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1 flammation on I/R in a murine model of total hepatic ischemia.
2 rvival was determined using a model of total hepatic ischemia.
3  more vulnerable to necrosis after transient hepatic ischemia.
4      Numerous clinical circumstances lead to hepatic ischemia.
5  attenuate tissue injury after an episode of hepatic ischemia.
6 leotidase may be a potential therapeutic for hepatic ischemia.
7 is rats underwent 60 minutes of partial warm hepatic ischemia.
8 ingly, male rats were subjected to 1 hour of hepatic ischemia (70%) followed by reperfusion; animals
9 ute kidney injury, myocardial, intestinal or hepatic ischemia, acute lung injury, or during organ tra
10 d to 4 groups: 1.Sham; 2.IR: 40 min of lobar hepatic ischemia and 2 hr reperfusion; 3.RIPC+IR: 6 cycl
11 e were subjected to 75 or 120 minutes of 70% hepatic ischemia and 3 hours of reperfusion.
12 C57BL/6 mice underwent 90 minutes of partial hepatic ischemia and 4 hours of reperfusion in the prese
13     Rats were killed after 60 min of partial hepatic ischemia and after 2, 6, 24, and 48 hr of reperf
14 deposited in liver parenchyma, and decreased hepatic ischemia and endothelial injury.
15 rculation, resulting in microscopic areas of hepatic ischemia and explaining the mechanism of IL-2-in
16                          These drugs lowered hepatic ischemia and inflammation, whereas pretreatment
17                 Cell transplantation-induced hepatic ischemia and recruitment of vasoconstrictors (e.
18                                              Hepatic ischemia and reperfusion (IR) injury is a major
19                                              Hepatic ischemia and reperfusion caused increased expres
20                                              Hepatic ischemia and reperfusion causes neutrophil-depen
21 y leukocyte protease inhibitor (SLPI) during hepatic ischemia and reperfusion in mice.
22                                              Hepatic ischemia and reperfusion injury (IRI) remains an
23                                              Hepatic ischemia and reperfusion injury (IRI), an exogen
24 a unique role for Neo1 in the development of hepatic ischemia and reperfusion injury and identified N
25                                   A model of hepatic ischemia and reperfusion injury in fatty and lea
26 d in a significant reduction of experimental hepatic ischemia and reperfusion injury, involving atten
27          Burn and sepsis are associated with hepatic ischemia and reperfusion injury.
28 ammation, we hypothesized that Neo1 enhances hepatic ischemia and reperfusion injury.
29 lanine, and proinflammatory cytokines during hepatic ischemia and reperfusion injury.
30 RA1, ADORA2A, ADORA2B, or ADORA3) attenuates hepatic ischemia and reperfusion injury.
31 ous SLPI on liver and lung injury induced by hepatic ischemia and reperfusion were evaluated.
32               C57BL/6 mice underwent partial hepatic ischemia and reperfusion with or without intrave
33              Using a murine model of partial hepatic ischemia and reperfusion, we evaluated the role
34 wild-type and IL-10(-/-) mice in response to hepatic ischemia and reperfusion.
35 uired for the full induction of injury after hepatic ischemia and reperfusion.
36                           Evidence for total hepatic ischemia and spontaneous shunts was demonstrated
37 cute liver damage and inflammation caused by hepatic ischemia and subsequent reperfusion.
38 ly elevated in vehicle-treated animals after hepatic ischemia and subsequent reperfusion.
39 ) mice were exposed to 90 minutes of partial hepatic ischemia and up to 24 hours of reperfusion.
40 ) mice were exposed to 90 minutes of partial hepatic ischemia and up to 24 hours of reperfusion.
41 ull mice were subjected to 60 min of partial hepatic ischemia, and at various times thereafter, blood
42                              This was due to hepatic ischemia, endothelial injury, and activation of
43 Analysis of microcirculatory events included hepatic ischemia, endothelial injury, including with gen
44 Rats were subjected to 60 minutes of partial hepatic ischemia followed by 0, 3, 6, 24, or 48 hours of
45 re subjected to 10 or 30 min of partial warm hepatic ischemia followed by 3 to 24 hr of reperfusion.
46         A mouse model of partial 90-min warm hepatic ischemia followed by 6 hr of reperfusion was use
47  STAT6 knockout mice underwent 90 minutes of hepatic ischemia followed by 8 hours of reperfusion.
48 before subjecting them to 90 minutes of warm hepatic ischemia followed by reperfusion for 6 or 24 hou
49                                Warm and cold hepatic ischemia followed by reperfusion leads to necrot
50 C57BL/6 mice underwent 90 minutes of partial hepatic ischemia followed by reperfusion with or without
51 ent mice were subjected to 90 min of partial hepatic ischemia followed by reperfusion.
52 mice were subjected to 90 minutes of partial hepatic ischemia followed by reperfusion.
