ライフサイエンスコーパス: hypertrophic scar

1 id, significant, and lasting improvements in hypertrophic scar.

2 Unlike humans, rats do not develop hypertrophic scars.

3 ore-after cohort study in burn patients with hypertrophic scars.

4 sses a wide spectrum, from chronic wounds to hypertrophic scars.

5 the development and treatment of keloids and hypertrophic scars.

6 ed to evaluate integrin roles in keloids and hypertrophic scars.

7 hyperproliferating situations, psoriasis and hypertrophic scars.

8 factors offers superior efficacy in reducing hypertrophic scars.

9 p-regulated in skin wounds and in normal and hypertrophic scars.

10 e and surgery to minimise the development of hypertrophic scarring.

11 preciation of its importance in fibrosis and hypertrophic scarring.

12 sential for normal healing and prevention of hypertrophic scarring.

13 enotype was typical except that he exhibited hypertrophic scarring.

14 is higher in keloids (63% +/- 3.6% SEM) and hypertrophic scars (45% +/- 2.7% SEM) than in normal ski

15 trospective study includes 128 patients with hypertrophic scars (56 underwent monotherapy and 72 unde

16 Now up to 70% of patients develop hypertrophic scars after burns.

17 Similar to the hypertrophic scar and keloids, the efficacy of glucortic

18 have therapeutic value in the prevention of hypertrophic scarring and in the treatment of fibrotic d

19 F-beta1) upregulation has been implicated in hypertrophic scars and keloids, but it is unclear if it

20 nd potentially prevent abnormal healing like hypertrophic scars and keloids.

21 s are histopathologically identical to human hypertrophic scars and persist for more than six months

22 ng scars are structurally identical to human hypertrophic scars and showed dramatic increases in volu

23 eases, 10(th) Revision (ICD-10) codes L91.0 (hypertrophic scar) and L90.5 (scar conditions and fibros

24 rmabrasion, wound healing, safety, scarring, hypertrophic scar, and keloid.

25 s cell carcinoma in situ, actinic cheilitis, hypertrophic scars, and keloids; it is useful for epider

26 Because keratinocytes in psoriasis and hypertrophic scars are activated, we conclude that K15 e

27 Keloids and hypertrophic scars are significant symptomatic clinical

28 Hypertrophic scars arise from aberrant wound healing and

29 w-up analysis; 28 (16.2%) of these developed hypertrophic scars, but the model was otherwise safe.

30 roliferative phase of wound healing produces hypertrophic scars by inhibiting cellular apoptosis thro

31 eferred to as combined therapy, for treating hypertrophic scars compared with only using fractional C

32 Hypertrophic scar contracture is considered to be a path

33 apoptosis of myofibroblasts and keloid- and hypertrophic scar-derived cells.

34 In hypertrophic scars, EMT-related genes were elevated alon

35 Preventing the formation of hypertrophic scars, especially those that are a result o

36 Keloids and hypertrophic scars (excessive scarring) are relatively u

37 These scar fibroblasts (hypertrophic scar fibroblasts (HTSFs)) retain the myofib

38 Complications included hypertrophic scar formation (35), atelectasis (12), pleu

39 cal delivery of S100A12 resulted in a marked hypertrophic scar formation in a validated rabbit hypert

40 To clarify the importance of apoptosis in hypertrophic scar formation, we examine the effects of m

41 f IL-1 signaling was effective in preventing hypertrophic scar formation.

42 and fibrosis than control mice in a model of hypertrophic scar formation.

43 We found that keloids and hypertrophic scars have marked alterations in fibroblast

44 A hypertrophic scar (HS) is a cutaneous condition characte

45 chanisms behind the pathogenesis of postburn hypertrophic scar (HS) remain unclear.

46 udy was performed involving 21 patients with hypertrophic scars (HS) (n = 9) and keloids (n = 12) res

47 Hypertrophic scar (HTS) formation is a common challenge

48 Hypertrophic scar (HTS) formation is a frequent postoper

49 aded control wounds in an established murine hypertrophic scar (HTS) model.

50 The genetic determinants of post-burn hypertrophic scarring (HTS) are unknown, and melanocorti

51 We used a hypertrophic scarring (HTS) mouse model in which Jun is

52 Hypertrophic scars (HTS), frequently seen after traumati

53 ity and thus excess scar-tissue formation of hypertrophic scars (HTS).

54 key functions of myofibroblasts derived from hypertrophic scars (HTSF) are constitutively activated b

55 e traumatic or thermal injury to the dermis, hypertrophic scars (HTSs) often develop and these scar f

56 e traumatic or thermal injury to the dermis, hypertrophic scars (HTSs) often develop in humans.

57 However, based on increased frequency of hypertrophic scarring in patients on testosterone, we hy

58 Keloids and hypertrophic scars in children are effectively treated w

59 to a healing wound is sufficient to produce hypertrophic scars in mice.

60 Hypertrophic scarring is a major source of morbidity.

61 One of the common interventions for treating hypertrophic scars is fractional carbon dioxide (CO2) la

62 trophic scar formation in a validated rabbit hypertrophic scar model compared with saline control.

63 rmal application in a preclinical rabbit ear hypertrophic scar model.

64 ), dislodged sternal bar (n = 3), and mildly hypertrophic scar (n = 12).

65 ned integrin expression in keloids (n = 11), hypertrophic scars (n = 5), radiation ulcers (n = 2), an

66 Hypertrophic scars occur following cutaneous wounding an

67 tic to prevent formation of a fibrotic scar (hypertrophic scar or keloid) or to prevent cutaneous fib

68 TRPC3 is highly expressed in human hypertrophic scar tissue and mechanical stimuli are know

69 ion of wound healing to attenuate or prevent hypertrophic scarring, well-designed trials to confirm t

70 monstrates additional features of keloid and hypertrophic scarring which we were not able to consider