ライフサイエンスコーパス: hairless mice

1 efect is brittle hair resulting in alopecia (hairless mice).

2 to generate PKCepsilon-overexpressing SKH-1 hairless mice.

3 d associated mechanisms of silibinin in SKH1 hairless mice.

4 on UVB-induced skin carcinogenesis in SKH-1 hairless mice.

5 e development of UVB-induced tumors in SKH-1 hairless mice.

6 was less pronounced in shaved haired than in hairless mice.

7 dothelial growth factor-A (VEGF-A) in normal hairless mice, a specific response to permeability barri

8 In vivo experiments performed using SKH1 hairless mice also confirmed increased dermal penetratio

9 pharmacokinetic studies performed using SKH1 hairless mice also confirmed the efficacy of SP50 in der

10 Here, 9-10 challenges with oxazolone (Ox) to hairless mice also produced a chronic Th2-like HR.

11 ion of imiquimod or S-28463 to the flanks of hairless mice and rats leads to increases in local conce

12 l was topically applied on the skin of SKH-1 hairless mice at a dose of 10 micromol/mouse (in 0.2 ml

13 Hairless mice carrying homozygous mutations in hairless

14 ess mice, PKCepsilon overexpression in SKH-1 hairless mice decreased the latency (12 weeks), whereas

15 Overall, 100% of hairless mice developed >12 tumors per mouse after 32 we

16 ocol, the nontransgenic littermates or SKH-1 hairless mice did not develop tumors or pigmented cysts

17 y and restoration of the calcium gradient in hairless mice exposed to 4 degrees C external temperatur

18 lopment, we bred Ptch(+/-)/C57BL6 with SKH-1 hairless mice, followed by brother-sister cross to get F

19 T, but not OHBT, when applied to the skin of hairless mice following acute barrier disruption by tape

20 of SC tocopherols to solar simulated UVR in hairless mice, (ii) the baseline levels and distribution

21 ependent depletion by solar simulated UVR in hairless mice; (ii) a gradient distribution within untre

22 me defenses after UVB radiation in Skh: HR-1 hairless mice, implicating antioxidant status in protect

23 e was developed and compared to control SKH1 hairless mice in terms of skin tumor induction and extra

24 In this study, we used SKH-1 hairless mice in which COX-1 was selectively deleted to

25 Here, we generated Keap1(flox/flox) SKH-1 hairless mice in which Nrf2 is disrupted (Keap1(flox/flo

26 a representative omega-3 PUFA, in wild type hairless mice induced expression of the Nrf2 target prot

27 PARalpha, on hyperproliferative epidermis in hairless mice, induced either by repeated barrier abroga

28 In hairless mice, inflammatory infiltrate was found around

29 SKH-1 hairless mice lacking the EP2 receptor were therefore st

30 rneum, by acetone application on the skin of hairless mice, led to a marked accumulation of HA in the

31 As compared with the wild-type hairless mice, PKCepsilon overexpression in SKH-1 hairle

32 rified anti-CMP EBA antibodies injected into hairless mice produced the clinical, histological, immun

33 uced squamous papillomas in SENCAR and SKH-1 hairless mice, respectively, to Pc4-PDT, and assessed it

34 CFU of either acapsular or SLS- strains into hairless mice resulted in lesions approximately 70% smal

35 Our use of hairless mice revealed this response to be largely indep

36 Hairless mice should facilitate comparison of various ta

37 Hairless mice (SKH1-hrBR) are used as a model for human

38 However, in SKH-1 hairless mice, the most common and highly sensitive mode

39 PKCepsilon FVB/N transgenic mice with SKH-1 hairless mice to generate PKCepsilon-overexpressing SKH-

40 n hydrophilic antioxidants, we exposed SKH-1 hairless mice to O3 concentrations of 0, 0.8, 1, and 10

41 Tumor onset in hairless mice was 10 weeks earlier than in haired litter

42 KH1 (nonpigmented) versus SKH2/J (pigmented) hairless mice, we evaluated how a pigment-dependent redu

43 To test this hypothesis, SKH-1 hairless mice were anesthetized and exposed for 2 h to O

44 SKH-1 hairless mice were exposed to a ultraviolet (UV) source

45 SKH-1 hairless mice were exposed to UVB alone for 15 weeks, an

46 Several groups of hairless mice were followed over a period of 18 mo to do

47 Hairless mice were injected with PAF or serotonin recept

48 f mtDNA mutations in UV-induced skin tumors, hairless mice were irradiated to produce tumors, and the

49 SKH-1 hairless mice were irradiated with ultraviolet B (UVB) t

50 SKH-1 hairless mice were irradiated with UVB and the skin remo

51 Tumors in hairless mice were more aggressive than in haired litter

52 Anesthetized hairless mice were scanned by using a 2.5-MHz transducer

53 Male SKH-1 hairless mice were subjected to full-thickness thermal i

54 SKH-1 hairless mice were topically treated with GTP (5 mg/0.2

55 Female SKH1 (hr/hr) albino hairless mice were treated 5 d per wk for 12 wk.

56 Hairless mice were treated topically with activators of

57 Hairless mice were treated with cyclophosphamide (100 mg

58 ed in drinking water (0.2%, wt/vol) to SKH-1 hairless mice, which were then exposed to multiple doses

59 ments with three separate mouse lines (SKH-1 hairless mice, wild-type FVB, and protein kinase C epsil

60 Topical treatment of normal hairless mice with 22(R)-hydroxycholesterol or 24(S),25-

61 reaction, initiated by treating the skin of hairless mice with a solution of dihydroxyacetone in buf

62 Moreover, topical treatment of hairless mice with ciglitazone or troglitazone increases

63 We treated Skh-1 hairless mice with daily doses of suberythemal UVB for 4

64 Hairless mice with Ercc1-deficient skin were hypersensit

65 Treatment of SKH-1 hairless mice with ultraviolet B light (UVB; 30 mJ/cm(2)

66 Treatment of SKH-1 hairless mice with UVB (30 mJ/cm(2)) twice a week for 20