53               Mice were subjected to partial hepatic ischemia followed by reperfusion.
54 mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 8 hours of reperfusio
55 mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 96 hours of reperfusi
56  T4 and steroid 48 hr before 15 min of total hepatic ischemia, followed by 24 hr of reperfusion.
57 mice were subjected to 90 minutes of partial hepatic ischemia, followed by up to 8 hours of reperfusi
58                                              Hepatic ischemia for 90 minutes and reperfusion for up t
59 serotype O55:B5 (EC) and 90 min of secondary hepatic ischemia in EC + I/R and saline-infused (normal
60 onditioning as a protective strategy against hepatic ischemia in humans.
61 ttent clamping (IC) using a model of partial hepatic ischemia in mice aged 20 to 24 months.
62 ificantly improved after 75 minutes of total hepatic ischemia in P-selectin deficient mice when compa
63 f ischemia were further studied in models of hepatic ischemia in rats.
64                             A model of total hepatic ischemia is currently not available in mice.
65           Furthermore, the potential role of hepatic ischemia, Kupffer cells, and cytokine release in
66 , improved cell engraftment independently of hepatic ischemia or inflammation, without improving live
67     Systemic administration of DAR decreases hepatic ischemia-related events and thus indirectly impr
68 mediator of inflammation and organ damage in hepatic ischemia reperfusion (I/R) injury.
69                                              Hepatic ischemia reperfusion injury (IRI) is a major cli
70                    The findings suggest that hepatic ischemia reperfusion injury may play a critical
71 tate aminotransferase, a surrogate marker of hepatic ischemia reperfusion injury, was the only consis
72 m and xenon have additionally been tested in hepatic ischemia reperfusion injury, whereas neon was on
73 sulfide (H2S) production and protection from hepatic ischemia reperfusion injury.
74 ble from wild-type mice in their response to hepatic ischemia reperfusion.
75     Octreotide exerts a protective effect in hepatic ischemia-reperfusion (HIR) injury.
76 ment NO. bioavailability and protect against hepatic ischemia-reperfusion (I-R) injury in type 2 diab
77     CD4+ T cells play a critical role during hepatic ischemia-reperfusion (I/R) injury although the m
78                                              Hepatic ischemia-reperfusion (I/R) injury continues to b
79 oprotection, we subjected CS-eNOS-Tg mice to hepatic ischemia-reperfusion (I/R) injury.
80                                              Hepatic ischemia-reperfusion (IR) injury is a common cli
81                                              Hepatic ischemia-reperfusion (IR) injury is frequently f
82                                              Hepatic ischemia-reperfusion (IR) results in Kupffer cel
83 L/6 mice were subjected to 60-minute partial hepatic ischemia-reperfusion and posttreated with sirtui
84 n of sirtuin 1 attenuates liver injury after hepatic ischemia-reperfusion by restoring mitochondrial
85                                              Hepatic ischemia-reperfusion can be associated with acut
86                                              Hepatic ischemia-reperfusion injury (I/R) occurs in the
87                                              Hepatic ischemia-reperfusion injury (IRI), an innate imm
88 play an essential role in the early phase of hepatic ischemia-reperfusion injury and determine the ex
89 ose tissue-derived mesenchymal stem cells in hepatic ischemia-reperfusion injury and the underlying m
90                                              Hepatic ischemia-reperfusion injury can result in organ
91                                              Hepatic ischemia-reperfusion injury is a disease pattern
92                                              Hepatic ischemia-reperfusion injury or sham operation.
93 ematopoietic Plexin C1 in the development of hepatic ischemia-reperfusion injury, and suggest that Pl
94 antibody and a Semaphorin 7A peptide reduced hepatic ischemia-reperfusion injury, as measured by the
95   Moreover, in animal models of peritonitis, hepatic ischemia-reperfusion injury, Salmonella infectio
96  role of Plexin C1 in a mouse model of early hepatic ischemia-reperfusion injury.
97 nt (PLXNC1) mice also demonstrated decreased hepatic ischemia-reperfusion injury.
98 ockout is crucial for reducing the extent of hepatic ischemia-reperfusion injury.
99  activation of sirtuin 1 is protective after hepatic ischemia-reperfusion injury.
100 e context of acetaminophen hepatotoxicity or hepatic ischemia-reperfusion injury.
101 e stress, and apoptosis in a rodent model of hepatic ischemia-reperfusion injury.
102                                              Hepatic ischemia-reperfusion is a major clinical problem
103                       The pathophysiology of hepatic ischemia-reperfusion is characterized by mitocho
104 zed that pulmonary injury is associated with hepatic ischemia-reperfusion resulting from descending t
105 hts into possible mechanisms responsible for hepatic ischemia-reperfusion-related acute lung injury a
106 rotects against inflammation and damage from hepatic ischemia/reperfusion (I/R) and other insults.
107 that drive sterile inflammatory injury after hepatic ischemia/reperfusion (I/R) injury are not comple
108                                              Hepatic ischemia/reperfusion (I/R) injury associated wit
109 nflammatory responses play critical roles in hepatic ischemia/reperfusion (I/R) injury associating wi
110                                              Hepatic ischemia/reperfusion (I/R) injury is associated
111 catalysis of heme, in the protection against hepatic ischemia/reperfusion (I/R) injury needs to be es
112 he liver to examine their role in total warm hepatic ischemia/reperfusion (I/R) injury with bowel con
113                    Using an in vivo model of hepatic ischemia/reperfusion (I/R) injury, we show that
114  critical mediator of leukocyte migration in hepatic ischemia/reperfusion (I/R) injury.
