ライフサイエンスコーパス: hepatic disease

1 der demographics especially with undiagnosed hepatic disease.

2 s utility for treating metabolically-related hepatic disease.

3 can be a life-saving treatment for end-stage hepatic disease.

4 r is necessary to advance cell therapies for hepatic disease.

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

6 rgery is performed in patients with advanced hepatic disease.

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

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

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

10 resection, most commonly because of advanced hepatic disease.

11 tiveness of bile acid therapy for preventing hepatic disease.

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

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

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

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

16 56 of them underwent resection of all gross hepatic disease.

17 scans has limited added utility in detecting hepatic disease.

18 iliary scintigraphy aids in the diagnosis of hepatic disease.

19 gene and cell transplantation therapies for hepatic diseases.

20 erapeutics, focusing on gastrointestinal and hepatic diseases.

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

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

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

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

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

26 h a variety of phenotypes, which mimic other hepatic diseases.

27 of liver transplantation for numerous human hepatic diseases.

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

29 dentify new therapeutic options for numerous hepatic diseases.

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

31 hat may underlie certain forms of autoimmune hepatic diseases.

32 d 9 patients with other chronic inflammatory hepatic diseases.

33 bundances on liver regeneration capacity and hepatic diseases.

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

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

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

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

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

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

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

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

42 proteins, we identify Polycystic Kidney and Hepatic Disease 1-Like 1 (PKHD1L1), a large, mostly extr

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

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

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

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

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

48 a re-emerging flavivirus that causes severe hepatic disease and mortality in humans.

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

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

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

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

53 on-viral nucleic acid delivery is limited to hepatic diseases and vaccines due to liver accumulation.

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

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

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

57 Hepatic disease associated with breast cancer is common

58 transcription and play an important role in hepatic disease by increasing the burden of proteotoxic

59 ogical status, age, pregnancy and underlying hepatic diseases, can affect the severity of disease.

60 bile acid reabsorption and is upregulated in hepatic diseases characterized by elevated bile acids, w

61 Hepatic disease complicates nearly 3% of all pregnancies

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

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

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

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

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

67 ure: HR: 3.258; 95% CI: 2.527-4.200; overall hepatic disease: HR: 4.128; 95% CI: 3.428-4.971).

68 s, HHV-6B may have triggered immune-mediated hepatic disease in genetically and immunologically predi

69 Therefore, Lrp1 is essential for RVF hepatic disease in mice.

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

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

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

73 significance of Lrp1, including its role in hepatic disease in vivo, however, remains to be determin

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

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

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

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

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

79 c potential of LRH-1 modulation in diabetes, hepatic diseases, inflammatory bowel diseases, atheroscl

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

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

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

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

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

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

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

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

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

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

90 e subjects who underwent FAPI PET/CT without hepatic disease or cancer diagnosis served as controls.

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

92 ent and liver biopsy revealed no evidence of hepatic disease or portal hypertension.

93 could model these personalized variations in hepatic disease phenotypes.

94 in innate and adaptive immunity orchestrate hepatic disease processes.

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

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

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

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

99 illness, thrombocytopenia, blood dyscrasias, hepatic disease, renal failure, antithrombotic medicatio

100 ups, presumably due to the wider spectrum of hepatic diseases represented in these samples.

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

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

103 Non-invasive assessment of hepatic disease severity represents a relevant issue to

104 Chronic hepatic diseases such as nonalcoholic steatohepatitis (N

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

106 Chronic hepatic diseases, such as cirrhosis, hepatocellular carc

107 at converge to induce deleterious effects in hepatic diseases, such as in the later stages, have pote

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

109 oma, cirrhosis, hepatic failure, and overall hepatic disease than those without HCV infection.

110 year-old Caucasian female with predominately hepatic disease that showed resistance to intravenous im

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

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

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

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

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

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

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

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