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1 ficant pathophysiological diversity of human alcoholic liver injury.
2 kin receptor-associated kinase-M (IRAK-M) in alcoholic liver injury.
3  functions as a protective factor preventing alcoholic liver injury.
4  mechanism of interindividual variability in alcoholic liver injury.
5 NF-alpha) production are key risk factors in alcoholic liver injury.
6 ial mechanisms of JNK1 activation related to alcoholic liver injury.
7  chemokine (C-C motif) receptor 2 (CCR2), in alcoholic liver injury.
8 were performed to study the role of MCP-1 in alcoholic liver injury.
9  a useful model to study the early stages of alcoholic liver injury.
10 es the hepatoprotection provided by IL-22 in alcoholic liver injury.
11 upplementation could provide protection from alcoholic liver injury.
12 age and reduction of ATP content, leading to alcoholic liver injury.
13  is a critical factor in the pathogenesis of alcoholic liver injury.
14 , plays an important role in protection from alcoholic liver injury.
15 ne metabolism and DNA damage while promoting alcoholic liver injury.
16  (PUFA) are important for the development of alcoholic liver injury.
17 activation are proposed as the mechanisms of alcoholic liver injury.
18 the presence of pathological liver injury in alcoholic liver injury.
19  play an important role in the initiation of alcoholic liver injury.
20  we investigated the role of LBP and CD14 in alcoholic liver injury.
21 t hypoxia is involved in mechanisms of early alcoholic liver injury.
22 al changes and thromboxane (TX) synthesis in alcoholic liver injury.
23 function are important to the development of alcoholic liver injury.
24 nsumption are frequently used to investigate alcoholic liver injury and define new therapeutic target
25      In conclusion, NOX4 is induced in early alcoholic liver injury and regulates CCR2/CCL2 mRNA stab
26 lus iron, agents important in development of alcoholic liver injury and which are toxic to E47 cells
27 A was significantly induced in patients with alcoholic liver injury, and was co-localized with alphaS
28     Here we describe a simple mouse model of alcoholic liver injury by chronic ethanol feeding (10-d
29 epatitis C virus (HCV) infection exacerbates alcoholic liver injury by mechanisms that include enhanc
30 abolites in this animal model of accelerated alcoholic liver injury can be ascribed to specific effec
31  identified but not of the predisposition to alcoholic liver injury, except perhaps for polymorphism
32              The importance of chemokines in alcoholic liver injury has been implicated.
33             As the role of this NOX in early alcoholic liver injury has not been addressed, we studie
34  of inflammatory cells is a major feature of alcoholic liver injury however; the signals and cellular
35 In conclusion, zinc supplementation prevents alcoholic liver injury in an metallothionein-independent
36                                   We induced alcoholic liver injury in male Sirt1LKO and control mice
37 d fatty liver, which mimics acute-on-chronic alcoholic liver injury in patients.
38 eine, endoplasmic reticulum (ER) stress, and alcoholic liver injury in the murine model of intragastr
39 ctivation in culture and in a mouse model of alcoholic liver injury in vivo, and its expression corre
40    Deficiency of MCP-1 protects mice against alcoholic liver injury, independent of CCR2, by inhibiti
41                                              Alcoholic liver injury is a major public health issue wo
42    Currently, the most widely used model for alcoholic liver injury is ad libitum feeding with the Li
43 sted the hypothesis that the pathogenesis of alcoholic liver injury is mediated by epigenetic changes
44 hat a critical factor in the pathogenesis of alcoholic liver injury is the enhanced ability of rat or
45 aride (LPS), how enteral LPS loading affects alcoholic liver injury is yet to be tested.
46                    Up-regulation of COX-2 in alcoholic liver injury occurred in the presence of proin
47 e of ALDH2 deficiency in the pathogenesis of alcoholic liver injury remains obscure.
48          With the essential role of TNFR1 in alcoholic liver injury, targeting TNFR1 by hepatitis vir
49                                              Alcoholic liver injury was achieved by pair feeding wild
50            This novel ER stress mechanism of alcoholic liver injury was studied in the model of intra
51      To test whether FOXO3 is protective for alcoholic liver injury, we fed alcohol to FOXO3(-/-) mic
52 urthermore, because TNF-alpha contributes to alcoholic liver injury, we tested the hypothesis that Eg
53             Typical histological features of alcoholic liver injury were present in posttransplant bi