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1 ed at different time points until 72 h after partial hepatectomy.
2 liver regeneration when applied 2 h prior to partial hepatectomy.
3 inistration of SB-258719 sixteen hours after partial hepatectomy.
4 nd 40 h (mitotic index in HE sections) after partial hepatectomy.
5 Male Wistar rats were subjected to 60-70% partial hepatectomy.
6 (Ad/BLOCK-iT/Nor-1(small hairpin RNA)) after partial hepatectomy.
7 iferative phases of liver regeneration after partial hepatectomy.
8 sing Cd39 are preferentially mobilized after partial hepatectomy.
9 support the selection of patients undergoing partial hepatectomy.
10 storation of liver volume and function after partial hepatectomy.
11 a, and its activation at 3 to 24 hours after partial hepatectomy.
12 in rat but not in regenerating livers after partial hepatectomy.
13 required for hepatocyte proliferation after partial hepatectomy.
14 at had undergone retrorsine pretreatment and partial hepatectomy.
15 erative than resident LSEC progenitors after partial hepatectomy.
16 a predictor of NAFLD and survival following partial hepatectomy.
17 ative chemotherapy treatments, and extent of partial hepatectomy.
18 ation, and increased the survival rate after partial hepatectomy.
19 d metabolism during liver regeneration after partial hepatectomy.
20 iated with decreased rates of survival after partial hepatectomy.
21 liver regeneration and mouse survival after partial hepatectomy.
22 e human blood clotting factor VIII, or after partial hepatectomy.
23 tic MMP-9 proteolytically cleaved VEGF after partial hepatectomy.
24 GPC3 TG mice during liver regeneration after partial hepatectomy.
25 tiation of liver regeneration in response to partial hepatectomy.
26 and had accelerated liver regeneration after partial hepatectomy.
27 hepatocytes in response to toxic injury and partial hepatectomy.
28 e progenitor cell niche following two-thirds partial hepatectomy.
29 nd sustain liver regeneration induced by 70% partial hepatectomy.
30 e liver after transplantation and two-thirds partial hepatectomy.
31 e proliferation and liver regeneration after partial hepatectomy.
32 ly inhibit liver proliferation in vivo after partial hepatectomy.
33 nderwent sham-operation or approximately 90% partial hepatectomy.
34 hour delay in hepatocyte proliferation after partial hepatectomy.
35 ssive accumulation of liver weight following partial hepatectomy.
36 atocyte fate during liver regeneration after partial hepatectomy.
37 ed capacity for liver regeneration following partial hepatectomy.
38 icantly accelerated liver regeneration after partial hepatectomy.
39 and endothelial cell proliferation following partial hepatectomy.
40 ced capacity to initiate DNA synthesis after partial hepatectomy.
41 /-) mice compared with control animals after partial hepatectomy.
42 generation following N-2-acetylaminofluorene/partial hepatectomy.
43 latory network driving the early response to partial hepatectomy.
44 injury with carbon tetrachloride exposure or partial hepatectomy.
45 osely followed liver function recovery after partial hepatectomy.
46 val of lymphocyte-deficient (Rag) mice after partial hepatectomy.
47 chronic hepatitis animal model and following partial hepatectomy.
48 )/M phase in Pbp(DeltaLiv) hepatocytes after partial hepatectomy.
49 s liver regeneration with low survival after partial hepatectomy.
50 iciency accelerates liver regeneration after partial hepatectomy.
51 tly impaired regeneration of the liver after partial hepatectomy.
52 did not compromise liver regeneration after partial hepatectomy.
53 d to 4-fold above baseline by 24 hours after partial hepatectomy.
54 id regeneration process following two-thirds partial hepatectomy.
55 he role of MMP-9 in liver regeneration after partial hepatectomy.
56 ase A (MMP-2) and gelatinase B (MMP-9) after partial hepatectomy.
57 row transplantation, ulcerative colitis, and partial hepatectomy.
58 regeneration and reduced steatosis following partial hepatectomy.
59 d in mice injected with Concanvalin A before partial hepatectomy.
60 , in the drinking water of mice subjected to partial hepatectomy.
61 iver regeneration in 157 patients undergoing partial hepatectomy.
62 tivation model of 2-acetylaminofluorene with partial hepatectomy.
