ライフサイエンスコーパス: hepatopathy

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1 hepatic innate immune responses, and diffuse hepatopathy.

2 This mouse displays severe and progressive hepatopathy.

3 ses of type I diabetes mellitus and glycogen hepatopathy.

4 s enrolled through August 2002, 18 developed hepatopathy.

5 n with calcium depositions, nephropathy, and hepatopathy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 Histopathology revealed acute hepatopathy including cellular swelling, cytoplasmic agg

27 Glycogen hepatopathy is the pathological overloading of hepatocyt

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

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

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

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

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

33 hese studies mechanistically link congestive hepatopathy to hepatic fibrosis.

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

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

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

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

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

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