ライフサイエンスコーパス: abscess formation

1 he peritoneal cavity of naive rats, promoted abscess formation.

2 l proliferation and modulating the course of abscess formation.

3 nfluences Ab responses to infection and skin abscess formation.

4 nism by which T cells control intraabdominal abscess formation.

5 que in their frequent association with brain abscess formation.

6 icitis with diffuse peritonitis or localized abscess formation.

7 extension into the adjacent soft tissues and abscess formation.

8 bial, hemorrhage, and bowel wall perforation/abscess formation.

9 is and reduces skin tissue invasion and deep-abscess formation.

10 utaneous nodules that can progress to dermal abscess formation.

11 equired for staphylococcal dissemination and abscess formation.

12 val in oxygenated tissues prior to anaerobic abscess formation.

13 teomyelitis, septic arthritis and metastatic abscess formation.

14 ed vaccine protection against staphylococcal abscess formation.

15 ell as SdrD and protein A, are necessary for abscess formation.

16 ins most commonly cause skin infections with abscess formation.

17 f S. aureus as antigens in a murine model of abscess formation.

18 reduction in virulence in a murine model of abscess formation.

19 of epithelial cell, and murine subcutaneous abscess formation.

20 cific virulence defects in a murine model of abscess formation.

21 ge volume of gas collection without signs of abscess formation.

22 e concurrent infection elsewhere or possible abscess formation.

23 licits chronic infection, resulting in brain abscess formation.

24 onance imaging technology to visualize brain abscess formation.

25 gens to induce a classic infectious process: abscess formation.

26 modulated the development of intraabdominal abscess formation.

27 This zwitterionic motif is essential for abscess formation.

28 staphylococcal virulence in mouse models of abscess formation.

29 rophylaxis, it dramatically increased kidney abscess formation and bacterial dissemination throughout

30 ages of a developmental program that enables abscess formation and bacterial persistence in host tiss

31 coccus aureus infections are associated with abscess formation and bacterial persistence; however, th

32 deficient (SCID) mouse model of amebic liver abscess formation and compared liver damage in neutrophi

33 allows definition of the fistula, associated abscess formation and its secondary extensions.

34 to SEB in the infected tissue and decreased abscess formation and proinflammatory cytokine levels, l

35 tment conferred long-term protection against abscess formation and resulted in significantly fewer to

36 n of FnBP reduces the risk of staphylococcal abscess formation and should be investigated further as

37 ysteine concentration significantly enhanced abscess formation and size.

38 rFnBF exhibited dose-dependent inhibition of abscess formation and, at a 100-microg dose, raised the

39 els of systemic infection: bacteremia, renal abscess formation, and lethality following high-dose int

40 g teeth (considered a sign of inflammation), abscess formation, and root exposure (penetration of bon

41 osteal reaction, serpentine bone resorption, abscess formation, and root penetration of the bone surf

42 se and human blood, provided protection from abscess formation, and stimulated pathogen-specific immu

43 sulitis associated with islet cell necrosis, abscess formation, and subsequent diabetes when transfer

44 ls transfer PS A-mediated protection against abscess formation, and that a soluble mediator produced

45 ve implicated T cells in the pathogenesis of abscess formation, and we have recently shown that CD4(+

46 gulates quorum-sensing, toxin production and abscess formation; and host-derived antimicrobial peptid

47 Bile leakage, bleeding, and abscess formation are major resection surface-related co

48 getations and a decreased incidence of renal abscess formation, as compared with animals inoculated w

49 u-1.4/1.1 bound to SEB in vivo and decreased abscess formation, as well as proinflammatory cytokine l

50 valuated for the prevention of mortality and abscess formation associated with experimental intraabdo

51 neate the mechanism by which T cells mediate abscess formation associated with intra-abdominal sepsis

52 Abscess formation associated with intra-abdominal sepsis

53 Two compounds were found to decrease liver abscess formation at 10 mg/kg ip with little or no effec

54 to synthesize PS B or PS C still facilitate abscess formation at levels comparable to those of wild-

55 MiR-142(-/-) mice exhibited abnormal abscess formation at S. aureus-infected skin wound sites

56 eased operative time, blood loss, and pelvic abscess formation but does not increase the rate of anas

57 Our results indicate that colonization and abscess formation by different phenotypes of S. epidermi

58 al neutrophils and are highly susceptible to abscess formation by gram-positive bacteria.

59 These results demonstrate that abscess formation by pathogenic bacteria is under the co

60 s provide a structure/function rationale for abscess formation by S. aureus and expand the sphere of

61 mouse model for the study of intraperitoneal abscess formation by S. aureus, a disease that occurs fr

62 usual free amino sugar that is essential for abscess formation by this polymer.

63 uced levels of arthritis, osteomyelitis, and abscess formation compared with control animals.

64 to anatomical plane, length, ramifications, abscess formation, enteric communication, external cutan

65 nd cause lethal infections with disseminated abscess formation, failing to elicit an adequate host re

66 neutralizing Ab specific for IL-17 prevented abscess formation following bacterial challenge in mice.

