ライフサイエンスコーパス: hepatopathy

1 r pIVCL as well as in humans with congestive hepatopathy.

2 hepatic innate immune responses, and diffuse hepatopathy.

3 This mouse displays severe and progressive hepatopathy.

4 ses of type I diabetes mellitus and glycogen hepatopathy.

5 s enrolled through August 2002, 18 developed hepatopathy.

6 n with calcium depositions, nephropathy, and hepatopathy.

7 ly identifying a novel tool to differentiate hepatopathies.

8 pathophysiology, diagnosis, and prognosis of hepatopathies.

9 iomyopathy (33%), isolated myopathy (15%) or hepatopathy (13%).

10 The greatest risk factor for development of hepatopathy after VAC therapy was age.

11 rgans affected is the liver, causing "sickle hepatopathy," an umbrella term for a variety of acute an

12 otype associated with hypogammaglobulinemia, hepatopathy and a spectrum of neurocognitive abnormaliti

13 evere bacterial and viral disease, recurrent hepatopathy and encephalopathy, and cardiac malformation

14 right HF, cardiorenal syndromes, congestive hepatopathy and frailty, which offer distinct targets fo

15 lation lead to the development of congestive hepatopathy and other life-threatening complications.

16 ic response to KD in mice with mitochondrial hepatopathy and warrant further investigations of dietar

17 setting of chronic heart failure congestive hepatopathy and-or the so-called cardiac cirrhosis are o

18 nd are associated with progressive myopathy, hepatopathy and/or encephalopathy, depending in part on

19 complete histological resolution of glycogen hepatopathy associated with control of glucose metabolis

20 A CerS2 null mouse displays hepatopathy because of depletion of C22-C24 ceramides, e

21 nge of clinical manifestations that included hepatopathy, bifid uvula, malignant hyperthermia, hypogo

22 Hepatopathies can cause major metabolic abnormalities in

23 my, and therefore, the risks of dactinomycin hepatopathy can be avoided.

24 the phenotypic correction of the preexisting hepatopathy, decreases in the incidence and sizes of HCC

25 tes phenotypical exposure risk such as toxic hepatopathy, diffuse fatty change and hepatocellular ade

26 omplex III (CIII) deficiency and progressive hepatopathy due to mutated BCS1L, a CIII assembly factor

27 tRNA(Glu) mutation, and reversible infantile hepatopathy, due to tRNA 5-methylaminomethyl-2-thiouridy

28 ethylglutaconic aciduria, dystonia-deafness, hepatopathy, encephalopathy, Leigh-like syndrome (MEGDHE

29 clusion criteria for SH by using established hepatopathy grading scales and clinical criteria were re

30 here were changes in many metabolites in the hepatopathy groups.

31 domain, is associated with a fatal neonatal hepatopathy; however, the molecular basis for dysfunctio

32 nine levels has been shown to cause a severe hepatopathy in a knockout mouse model.

33 Diabetic liver lesions include glycogenic hepatopathy (in which poor diabetic control leads to swo

34 Histopathology revealed acute hepatopathy including cellular swelling, cytoplasmic agg

35 ior vena cava (pIVCL) to simulate congestive hepatopathy-induced portal hypertension in mice; some mi

36 Glycogen hepatopathy is the pathological overloading of hepatocyt

37 ronic passive hepatic congestion (congestive hepatopathy) leads to hepatic fibrosis; however, the mec

38 The major clinical features are hepatopathy, peripheral neuropathy, corneal anesthesia a

39 For thioacetamide (TAA)-induced hepatopathy rats, we observe that the proposed sensor ca

40 ed cardiomyopathy, exercise intolerance, and hepatopathy, reflecting the central role of the enzyme i

41 rapy (immediate causes of death were sepsis; hepatopathy, severe immune dysfunction, and pseudomonal

42 e pediatric renal tumor setting after severe hepatopathy (SH), including sinusoidal obstruction syndr

43 ed a murine experimental model of congestive hepatopathy through partial ligation of the inferior ven

44 hese studies mechanistically link congestive hepatopathy to hepatic fibrosis.

45 patients under 36 months of age, the risk of hepatopathy was 15%, with two deaths.

46 ildren 3 years of age or older, the risk for hepatopathy was 4%, with two deaths.

47 The onset of hepatopathy was 5 to 16 days from the start of a treatme

48 n detect liver that undergoes acute-moderate hepatopathy with a p-value less than 0.05.

49 Two of the individuals had infantile hepatopathy with fibrosis and steatosis, leading in one

50 s system) during the search for the cause of hepatopathy with very low values of serum ceruloplasmin.