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1 re length of protocol and carcinogenicity of retrorsine.
2 gative (DPPIV-) Fischer host rats exposed to retrorsine.
4 patocyte transplantation in rats primed with retrorsine and partial hepatectomy showed accelerated ki
5 By contrast, in animals preconditioned with retrorsine and partial hepatectomy, cell transplantation
7 ion, recipient animals were conditioned with retrorsine and two-thirds partial hepatectomy (PH), whic
8 treated with 2 doses (30 mg/kg body weight) retrorsine (at 6 and 8 weeks of age) followed by PH 5 we
9 presence of 2-acetylaminofluorene (2AAF) or retrorsine, both of which are injury models that favor s
10 rats treated with the pyrrolizidine alkaloid retrorsine can be accomplished through the activation, e
11 ulation was induced in the host by injecting retrorsine, creating a portacaval shunt, and performing
14 ls in the organoid cultures, we utilized the retrorsine/DPPIV system of hepatocyte transplantation to
15 tic indices for hepatocytes in the livers of retrorsine-exposed and control rats up to 14 days post-P
16 protein are localized to the mitochondria of retrorsine-exposed rat livers after PH during the same t
18 ation of primary liver cell dispersions from retrorsine-exposed rats 6-8 days and 13-15 days after PH
21 riched SHPC populations can be isolated from retrorsine-exposed rats and established in short-term cu
22 nduced blockade of hepatocyte proliferation, retrorsine-exposed rats are able to reconstitute complet
23 ighest (approximately 6.0%) in the livers of retrorsine-exposed rats at 1 day post-PH, gradually decl
25 tration of 4,4'-methylenedianiline (DAPM) to retrorsine-exposed rats impaired the emergence of SHPC c
26 n after surgical partial hepatectomy (PH) in retrorsine-exposed rats is accomplished through the outg
27 tic protein Bax are increased in livers from retrorsine-exposed rats relative to the levels observed
28 ration secondary to bile duct destruction in retrorsine-exposed rats treated with 4,4'-diaminodipheny
34 These observations combine to suggest that retrorsine-injured hepatocytes are removed after PH via
37 rats treated with the pyrrolizidine alkaloid retrorsine is accomplished through the activation, expan
38 ce of SHPCs to the mitoinhibitory effects of retrorsine may be directly related to a lack of CYP enzy
39 tocyte-like progenitor cells observed in the retrorsine model reflect a novel mechanism of complete l
41 ibitory effect of the pyrrolizidine alkaloid retrorsine on hepatocytes in the resident liver while tr
44 rategy for hepatocyte transplantation, using retrorsine/partial hepatectomy (PH) in a DPPIV- mutant F
45 ly 10 cell doublings) under the influence of retrorsine/partial hepatectomy, and both repopulation an
46 as augmented in bile ducts and oval cells in retrorsine/partial hepatectomy-treated liver, and this c
47 Tissues from DPPIV chimeric livers after retrorsine/PH treatment showed large numbers of SHPC clu
49 ial hepatectomy into the liver of normal and retrorsine (Rs) treated syngeneic dipeptidyl peptidase I
50 rat liver by transplanted hepatocytes using retrorsine (RS), a pyrrolizidine alkaloid that alkylates
54 portally (2 x 10(6) cells) into the liver of retrorsine-treated Dipeptidyl peptidase IV- mutant Fisch
55 yl peptidase IV (DPPIV)-positive donors into retrorsine-treated DPPIV-negative recipients subjected t
56 her (F)344 rats to repopulate the normal and retrorsine-treated liver was studied throughout a 6-mont
60 h severe-combined immunodeficiency underwent retrorsine treatment and either partial hepatectomy befo
61 PPIV-positive hepatocytes, were subjected to retrorsine treatment followed by partial hepatectomy (PH
62 senkirkine, senecionine, seneciphylline and retrorsine were determined by ultra-performance liquid c
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