63 MSCs supported survival after partial hepatectomy.
64 e (GH) signaling, was strongly induced after partial hepatectomy.
65 ver regeneration and clinical outcomes after partial hepatectomy.
66 rbol esters and the in vivo activation after partial hepatectomy.
67 difference to the 10-fold volume removal of partial hepatectomy.
68 difference to the 10-fold volume removal of partial hepatectomy.
69 nd a much higher rate of proliferation after partial hepatectomy.
70 fects the recovery of the living donor after partial hepatectomy.
71 eceptor blockade on liver regeneration after partial hepatectomy.
72 2-acetylaminofluorene treatment followed by partial hepatectomy (2-AAF/PH) by using rat genome 230 2
73 We addressed this question by performing 2/3 partial hepatectomy (2/3 PH) on mice with hepatocyte-spe
76 ) cells that give rise to regeneration after partial hepatectomy, (3) cells responsible for progenito
77 Wild-type and Zip14(-/-) mice that underwent partial hepatectomy (70% of liver removed) were used as
81 ) mice had impaired liver regeneration after partial hepatectomy and 50% mortality, indicating that N
82 -Fc (fragment, crystallizable) to mice after partial hepatectomy and acetaminophen intoxication, and
83 liver regeneration, which is required after partial hepatectomy and acute or chronic liver injury.
84 e proliferation and liver regeneration after partial hepatectomy and alters gene expression profiles
85 e two hours prior to and sixteen hours after partial hepatectomy and by intraperitoneal administratio
86 d experimental models of liver regeneration (partial hepatectomy and carbon tetrachloride treatment),
87 ranscriptional programs of adult liver after partial hepatectomy and contrasted these with developing
88 acid synthesis is reduced immediately after partial hepatectomy and during the early stage of liver
90 ety of hepatotrophic growth signals, such as partial hepatectomy and hepatocyte growth factor, can be
91 l liver regeneration can be induced upon 70% partial hepatectomy and is accompanied by an increase in
92 n vivo during mouse liver regeneration after partial hepatectomy and is strongly overexpressed in pre
93 signal, is activated in myeloid cells after partial hepatectomy and its conditional deletion results
95 d (by SB-258719 and SB-269970) at 16 h after partial hepatectomy and peaked at 32 h ([(3)H]-thymidine
96 tomy (incidental tumors, 2 stage), including partial hepatectomy and portal LN dissection, with or wi
97 models of liver regeneration after extended partial hepatectomy and portal vein ligation for multipl
98 lectively augmented liver regeneration after partial hepatectomy and portal vein ligation, and increa
99 and/or Epac2 are deleted, were subjected to partial hepatectomy and the regenerating liver was analy
100 usoidal endothelial cell responses following partial hepatectomy and to dissect purinergic and growth
101 that CD81 levels also increased 2 days after partial hepatectomy and toward the end of regeneration.
103 of hepatocyte proliferation (days 1-3 after partial hepatectomy) and subsequent reconstitution of th
104 s during mouse liver regeneration induced by partial hepatectomy, and DNA replication was determined
105 n the initiation of liver regeneration after partial hepatectomy, and new cytokines and receptors tha
106 hat follows CCl(4)-induced liver injury, 70% partial hepatectomy, and postnatal liver development wer
107 on, progression-free survival, conversion to partial hepatectomy, and viable HCC within the tumor spe
110 ed glycogen, and proliferated in response to partial hepatectomy, as neighboring native hepatocytes.
