ライフサイエンスコーパス: affected mice

1 Galactosylceramide increased the lifespan of affected mice.

2 s absent in the CUH and CE structures of the affected mice.

3 e LBs of the type II cells isolated from the affected mice.

4 intact RBCs derived from healthy and disease-affected mice.

5 ular nucleus (VN) and cerebellum of severely affected mice.

6 k1 V657F) was found to be recurrent in other affected mice.

7 fibers in skin is increased, compared to non-affected mice.

8 ydronephrosis and obstructive nephropathy in affected mice.

9 re associated with renal disease severity in affected mice.

10 S has been limited by postnatal lethality in affected mice.

11 serum levels of estrogen and progesterone in affected mice.

12 in the thoracolumbar spinal cord of colitis-affected mice.

13 lesterol, manifested in fatal wasting of the affected mice.

14 M2 macrophage markers than those from cGVHD-affected mice.

15 As for CCR2 were also detected in the CNS of affected mice.

16 and soleus but reduced in the diaphragm from affected mice.

17 rine but decreased in liver homogenates from affected mice.

18 ronal intranuclear inclusions are present in affected mice.

19 ected mice but became transmural in severely affected mice.

20 le histopathology and functional outcomes in affected mice.

21 n mitigated glycolytic muscle wasting in LLC-affected mice.

22 a and hyperinflammation in the most severely affected mice.

23 he tumor and improved survival rate of tumor-affected mice.

24 Affected mice and humans both manifest an X-linked pheno

25 Non-treated periodontitis-affected mice and non-ligated mice were used as controls

26 ly, the excessive amount of IFNgamma seen in affected mice appears to be driven by increased antigen

27 Tissues from affected mice are devoid of beta-gal mRNA and totally de

28 ipheral T cell phenotypes of our patient and affected mice are distinct.

29 At birth, optic nerves of affected mice are smaller than those of wild-type mice,

30 lum and spinal cord of untreated and treated affected mice at different ages.

31 as localized to the lamina propria of mildly affected mice but became transmural in severely affected

32 The basal cells of affected mice ceased to proliferate, and expressed the p

33 Although affected mice consumed more food than control animals, t

34 In mildly affected mice, cysts were not randomly distributed throu

35 ion and an early stop codon into the mRNA of affected mice (designated Grm6(nob3)).

36 graphy and haemodynamic analyses showed that affected mice develop aortic stenosis and regurgitation.

37 inoculated with virus-containing plasma from affected mice developed splenomegaly, which was caused b

38 Affected mice developed thick skin due to formation of c

39 exsanguination after tail snipping, and two affected mice died of umbilical cord bleeding.

40 t only lymph node cells from alopecia areata affected mice displayed an increased response with T cel

41 Affected mice displayed hypertrophic cells with AT2 and

42 Affected mice displayed ocular lesions typical of rd8, w

43 Pathologically, affected mice exhibit neuronal abnormalities (in perikar

44 Affected mice exhibited hemorrhage and neuronal cell dea

45 Furthermore, the homozygous affected mice exhibited hyperproliferation of the epider

46 The affected mice exhibited malformed glial borders, larger

47 Assay of cryoprecipitate from the plasma of affected mice failed to show factor VIII light chain.

48 Affected mice had a nonsense mutation in the thyroid hor

49 In addition, all affected mice had a progressive renal hemosiderosis conc

50 Mouse embryonic fibroblasts from the affected mice had increased expression of a subset of TG

51 Although the brains of 263K-affected mice had little immunoblot-detectable PrP(Res),

52 The affected mice had reduced sperm number and motility and

53 The affected mice have a mild motor deficit but do not devel

54 gnificant MMR signal in nonarthritic paws of affected mice (i.e., mice displaying symptoms of arthrit

55 h node and spleen cells from alopecia areata affected mice injected into normal haired littermates tr

56 uscle invasion, rapid growth, and, in 20% of affected mice, intravascular lung metastasis.

57 The lifespan of affected mice is 8-12 months, with occasional mice livin

58 ubule-associated protein 210 (GMAP-210); the affected mice lacked this protein.

59 Additional SP supply to the skin of AA-affected mice leads to a significant increase of mast ce

60 reover, systemic ASO injection into severely affected mice leads to reversal of muscle pathology with

61 the lesions, and Treg cell depletion in the affected mice led to an interstitial spread of the disea

62 Additionally, the serum cytokine profile of affected mice mimics data in human PBC.

63 tion in the severity of kidney disease among affected mice motivated a second genome-wide search, ide

64 Affected mice of both strains have no plasma factor VIII

65 In individual affected mice, only a weak correlation was observed betw

66 AqH was collected from eyes of affected mice periodically after immunization and then e

67 ure death compared to traditional dystrophin-affected mice prompted us to take a further look into fi

68 Autoantibodies and autoreactive T cells from affected mice recognized a approximately 50-kDa protein

69 Postmortem examination of affected mice revealed dehydration and luminal cecal flu

70 Histochemical analysis of the severely affected mice revealed that their Purkinje cell dendriti

71 Affected mice show high serum levels of inhibin-alpha-ne

72 Affected mice show significant loss of motor neurons wit

73 ared with age-matched heterozygous controls, affected mice showed impaired conditioned fear response

74 Affected mice showed limb weakness and paresis with moto

75 Affected mice showed marked perturbations of cardiac gap

76 Although these same muscles in non-affected mice showed marked variation in patterns of gen

77 Homozygous affected mice showed ragged and dilapidated cuticle of t

78 Affected mice showed reduced survival, severely decrease

79 s causes sudden death, with less than 13% of affected mice surviving after 14 days.

80 Currently, there are 10 affected mice surviving at 4 months of age.

81 In affected mice, the retinal outer nuclear and plexiform l

82 od reproducibly provides large numbers of AA-affected mice to study the pathogenesis and treatment of

83 expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitted hair

84 Affected mice usually die of renal and liver failure by

85 Lifespan of the affected mice was greatly reduced (median survival, 138

86 Affected mice were identified by recording the light-evo

87 Electroretinograms demonstrated that affected mice were virtually non-responsive to light by

88 ssessed five different skeletal muscles from affected mice, which are representative of muscles with

89 A-associated asthma-like disease by treating affected mice with OVA-pulsed DC10 generated from wild-t

90 ce junction were evident in spermatozoa from affected mice, with consequent deficits in motility.