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1 d memory T-cell responses with no measurable liver toxicity.
2 rved for tolerability, glycemic control, and liver toxicity.
3  be withdrawn within weeks on the grounds of liver toxicity.
4 a and IL-18 fully protected the mice against liver toxicity.
5 ect that needs to be overcome is nonspecific liver toxicity.
6 onistic antibodies resulted in dose-limiting liver toxicity.
7  to liver cells and results in dose-limiting liver toxicity.
8               Dose escalation was limited by liver toxicity.
9 rstanding how covalent binding could lead to liver toxicity.
10 tifying patients most susceptible to tacrine liver toxicity.
11 re chemotherapy- and/or radiotherapy-induced liver toxicity.
12 cute myocardial infarction, and drug-induced liver toxicity.
13  did not induce adverse immune activation or liver toxicity.
14 served antitumor efficacy from the on-target liver toxicity.
15 s toxic to reproduction and that it exhibits liver toxicity.
16  function, lipid metabolism and TCDD-induced liver toxicity.
17  an important component of pesticide-induced liver toxicity.
18 o antitumor efficacy, without weight loss or liver toxicity.
19 persistence of activated T cells may lead to liver toxicity.
20 ide effects like bone marrow suppression and liver toxicity.
21  (p for trend < 0.0001), indicating possible liver toxicity.
22 lpha-amanitin have been limited owing to its liver toxicity.
23 dard of care (sorafenib), without increasing liver toxicity.
24 ATRA and idarubicin, with a low incidence of liver toxicity.
25 cing secondary disease such as steatosis and liver toxicity.
26        There have also been suspicions about liver toxicity.
27 ed CYP2E1 plays an important role in alcohol liver toxicity.
28 veral diseases, including cancer and alcohol liver toxicity.
29 pl2 in sterile inflammation and drug-induced liver toxicity.
30 L12-, IFN-gamma-, and concanavalin A-induced liver toxicity.
31 ppresses proinflammatory cytokine-associated liver toxicity.
32 e (C-C motif) ligand 5 (CCL5) and subsequent liver toxicity.
33 d was applied to study acetaminophen-induced liver toxicity.
34 mmadeltaT cells during AdLacZ-mediated acute liver toxicity.
35 ion-defective adenovirus (Ad)-mediated acute liver toxicity.
36 ated in the development of Ad-mediated acute liver toxicity.
37 t-market attrition of pharmaceuticals due to liver toxicity.
38 trains in the study of acetaminophen-induced liver toxicity.
39 emplified using a study on hydrazine-induced liver toxicity.
40 and Drug Administration (FDA) for reasons of liver toxicity.
41 pecific compositional changes and spleen and liver toxicities.
42 th ipilimumab (anti-CTLA4), with significant liver toxicities.
43  peripheral neuropathy (2 patients, 5%), and liver toxicity (2 patients, 5%).
44  outcomes (hyponatremia 44% vs 67% (p=0.29); liver toxicity 6% vs 0% (p=1.0)).
45 n unraveling the mechanisms underlying early liver toxicity after adenovirus infusion, particularly t
46 le for gammadeltaT cells in initiating acute liver toxicity after AdLacZ administration, driven in pa
47              We examined the hypothesis that liver toxicity after cyclophosphamide and total body irr
48                 Management and prevention of liver toxicity among HIV-infected patients treated with
49 discovered common biomarkers of drug-induced liver toxicity among six heterogeneous compounds.
50 kylating agent azoxymethane resulted in both liver toxicity and an increased incidence of precancerou
51 n restoring tissue integrity following acute liver toxicity and establish a role of endothelial cells
52 hich stem from diverse etiologies, result in liver toxicity and fibrosis and may progress to cirrhosi
53 s exposure is one of the primary factors for liver toxicity and hepatocarcinoma.
54 pplications is restricted due to significant liver toxicity and immunogenicity.
55 cumulation resulted in significantly reduced liver toxicity and increased transduction efficiency of
56 2 to 3 days in TCZ-treated patients, whereas liver toxicity and infectious complications were similar
57 tion, using a murine model of CCl(4)-induced liver toxicity and mice genetically deficient in C5.
58 data and applied to proprietary data for the liver toxicity and MNT in vivo endpoints were investigat
59 d of follow-up (18-53 weeks), only transient liver toxicity and no renal toxicity had been observed.
60 lites of cyclophosphamide leads to increased liver toxicity and nonrelapse mortality and lower overal
61 amide synthases (CerS) and causes kidney and liver toxicity and other disease.
62 lusion: Pretreatment cytokine levels predict liver toxicity and overall survival.
63 umulate these chemical pollutants and suffer liver toxicity and pathology.
