ライフサイエンスコーパス: hepatic disease

1 s utility for treating metabolically-related hepatic disease.

2 s such as the metabolic syndrome, cancer and hepatic disease.

3 rgery is performed in patients with advanced hepatic disease.

4 es and have been implicated in lipid-induced hepatic disease.

5 ohol abuse and may predispose to more severe hepatic disease.

6 rapidly and are seen in cardiac, renal, and hepatic disease.

7 resection, most commonly because of advanced hepatic disease.

8 tiveness of bile acid therapy for preventing hepatic disease.

9 nd point was major cardiovascular, renal, or hepatic disease.

10 tate, 35-80 years of age and free from known hepatic disease.

11 n 3 of 22 livers from patients with nonviral hepatic disease.

12 cured 58% of patients, 72% of those without hepatic disease.

13 56 of them underwent resection of all gross hepatic disease.

14 scans has limited added utility in detecting hepatic disease.

15 iliary scintigraphy aids in the diagnosis of hepatic disease.

16 pecies are associated with intestinal and/or hepatic diseases.

17 l drug targets to treat common metabolic and hepatic diseases.

18 e the prevention, diagnosis and treatment of hepatic diseases.

19 with advanced cardiac, pulmonary, renal, and hepatic diseases.

20 of liver transplantation for numerous human hepatic diseases.

21 derstand, diagnose, treat, and prevent human hepatic diseases.

22 ikely to be important in the pathogenesis of hepatic diseases.

23 hat may underlie certain forms of autoimmune hepatic diseases.

24 d 9 patients with other chronic inflammatory hepatic diseases.

25 s, representing the end stage of progressive hepatic diseases.

26 es (40.0% v 33.1%), dyspnea (49.4% v 28.5%), hepatic diseases (0.8% v 0.2%), and infections (sepsis:

27 ) were cross-bred with polycystic kidney and hepatic disease 1 (Pkhd1(del2/del2)) mice (which have in

28 Mutations of the polycystic kidney and hepatic disease 1 (PKHD1) gene have been shown to cause

29 d parent, or biallelic polycystic kidney and hepatic disease 1 (PKHD1) mutations.

30 ons at a single locus, polycystic kidney and hepatic disease 1 (PKHD1), are responsible for all typic

31 r this disease, termed polycystic kidney and hepatic disease 1 (PKHD1), was mapped on human chromosom

32 es a novel mutation in polycystic kidney and hepatic disease 1 (Pkhd1).

33 The PKHD1 (polycystic kidney and hepatic disease 1) gene responsible for autosomal recess

34 all causes of death; 12.48 (9.34-16.66) for hepatic diseases; 1.35 (1.15-1.57) for extrahepatic dise

35 nary disease, 77%; cardiac disease, 73%; and hepatic disease, 3%.

36 dy of molecular and genetic aspects of human hepatic disease and development and provide a platform f

37 the possibility of using such cells to model hepatic disease and development.

38 best case' substantially reduces HCV-related hepatic disease and HCV-related liver mortality by 2020

39 f cholesterol and other lipids that leads to hepatic disease and progressive neurological impairment.

40 Glycyrrhizin, clinically used for chronic hepatic diseases and itching dermatitis, modulates the p

41 ocellular division that is a feature of many hepatic diseases and malignancies, physiologic liver gro

42 ntal questions regarding the pathogenesis of hepatic diseases and provide the mechanistic rationale t

43 ) had cardiac disease, 25 patients (24%) had hepatic disease, and 19 patients (18%) had pulmonary dis

44 f cytochrome P450-inducing drugs, underlying hepatic disease, and unique genetic makeup.

45 TTV's aetiological role in hepatic and extra-hepatic disease, are urgently needed.

46 Hepatic disease associated with breast cancer is common

47 Hepatic disease complicates nearly 3% of all pregnancies

48 luated as therapeutic agents for a number of hepatic diseases due to their lipid-lowering and antiinf

49 he clinical course is often dominated by the hepatic disease, either because of hormone secretion or

50 However, there are many gastrointestinal and hepatic diseases for which obesity is the direct cause (

51 aluate improvement in time to recurrence and hepatic disease-free survival, not overall survival.

52 any significant advances in the treatment of hepatic diseases have been achieved recently.

53 er hepaticus- and Helicobacter bilis-related hepatic disease in mice.

54 To analyze the contribution of the hepatic disease in Niemann-Pick C disease progression an

55 ent is vital in the appropriate diagnosis of hepatic disease in pregnancy.

56 logy and biology that employ mouse models of hepatic diseases in an effort to better understand, diag

57 to first clinical event (CV event, renal or hepatic disease, incident diabetes, thrombotic/embolic e

58 enesis in a spectrum of chronic inflammatory hepatic diseases including alcoholic liver disease (ALD)

59 d cell death) have been demonstrated in many hepatic diseases including chronic hepatitis C.

60 se (NAFLD) and may predispose to more severe hepatic disease, including hepatocellular carcinoma.

61 Its role in hepatic cell death and hepatic diseases is not clear.

62 ased hepatic function, because of underlying hepatic disease, lead to the extremely high mortality ra

63 onse and is known to be the cause of several hepatic diseases leading to cirrhosis and hepatocellular

64 For many inherited and acquired hepatic diseases, liver transplantation is the only poss

65 ssue in lymph nodes rescues mice from lethal hepatic disease; lymph nodes therefore might be used as

66 gy assays and allow the creation of in vitro hepatic disease models.

67 idence of extrahepatic malignancy or chronic hepatic disease [n = 95]).

68 t be considered at all ages in patients with hepatic disease, neurological disease, or psychiatric sy

69 eases such as dementia and stroke, renal and hepatic diseases, obesity, anemia, malignancy, coagulopa

70 rugs and other interventions for high impact hepatic diseases often target biochemical pathways such

71 ion with syncope or melaena, and evidence of hepatic disease or cardiac failure.

72 could model these personalized variations in hepatic disease phenotypes.

73 ns aimed at answering important questions of hepatic disease prognosis, pathogenesis, and treatment.

74 velopmentally and biochemically characterize hepatic disease progression and bile acid products.

75 ngiocytes and serum by 32%-39% and inhibited hepatic disease progression, leading to 22%-60% reductio

76 ing fibrosis, as it is a strong indicator of hepatic disease-related mortality.

77 ing longer and developing end-stage renal or hepatic disease requiring transplantation.

78 but the mechanisms involved in establishing hepatic disease secondarily remain poorly understood.

79 econdary" LF (n = 5) which resulted from non-hepatic diseases such as sepsis.

80 Chronic hepatic diseases, such as cirrhosis, hepatocellular carc

81 overload on mitochondrial function in other hepatic diseases, such as non-alcoholic fatty liver dise

82 cirrhosis and 115 without history of chronic hepatic diseases) underwent magnetic resonance (MR) imag

83 replacement and without a medical history of hepatic disease, underwent a percutaneous cholecystostom

84 colorectal cancer, a subset of patients with hepatic disease was also analyzed; findings were similar

85 terparts, unless chronic transfusion-related hepatic disease was superimposed.

86 further the implication of IL-22/IL-22BP in hepatic disease, we analyzed common genetic variants of

87 use and for major cardiovascular, renal, and hepatic disease were 1.8 (95% CI, 1.2 to 2.9; P=0.007) a

88 ve for many clotting disorders and for other hepatic diseases where recombinant proteins may be unaff

89 mplications for patients with both renal and hepatic disease, who may be at risk of Phe overloading a