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1 iver cells and may play an important role in hepatic regeneration.
2 before liver resection suffered from delayed hepatic regeneration.
3 is required for gammadeltaT cells to promote hepatic regeneration.
4  with regenerative growth factors to promote hepatic regeneration.
5 a specific inhibitor of Zn-HDAC activity) on hepatic regeneration.
6 jury, limit vascular inflammation, and boost hepatic regeneration.
7 ony-stimulating factor (G-CSF) could promote hepatic regeneration.
8 Ogenitor Cells (sprocs) play a vital role in hepatic regeneration.
9 tosis resulted in significant suppression of hepatic regeneration.
10 inophen-induced injury, which contributes to hepatic regeneration.
11 systemic milieu that does not support normal hepatic regeneration.
12 mia/reperfusion but is also mitogenic during hepatic regeneration.
13 uld impair hepatocellular function and limit hepatic regeneration.
14 70), after two-thirds hepatectomy to prevent hepatic regeneration.
15 cumulation would be associated with impaired hepatic regeneration.
16  MIP-2 doses after hepatic injury accelerate hepatic regeneration.
17 f CREB by phosphorylation that occurs during hepatic regeneration.
18 gave rise to donor-derived hematopoietic and hepatic regeneration.
19 ide-1/glucagon receptor agonist, on NASH and hepatic regeneration.
20 n in the rat has been useful in the study of hepatic regeneration.
21 ion of glucuronidation during the process of hepatic regeneration.
22 liver injuries alter metabolism and initiate hepatic regeneration.
23 ing to liver injury, but is also involved in hepatic regeneration.
24 enol glucuronide formation was unaffected by hepatic regeneration 1, 2, and 5 days posthepatectomy wh
25 not the cellular alterations associated with hepatic regeneration affect the efficacy and toxicity of
26 ss the effects of undifferentiated UCMSCs in hepatic regeneration after an acute liver injury, we tra
27 F) and epidermal growth factor (EGF) mediate hepatic regeneration after liver injury.
28 markers of lipid metabolism and insufficient hepatic regeneration after liver surgery suggest a criti
29  systemic inflammatory reactions may trigger hepatic regeneration after major tissue loss.
30 lar matrix remodeling events associated with hepatic regeneration after partial hepatectomy.
31           In conclusion, the early stages of hepatic regeneration after resection provide an environm
32 g protein (ENA-78), a CXC chemokine, retards hepatic regeneration after resection.
33 nisms prevail: (1) cirrhosis associated with hepatic regeneration after tissue damage caused by hepat
34 f CD39 activity is associated with decreased hepatic regeneration and failure of vascular reconstitut
35 ighlights the role of activated HPCs in both hepatic regeneration and fibrosis during liver injury.
36 te that IL-6 can function acutely to improve hepatic regeneration and repair, but that more chronic e
37                  Analysis of liver function, hepatic regeneration, and comprehensive genomic and meta
38 th elevated portal venous pressure, impaired hepatic regeneration, and postoperative morbidity.
39 ects of the signaling mechanisms involved in hepatic regeneration are under active investigation.
40                        Therefore, we studied hepatic regeneration at day 1, day 2, and day 4 in a mod
41                             bFGF accelerated hepatic regeneration by 42%, 19%, 16%, and 16% on postop
42                            TNP-470 inhibited hepatic regeneration by 46%, 74%, 67%, and 64% on postop
43         We have shown that G-CSF facilitates hepatic regeneration by increasing the migration of BM-d
44                   gammadeltaT cells regulate hepatic regeneration by producing IL-22 and IL-17, which
45 treated mice exhibited significantly reduced hepatic regeneration compared with controls, as assessed
46            Remarkably, DNA damage/repair and hepatic regeneration directed by G-CSF concerned rebalan
47 vestigated the time course of changes during hepatic regeneration for Na, K-ATPase activity, lipid co
48 ataxia telangiectasia mutated gene restricts hepatic regeneration in acute liver failure.
49 c liver failure, and erythropoietin promoted hepatic regeneration in animal studies.
50 brosis, reduced liver injury, and stimulated hepatic regeneration in fibrotic mice with or without he
51  Interleukin 6 (IL-6) is a potent inducer of hepatic regeneration in normal and ischemic livers.
52 ent may be useful in assessing the degree of hepatic regeneration in patients with clinical liver dis
53 gon-like peptide-2 (GLP-2) critically affect hepatic regeneration in rodent models.
54 M-HSCs) have been shown to act as source for hepatic regeneration in rodent models; however, their ab
55   These results indicate major impairment of hepatic regeneration in steatotic livers.
56 emic endotoxemia, which normally accompanies hepatic regeneration induced by PH, also decreased clear
57                                              Hepatic regeneration is a heterogeneous phenomenon invol
58                                       During hepatic regeneration, MMP-9 was detected in the urine at
59 ectomy rat model to elucidate the effects of hepatic regeneration on the various components of the mi
60 RK activation and promoted STAT3-independent hepatic regeneration (PCNA, Cyclin D1, Ki67) following a
61  and enhanced the proliferative capacity and hepatic regeneration ratio in mice on the MCD diet.
62 partial hepatectomy (PH) of 70% to stimulate hepatic regeneration showed decreased asialoglycoprotein
63 nvestigated the role of gammadeltaT cells in hepatic regeneration using mice with disruptions in Tcrd
64                                     Although hepatic regeneration was associated with a reduced chole
65                                              Hepatic regeneration was determined by liver weight/tota
66  to ischemia and hepatectomy showed impaired hepatic regeneration when compared with wild-type mice s
67  and consistently inverse time course during hepatic regeneration with a significant decrease of GLP-
68 lts provide a therapeutic roadmap to achieve hepatic regeneration without provoking fibrosis.