ライフサイエンスコーパス: chemical injury

1 ssed 10 participants (15 eyes) with an acute chemical injury.

2 is a useful tool in the management of ocular chemical injury.

3 of limbal ischemia following an acute ocular chemical injury.

4 on that are characteristic of mechanical and chemical injury.

5 cytokine-mediated rather than the result of chemical injury.

6 cals to define the molecular pathogenesis of chemical injury.

7 s kidney injury molecule-1 after nephrotoxic chemical injury.

8 ndergoing classical apoptosis in response to chemical injury.

9 s contradicted those expected from a caustic chemical injury.

10 mor suppressor might alter susceptibility to chemical injury.

11 elicited by elastase perfusion or periaortic chemical injury.

12 ght to provide protection from bacterial and chemical injury.

13 , and relative resistance, of melanocytes to chemical injury.

14 idly regenerates in response to bacterial or chemical injury.

15 t activation were specifically induced after chemical injury.

16 otential use for therapeutic treatment after chemical injury.

17 atogenesis as well as regeneration following chemical injury.

18 ent the single highest-risk group for ocular chemical injuries.

19 an function following surgical resection and chemical injuries.

20 ve capacity following partial hepatectomy or chemical injuries.

21 ognosis of patients with serious thermal and chemical injuries.

22 management strategies of ocular thermal and chemical injuries.

23 tion or affect final visual acuity in severe chemical injuries.

24 therapeutic in the acute treatment of ocular chemical injuries.

25 including infectious etiologies, trauma, and chemical injuries.

26 ction (54.17%), autoimmune disease (20.83%), chemical injury (12.5%), and other (12.5%).

27 patients presenting in early stage of severe chemical injury, 38 eyes (median age 11 years) managed w

28 The most frequent cause of blindness was chemical injuries (71%).

29 ctor for prostate carcinogenesis, with diet, chemical injury and an altered microbiome being causally

30 iota fortifies the intestinal barrier during chemical injury and infectious challenges.

31 icient to increase mucosal susceptibility to chemical injury and inflammation.

32 e lay emphasis on the importance identifying chemical injury and recommend that medication attention

33 n migrate to the RPE layer after physical or chemical injury and regenerate a portion of the damaged

34 ion as a protective UPR-mediated response to chemical injury, and uncover an essential role for MDR e

35 Ocular thermal and chemical injuries are a true ocular emergency and requir

36 djuvant to standard medical therapy in acute chemical injury, are equally efficacious.

37 f the pathophysiology of a radiant energy or chemical injury as well as advancements in ocular surfac

38 However, caustic chemical injuries develop rapidly whereas esophagitis mi

39 The best visual prognosis is observed in chemical injury eyes, whereas the worst prognosis is in

40 rface epithelial cells are exposed to lethal chemical injury from refluxed acid.

41 n was noted in 3 out of the 7 laminae in the chemical injury group and 8 out of the 12 laminae in the

42 raft failures, 6 (7 laminae) belonged to the chemical injury group, and 10 (12 laminae) to the Steven

43 Chemical injuries in pediatric patients are more commonl

44 with grade 4 and above (Dua classification) chemical injuries in the early stage.

45 es were implanted in 15 eyes of 14 patients (chemical injury in 9 [10 eyes] and Stevens-Johnson syndr

46 se of AI for assessing corneal damage due to chemical injury in live rabbits remains lacking.

47 photochemical injury in the carotid artery, chemical injury in the carotid artery or mesenteric arte

48 lipoxin A(4), and 18-HEPE are produced after chemical injury in the lungs, and that exogenous treatme

49 Chemical injury induced by DSS leads to a loss of both L

50 Exploiting a chemical injury model that overexpresses vimentin and GF

51 neal graft failure (n = 50; 44%) followed by chemical injury (n = 30; 27%).

52 subjected to either adriamycin-induced acute chemical injury or genetic deletion of the podocin-encod

53 f these cases, as seen in an animal model of chemical injury or in late mustard gas keratitis.

54 Common top-eye emergencies (TEE) include chemical injuries, orbital-preseptal cellulitis, and orb

55 of managing repeat graft failure and ocular chemical injury outside of North America, with similar v

56 Chemical injuries to the eye are emergencies with limite

57 Gastric aspiration pneumonia involves chemical injury to the alveoli of the lungs with inflamm

58 In vivo thrombus formation after chemical injury to the carotid artery revealed a severe

59 Upon chemical injury to the intestine, mice deficient in RAB1

60 are activated in response to a mechanical or chemical injury to their tissue niche.

61 echanical hypersensitivity produced by these chemical injuries was prevented by 1NM-PP1 inhibition of

62 of SJS was 36.7 months and among patients of chemical injury was 43 months.

63 actors associated with final visual outcome: chemical injury was associated with better final vision

64 Severe (grade 3 and 4) ocular chemical injury was seen in 94 patients (70.1%).

65 Bilateral chemical injuries were seen in 24 patients (17.9%).

66 Case records of patients with ocular chemical injury who presented to the Dr.

67 Records of patients with severe ocular chemical injury who underwent AMG alone (between 2009 an

68 60 patients with Roper-Hall grade IV ocular chemical injury with a minimum follow-up of 12 months we

69 s (6), corneal scar (6), corneal keloid (3), chemical injury with limbal stem cell deficiency (2), an

70 iferative response to bacterial infection or chemical injury within the bladder is regulated by signa