64 dentified was evaluated in mouse and rat for liver toxicity and systemic exposure, respectively, prov
65 cal awareness regarding zanubrutinib-induced liver toxicity and the importance of drug withdrawal in
66 5 x 10(5)CFU of Brucella, (ii) the extent of liver toxicity, and (iii) the minimum immunizing dose of
67 nsidered in future studies for prevention of liver toxicity, and HGF should be explored further to de
68 nsidered in future studies for prevention of liver toxicity, and HGF should be explored further to de
69 luding adverse events with serious outcomes, liver toxicity, and muscle toxicity without rhabdomyolys
70 tritional abnormalities, including alopecia, liver toxicity, and runting.
71 he MONO study were fever, hypotension, acute liver toxicity, and vascular leak syndrome.
72                                        Early liver toxicity as determined by serum glutamic-pyruvic t
73                                        Acute liver toxicity (as measured with liver enzyme elevation)
74 f urelumab has been hampered by inflammatory liver toxicity at doses >1 mg/kg.
75 n dosing algorithms were not associated with liver toxicity at EOT.
76             No clinical symptoms or signs of liver toxicity attributable to vitamin A excess were det
77                   Obesity increases risk for liver toxicity by the anti-leukemic agent asparaginase,
78 f HIV infection, increasing the incidence of liver toxicity caused by antiretroviral medications.
79 at such a discrepancy could be due to severe liver toxicity caused by bortezomib and LPS co-treatment
80                                              Liver toxicity caused by high-dose myeloablative therapy
81 IH greatly exacerbated acetaminophen-induced liver toxicity, causing fulminant hepatocellular injury.
82             Iron overload is associated with liver toxicity, cirrhosis, and hepatocellular carcinoma
83                                       Recent liver toxicity concerns with UPA, diminished enthusiasm
84                                 The observed liver toxicity confirms the results of gamma camera and
85 se events of special interest were potential liver toxicity, corrected QT prolongation, and adrenal i
86 refore, we investigated whether FIAU-induced liver toxicity could be detected in chimeric TK-NOG mice
87                                 FIAU-induced liver toxicity could be readily detected using chimeric
88 ate-phase drug developmental failures due to liver toxicity could potentially be reduced through the
89                         The lack of relevant liver toxicity despite high applied (90)Y activities and
90                                              Liver toxicity did not develop in control mice that were
91 es some protection against cardiotoxicity or liver toxicity during cancer treatment.
92 eated with azoxymethane (AOM) and markers of liver toxicity examined.
93                                              Liver toxicity following an overdose of acetaminophen is
94                             The experimental liver toxicity from the different treatments was confirm
95                                However, mild liver toxicities have been observed in some patients rec
96 ach to integrate these data to help identify liver toxicity hazards.
97                                              Liver toxicity (hepatotoxicity) is a critical issue in d
98 line liver function were not associated with liver toxicity; however, levels of sTNFR1 (P = 0.045) an
99 ical consequences derived from HAART-related liver toxicity, hypersensitivity reactions and lactic ac
100 pt that it resulted in serologic evidence of liver toxicity in 6 percent of the women.
101 V) serotype 2 vectors has been implicated in liver toxicity in a recent human gene therapy trial of h
102                The results of antidepressant liver toxicity in all phases of clinical trials should b
103 ubsequent autologous recovery, and transient liver toxicity in dogs treated with (211)At doses less t
104 44 mg/kg/d po) for 14 d, which did not cause liver toxicity in human trial participants, did not caus
105                In addition, we observed less liver toxicity in mice injected with the Av4orf3nBg vect
106 y in human trial participants, did not cause liver toxicity in mice with humanized livers.
107 cted susceptibility to acetaminophen-induced liver toxicity in mice.
108  The approach is illustrated with a study of liver toxicity in rats using NMR spectra of urine follow
109 to one of 13 endpoints indicative of lung or liver toxicity in rodents, or of breast cancer, multiple
110 45) and HGF (P = 0.005) were associated with liver toxicity in univariate models.
111 icantly reduced infection of liver cells and liver toxicity in vivo.
112                       We previously observed liver toxicity-including hepatocyte turnover, loss of ge
113 ow that PPARbeta/delta is protective against liver toxicity induced by AOM and CCl(4), suggesting tha
114                   In contrast to evidence of liver toxicity, inflammation, and cellular infiltration
115 essing a new chemical entity's potential for liver toxicity is an important consideration for the lik
116 ose, its importance in acetaminophen-induced liver toxicity is not well understood, primarily due to
117 ochemicals and pharmaceuticals for potential liver toxicity is required for regulatory approval and i
118                                              Liver toxicity is the major concern for use of recombina
119                        Acetaminophen-induced liver toxicity is the most frequent precipitating cause
120                                    The FDA's Liver Toxicity Knowledge Base (LTKB) evaluated >1000 dru
121 s National Center for Toxicological Research Liver Toxicity Knowledge Base (NCTR-LTKB), the inhibitor
122 ntial for DILI concern, as classified in the Liver Toxicity Knowledge Base database.
