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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 rats showed an increase in echointensity from 37.1 +
5 DEN treatment also reduced survival of LKO mice compared
6 DEN treatment induced p53-independent PUMA expression, P
7 DEN-1 was subsequently detected by RT-PCR from cell cult
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
26 not develop liver cancer with age and after DEN injections due to failure to activate gankyrin and e
27 ver nuclear extracts of both genotypes after DEN exposure, the complex formed in MTKO mice was predom
28 e, treatment with an IRAK1/4 inhibitor after DEN administration reduced serum IL-6 levels and liver t
31 Apoptosis assays performed monthly after DEN treatment showed no differences between mutant and w
33 mmatory cytokines in LKO liver shortly after DEN exposure indicates predisposition of a pro-tumorigen
35 S exhibited hepatoprotective effects against DEN/CCl4-induced injury by reducing DCLK1 expression and
38 in 16007), DEN-2 (16681), DEN-3 (16562), and DEN-4 (1036) viruses by over 4 log10, in most cases to b
39 , TrxR1-null livers showed altered basal and DEN-exposed metabolomic profiles compared with WT livers
41 so seen in the (D)(V/K) results with DMN and DEN for the minor products resulting from the denitrosat
45 parameters measured for oxidation of DMN and DEN to the aldehydes and for oxidation of the aldehydes
49 rom mosquito-borne flaviviruses (WN-rED3 and DEN-rED3) were similar to each other yet distinct from r
53 Analyses of WA-treated HepG2-xenografts and DEN-induced-HCC tumors showed elevated levels of ERK, RS
55 lly hybridized to labeled sense or antisense DEN-2 RNA derived from the target region of the genome.
57 ocyte-specific deletion of IKKbeta augmented DEN-induced hepatocyte death and cytokine-driven compens
59 matically reduced the LNP's ability to boost DEN-80E specific immune responses, highlighting the cruc
61 to TNF-alpha, whose expression is induced by DEN, and JNK activity is required for normal hepatocyte
63 n be initiated by exposure to the carcinogen DEN, which has been shown to rely upon activation of NF-
64 se FGF21 is induced in response to chemical (DEN treatment) and genetic-induced hepatocarcinogenesis
66 sions produced by the tetravalent ChimeriVax-DEN vaccine were significantly less severe than those ob
67 yellow fever virus-dengue virus (ChimeriVax-DEN) vaccine candidates against dengue virus types 1 to
68 onstruct chimeric YF/DEN viruses (ChimeriVax-DEN), the premembrane (prM) and envelope (E) genes of ye
69 s influenced cancer progression, we compared DEN-induced cancer malignancy under chronically low oxid
71 in impairs the liver's ability to counteract DEN-induced oxidative stress and enhances tumorigenesis
72 emonstrating that RIPK1 deficiency decreases DEN-induced liver tumor formation in a TNFR1-dependent m
74 lammatory cytokines induced during a dengue (DEN) virus infection plays a role in either protection o
75 a worst-case recombinant, ChimeriVax-dengue (DEN) 4 virus was chimerized with the WT Asibi yellow fev
78 s of previously described monovalent dengue (DEN) virus vaccine candidates were compared to a tetrava
84 ing HCC in response to a Diethylnitrosamine (DEN)/Phenobarbital (PB) liver tumor-induction protocol.
86 o rats were administered diethylnitrosamine (DEN) orally for 12 weeks to induce hepatic fibrosis.
87 eed oil extracts against diethylnitrosamine (DEN) and phenobarbital (PB) induced hepatic injury in ra
89 f c-Fos protects against diethylnitrosamine (DEN)-induced HCCs, whereas liver-specific c-Fos expressi
91 (NO) in spontaneous and diethylnitrosamine (DEN)-initiated and/or phenobarbital (Pb)-promoted HCC de
92 arcinogenesis induced by diethylnitrosamine (DEN) produced large carcinomas in all AhR-/- mice but mo
95 to the liver carcinogen diethylnitrosamine (DEN) and fed diets with well-defined sugar and fat conte
101 y the genotoxic chemical diethylnitrosamine (DEN), a hepatic carcinogen that is not an AHR ligand.
