コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ccumulation that contributes to AhR-mediated hepatotoxicity.
2 mice exhibited increased liver steatosis and hepatotoxicity.
3 osomal cholesterol (LC) accumulation in APAP hepatotoxicity.
4 n time and reduced immunogenicity as well as hepatotoxicity.
5 ven platelet activation participates in APAP hepatotoxicity.
6 rse reactions, including agranulocytosis and hepatotoxicity.
7 future therapeutic targets for APAP-induced hepatotoxicity.
8 lammation, liver neutrophil recruitment, and hepatotoxicity.
9 3 events of which one was a possibly related hepatotoxicity.
10 onhematopoietic cell PAR-4 signaling to APAP hepatotoxicity.
11 n patients without serious adverse events or hepatotoxicity.
12 fect of FABP1 on acetaminophen (AAP)-induced hepatotoxicity.
13 as sparse for some comparisons, particularly hepatotoxicity.
14 g, are a major mechanism contributing to BQA hepatotoxicity.
15 times the upper limit of normal or clinical hepatotoxicity.
16 effector differentiation resulting in overt hepatotoxicity.
17 ls to minimize off-target effects and reduce hepatotoxicity.
18 off-target toxicities, including concerns of hepatotoxicity.
19 d ROS and RNS for direct evaluation of acute hepatotoxicity.
20 ted with bacterial translocation during APAP hepatotoxicity.
21 possible that HMGB1 mediates gut BT in APAP hepatotoxicity.
22 ivated kinase (AMPK) in acetaminophen (APAP) hepatotoxicity.
23 x) 32, a key gap junction protein, to induce hepatotoxicity.
24 h increased liver triglyceride deposition or hepatotoxicity.
25 tioxidant and antitumour activities, without hepatotoxicity.
26 thout concomitant increase in the off-target hepatotoxicity.
27 mice were resistant to acetaminophen-induced hepatotoxicity.
28 licity contributes significantly to risk for hepatotoxicity.
29 nine nucleotide) consistent with AZA-induced hepatotoxicity.
30 ved transgene expression and largely avoided hepatotoxicity.
31 ptive response mechanisms in arsenic induced hepatotoxicity.
32 d-to-treat patients with severe APAP-induced hepatotoxicity.
33 d Fizz1, increased liver repair, and reduced hepatotoxicity.
34 trations that were paralleled by evidence of hepatotoxicity.
35 on, and protection of mice from APAP-induced hepatotoxicity.
36 a major role in acetaminophen (APAP)-induced hepatotoxicity.
37 NK activation and thus promotes drug-induced hepatotoxicity.
38 believed to be responsible for the observed hepatotoxicity.
39 nt hepatic failure and acetaminophen-induced hepatotoxicity.
40 brate, fully protects mice from APAP-induced hepatotoxicity.
41 er injury and in liver neutrophil influx and hepatotoxicity.
42 chloroquine further exacerbated APAP-induced hepatotoxicity.
43 utophagy by rapamycin inhibited APAP-induced hepatotoxicity.
44 the embolization materials exhibited evident hepatotoxicity.
45 ive diagnosis to some cases of presumed drug hepatotoxicity.
46 XCR2-FPR1 antagonism significantly prevented hepatotoxicity.
47 linically relevant sensitizer to TNF-induced hepatotoxicity.
48 eir depletion is associated with exacerbated hepatotoxicity.
49 ull mice did not afford protection from APAP hepatotoxicity.
50 ned LEF+MTX, should be monitored closely for hepatotoxicity.
51 ecreased acetaminophen (APAP) metabolism and hepatotoxicity.
52 expression in liver tissue without producing hepatotoxicity.
53 n hepatocytes can lead to protoporphyria and hepatotoxicity.
54 T, as a potential therapeutic target in APAP hepatotoxicity.
55 NK1 or JNK2 plays a role in this potentiated hepatotoxicity.
56 X receptor (LXR) in preventing APAP-induced hepatotoxicity.
57 a multi-gene expression signature to predict hepatotoxicity.
58 uide us to the targets of the dioxin-induced hepatotoxicity.
59 AIP protein is essential for dioxin-induced hepatotoxicity.
60 ng pathways that may also contribute to APAP hepatotoxicity.
61 me otherwise healthy individuals develop VPA hepatotoxicity.
62 th an increased risk of developing fatal VPA hepatotoxicity.
63 ncy in the liver of adult mice but increased hepatotoxicity.
64 aspirin reduced mortality from acetaminophen hepatotoxicity.
65 odulation of susceptibility to acetaminophen hepatotoxicity.
66 h suspected or known chemotherapy-associated hepatotoxicity.