123 n sensitivity to TRAIL, and that substantial liver toxicity might result if TRAIL were used in human
124                 Only transient, mostly minor liver toxicity (no grade 4) was recorded.
125                               The hazards of liver toxicity, nonrelapse mortality, tumor relapse, and
126                            Also, no signs of liver toxicity occurred after the rAAV-AGA administratio
127 OLG was strongly associated with VPA-induced liver toxicity (odds ratio = 23.6, 95% confidence interv
128                       Updated information on liver toxicity of current antiretroviral drugs, includin
129 a high response rate (85%) without increased liver toxicity of grade 3 or higher (6% vs. 12% in the p
130  an important causal role in the nonspecific liver toxicity of LMB-2.
131 kDa gene had no significant influence on the liver toxicity of the vectors in this system.
132 GI, and liver (18%; 12 patients) and grade 4 liver toxicities (one patient) were also observed.
133                                        After liver toxicity (one death from venoocclusive disease [VO
134                               No significant liver toxicity or cFIX-specific antibodies have been det
135 ding to treatment discontinuation related to liver toxicity or diarrhea.
136 or for at least 7 months, with no detectable liver toxicity or meaningful off-target effects.
137 the XRCC3 241Met variant had reduced risk of liver toxicity (OR = 0.32; 95%CI, 0.11-0.95).
138                                  LXR-induced liver toxicity, poor drug aqueous solubility and low lev
139             The overall gastrointestinal and liver toxicity profile was consistent with the profile i
140 ence of hyponatraemia (sNa</=132 mmol/L) and liver toxicity (proportion of patients alanine transamin
141                              All evidence of liver toxicity resolved except for persistent hypofibrin
142 imary hepatocytes for use in high-throughput liver toxicity studies.
143 NMR spectroscopic study of hydrazine-induced liver toxicity study in rats.
144 the IL-2 mutant also exhibits lower lung and liver toxicity than does wtIL-2 when used at high doses
145 s substantial, dose-dependent, dose-limiting liver toxicity that was manifest as elevated serum trans
146  and tumorigenesis, and the relevance of TCS liver toxicity to humans should be evaluated.
147 ration of HAdV-5 vectors can result in acute liver toxicity, transaminitis, thrombocytopenia, and inj
148 ardiotoxicity, two acute kidney failure, one liver toxicity, two respiratory failure, one thromboembo
149 ed stop criteria: one IV-D patient developed liver toxicity; two patients in each group developed bra
150 ces and alternative mechanisms including gut-liver toxicity warrant investigation.
151                                              Liver toxicity was also blocked by indomethacin, which a
152                                              Liver toxicity was assessed through physical examination
153               In addition, the LMB-2-induced liver toxicity was blocked by a specific TNF binding pro
154                               Dose-dependent liver toxicity was detected in chimeric mice treated wit
155                                 APAP-induced liver toxicity was mirrored by significantly increased p
156 ur polyamides after injection, dose-limiting liver toxicity was only observed for three polyamides.
157                                              Liver toxicity was scored by the development of sinusoid
158 grade 3 or 4 thrombocytopenia, asthenia, and liver toxicity was significantly higher in the experimen
159                 Grade 3 to 4 hematologic and liver toxicities were greater in the GO arm.
160       Severe TRAEs associated with renal and liver toxicities were uncommon.
161  doses of 3.6 to 8.8 mCi/kg Bi, but signs of liver toxicity were noted in all dogs.
162  of anemia, hypokalemia, hypomagnesemia, and liver toxicity were similar.
163 erase (GGT) and direct bilirubin, markers of liver toxicity, were obtained from blood samples collect
164     Importantly, AdMKTK + GCV did not induce liver toxicity, whereas substantial toxicity was seen wi
165  receptor agonist (GW3965) and abolished its liver toxicity while still preserving its therapeutic fu
166 role of PPARbeta/delta in chemically induced liver toxicity, wild-type and PPARbeta/delta-null mice w
167                   However, concern regarding liver toxicity with systemic therapy makes local deliver
168 ; and 5) safety concerns regarding increased liver toxicity with ximelagatran without a significant o
169 of the mechanisms that lead to idiosyncratic liver toxicity would be extremely beneficial for the dev

 
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