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1 is rats underwent 60 minutes of partial warm hepatic ischemia.
2 flammation on I/R in a murine model of total hepatic ischemia.
3 rvival was determined using a model of total hepatic ischemia.
4  more vulnerable to necrosis after transient hepatic ischemia.
5      Numerous clinical circumstances lead to hepatic ischemia.
6  attenuate tissue injury after an episode of hepatic ischemia.
7 leotidase may be a potential therapeutic for 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 ury of eosinophil-deficient mice and reduced hepatic ischemia and reperfusion injury in wild-type mic
27 d in a significant reduction of experimental hepatic ischemia and reperfusion injury, involving atten
28          Burn and sepsis are associated with hepatic ischemia and reperfusion injury.
29 ammation, we hypothesized that Neo1 enhances hepatic ischemia and reperfusion injury.
30 lanine, and proinflammatory cytokines during hepatic ischemia and reperfusion injury.
31 RA1, ADORA2A, ADORA2B, or ADORA3) attenuates hepatic ischemia and reperfusion injury.
32 ous SLPI on liver and lung injury induced by hepatic ischemia and reperfusion were evaluated.
33               C57BL/6 mice underwent partial hepatic ischemia and reperfusion with or without intrave
34              Using a murine model of partial hepatic ischemia and reperfusion, we evaluated the role
35 wild-type and IL-10(-/-) mice in response to hepatic ischemia and reperfusion.
36 uired for the full induction of injury after hepatic ischemia and reperfusion.
37 tion revealed exacerbated liver injury after hepatic ischemia and reperfusion.
38                           Evidence for total hepatic ischemia and spontaneous shunts was demonstrated
39 cute liver damage and inflammation caused by hepatic ischemia and subsequent reperfusion.
40 ly elevated in vehicle-treated animals after hepatic ischemia and subsequent reperfusion.
41 ) mice were exposed to 90 minutes of partial hepatic ischemia and up to 24 hours of reperfusion.
42 ) mice were exposed to 90 minutes of partial hepatic ischemia and up to 24 hours of reperfusion.
43 ull mice were subjected to 60 min of partial hepatic ischemia, and at various times thereafter, blood
44                              This was due to hepatic ischemia, endothelial injury, and activation of
45 Analysis of microcirculatory events included hepatic ischemia, endothelial injury, including with gen
46 Rats were subjected to 60 minutes of partial hepatic ischemia followed by 0, 3, 6, 24, or 48 hours of
47 re subjected to 10 or 30 min of partial warm hepatic ischemia followed by 3 to 24 hr of reperfusion.
48         A mouse model of partial 90-min warm hepatic ischemia followed by 6 hr of reperfusion was use
49  STAT6 knockout mice underwent 90 minutes of hepatic ischemia followed by 8 hours of reperfusion.
50 before subjecting them to 90 minutes of warm hepatic ischemia followed by reperfusion for 6 or 24 hou
51                                Warm and cold hepatic ischemia followed by reperfusion leads to necrot
52 C57BL/6 mice underwent 90 minutes of partial hepatic ischemia followed by reperfusion with or without
53 ent mice were subjected to 90 min of partial hepatic ischemia followed by reperfusion.
54 mice were subjected to 90 minutes of partial hepatic ischemia followed by reperfusion.
55               Mice were subjected to partial hepatic ischemia followed by reperfusion.
56 mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 8 hours of reperfusio
57 mice were subjected to 90 minutes of partial hepatic ischemia followed by up to 96 hours of reperfusi
58  T4 and steroid 48 hr before 15 min of total hepatic ischemia, followed by 24 hr of reperfusion.
59 mice were subjected to 90 minutes of partial hepatic ischemia, followed by up to 8 hours of reperfusi
60                                              Hepatic ischemia for 90 minutes and reperfusion for up t
61 serotype O55:B5 (EC) and 90 min of secondary hepatic ischemia in EC + I/R and saline-infused (normal
62 onditioning as a protective strategy against hepatic ischemia in humans.
63 ttent clamping (IC) using a model of partial hepatic ischemia in mice aged 20 to 24 months.
64 ificantly improved after 75 minutes of total hepatic ischemia in P-selectin deficient mice when compa
65 f ischemia were further studied in models of hepatic ischemia in rats.
66          Postoperative complications such as hepatic ischemia injury or apparent immune cell accumula
67                             A model of total hepatic ischemia is currently not available in mice.
68           Furthermore, the potential role of hepatic ischemia, Kupffer cells, and cytokine release in
69 , improved cell engraftment independently of hepatic ischemia or inflammation, without improving live
70     Systemic administration of DAR decreases hepatic ischemia-related events and thus indirectly impr
71 mediator of inflammation and organ damage in hepatic ischemia reperfusion (I/R) injury.
72                                              Hepatic ischemia reperfusion (I/R) is a clinically relev
73 neth cells and IL-17A play critical roles in hepatic ischemia reperfusion (IR) injury, we tested whet
74                                              Hepatic ischemia reperfusion injury (IRI) is a major cli
75                    The findings suggest that hepatic ischemia reperfusion injury may play a critical
76 tate aminotransferase, a surrogate marker of hepatic ischemia reperfusion injury, was the only consis
77 m and xenon have additionally been tested in hepatic ischemia reperfusion injury, whereas neon was on
78 sulfide (H2S) production and protection from hepatic ischemia reperfusion injury.