67 e and components involved in ethanol-induced hepatotoxicity.
68 s is not the cause of many aspects of dioxin hepatotoxicity.
69 afety profile, with no evidence of increased hepatotoxicity.
70 EtOH-induced hepatic lipid accumulation and hepatotoxicity.
71 tribution and long half-life without obvious hepatotoxicity.
72 inone-imines and, as such, the potential for hepatotoxicity.
73 ted myeloid cells and macrophages and lethal hepatotoxicity.
74 g BA homoeostasis and protecting from the BA hepatotoxicity.
75 d the molecular mechanisms of TDCIPP-induced hepatotoxicity.
76 mice from lethal LPS/D-Galactosamine-induced hepatotoxicity.
77 ty, metastatic infection, nephrotoxicity, or hepatotoxicity.
78 abetes mellitus, cardiovascular disease, and hepatotoxicity.
79 ether the implicated agent is known to cause hepatotoxicity.
80 nificant risk factors for the development of hepatotoxicity.
81 iate inflammatory conditions in mice without hepatotoxicity.
82 h solubility, lack of CYP inhibition and low hepatotoxicity.
83 ly suitable for minimizing radiation-induced hepatotoxicity.
84 d CCL-4 were higher in subjects experiencing hepatotoxicity.
85 ency along with a higher propensity to cause hepatotoxicity.
86 hat manifests as severe photosensitivity and hepatotoxicity.
87 ling pathways without causing any detectable hepatotoxicity.
88 iabetes mellitus, cardiovascular disease, or hepatotoxicity.
89 levels and were predisposed to APAP-induced hepatotoxicity.
90 -mediated CYP450 induction, and drug-induced hepatotoxicity.
91 tor lepirudin and PAR-4 deficiency attenuate hepatotoxicity.
92 ost common grade 3 and 4 adverse events were hepatotoxicity (188 [8%]), hypertension (99 [4%]), cardi
93 ALF etiologies included acetaminophen (APAP) hepatotoxicity (29%), indeterminate ALF (23%), idiosyncr
94 relationship between nucleotide sequence and hepatotoxicity, a structure-toxicity analysis was perfor
97 The primary safety endpoint was incidence of hepatotoxicity: alanine aminotransferase of greater than
99 Acetaminophen (APAP, paracetamol)-induced hepatotoxicity, although treatable by timely application
100 minophen (APAP) overdose is a major cause of hepatotoxicity and acute liver failure in the U.S., but
101 event linking the bioactivation of drugs to hepatotoxicity and as a more direct and mechanistic indi
102 in exploring both markers and mechanisms of hepatotoxicity and can readily be extended to clinical s
104 chanisms associated with dronedarone-induced hepatotoxicity and clinical drug-drug interactions.
105 er profiling in studies exploring xenobiotic hepatotoxicity and clinical investigations of liver dise
106 ular steatosis is a hallmark of drug-induced hepatotoxicity and early-stage fatty liver disease.
108 ompounds exhibited in vitro neurotoxicity or hepatotoxicity and hence they had improved safety profil
111 racellular 4-HNE accumulation on TNF-induced hepatotoxicity and its potential implication in the path
113 on in APAP-induced chemical stress, both the hepatotoxicity and localised Nrf2-luc response were amel
114 o the clinical presentation of acetaminophen-hepatotoxicity and may inform future mechanistic studies
117 tment, after administration of the codrug no hepatotoxicity and no induction of the cytochrome P450 s
120 s from the areas of preclinical and clinical hepatotoxicity and safety assessment, from industry, aca
121 alp3 inflammasome) for acetaminophen-induced hepatotoxicity and some potential therapeutic approaches
122 ing macroautophagy pharmacologically reduced hepatotoxicity and steatosis associated with acute ethan
123 oxygen species generated during drug-induced hepatotoxicity and suggest that induction of UCP2 may al
124 om a polyfunctional T cell activation caused hepatotoxicity and the rapid induction of apoptotic sign
125 mechanisms involved in acetaminophen-induced hepatotoxicity and the role of chemokine (C-X-C motif) r
127 dospicine is consistent with observed canine hepatotoxicity, and considering the higher in vitro tran
128 nous and endogenous hepatic targets, reduced hepatotoxicity, and extended RNAi stability by more than
129 um T3 (3,3 ,5-triiodo-l-thyronine), maternal hepatotoxicity, and increased multinucleated germ cells
131 are unreactive with thiols, display reduced hepatotoxicity, and retain Hsp90 and growth-inhibitory a