102 njection of 10 micro g/g diethylnitrosamine (DEN) and continued administration of phenobarbital (PB)
106 ation of liver cancer in diethylnitrosamine (DEN)-treated CUGBP1-S302A mice showed these mice develop
107 hout the tumor initiator diethylnitrosamine (DEN) at 5 weeks of age and then orally inoculated with H
109 itrosamine (DMN) and N,N-diethylnitrosamine (DEN), to alkyl diazohydroxides (which are DNA-alkylating
110 l, were susceptible to N-diethylnitrosamine (DEN)-induced liver cancer, indicating that loss of these
111 nitrosodiethylamine [N,N-diethylnitrosamine (DEN)], the intrinsic KIE was slightly lower and was not
112 ed with a combination of diethylnitrosamine (DEN) and CCl4, along with either LPS or E. coli infectio
113 en a single injection of diethylnitrosamine (DEN) followed by weekly doses of carbon tetrachloride to
114 were given injections of diethylnitrosamine (DEN) to induce liver cancer and alpha-galactosylceramide
115 raperitoneal delivery of diethylnitrosamine (DEN), a known carcinogen, induced HCC at 6 months in TG
116 , low-dose injections of diethylnitrosamine (DEN), a mouse model induced by carbon tetrachloride (CCl
117 er a single injection of diethylnitrosamine (DEN), SV1 hepatocyte transgenic mice developed more hist
118 main cellular origin of diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) and are high
120 peritoneal injections of diethylnitrosamine (DEN); 2 weeks later, some mice also received left and me
121 Using the procarcinogen diethylnitrosamine (DEN) to initiate tumorigenesis in mice, we discovered th
126 WT) mice were exposed to diethylnitrosamine (DEN) and induction of HCC was monitored at 23 and 33 wee
127 much more susceptible to diethylnitrosamine (DEN)-induced acute liver injury and liver carcinogenesis
130 Cre; Rosa(YFP) mice with diethylnitrosamine (DEN), followed by multiple injections of carbon tetrachl
133 iters of all four DEN virus serotypes, i.e., DEN-1 (strain 16007), DEN-2 (16681), DEN-3 (16562), and
134 -derived dendritic cell cultures with either DEN or Sindbis virus, another positive-strand RNA virus,
136 RB deletion in the mouse liver enhances DEN-induced tumorigenesis, associated with increased hep
138 satory proliferation and prevented excessive DEN-induced carcinogenesis in Ikkbeta(Deltahep) mice.
144 mutagenic O6-ethyldeoxyguanosines following DEN challenge in livers of GSNOR-deficient (GSNOR(-/-))
146 otably, short-term iNOS inhibition following DEN treatment had little effect on carcinogenesis in wil
147 osis and compensatory regeneration following DEN treatment, and does not require the HBV X protein.
148 precursors improves cell survival following DEN treatment to a level indistinguishable from ACC-defi
151 0 microM 3'CS reduced the titers of all four DEN virus serotypes, i.e., DEN-1 (strain 16007), DEN-2 (
153 with TV-1 and TV-3 seroconverted to the four DEN components by day 28 with neutralization titers rang
162 tes are the cell of origin of HCA and HCC in DEN/carbon tetrachloride and DEN/TCPOBOP induced liver t
163 iated compensatory proliferation observed in DEN-injured ERRalpha-null livers is concomitant with inc
164 Mechanistically, hepatocyte proliferation in DEN-treated P2y(2)r (-/-) mice was reduced, which correl
166 Despite the oncogenic function of STAT3 in DEN-induced liver tumor, hepatocyte-specific STAT3 knock
167 umors and surrounding normal liver tissue in DEN-treated HNF4alpha knockout mice showed significant i
169 gamma and TNF-alpha responses to inactivated DEN Ags were detected in up to 0.54 and 1.17% of total c
171 also suppressed diethylnitrosamine-induced (DEN-induced) hepatocarcinogenesis, as an increased numbe
172 1 showed reduced diethylnitrosamine-induced (DEN-induced) liver tumorigenesis that correlated with in
173 ack of RIPK1 kinase activity did not inhibit DEN-induced liver tumor formation, showing that kinase-i
174 eriments showed that 5'SL and 3'CS inhibited DEN-2 virus replication in a dose-dependent and sequence
175 beta receptor-mediated action limits initial DEN replication in extraneural sites and controls subseq
177 controls were given a single intraperitoneal DEN injection and followed for 6-12 months for hepatic t
178 an isolate, which can be used to investigate DEN pathogenesis and to evaluate candidate vaccines and
179 s in which translation factors are limiting, DEN can alternate between canonical cap-dependent transl
183 tudy, the use of a dopant enriched nitrogen (DEN)-gas combined with sheathless capillary electrophore
185 umor cells in mice with diethyl nitrosamine (DEN)-initiated, Western alcohol diet-promoted liver tumo
190 el that is more relevant to DHF/DSS, a novel DEN strain, D2S10, was generated by alternately passagin
191 crucial for both early and late clearance of DEN infection in mice, and (iii) the IFN system plays a
198 In mice given a single i.p. injection of DEN, AHR antagonized liver tumor formation and growth by
202 tion after PH, as well as the progression of DEN-induced tumors, providing evidence for a functional
203 ed hepatocyte proliferation and promotion of DEN-induced hepatic tumors secondary to aberrant c-Myc a
204 Although hepatocytes in nontumor regions of DEN-exposed livers were quiescent regardless of RB statu
205 for their ability to inhibit replication of DEN virus serotype 2 (DEN-2 virus) in mammalian cell cul
206 and characterized the cytokine responses of DEN virus-specific memory CD4+ T cells in PBMC of six vo
209 ted responses seem to act at later stages of DEN disease by restricting viral replication in the peri
210 Disruption of TrxR1 in a marked subset of DEN-initiated cancer cells had no effect on their subseq
211 -PMO showed relatively little suppression of DEN-2 virus titer (0.1 and 0.9 log10, respectively).
