccine in a formal neurovirulence
230 r structures clarify the previously reported DEN MTase structure, suggest novel protein-cap interacti
231 y of the four related dengue virus serotypes DEN-1, -2, -3 and -4, which are transmitted to people by
232 rotein from all four Dengue virus serotypes (DEN-80E) formulated with ionizable cationic lipid nanopa
233 nificant advance in animal models for severe DEN disease, and it begins to provide mechanistic insigh
235 ced HCCs with constitutive Notch2 signaling (DEN(N2ICD) HCCs) exhibit a marked increase in size, prol
236 t to liver tumorigenesis induced by a single DEN injection, whose tumorigenesis was associated with m
237 and TV-3, possess properties of a successful DEN vaccine and can be considered for evaluation in clin
238 expression of GCIP in mouse liver suppressed DEN-induced hepatocarcinogenesis at an early stage of tu
239 of a small-animal model that mimics systemic DEN disease without neurovirulence has been an obstacle,
241 and DEN4 viruses suggests that a tetravalent DEN vaccine could be generated by introduction of the De
244 l examination of liver tissue confirmed that DEN-treated ATX mice developed approximately twice as ma
250 at translational enhancement provided by the DEN 3' UTR is attributable to the cumulative contributio
251 try site but requires the interaction of the DEN 5' and 3' UTRs for activity, suggesting a novel stra
254 ession of 5'- and 3'-terminal regions of the DEN serotype 2 genome by using luciferase reporter mRNAs
256 targeting the 3'-terminal nucleotides of the DEN-2 virus genome and a random-sequence P4-PMO showed r
263 EGFR inhibitor erlotinib delivered prior to DEN-induced injury was sufficient to block compensatory
266 designed to express irRNA were resistant to DEN-2 challenge, with more than 95% of the cells showing
269 played normal tumor formation in response to DEN, demonstrating that RIPK1 deficiency decreases DEN-i
270 ta is critical for early immune responses to DEN infection, (ii) IFN-gamma-mediated immune responses
272 examined whether increased susceptibility to DEN-induced hepatocarcinogenesis in Ikkbeta(Deltahep) mi
274 ) T cells had no increased susceptibility to DEN; however, RAG mice (deficient in both B and T cells)
278 ese defects and reversed unresponsiveness to DEN-induced liver injury and malignant development.
279 ed to a tetravalent formulation of wild-type DEN viruses (T-wt) for replication in SCID mice transpla
280 el of toxin-induced hepatic neoplasia, using DEN and 3,3',5,5'-tetrachloro-1,4-bis(pyridyloxy)benzene
283 c RNAs of flaviviruses such as dengue virus (DEN) have a 5' m7GpppN cap like those of cellular mRNAs
286 n appropriate animal model for dengue virus (DEN), which causes dengue fever and dengue hemorrhagic f
288 mice and treated the resulting animals with DEN/Phenobarbital, an established protocol for liver car
290 e hepatobiliary cysts, which correlated with DEN-induced transcriptional activation of Cdc25a mediate
294 for liver tumorigenesis in mice treated with DEN, and identifies an important role for ACC enzymes in
295 hepatitis in WT and KO mice with or without DEN that correlated with significant upregulation of Tnf
296 introduction of the Delta30 mutation into wt DEN viruses belonging to each of the four serotypes.
298 describe construction of three additional YF/DEN chimeras using premembrane (prM) and envelope (E) ge
300 r, four of nine monkeys in the monovalent YF/DEN groups developed low levels of viremia, whereas no v
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