ライフサイエンスコーパス: chemical injury

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1 on that are characteristic of mechanical and chemical injury.

2 ndergoing classical apoptosis in response to chemical injury.

3 s contradicted those expected from a caustic chemical injury.

4 mor suppressor might alter susceptibility to chemical injury.

5 elicited by elastase perfusion or periaortic chemical injury.

6 ght to provide protection from bacterial and chemical injury.

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

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

9 cals to define the molecular pathogenesis of chemical injury.

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

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

12 ve capacity following partial hepatectomy or chemical injuries.

13 ognosis of patients with serious thermal and chemical injuries.

14 management strategies of ocular thermal and chemical injuries.

15 an function following surgical resection and chemical injuries.

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

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

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

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

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

21 However, caustic chemical injuries develop rapidly whereas esophagitis mi

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

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

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

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

26 Chemical injuries in pediatric patients are more commonl

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

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

29 Exploiting a chemical injury model that overexpresses vimentin and GF

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

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

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

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

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

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

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

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

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

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

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

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

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