115 ed mitochondrial function that is evident in hepatic ischemia/reperfusion (I/R) injury.
116                                              Hepatic ischemia/reperfusion (I/R) is a major adverse re
117                                              Hepatic ischemia/reperfusion (I/R) leads to liver injury
118                                              Hepatic ischemia/reperfusion (I/R) results in a neutroph
119                          In a model of mouse hepatic ischemia/reperfusion (I/R), recombinant adenovir
120        Platelets play a critical role during hepatic ischemia/reperfusion (I/R).
121  regeneration of functional liver mass after hepatic ischemia/reperfusion (I/R).
122 iverse roles in the acute injury response to hepatic ischemia/reperfusion (I/R).
123 g with HMGB1 results in protection following hepatic ischemia/reperfusion (I/R).
124 ese Zucker rats are susceptible to increased hepatic ischemia/reperfusion (I/RP) injury.
125 ever, their in vivo functional importance in hepatic ischemia/reperfusion (IR) injury is perplexing.
126                                              Hepatic ischemia/reperfusion (IRI) injury remains a majo
127                                 In addition, hepatic ischemia/reperfusion caused significant increase
128   Therefore, we investigated the response to hepatic ischemia/reperfusion in STAT4-deficient mice.
129                                              Hepatic ischemia/reperfusion in wild-type and STAT6 knoc
130                                              Hepatic ischemia/reperfusion increased expression of TNF
131 (ALT) levels and histological improvement of hepatic ischemia/reperfusion injuries.
132              However, in swine that survived hepatic ischemia/reperfusion injury (45 minutes of ische
133 stic target of rapamycin (mTOR) signaling in hepatic ischemia/reperfusion injury (HIRI) in normal and
134 NK cells in dictating outcomes after partial hepatic ischemia/reperfusion injury (IRI).
135                              Amelioration of hepatic ischemia/reperfusion injury after inhibition of
136 ate that SLPI has protective effects against hepatic ischemia/reperfusion injury and suggest that end
137 The data suggest that IL-10 protects against hepatic ischemia/reperfusion injury by suppressing NFkap
138 sought to determine the role of PPARgamma in hepatic ischemia/reperfusion injury in mice.
139 er the LPS signaling pathway is activated by hepatic ischemia/reperfusion injury in the transplant se
140                                              Hepatic ischemia/reperfusion injury involves a complex i
141                                              Hepatic ischemia/reperfusion injury is caused primarily
142                                              Hepatic ischemia/reperfusion injury is initiated by the
143                             We observed that hepatic ischemia/reperfusion injury leads to: (1) a coin
144 ies with isolated cells and a mouse model of hepatic ischemia/reperfusion injury revealed that NOX2 f
145  have previously employed an animal model of hepatic ischemia/reperfusion injury, and have shown that
146  Furthermore, P5779 can protect mice against hepatic ischemia/reperfusion injury, chemical toxicity,
147 R1, and IL-6 levels, are increased following hepatic ischemia/reperfusion injury, implying that TACE
148 Rgamma activation is hepatoprotective during hepatic ischemia/reperfusion injury, mice were treated w
149                 In an in vivo model of mouse hepatic ischemia/reperfusion injury, recombinant adenovi
150 rtant therapeutic intervention strategies in hepatic ischemia/reperfusion injury.
151  (IL-12) in the induction and development of hepatic ischemia/reperfusion injury.
152 he roles of MIP-2 and KC in the induction of hepatic ischemia/reperfusion injury.
153 rovide sensitive and quantitative markers of hepatic ischemia/reperfusion injury.
154 ctions, which contribute to the pathology of hepatic ischemia/reperfusion injury.
155 ns but also protection from tissue injury in hepatic ischemia/reperfusion injury.
156 tical role in the inflammatory cascade after hepatic ischemia/reperfusion injury.
157 mplying that TACE plays an important role in hepatic ischemia/reperfusion injury.
158                      Liver injury induced by hepatic ischemia/reperfusion is characterized by activat
159 pathways that are activated by the stress of hepatic ischemia/reperfusion remain unknown.
160 as to determine whether IL-10 could suppress hepatic ischemia/reperfusion-induced NFkappaB activation
161 us regulator of the inflammatory response to hepatic ischemia/reperfusion.
162 hil-dependent hepatic injury associated with hepatic ischemia/reperfusion.
163 bjected to 70% hepatectomy and 30 minutes of hepatic ischemia showed significantly reduced regenerati
164 t) following 30, 45, and 90 minutes of acute hepatic ischemia, the systemic release of eight differen
165 R4 knockout (KO) mice were subjected to warm hepatic ischemia, there was significant protection in th
166 vival was observed after 75 minutes of total hepatic ischemia using both protective protocols, wherea
167                              Seventy percent hepatic ischemia was induced in male adult rats by placi
168 ncapsulated clodronate 48 h before 35 min of hepatic ischemia with bowel congestion, followed by 6 or

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