132 monocyte-derived macrophages aggravate APAP hepatotoxicity, and the pharmacological inhibition of ei
133 for MLK3 in APAP-induced JNK activation and hepatotoxicity, and they suggest MLK3 as a possible targ
135 RF1 delivery to Junb-deficient mice restored hepatotoxicity, and we demonstrate that Ifng is a direct
136 epatitis C virus (HCV) disease, drug-induced hepatotoxicity, and, possibly, direct damage from HIV in
138 ts that seem to have the least potential for hepatotoxicity are citalopram, escitalopram, paroxetine,
140 depressants associated with greater risks of hepatotoxicity are iproniazid, nefazodone, phenelzine, i
141 sing rAAV-shRNAs we have now determined that hepatotoxicity arises when exogenous shRNAs exceed 12% o
142 in productions were monitored during a 5-day hepatotoxicity assessment in which human primary hepatoc
144 gion have been associated with idiosyncratic hepatotoxicity attributed to flucloxacillin, ximelagatra
145 s from HDS versus medications, patients with hepatotoxicity attributed to medications or HDS were enr
146 hed hepatic NADP and protected the mice from hepatotoxicity, based on markers such as increased level
147 hepatotoxicity of TDCIPP, the expression of hepatotoxicity biomarker genes, liver histopathology and
148 not only for discerning a compound's general hepatotoxicity but also for determining its toxic concen
150 vo sensitizes the liver to TNF-alpha-induced hepatotoxicity by a mechanism involving the activation o
152 idinyl ketolides that focus on mitigation of hepatotoxicity by minimizing hepatic turnover and time-d
153 cumulation determines susceptibility to APAP hepatotoxicity by modulating mitophagy, and imply that g
155 ing high affinity modifications such as LNA, hepatotoxicity can occur as a result of unintended off-t
156 Induced Liver Injury Network (DILIN) studies hepatotoxicity caused by conventional medications as wel
159 ury," "liver failure," "DILI," "hepatitis," "hepatotoxicity," "cholestasis," and "aminotransferase,"
160 he diurnal variation in acetaminophen (APAP) hepatotoxicity (chronotoxicity) reportedly is driven by
161 ficantly with less bone destruction and less hepatotoxicity compared with equimolar doses of free doc
162 ctive antiretroviral therapy (HAART)-related hepatotoxicity complicates the management of patients in
165 2(-/-) mice were used to identify changes of hepatotoxicity, damage to mitochondria, and production o
167 ice, however, were sensitive to APAP-induced hepatotoxicity despite activation of PPARalpha with Wy-1
170 SMase(-/-) mice and hepatocytes against APAP hepatotoxicity, effects that were reversed by chloroquin
171 zonation patterns of P450 isozyme levels and hepatotoxicity emerge following dosing with different co
172 umab ozogamicin is associated with increased hepatotoxicity, especially after follow-up HSCT, compare
174 ns of an extensive antioxidant screening and hepatotoxicity evaluation against HepG2, a human hepatob
175 g set of in vivo rodent experiments for drug hepatotoxicity evaluation, we discovered common biomarke
176 e viral hepatitis coinfections, drug-related hepatotoxicity, fatty liver disease, and direct and indi
179 he expression of several biomarker genes for hepatotoxicity (gck, gsr and nqo1) and caused hepatic va
182 ome-wide association study of flucloxacillin hepatotoxicity has yielded groundbreaking results and ma
184 ssays/techniques in order to investigate the hepatotoxicity; however, only the covalent binding in ra
189 Thus, this model allows for investigation of hepatotoxicity in human liver tissue upon applying drug
191 ion are likely to be critical events in APAP hepatotoxicity in humans, resulting in necrotic cell dea
196 e nanoprobes achieve real-time monitoring of hepatotoxicity in living animals, thereby providing a co
201 requency of, and potential risk factors for, hepatotoxicity in patients in this trial and after treat
202 There was a higher rate of grade 3 or 4 hepatotoxicity in patients on BIBF 1120 (51.2%) compared
203 e effective noninvasive tools for monitoring hepatotoxicity in patients receiving methotrexate for ps
204 e is a need for noninvasive tools to monitor hepatotoxicity in patients with psoriasis who are receiv
207 protected wildtype mice against APAP-induced hepatotoxicity in the absence of PPARalpha activation.
