ライフサイエンスコーパス: diabetic mouse

1 itis, uveitis, and diabetes in the non-obese diabetic mouse.

2 ent type 1 diabetes mellitus in the nonobese diabetic mouse.

3 an and the orthologous I-Ag7 in the nonobese diabetic mouse.

4 betogenic CD4+ T cell clones in the nonobese diabetic mouse.

5 creas of the interferon (IFN) gamma-nonobese diabetic mouse.

6 on of renal VDR was examined in the nonobese diabetic mouse.

7 ly class II allele expressed by the nonobese diabetic mouse.

8 In the nonobese diabetic mouse, a predominant component of the autoreact

9 adenine dinucleotide (NAD) depletion and in diabetic mouse and human livers.

10 GPR109A expression was increased in diabetic mouse and human retina.

11 observations have been made in the nonobese diabetic mouse and in clinical insulin-dependent diabete

12 mined the effect of exogenous SP delivery on diabetic mouse and rabbit wounds.

13 lin mRNA and protein expression in different diabetic mouse and rat models, including streptozotocin-

14 ore easily, such as those from the non-obese diabetic mouse, and display them in a more intuitive way

15 n the Toll-like receptor 4-defective C3H/HeJ diabetic mouse, arguing that the dramatic increase in co

16 ) expression in streptozotocin (STZ)-induced diabetic mouse arteries and in human coronary smooth mus

17 increased in endothelial cells of obese and diabetic mouse blood vessels.

18 ntitative analysis of PPI species present in diabetic mouse cortex and liver, and it allowed us to un

19 ies in type 1 diabetes (T1D) in the nonobese diabetic mouse demonstrated that a crucial insulin epito

20 Adult diabetic mouse fibroblast migration exhibited a 75% redu

21 ncrease of miR-200b/c levels was detected in diabetic mouse glomeruli and TGF-beta-treated MMC.

22 The NOD (nonobese diabetic) mouse has been studied as an animal model for

23 ction of adenovirus encoding PLN-Ab into the diabetic mouse heart enhanced contractility when measure

24 In 8-week diabetic mouse heart, CTGF and TGFbeta expression increa

25 ctors (AAVs) for the capacity to protect the diabetic mouse heart.

26 by which Nrf2 suppresses oxidative stress in diabetic mouse heart.

27 Treatment of both types of diabetic mouse hearts with an INaP blocker also shortene

28 We developed a transgenic (Tg) diabetic mouse in which eNOS is systemically overexpress

29 is is reminiscent of studies in the nonobese diabetic mouse, in which I-A(g7) is relatively unstable,

30 In the nonobese diabetic mouse, insulin-dependent diabetes is an autoimm

31 t diabetic nephropathy and that the Dcn(-/-) diabetic mouse is a useful new model of progressive diab

32 n from insulitis to diabetes in the nonobese diabetic mouse is typically associated with Th1 pancreat

33 The NOD (nonobese diabetic) mouse is a good animal model for human IDDM.

34 Streptozotocin-induced diabetic mouse kidney cDNA was prepared and subtracted b

35 sentational difference analyses of cDNA from diabetic mouse kidney were performed.

36 sentational difference analysis of cDNA from diabetic mouse kidney.

37 Sgk mRNA was selectively increased in diabetic mouse kidneys.

38 to validate the presence of DMPO adducts in diabetic mouse livers.

39 ssels in the low-dose streptozotocin-induced diabetic mouse model (10 animals) was performed.

40 We found CD44 deficiency in a diabetic mouse model ameliorates insulin resistance and

41 t reduction in a high-fat diet (HFD) induced diabetic mouse model and a genetically engineered T2DM r

42 ogenesis in cardiac mitochondria of a type 1 diabetic mouse model and proposed that mitochondria are

43 d contractile function observed in the db/db diabetic mouse model appears to be related to decreased

44 Furthermore, a diabetic mouse model exhibited lower FAS levels and a de

45 enable rapid reversal of blood glucose in a diabetic mouse model following glucose challenge, with s

46 lin(+) cells can suppress hyperglycemia in a diabetic mouse model for at least 6 months and regenerat

47 Analysis of PDGF-CC in vivo in a diabetic mouse model of delayed wound healing showed tha

48 ptide I-A(g7) dimers for use in the nonobese diabetic mouse model of diabetes.

49 The nonobese diabetic mouse model of human T1DM reveals that T cells

50 ession is very controversial in the nonobese diabetic mouse model of IDDM, but to our knowledge, it h

51 could fully mimic the effect of fibrin in a diabetic mouse model of impaired wound healing, demonstr

52 In the nonobese diabetic mouse model of T1D, administration of ML351 dur

53 radicals (MBRs) in a streptozotocin-induced diabetic mouse model were uniquely detected by combining

54 P2 axis in vivo, the New Zealand obese (NZO) diabetic mouse model, characterized by beta-cell loss un

55 In a streptozotocin-induced diabetic mouse model, compound 2 potentiated the glucose

56 rd with prior observations from the nonobese diabetic mouse model, suggesting a mechanism shared by m

57 In the nonobese diabetic mouse model, there is new evidence that insulin

58 anilloid 1 (TRPV1) on DPN in the STZ-induced diabetic mouse model, we found that a proportion of STZ-

59 In parallel, using streptozotocin-induced diabetic mouse model, we found that treatment with oxyto

60 glucose uptake was demonstrated in a type 1 diabetic mouse model, with significant recovery after ac

61 vival and number in a streptozotocin-induced diabetic mouse model.

