ライフサイエンスコーパス: necrotic lesion

1 s to be triggered at the periphery of the HR necrotic lesion.

2 , inhibited tumor growth and led to smaller, necrotic lesions.

3 s, Pst DC3000 induced accelerated coalescing necrotic lesions.

4 lated in capillaries and neurons surrounding necrotic lesions.

5 to causes MAPKKKalpha-dependent formation of necrotic lesions.

6 restricted to myocytes surrounding piecemeal necrotic lesions.

7 e infection was associated with larger, more necrotic lesions.

8 ulated factors involved in the production of necrotic lesions.

9 aic virus, or tobacco etch virus resulted in necrotic lesions.

10 Arabidopsis is characterized by spontaneous necrotic lesions, accumulation of reactive oxygen specie

11 sis and treatment can prevent progression of necrotic lesions and bone collapse.

12 Necrotic lesions and necrotic cell death characterize se

13 th lower blood urea nitrogen levels, reduced necrotic lesions, and higher survival rates.

14 ion with the wild-type GAS isolate generated necrotic lesions, and in some animals the GAS disseminat

15 in aconitase activity, stunting, spontaneous necrotic lesions, and increased resistance to paraquat.

16 eins, and manganite [Mn(III)] accumulated in necrotic lesions apparently through low Mn sequestration

17 tion process and coincided with formation of necrotic lesions approximately 5 days after inoculation.

18 wth and sporadic development of chlorotic or necrotic lesions at inoculation sites.

19 ed approaches are an important complement to necrotic lesion-based approaches and should be used in c

20 ed-9 specifically abrogated the formation of necrotic lesions, but not other symptoms, in tomato leav

21 es of seedlings showed significantly smaller necrotic lesions compared with nonprimed plants, coincid

22 nt, speckle, is characterized by spontaneous necrotic lesion formation on leaves, root, and stems, si

23 rapid weight loss, bacteremia, and abdominal necrotic lesion formation.

24 shift within the lobule in parallel with the necrotic lesion in these animals.

25 pregulate p50 transcription and induce local necrotic lesions in an A. tumefaciens infiltration assay

26 uronal cell loss, demyelination, gliosis and necrotic lesions in post-mortem material.

27 oduced high levels of ethylene and developed necrotic lesions in response to an acute O3 exposure tha

28 We used C3HeB/FeJ mice, which develop necrotic lesions in response to Mycobacterium tuberculos

29 protein gene PR-1a and developed spontaneous necrotic lesions in the absence of any pathogen.

30 treatment groups showed significantly fewer necrotic lesions in the cerebral cortex, caudate nucleus

31 gene completely lack chlorophyll and develop necrotic lesions in the light.

32 The appearance of multiple granulomatous-necrotic lesions in the liver correlates with a marked i

33 This study revealed necrotic lesions in the peripheries of Ahr-/- fetal live

34 infection and contribute to the formation of necrotic lesions in tuberculosis.

35 c, but not normoglycemic, animals showed pan-necrotic lesions ('infarction') after 4 h of recirculati

36 red delivery of antifungals to hyphae within necrotic lesions is thought to contribute to therapeutic

37 dence of muscle regeneration due to previous necrotic lesions likely caused by earlier SINV infection

38 t Slo was not necessary for the formation of necrotic lesions, nor was it necessary for escape from t

39 ase in Opn transcription was demonstrated in necrotic lesions of both DCC-susceptible C3H/He and B6.C

40 onse to B. cinerea, measured as expansion of necrotic lesions on leaves and accumulation of the antim

41 These promoter::p50 constructs induce local necrotic lesions on NN tobacco plants in an Agrobacteriu

42 he PPO-silenced plants developed spontaneous necrotic lesions on their leaves in the absence of patho

43 ct plants, but they can colonize and develop necrotic lesions on wounded leaves and stems.

44 Histopathologic examination of the necrotic lesion revealed bacteria throughout inflamed su

45 was more likely than the wild type to yield necrotic lesions, suggesting that mucoidy contributes to

46 o, causing disease symptoms characterized by necrotic lesions surrounded by chlorosis.

47 to be strongly reduced in its production of necrotic lesion symptoms.

48 ) and csrRS(-) bacteria yielded larger, more necrotic lesions than did either strain at twice the ino

49 es and was characterized by an initial focal necrotic lesion that rapidly progressed to invasion of t

50 d growth alterations and their leaves showed necrotic lesions that appeared similar to lesions charac

51 D mice verified that they do not exhibit the necrotic lesions that are usually associated with SCD.

52 , in a developmentally programmed manner, of necrotic lesions that expand to kill leaves cell autonom

53 e mice, young B10.T(6R) mice did not develop necrotic lesions throughout the liver.

54 ys enhanced stress responses and spontaneous necrotic lesions under drought conditions in the absence

55 seedlings silenced for Sl2/3-MMP expression, necrotic lesions were observed at the base of the hypoco

56 drug-tolerant persister population only when necrotic lesions were present.

57 Focal necrotic lesions were seen in all cases at MR, and five

58 e vascular changes that precede the onset of necrotic lesions with the thalamus of the pyrithiamine-i

59 ith PB or betaNF shifted the location of the necrotic lesion within the lobule from zone 2, as observ