ライフサイエンスコーパス: affected mice

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

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

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

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

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

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

7 ydronephrosis and obstructive nephropathy in affected mice.

8 re associated with renal disease severity in affected mice.

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

10 serum levels of estrogen and progesterone in affected mice.

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

12 le histopathology and functional outcomes in affected mice.

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

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

15 rine but decreased in liver homogenates from affected mice.

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

17 ronal intranuclear inclusions are present in affected mice.

18 ected mice but became transmural in severely affected mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

32 Affected mice developed thick skin due to formation of c

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

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

35 Affected mice displayed ocular lesions typical of rd8, w

36 Pathologically, affected mice exhibit neuronal abnormalities (in perikar

37 Affected mice exhibited hemorrhage and neuronal cell dea

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

39 The affected mice exhibited malformed glial borders, larger

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

41 Affected mice had a nonsense mutation in the thyroid hor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 Affected mice of both strains have no plasma factor VIII

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

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

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

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

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

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

63 Affected mice show significant loss of motor neurons wit

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

65 Affected mice showed limb weakness and paresis with moto

66 Affected mice showed marked perturbations of cardiac gap

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

68 Homozygous affected mice showed ragged and dilapidated cuticle of t

69 Affected mice showed reduced survival, severely decrease

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

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

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

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

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

75 Affected mice usually die of renal and liver failure by

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

77 Affected mice were identified by recording the light-evo

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

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

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

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