111 les collected from 55 patients who underwent partial hepatectomy at the Royal Infirmary Edinburgh bet
112 cy underwent retrorsine treatment and either partial hepatectomy before transplantation or carbon tet
115 nic mice accelerate liver regeneration after partial hepatectomy but are not protected from hepatocyt
116 ice exhibited accelerated regeneration after partial hepatectomy but no signs of neoplastic or preneo
117 atocyte proliferation and survival following partial hepatectomy, but also acts in concert with other
118 for an efficient early cytokine response to partial hepatectomy, but is inhibitory to later growth f
119 a critical role in liver regeneration after partial hepatectomy, but their role in TCPOBOP-induced d
120 ibition accelerated liver regeneration after partial hepatectomy by 40%, whereas systemic MMP inhibit
121 n important role in liver regeneration after partial hepatectomy by affecting matrix remodeling, as w
122 irst round of hepatocyte proliferation after partial hepatectomy by preventing increases in growth ho
123 ocytes, p38gamma induces proliferation after partial hepatectomy by promoting the phosphorylation of
124 n of the hepatovascular mass (days 4-8 after partial hepatectomy) by inhibiting upregulation of the e
127 n animals preconditioned with retrorsine and partial hepatectomy, cell transplantation after ETN pret
128 dly inhibited hepatocyte proliferation after partial hepatectomy, confirming its pivotal role in cell
129 that accumulate in regenerating livers after partial hepatectomy, contributes to this process by regu
133 proliferation in p21 null mice subjected to partial hepatectomy, establishing the functional signifi
134 e previously reported that mice subjected to partial hepatectomy exhibit rapid development of hypogly
137 F15/19 levels improve survival of mice after partial hepatectomy, FGF19 mitogenic activity is associa
138 , respectively; whereas liver radiation plus partial hepatectomy followed by cell transplantation pro
140 rategy to stimulate liver regeneration after partial hepatectomy for colorectal liver metastases (CRL
142 encouraging results have been reported with partial hepatectomy for solitary metastases, with percut
143 n the liver of wild type mice in response to partial hepatectomy, further supporting a role for these
144 ice to deplete hepatocyte alphavbeta8, after partial hepatectomy, hepatocyte proliferation and liver-
145 rmous regenerative capacity such that, after partial hepatectomy, hepatocytes rapidly replicate to re
146 omic analysis of seven time points following partial hepatectomy identified the epigenetic regulator
147 d HCC model) that underwent RF ablation, 35% partial hepatectomy (ie, left lobectomy), or a sham oper
152 exposure on liver regeneration following 70% partial hepatectomy in mice lacking the Cip/Kip inhibito
153 cell proliferation, were assessed following partial hepatectomy in mice that do not express CD39, th
158 e implantation of 2-acetylaminofluorene with partial hepatectomy in rats or on feeding a 3,5-diethoxy
159 ivation models of 2-acetylaminofluorene with partial hepatectomy in rats, and 3,5-diethoxycarbonyl-1,
162 into wild-type (WT) rats that had undergone partial hepatectomy in the presence of 2-acetylaminofluo
167 is study utilizing surgical liver resection (partial hepatectomy) in various complement-deficient mic
168 st that the hypoglycemia that develops after partial hepatectomy induces systemic lipolysis followed
169 Liver regeneration triggered by two-thirds partial hepatectomy is accompanied by elevated hepatic l
170 so suggests that AhR functionality following partial hepatectomy is dependent on a p21(Cip1)-regulate
173 well tolerated, and liver regeneration after partial hepatectomy is not impaired, indicating that reg
175 s no obvious consequences for normal livers, partial hepatectomy leads to severe liver necrosis and r
178 We investigated these mechanisms using the partial hepatectomy model in mice given standard or 10%
179 were subjected to the 2-acetylaminofluorene/partial hepatectomy model of oval cell-mediated liver re
189 1-Fc increased innate immunity in mice after partial hepatectomy or acetaminophen-induced injury, wit
190 e injury, such as rodent LR after two-thirds partial hepatectomy or administration of damaging chemic
191 e liver regeneration/repair after either 70% partial hepatectomy or carbon tetrachloride-induced live
193 ant hepatocyte proliferation following liver partial hepatectomy or damage resulting from carbon tetr
194 cetylaminofluorene-treated rats subjected to partial hepatectomy or in D-galactosamine-treated rats.
196 ing Med1 did not regenerate following either partial hepatectomy or treatment with certain nuclear re
198 generated a TSP-1-deficient mouse model of a partial hepatectomy (PH) and explored TSP-1 induction, p
199 ncreased in young livers proliferating after partial hepatectomy (PH) and in human liver tumors.
201 during liver regeneration in rats after 70% partial hepatectomy (PH) at early and mid time points to
202 CcnE2, and Cdk2 for liver regeneration after partial hepatectomy (PH) by generating corresponding dou
205 the wave of cell proliferation that follows partial hepatectomy (PH) identified approximately 1,400
206 rowth during embryonic development and after partial hepatectomy (PH) in adults is characterized by t
207 nor (30%), standard (60%), or extended (80%) partial hepatectomy (PH) in mice with and without liver
208 Liver regeneration is impaired following partial hepatectomy (PH) in mice with genetic obesity an
212 ined the intrinsic hepatic innervation after partial hepatectomy (PH) in rats and the presence and pa
214 ver NK cells undergo phenotypic changes post-partial hepatectomy (PH) in vivo, including increased cy
215 BACKGROUND & AIMS: Liver regeneration after partial hepatectomy (PH) increases the protein folding b
216 gnaling during liver regeneration (LR) after partial hepatectomy (PH) is observed in several species.