212 tration of an antioxidant around the time of DEN exposure blocked prolonged JNK activation and compen
214 he enhanced repeatability fosters the use of DEN-gas sheathless CE-ESI-MS in protein glycosylation an
216 ogenesis and hepatocarcinogenesis in mice on DEN challenge by up-regulating several genes involved in
217 ed the influence of cellular growth state on DEN type 2 (DEN2) replication in mosquito and human cell
220 effect was observed for RNAs with globin or DEN 5' sequences, indicating no codependency between vir
221 In contrast, mice infected with the parental DEN strain developed paralysis at late times after infec
222 ce infected with D2S10, but not the parental DEN strain, significant levels of serum tumor necrosis f
223 mice with diethylnitrosamine/phenobarbital (DEN/PB), which induces formation of liver cancer, actual
224 l and seed oil extracts pre, during and post DEN administration improved liver functions, decreased t
228 trate that IFNR-dependent control of primary DEN infection involves both STAT1-dependent and STAT1-in
231 1-independent responses in mice with primary DEN infection included the early activation of B and NK
237 t to demonstrate the safety of a recombinant DEN virus tetravalent vaccine in a formal neurovirulence
238 r structures clarify the previously reported DEN MTase structure, suggest novel protein-cap interacti
239 y of the four related dengue virus serotypes DEN-1, -2, -3 and -4, which are transmitted to people by
240 rotein from all four Dengue virus serotypes (DEN-80E) formulated with ionizable cationic lipid nanopa
241 nificant advance in animal models for severe DEN disease, and it begins to provide mechanistic insigh
243 ced HCCs with constitutive Notch2 signaling (DEN(N2ICD) HCCs) exhibit a marked increase in size, prol
244 t to liver tumorigenesis induced by a single DEN injection, whose tumorigenesis was associated with m
245 and TV-3, possess properties of a successful DEN vaccine and can be considered for evaluation in clin
246 expression of GCIP in mouse liver suppressed DEN-induced hepatocarcinogenesis at an early stage of tu
247 of a small-animal model that mimics systemic DEN disease without neurovirulence has been an obstacle,
254 at translational enhancement provided by the DEN 3' UTR is attributable to the cumulative contributio
258 try site but requires the interaction of the DEN 5' and 3' UTRs for activity, suggesting a novel stra
261 ession of 5'- and 3'-terminal regions of the DEN serotype 2 genome by using luciferase reporter mRNAs
263 targeting the 3'-terminal nucleotides of the DEN-2 virus genome and a random-sequence P4-PMO showed r
269 EGFR inhibitor erlotinib delivered prior to DEN-induced injury was sufficient to block compensatory
272 designed to express irRNA were resistant to DEN-2 challenge, with more than 95% of the cells showing
275 played normal tumor formation in response to DEN, demonstrating that RIPK1 deficiency decreases DEN-i
276 ta is critical for early immune responses to DEN infection, (ii) IFN-gamma-mediated immune responses
278 examined whether increased susceptibility to DEN-induced hepatocarcinogenesis in Ikkbeta(Deltahep) mi
280 ) T cells had no increased susceptibility to DEN; however, RAG mice (deficient in both B and T cells)
282 Nlrp12(-/-) mice were highly susceptible to DEN-induced HCC with increased inflammation, hepatocyte
285 ese defects and reversed unresponsiveness to DEN-induced liver injury and malignant development.
286 ed to a tetravalent formulation of wild-type DEN viruses (T-wt) for replication in SCID mice transpla
287 el of toxin-induced hepatic neoplasia, using DEN and 3,3',5,5'-tetrachloro-1,4-bis(pyridyloxy)benzene
290 c RNAs of flaviviruses such as dengue virus (DEN) have a 5' m7GpppN cap like those of cellular mRNAs
293 n appropriate animal model for dengue virus (DEN), which causes dengue fever and dengue hemorrhagic f
294 mice and treated the resulting animals with DEN/Phenobarbital, an established protocol for liver car
295 e hepatobiliary cysts, which correlated with DEN-induced transcriptional activation of Cdc25a mediate
298 for liver tumorigenesis in mice treated with DEN, and identifies an important role for ACC enzymes in
299 hepatitis in WT and KO mice with or without DEN that correlated with significant upregulation of Tnf