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1 functions as a protective factor preventing alcoholic liver injury.
2 mechanism of interindividual variability in alcoholic liver injury.
3 NF-alpha) production are key risk factors in alcoholic liver injury.
4 ial mechanisms of JNK1 activation related to alcoholic liver injury.
5 chemokine (C-C motif) receptor 2 (CCR2), in alcoholic liver injury.
6 were performed to study the role of MCP-1 in alcoholic liver injury.
7 a useful model to study the early stages of alcoholic liver injury.
8 es the hepatoprotection provided by IL-22 in alcoholic liver injury.
9 upplementation could provide protection from alcoholic liver injury.
10 age and reduction of ATP content, leading to alcoholic liver injury.
11 is a critical factor in the pathogenesis of alcoholic liver injury.
12 , plays an important role in protection from alcoholic liver injury.
13 ne metabolism and DNA damage while promoting alcoholic liver injury.
14 (PUFA) are important for the development of alcoholic liver injury.
15 activation are proposed as the mechanisms of alcoholic liver injury.
16 the presence of pathological liver injury in alcoholic liver injury.
17 play an important role in the initiation of alcoholic liver injury.
18 we investigated the role of LBP and CD14 in alcoholic liver injury.
19 t hypoxia is involved in mechanisms of early alcoholic liver injury.
20 function are important to the development of alcoholic liver injury.
21 al changes and thromboxane (TX) synthesis in alcoholic liver injury.
22 kin receptor-associated kinase-M (IRAK-M) in alcoholic liver injury.
24 lus iron, agents important in development of alcoholic liver injury and which are toxic to E47 cells
25 A was significantly induced in patients with alcoholic liver injury, and was co-localized with alphaS
27 epatitis C virus (HCV) infection exacerbates alcoholic liver injury by mechanisms that include enhanc
28 abolites in this animal model of accelerated alcoholic liver injury can be ascribed to specific effec
29 identified but not of the predisposition to alcoholic liver injury, except perhaps for polymorphism
32 of inflammatory cells is a major feature of alcoholic liver injury however; the signals and cellular
33 In conclusion, zinc supplementation prevents alcoholic liver injury in an metallothionein-independent
36 eine, endoplasmic reticulum (ER) stress, and alcoholic liver injury in the murine model of intragastr
37 ctivation in culture and in a mouse model of alcoholic liver injury in vivo, and its expression corre
38 Deficiency of MCP-1 protects mice against alcoholic liver injury, independent of CCR2, by inhibiti
40 Currently, the most widely used model for alcoholic liver injury is ad libitum feeding with the Li
41 sted the hypothesis that the pathogenesis of alcoholic liver injury is mediated by epigenetic changes
42 hat a critical factor in the pathogenesis of alcoholic liver injury is the enhanced ability of rat or
50 urthermore, because TNF-alpha contributes to alcoholic liver injury, we tested the hypothesis that Eg
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