79 ble from wild-type mice in their response to hepatic ischemia reperfusion.
80     Octreotide exerts a protective effect in hepatic ischemia-reperfusion (HIR) injury.
81 ment NO. bioavailability and protect against hepatic ischemia-reperfusion (I-R) injury in type 2 diab
82     CD4+ T cells play a critical role during hepatic ischemia-reperfusion (I/R) injury although the m
83                                              Hepatic ischemia-reperfusion (I/R) injury continues to b
84                                              Hepatic ischemia-reperfusion (I/R) injury, which mainly
85 oprotection, we subjected CS-eNOS-Tg mice to hepatic ischemia-reperfusion (I/R) injury.
86                                              Hepatic ischemia-reperfusion (IR) injury is a common cli
87                                              Hepatic ischemia-reperfusion (IR) injury is frequently f
88                                              Hepatic ischemia-reperfusion (IR) injury is the most com
89                                              Hepatic ischemia-reperfusion (IR) results in Kupffer cel
90 14 expression increased in mice subjected to hepatic ischemia-reperfusion (IR) surgery and during hyp
91 L/6 mice were subjected to 60-minute partial hepatic ischemia-reperfusion and posttreated with sirtui
92 n of sirtuin 1 attenuates liver injury after hepatic ischemia-reperfusion by restoring mitochondrial
93                                              Hepatic ischemia-reperfusion can be associated with acut
94 (AKI) frequently arises as a complication of hepatic ischemia-reperfusion injury (HIRI), yet simultan
95                                              Hepatic ischemia-reperfusion injury (I/R) occurs in the
96 ine whether/how CEACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcom
97                                              Hepatic ischemia-reperfusion injury (IRI) is a common co
98                                              Hepatic ischemia-reperfusion injury (IRI) is the leading
99 gous blood for 2 h, and surrogate markers of hepatic ischemia-reperfusion injury (IRI) were assessed
100                                              Hepatic ischemia-reperfusion injury (IRI), an innate imm
101 referential liver uptake to directly prevent hepatic ischemia-reperfusion injury (IRI), which is a re
102 ciated molecular pattern that contributes to hepatic ischemia-reperfusion injury (IRI).
103 play an essential role in the early phase of hepatic ischemia-reperfusion injury and determine the ex
104 ose tissue-derived mesenchymal stem cells in hepatic ischemia-reperfusion injury and the underlying m
105                                              Hepatic ischemia-reperfusion injury can result in organ
106                                              Hepatic ischemia-reperfusion injury is a disease pattern
107                                              Hepatic ischemia-reperfusion injury or sham operation.
108                                              Hepatic ischemia-reperfusion injury remains a significan
109 ematopoietic Plexin C1 in the development of hepatic ischemia-reperfusion injury, and suggest that Pl
110 antibody and a Semaphorin 7A peptide reduced hepatic ischemia-reperfusion injury, as measured by the
111   Moreover, in animal models of peritonitis, hepatic ischemia-reperfusion injury, Salmonella infectio
112 e context of acetaminophen hepatotoxicity or hepatic ischemia-reperfusion injury.
113  role of Plexin C1 in a mouse model of early hepatic ischemia-reperfusion injury.
114  in two models of surgical stress: renal and hepatic ischemia-reperfusion injury.
115 s a putative biomarker for the assessment of hepatic ischemia-reperfusion injury.
116 nt (PLXNC1) mice also demonstrated decreased hepatic ischemia-reperfusion injury.
117 ockout is crucial for reducing the extent of hepatic ischemia-reperfusion injury.
118 e stress, and apoptosis in a rodent model of hepatic ischemia-reperfusion injury.
119  activation of sirtuin 1 is protective after hepatic ischemia-reperfusion injury.
120                                              Hepatic ischemia-reperfusion is a major clinical problem
121                       The pathophysiology of hepatic ischemia-reperfusion is characterized by mitocho
122 zed that pulmonary injury is associated with hepatic ischemia-reperfusion resulting from descending t
123 hts into possible mechanisms responsible for hepatic ischemia-reperfusion-related acute lung injury a
124 rotects against inflammation and damage from hepatic ischemia/reperfusion (I/R) and other insults.
125 that drive sterile inflammatory injury after hepatic ischemia/reperfusion (I/R) injury are not comple
126                                              Hepatic ischemia/reperfusion (I/R) injury associated wit
127 nflammatory responses play critical roles in hepatic ischemia/reperfusion (I/R) injury associating wi
128                                              Hepatic ischemia/reperfusion (I/R) injury is associated
129 catalysis of heme, in the protection against hepatic ischemia/reperfusion (I/R) injury needs to be es
130 he liver to examine their role in total warm hepatic ischemia/reperfusion (I/R) injury with bowel con
131                    Using an in vivo model of hepatic ischemia/reperfusion (I/R) injury, we show that
132  critical mediator of leukocyte migration in hepatic ischemia/reperfusion (I/R) injury.
