ライフサイエンスコーパス: foal

1 ete prevention of infection occurring in one foal.

2 etween SCID foals and the reconstituted SCID foal.

3 m an immune-reconstituted EIAV-infected SCID foal.

4 rhodococcal pneumonia, CTL were evaluated in foals.

5 ntly killed infected targets from 3-week-old foals.

6 ined from four EIAV-infected immunocompetent foals.

7 iate between that seen in SCID mice and SCID foals.

8 causes severe pyogranulomatous pneumonia in foals.

9 rology for diagnosis of R. equi pneumonia in foals.

10 were affected as severely as immunocompetent foals.

11 her SCID or immunocompetent thrombocytopenic foals.

12 (1 Arabian and 1 Arabian-pony cross), and 2 foals (1 Arabian and 1 Arabian-pony cross) with severe c

13 young adult Arabian horses, two 1-month-old foals (1 Arabian and 1 Arabian-pony cross), and 2 foals

14 g infection in both SCID and immunocompetent foals: 51 and 68%, respectively, relative to the preinfe

15 In severe combined immunodeficiency (SCID) foals, a 5 bp deletion at codon 9480 results in a frames

16 In three SCID foals, a novel neutralization-resistant variant arose th

17 Plasma was infused into young horses (foals) affected with severe combined immunodeficiency (S

18 These antibodies cross-reacted with both foal and adult PBAC.

19 virus was isolated from feces of a diarrheic foal and serially propagated in human rectal adenocarcin

20 All strains of R. equi isolated from foals and approximately a third isolated from humans con

21 Immunocompetent Arabian foals and Arabian foals with severe combined immunodefic

22 differences between SCID and immunocompetent foals and between SCID foals and the reconstituted SCID

23 ere recognized by sera from R. equi-infected foals and immune adult horses.

24 severe, life-threatening pneumonia in young foals and in people with underlying immune deficiencies.

25 ival within macrophages and for virulence in foals and mice.

26 growth of the organism and for virulence in foals and murine in vivo model systems.

27 D and immunocompetent foals and between SCID foals and the reconstituted SCID foal.

28 pneumonia with abscessation in young horses (foals) and in immunocompromised people, such as persons

29 genetic immunodeficiencies in mice, Arabian foals, and recently in Jack Russell terriers have been a

30 ere than its murine counterpart in that SCID foals are incapable of forming either coding or signal j

31 nt CTL activity was present in three of five foals at 6 weeks of age, and significant specific lysis

32 specific lysis was induced by PBMC from all foals at 8 weeks of age.

33 threatening pyogranulomatous pneumonia, most foals develop a protective immune response that lasts th

34 f abortion in pregnant mares, death in young foals, establishment of the carrier state in stallions,

35 to 89% in three SCID and two immunocompetent foals examined.

36 ce in DNA-PK(CS) expression in SCID mice and foals explains the more severe phenotype of equine SCID,

37 tion of all available information about each foal, including clinical presentation, diagnostic test r

38 five severe combined immunodeficient (SCID) foals infected with EIAV.

39 Foals infected with equine infectious anemia virus becom

40 In contrast, SCID foals infused with nonimmune plasma developed acute dise

41 s is that the mutant DNA-PKCS allele in SCID foals inhibits signal end resolution.

42 the genetic SCID disease observed in Arabian foals is explained by a defect in V(D)J recombination th

43 B-17 SCID mice, the molecular defect in SCID foals is in the catalytic subunit of the DNA-dependent p

44 on for the differences between SCID mice and foals is that the mutant DNA-PKCS allele in SCID foals i

45 pathogen that primarily causes pneumonia in foals less than six months in age and immunocompromised

46 protein carbonyls, during chill storage, of foal liver pate reflects the intense oxidative degradati

47 nd protein changes, during chill storage, of foal liver pate was studied.

48 on) increased during refrigerated storage of foal liver pate, with the contents in the HF group being

49 olic rates of chronically catheterized fetal foals (n = 24) were measured at different gestational ag

50 ess effects of plasma or serum from infected foals on megakaryocyte (MK) growth and maturation in vit

51 ficant differences in lipid oxidation, since foal pates with higher fat content (HF) showed significa

52 ies resulted in larger placentae and heavier foals relative to PinP (P < 0.05).

53 TinP had smaller placentae and lighter foals relative to TinT (P < 0.05).

54 Growth-enhanced (PinT) foals showed elevated basal arterial blood pressure and

55 Conversely, growth-restricted (TinP) foals showed no change in basal arterial blood pressure,

56 case in C.B-17 SCID mice and in Arabian SCID foals, the defective factor in these SCID puppies is DNA

57 n and deletion of 83 amino acids; as in SCID foals, the mutant protein is unstable.

58 between immunocompetent and immunodeficient foals was not statistically significant.

59 ophages and in the lungs of R. equi-infected foals, we hypothesized that vapG could be an important v

60 Values for maternal and foal weights and placental area at birth were larger in

61 Maternal and foal weights and placental microscopic area were measure

62 young adult Arabian-pony crosses and 1 SCID foal were then inoculated with plasma containing only EH

63 s not dependent on the immune response: SCID foals were affected as severely as immunocompetent foals

64 Four of five SCID foals were completely protected against homologous chall

65 Treated SCID foals were protected against clinical disease, with comp

66 ood mononuclear cells (PBMC) from 3-week-old foals were unable to lyse either autologous perinatal or

67 ole blood samples, and serum samples from 56 foals with pneumonia were analyzed.

68 Immunocompetent Arabian foals and Arabian foals with severe combined immunodeficiency (SCID), whic

69 Rhodococcus equi isolated from young horses (foals) with R. equi pneumonia, carry an 80-90 kb virulen

70 neutralizing immune plasma in young horses (foals) with severe combined immunodeficiency (SCID).