ライフサイエンスコーパス: nonhepatic

1 Therefore, the nonhepatic action of GlcNAc-TIII promotes hepatocyte pro

2 Zf9 mRNA also is expressed widely in nonhepatic adult rat tissues and the fetal liver.

3 icol acetyltransferase reporter gene in both nonhepatic and hepatic cells.

4 deoxycholic acid, similar rates and types of nonhepatic autoimmune diseases, and/or subsequent develo

5 l CT scans were obtained in 80 patients with nonhepatic cancer and no hepatic metastases visible at C

6 athy, persistent ascites, or death excluding nonhepatic causes of these conditions.

7 Nonhepatic causes such as celiac disease, thyroid, and m

8 ty among older recipients was largely due to nonhepatic causes, including infectious, cardiac, and ne

9 T3 regulation of ACCalpha transcription in nonhepatic cell cultures such as chick embryo fibroblast

10 he dedifferentiated cell line HepG2.1 or the nonhepatic cell line HeLa.

11 detected in mouse livers and in hepatic and nonhepatic cell lines overexpressing STAT3/c-Fos/HNF-1.

12 3 in cell lines of hepatic origin but not in nonhepatic cell lines.

13 Thus, unlike many nonhepatic cell types, rat hepatocytes are resistant to

14 In contrast, the "urea cycle" enzymes in nonhepatic cells are regulated by a wide range of pro- a

15 nduction of the reporter gene in transfected nonhepatic cells but not in liver cells.

16 d receptor alpha, support HBV replication in nonhepatic cells by controlling pregenomic RNA synthesis

17 factor activated by IL-6 in both hepatic and nonhepatic cells efficiently interacts with the SAS.

18 In addition, nonhepatic cells have been rendered more efficient at su

19 lular injury is unclear, because findings in nonhepatic cells have implicated autophagy as both a med

20 ithin the nuclear compartment of hepatic and nonhepatic cells in a manner independent of the Arnt pro

21 Cholesterol elimination from nonhepatic cells involves metabolism to side-chain oxyst

22 In both hepatic and nonhepatic cells, IL-6 -mediated IGFBP-1 promoter activa

23 and its abnormal expression, particularly in nonhepatic cells, is implicated in the pathogenesis of t

24 In nonhepatic cells, lipid synthesis is controlled by stero

25 of apoptotic cell death in both hepatic and nonhepatic cells.

26 ired, it greatly enhances HCV replication in nonhepatic cells.

27 only SAA1 gene but also other liver genes in nonhepatic cells.

28 r signaling pathways leading to apoptosis in nonhepatic cells.

29 ytokine-mediated SAA gene expression in some nonhepatic cells.

30 f advanced liver disease), or too old or had nonhepatic comorbid conditions, substance abuse problems

31 periphery and describes a unique role for a nonhepatic complement source.

32 ession of p450 on apoptosis were observed in nonhepatic COS1 and hepatic HepG2 cells.

33 Studies of nonhepatic disease have linked hypotension and cognitive

34 patic decompensation, or another significant nonhepatic disease.

35 th reduced hazard for a range of hepatic and nonhepatic events; (2) an association between SVR and be

36 the mechanism controlling cytokine-induced, nonhepatic expression of the SAA gene.

37 epatic tissues (presumably visceral fat) and nonhepatic fractional spillover (R = 0.81, P < 0.01), co

38 equences on the liver, with little effect on nonhepatic glucose metabolism, whereas insulin delivered

39 These data show that postabsorptive nonhepatic glucose production in humans may contribute t

40 Nonhepatic glucose uptake ( micromol.kg(-1).min(-1)) in

41 basal insulin LY2605541 (LY) on hepatic and nonhepatic glucose uptake (non-HGU) was evaluated.

42 ulmonary administration of insulin increases nonhepatic glucose uptake compared with infusion, and sk

43 were greatest in the PoHI and Pe327 groups, nonhepatic glucose uptake increased most in the PeHI gro

44 Glucose infusion rate, nonhepatic glucose uptake, and tracer-determined glucose

45 Intraportal 5-HT enhances NHGU but blunts nonhepatic glucose uptake, raising the possibility that

46 demonstrate successful lineage conversion of nonhepatic human cells into mature hepatocytes with pote

47 HCV RNAs can replicate in mouse hepatoma and nonhepatic human epithelial cells.

48 of 60 years, the excess mortality was due to nonhepatic, largely age-related problems.

49 line for recurrence-free survival period for nonhepatic malignancies before LTx, based on the type an

50 , mean age 56.9+/-12.8 years) had documented nonhepatic malignancies.

51 he data for patients with a prior history of nonhepatic malignancy and its recurrence post-LTx are li

52 The rate of recurrence of nonhepatic malignancy was 3% and de novo cancer was 6% i

53 nophen-induced acute liver failure (n = 13), nonhepatic multiple organ failure (n = 28), chronic live

54 VA distribution and kinetics in individual, nonhepatic organs is limited.We examined retinol uptake

55 d.We examined retinol uptake and turnover in nonhepatic organs, including skin, brain, and adipose ti

56 Cell lines of nonhepatic origin do not independently support HBV repli

57 f this study was to examine the patient with nonhepatic pre-LTx malignancies, and their recurrence po

58 al model was developed and demonstrated that nonhepatic splanchnic spillover rates in study A and stu

59 s, assumptions regarding actual spillover in nonhepatic splanchnic tissues were required for the spil

60 significant effect on AAV gene transfer into nonhepatic tissue, indicating that there are distinct ti

61 of [3H]oleate was observed in both liver and nonhepatic tissues (approximately 50% each).

62 ificant correlation between FFA release from nonhepatic tissues (presumably visceral fat) and nonhepa

63 of XAP2 is low in liver compared with other nonhepatic tissues and the AHR exhibits high ligand-indu

64 On the other hand, nonhepatic tissues are much less sensitive to insulin an

65 ow level of Delta-6 desaturase expression in nonhepatic tissues may need to be reevaluated.

66 the liver and the 5 nonessential proteins in nonhepatic tissues sets up a dichotomy that takes advant

67 ow that bile acids selectively accumulate in nonhepatic tissues under two conditions of impaired live

68 apeutic agent for various diseases affecting nonhepatic tissues, but great caution is required for ve

69 umican, an important mediator of fibrosis in nonhepatic tissues, whereas FABP-1 is paradoxically unde

70 rp) metabolism via the kynurenine pathway in nonhepatic tissues.

71 rp) metabolism via the kynurenine pathway in nonhepatic tissues.

72 nnot act on the liver without also affecting nonhepatic tissues.

73 subtypes that are found in both hepatic and nonhepatic tissues.

74 cell culture lines derived from hepatic and nonhepatic tissues.

75 tients with chronic myelogenous leukemia and nonhepatic toxicities between the two groups was not sta

76 gressed, two refused treatment, and five had nonhepatic toxicities).

77 o enhance their antiviral effects and reduce nonhepatic toxicity.

78 The use of a nonhepatic transplant site may avoid intrahepatic compli

79 ntly correlated with AADC expression (n = 15 nonhepatic tumors; maximum standardized uptake value, P