133 ed mitochondrial function that is evident in hepatic ischemia/reperfusion (I/R) injury.
134                                              Hepatic ischemia/reperfusion (I/R) is a major adverse re
135                                              Hepatic ischemia/reperfusion (I/R) leads to liver injury
136                                              Hepatic ischemia/reperfusion (I/R) results in a neutroph
137                          In a model of mouse hepatic ischemia/reperfusion (I/R), recombinant adenovir
138        Platelets play a critical role during hepatic ischemia/reperfusion (I/R).
139  regeneration of functional liver mass after hepatic ischemia/reperfusion (I/R).
140 iverse roles in the acute injury response to hepatic ischemia/reperfusion (I/R).
141 g with HMGB1 results in protection following hepatic ischemia/reperfusion (I/R).
142 ese Zucker rats are susceptible to increased hepatic ischemia/reperfusion (I/RP) injury.
143 ever, their in vivo functional importance in hepatic ischemia/reperfusion (IR) injury is perplexing.
144                                              Hepatic ischemia/reperfusion (IRI) injury remains a majo
145                                 In addition, hepatic ischemia/reperfusion caused significant increase
146   Therefore, we investigated the response to hepatic ischemia/reperfusion in STAT4-deficient mice.
147                                              Hepatic ischemia/reperfusion in wild-type and STAT6 knoc
148                                              Hepatic ischemia/reperfusion increased expression of TNF
149 (ALT) levels and histological improvement of hepatic ischemia/reperfusion injuries.
150              However, in swine that survived hepatic ischemia/reperfusion injury (45 minutes of ische
151 stic target of rapamycin (mTOR) signaling in hepatic ischemia/reperfusion injury (HIRI) in normal and
152 NK cells in dictating outcomes after partial hepatic ischemia/reperfusion injury (IRI).
153                              Amelioration of hepatic ischemia/reperfusion injury after inhibition of
154 ate that SLPI has protective effects against hepatic ischemia/reperfusion injury and suggest that end
155 The data suggest that IL-10 protects against hepatic ischemia/reperfusion injury by suppressing NFkap
156 sought to determine the role of PPARgamma in hepatic ischemia/reperfusion injury in mice.
157 er the LPS signaling pathway is activated by hepatic ischemia/reperfusion injury in the transplant se
158                                              Hepatic ischemia/reperfusion injury involves a complex i
159                                              Hepatic ischemia/reperfusion injury is a complication of
160                                              Hepatic ischemia/reperfusion injury is caused primarily
161                                              Hepatic ischemia/reperfusion injury is initiated by the
162                             We observed that hepatic ischemia/reperfusion injury leads to: (1) a coin
163 ies with isolated cells and a mouse model of hepatic ischemia/reperfusion injury revealed that NOX2 f
164  have previously employed an animal model of hepatic ischemia/reperfusion injury, and have shown that
165  Furthermore, P5779 can protect mice against hepatic ischemia/reperfusion injury, chemical toxicity,
166 R1, and IL-6 levels, are increased following hepatic ischemia/reperfusion injury, implying that TACE
167 Rgamma activation is hepatoprotective during hepatic ischemia/reperfusion injury, mice were treated w
168                 In an in vivo model of mouse hepatic ischemia/reperfusion injury, recombinant adenovi
169 rtant therapeutic intervention strategies in hepatic ischemia/reperfusion injury.
170  (IL-12) in the induction and development of hepatic ischemia/reperfusion injury.
171 he roles of MIP-2 and KC in the induction of hepatic ischemia/reperfusion injury.
172 rovide sensitive and quantitative markers of hepatic ischemia/reperfusion injury.
173 ctions, which contribute to the pathology of hepatic ischemia/reperfusion injury.
174 ns but also protection from tissue injury in hepatic ischemia/reperfusion injury.
175 tical role in the inflammatory cascade after hepatic ischemia/reperfusion injury.
176 mplying that TACE plays an important role in hepatic ischemia/reperfusion injury.
177                      Liver injury induced by hepatic ischemia/reperfusion is characterized by activat
178 pathways that are activated by the stress of hepatic ischemia/reperfusion remain unknown.
179 as to determine whether IL-10 could suppress hepatic ischemia/reperfusion-induced NFkappaB activation
180 us regulator of the inflammatory response to hepatic ischemia/reperfusion.
181 hil-dependent hepatic injury associated with hepatic ischemia/reperfusion.
182 bjected to 70% hepatectomy and 30 minutes of hepatic ischemia showed significantly reduced regenerati
183 t) following 30, 45, and 90 minutes of acute hepatic ischemia, the systemic release of eight differen
184 R4 knockout (KO) mice were subjected to warm hepatic ischemia, there was significant protection in th
185 ducible factor 1 alpha under stress enhances hepatic ischemia tolerance in mice and humans.
186 vival was observed after 75 minutes of total hepatic ischemia using both protective protocols, wherea
187                              Seventy percent hepatic ischemia was induced in male adult rats by placi
188 ncapsulated clodronate 48 h before 35 min of hepatic ischemia with bowel congestion, followed by 6 or

 
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