62 ractionation of an ethanolic extract using a diabetic mouse model.

63 nhibits diabetes development in the nonobese diabetic mouse model.

64 S-IV on renal injury in db/db mice, a type 2 diabetic mouse model.

65 to normoglycemia in a streptozotocin-induced diabetic mouse model.

66 gression of diabetic nephropathy in a type 1 diabetic mouse model.

67 evelopment of type 1 diabetes in a non-obese diabetic mouse model.

68 lcoholic steatohepatitis (NASH) in an obese, diabetic mouse model.

69 vivo and in situ in a streptozotocin-induced diabetic mouse model.

70 N neurons and a shift toward excitation in a diabetic mouse model.

71 before and after photothrombotic stroke in a diabetic mouse model.

72 nase reduced glomerular AT1R expression in a diabetic mouse model.

73 ograft rejection in a streptozotocin-induced diabetic mouse model.

74 full-thickness excisional wounds in a db/db diabetic mouse model; QHREDGS showed significantly accel

75 In diabetic patients and diabetic mouse models (streptozotocin/high-fat diet-indu

76 nd that miR-7a levels are decreased in obese/diabetic mouse models and human islets from obese and mo

77 fections in type 1 (T1D) versus type 2 (T2D) diabetic mouse models and in patients with S. aureus inf

78 beta cells, islets of Txnip-deficient mice, diabetic mouse models and primary human islets.

79 toms of large-fiber DPN in type 1 and type 2 diabetic mouse models are related to alterations in musc

80 these islets in immunocompetent and nonobese diabetic mouse models are underway.

81 d "type 1" and B6.BKS(D)-Lepr(db)/J "type 2" diabetic mouse models on OCT; immunohistochemistry in ty

82 d CDDO-Me has potent anti-diabetic action in diabetic mouse models that is mediated at least in part

83 ized that superimposition of hypertension on diabetic mouse models would accelerate DKD.

84 in production was assessed directly in obese diabetic mouse models, and proinsulin biosynthesis was f

85 and associated metabolic dysfunction in two diabetic mouse models.

86 DLR-N were reduced in both type 1 and type 2 diabetic mouse models.

87 se and insulin levels in the ob/ob and db/db diabetic mouse models.

88 In the nonobese diabetic mouse (NOD) model, administration of IL-10/Fc f

89 he inflamed lacrimal gland (LG) of non-obese diabetic mouse (NOD), a classic mouse model of SjS.

90 ghly pathogenic CD8 T cells in the non-obese diabetic mouse, one of the best animal models for human

91 tosis and the migration and proliferation of diabetic mouse primary dermal fibroblasts and 3T3 fibrob

92 were transplanted to streptozotocin-induced diabetic mouse recipients.

93 sion and phosphorylation were upregulated in diabetic mouse renal proximal tubule epithelial cells, w

94 es increased the generation of superoxide by diabetic mouse retina more at night than during the day.

95 droxydocosapentaenoic acid were increased in diabetic mouse retinas and in the retinas and vitreous h

96 ned to determine whether neurons are lost in diabetic mouse retinas and whether the loss involves an

97 crease in dopaminergic amacrine cells in the diabetic mouse retinas, compared with the nondiabetic co

98 The data suggest that in diabetic mouse retinas, neurons in the ganglion cell lay

99 se in the number of acellular capillaries in diabetic mouse retinas, which were not reversible with i

100 , and this autophosphorylation is reduced in diabetic mouse retinas.

101 nsulin receptor (IR) and PTP1B in normal and diabetic mouse retinas.

102 Further, PTP1B activity was increased in diabetic mouse retinas.

103 etic foot skin, ob/ob and diet-induced obese diabetic mouse skin, and in mouse KCs exposed to increas

104 se skin, but the level of VEGF is reduced in diabetic mouse skin, and its release from human MCs is r

105 In diabetic mouse skin, hyperglycaemia inhibits the express

106 Type 1 diabetes in the nonobese diabetic mouse stems from an infiltration of the pancrea

107 acerbated autoimmune disease in the nonobese diabetic mouse strain as a result of a marked reduction

108 The model was the obese diabetic mouse strain BKS.Cg-m +/+ Lepr(db)/J, a model o

109 tect against type I diabetes in the nonobese diabetic mouse strain may, in some cases, be due to nega

110 of the CD28/B7 pathway early in the nonobese diabetic mouse strain, using CD28-/- and CTLA41g transge

111 and the other using T cells in the nonobese diabetic mouse strain, which develops spontaneous diabet

112 NOD mice compared with thymus of several non-diabetic mouse strains.

113 In the diabetic mouse, the laminin alpha5 chain content of the

114 p90RSK activity was increased in diabetic mouse vessels, and fluoromethyl ketone-methoxye

115 dysfunction in the heart of the Akita type 1 diabetic mouse was due to a decrease in the level of the

116 ormed in the salivary gland of the non-obese diabetic mouse, which displays chronic inflammation.

117 sphorylation of MRA and coronary artery from diabetic mouse, which was reduced by AG1478.

118 xpression was significantly downregulated in diabetic mouse wounds.