217 wild-type (WT) littermates were used in the partial hepatectomy (PH) model for compensatory regenera
221 ays are involved in liver regeneration after partial hepatectomy (PH) to initiate growth, protect liv
223 e the role of PXR in liver regeneration, 2/3 partial hepatectomy (PH) was performed on wild-type and
224 3 (HFD groups) weeks of treatment with G49, partial hepatectomy (PH) was performed, and all mice wer
225 atocyte DNA and prevents proliferation after partial hepatectomy (PH), allowing selective expansion o
226 lysis of murine liver regeneration after 70% partial hepatectomy (PH), an established model of adult
227 in initiating liver regeneration (LR) after partial hepatectomy (PH), by regulating expression of Cy
229 Different surgical procedures, including partial hepatectomy (PH), intraoperative portal vein lig
230 ays are involved in liver regeneration after partial hepatectomy (PH), to initiate growth, protect li
242 appropriate regenerative response following partial hepatectomy (PHTx) compared to wildtype controls
243 t liver injury and regeneration induced by a partial hepatectomy (PHx) could have different effects o
244 on in the remnant liver of the rat after 70% partial hepatectomy (PHx) during the early phase respons
245 ogen) deposition was recently reported after partial hepatectomy (PHx) in mice, but the role of fibri
249 the rat 2-acetylaminofluorene (2AAF) and 2/3 partial hepatectomy (PHx) liver regeneration model.
250 L-2Rgamma(-/-) (NSG) mice that had undergone partial hepatectomy (PHx) represented the best combinati
251 ut (DeltaKlf6), cell proliferation following partial hepatectomy (PHx) was increased compared to cont
252 ver regeneration in rat following two-thirds partial hepatectomy (PHx) was investigated using RNA int
256 6(-/-) ), we challenged liver function after partial hepatectomy (PHx), inducing acute proliferative
259 y also impaired liver regeneration following partial hepatectomy (PHx), the effect of CR2-Crry in thi
269 ds are currently used in preclinical models: partial hepatectomy, portal ligature or embolization, an
273 severely inhibited in DeltaEGFR livers after partial hepatectomy, revealing a new function for EGFR k
274 cle progression and liver regeneration after partial hepatectomy, suggesting that DBC1/DN-DBC1 transi
275 che may play a smaller role in recovery from partial hepatectomy than BM LSEC progenitors, but, when
280 ithin a milieu of chronic inflammation links partial hepatectomy to accelerated hepatocarcinogenesis;
281 Concanvalin A was injected 4 days before partial hepatectomy to natural killer T cells- deficient
282 d in bile ducts and oval cells in retrorsine/partial hepatectomy-treated liver, and this correlated w
285 oung mice inhibits liver proliferation after partial hepatectomy via the cyclin D3-C/EBPalpha pathway
289 A model of liver regeneration after 70% partial hepatectomy was used, followed by examination of
290 Using a model of liver regeneration after partial hepatectomy, we found that DN-DBC1 is down-regul
291 k2, cyclin A2/Cdk2, and cyclin B1/Cdk1 after partial hepatectomy were altered in regenerating RXRalph
293 tocyte proliferation that occurred following partial hepatectomy were not observed in Zip14(-/-) mice
294 , and a dramatic reduction in survival after partial hepatectomy, whereas additional global deletion
295 ped hepatocellular carcinomas 6 months after partial hepatectomy, whereas Nemo(Deltahepa) mice fed th
296 n contrast to the regenerative process after partial hepatectomy, which is driven by the replication
297 ted kinases and AKT activation 3 hours after partial hepatectomy, which, however, is alleviated by te
299 ed bi-1(+/+) and bi-1(-/-) mice subjected to partial hepatectomy with respect to the kinetics of live
300 dramatically impedes tumorigenesis following partial hepatectomy without compromising survival or liv