208 iver injury now accounts for 20% of cases of hepatotoxicity in the United States based on research da
210 on, neuroprotective effects, lacks tacrine's hepatotoxicity in vitro and in vivo, and shows the same
212 ort a luminescent approach to evaluate acute hepatotoxicity in vivo by chromophore-conjugated upconve
216 first treatment, 13 (1%) of 996 patients had hepatotoxicity (including one [<1%] possible Hy's law ca
217 bes investigator-assessed treatment-emergent hepatotoxicity, including sinusoidal obstruction syndrom
218 stases has raised awareness of the potential hepatotoxicities induced by systemic drugs and the effec
219 ammatory macrophages have been implicated in hepatotoxicity induced by the analgesic acetaminophen (A
222 strate that the off-target RNA knockdown and hepatotoxicity is attenuated by RNase H1 knockdown, and
223 f compensatory liver regeneration after APAP hepatotoxicity is critical for final recovery, but the m
225 Standard preclinical evaluation of drug hepatotoxicity is generally performed using in vivo anim
228 reported to be responsible for APAP-induced hepatotoxicity, it is not known whether APAP can modulat
229 g/day are associated with increased risk for hepatotoxicity, many drugs are safe at such dosages.
230 o exhibited significantly elevated levels of hepatotoxicity markers in circulation, a 58% increase in
234 oral medications and observed high risk for hepatotoxicity (odds ratio [OR], 14.05; P < 0.001) for d
235 y an LXR agonist conferred resistance to the hepatotoxicity of APAP, whereas the effect of LXR agonis
237 s represents a powerful tool to evaluate the hepatotoxicity of drugs that are metabolized by CYP2E1.
239 and reveal possible strategies for reducing hepatotoxicity of short- and long-term clinical gene sil
241 nt gut microbial influences in modifying the hepatotoxicity of tacrine, providing insights for person
244 for clinician awareness regarding potential hepatotoxicity of varenicline, particularly among patien
247 ect outcomes in the context of acetaminophen hepatotoxicity or hepatic ischemia-reperfusion injury.
250 ith adverse drug reactions (ADRs), including hepatotoxicity; oxidative metabolism of 1 has been impli
252 alogues developed a variety of clearance and hepatotoxicity patterns that were strikingly similar to
253 andardized system for categorizing drugs for hepatotoxicity potential will help develop objective and
254 ritical protective role against APAP-induced hepatotoxicity, primary cultured mouse hepatocytes and g
260 lly explore the application of stem cells in hepatotoxicity safety assessment and to make recommendat
261 complementary to animal testing, for initial hepatotoxicity screening or mechanistic studies of candi
263 t urine samples generated in an experimental hepatotoxicity study of galactosamine (galN) and the con
265 ite alterations associated with hallmarks of hepatotoxicity such as gamma-glutamyl dipeptides, acylca
266 r 4 of the first 8 patients developed severe hepatotoxicity suggestive of veno-occlusive disease.
267 Recently, a liver tissue model conducive to hepatotoxicity testing was developed by bioprinting hepa
269 ong cholinesterase inhibitory activity, less hepatotoxicity than tacrine, and the best neuroprotectiv
272 , or R341C in mice predisposes to acute APAP hepatotoxicity, thereby providing direct evidence for th
274 tent environmental contaminant which elicits hepatotoxicity through activation of the aryl hydrocarbo
275 ombination of high potency to tumors and low hepatotoxicity to provide a pronounced survival benefit
276 coholic fatty liver disease and drug-induced hepatotoxicity, together with development of hepatocellu
277 In order to understand the mechanism of this hepatotoxicity, transcriptional profiles were collected
278 inhibitors used were shown to cause relevant hepatotoxicity under nearly all conditions, but particul
279 se 3 (GSK3) in liver regeneration after APAP hepatotoxicity using a pharmacological inhibition strate
280 d the effect of bile acid modulation on APAP hepatotoxicity using C57BL/6 mice, which were fed a norm
283 ical and hepatocellular carcinomas), and the hepatotoxicity was evaluated using a porcine liver prima
284 ical and hepatocellular carcinomas), and the hepatotoxicity was evaluated using a porcine liver prima
285 er a median follow-up period of 14.7 months, hepatotoxicity was found to be a frequent and often seve
287 he chronic toxicity of fialuridine for which hepatotoxicity was mimicked after repeated-dosing in the
291 Rates of investigator-assessed drug-related hepatotoxicity were 0.4% and 2.7%, respectively (P<0.001
294 me and the role of CYP2E1 in ethanol-induced hepatotoxicity were investigated using liquid chromatogr
297 Paracetamol (APAP) has been known to induce hepatotoxicity when exceeding therapeutic doses and was
298 ered 90 minutes post-APAP) protected against hepatotoxicity, whereas mice treated with APAP alone dev
299 not secondary to alteration of APAP-induced hepatotoxicity, which remained unchanged after GSK3 inhi
WebLSDに未収録の専門用語（用法）は "新規対訳" から投稿できます。