67 B7 pathway in animals with CTLA4Ig prevented abscess formation following challenge with different bac

68 s site, graft thrombosis, and intraabdominal abscess formation have been well documented after pancre

69 In models of staphylococcal s.c. abscess formation, hindpaw infection, and surgical wound

70 ng the infection site play a pivotal role in abscess formation; however, the abscess is not formed in

71 at the time of bacterial challenge prevented abscess formation in a dose-dependent manner.

72 mutant was not able to induce intraabdominal abscess formation in a mouse model, whereas the parent s

73 these genes are also required for S. aureus abscess formation in a murine infection model.

74 entral nervous system involvement with brain abscess formation in a patient with chronic granulomatou

75 m in this anaerobe required for survival and abscess formation in a peritoneal cavity infection model

76 ps) confer protection against intraabdominal abscess formation in a T cell-dependent manner.

77 The minimum dose that led to colonization or abscess formation in all mouse strains was 10(7) or 10(8

78 ity to delay the development of amebic liver abscess formation in an E. histolytica infected hamster

79 ated the role of S. aureus CPs in modulating abscess formation in an experimental animal model of int

80 hese polypeptides provide protection against abscess formation in animal models of staphylococcal dis

81 The regulation of abscess formation in animals is dependent on T lymphocyt

82 ified CP5 and CP8 facilitated intraabdominal abscess formation in animals when given i.p. with a ster

83 stimulate T-cell proliferation and regulate abscess formation in bacterial infection.

84 ingular ability of this organism to modulate abscess formation in experimental rodent models resides

85 Notably, liver abscess formation in hamsters by the pAP-R2 transfectant

86 de complex is the major virulence factor for abscess formation in human hosts.

87 not in periodontal ligament; (2) it reduces abscess formation in injured teeth; (3) it does not bloc

88 A and provide protection from staphylococcal abscess formation in mice.

89 R2-/- mice exhibited impaired intraabdominal abscess formation in response to B. fragilis.

90 nd reduced the incidence and the severity of abscess formation in response to inoculation with S. aur

91 tivated CD4(+) T cells, were associated with abscess formation in Th2-impaired (STAT6(-/-)) mice, whi

92 ficantly increased bone destruction and more abscess formation in the apical area compared with WT mi

93 To determine the contribution of PS A to abscess formation in the context of the intact organism,

94 hock to a chronic infection characterized by abscess formation in the lungs, liver, and spleen.

95 nt but not an exclusive role in amebic liver abscess formation in the mouse model.

96 n lesion 3 and 5 days postinfection revealed abscess formation in the s.c. tissues, and abundant spir

97 colonization of implanted PVC catheters and abscess formation in three different mouse strains.

98 Abscess formation in vivo and T-cell activation in vitro

99 induces T cell-dependent protection against abscess formation in vivo.

100 ry cytokine or chemokine expression or brain abscess formation in vivo.

101 lication in a murine model of staphylococcal abscess formation, indicating that carbon catabolite rep

102 treated with CP8 s.c. were protected against abscess formation induced by homologous or heterologous

103 These results indicate that abscess formation is a major mechanism of host resistanc

104 strate that PS A-mediated protection against abscess formation is dependent upon a CD4+ T cell-depend

105 ued innate responses during late-stage brain abscess formation is not known but is important, because

106 Abscess formation is not unique to staphylococcal infect

107 S-variant infection, and the cords initiated abscess formation leading to rapid larval death.

108 xia, ileus, wound infection, intra-abdominal abscess formation, operative time, and postoperative hos

109 oteins, Emp and Eap, are either required for abscess formation or contribute to persistence.

110 1; P = .01) and no differences in fistula or abscess formation or in pouch failure.

111 tive hemorrhage (P = 0.174), intra-abdominal abscess formation (P = 0.199), biliary leakage (P = 0.38

112 terial polysaccharides (Zps) known to induce abscess formation required CD28-B7 costimulation and, wh

113 le SCV phenotype led to colonization only or abscess formation, respectively.

114 y before or after challenge protects against abscess formation subsequent to challenge with different

115 xpressed in infected tissues at the sites of abscess formation, suggesting that abscesses are iron-st

116 used by Actinomyces species characterized by abscess formation, tissue fibrosis, and draining sinuses

117 high)) and thus were more active in inducing abscess formation via a WTA-dependent and T-cell-mediate

118 ntermuscularly administered rFnBF to prevent abscess formation was determined in a guinea pig model o

119 Intra-abdominal abscess formation was more common following laparoscopic

120 mice survived after the infection; however, abscess formation was not demonstrated to occur in burne

121 In contrast, no improvement in abscess formation was observed in animals treated with p

122 s lower in animals treated with antibiotics; abscess formation was reduced and pseudocysts were small

123 a propria, transmural involvement, and micro abscess formation was suggestive of Crohn's disease.

124 Progression of the infection (usually abscess formation) was monitored by examining mice for b

125 Organ invasion by hyphae and early abscess formation were evident 6 and 24 hours after infe

126 However, they may lead to abscess formation with an estimated incidence of about 0

127 Animal models of liver abscess formation with Entamoeba histolytica suggest tha

128 Each of the PDD isolates induced abscess formation, with strain 3A causing cutaneous ulce

129 e of state from solid to gas without sign of abscess formation within 2 days after TAE was described

130 Using a mouse model of Staphylococcus aureus abscess formation within a cutaneous wound, combined wit

131 me, estimated blood loss, and rate of pelvic abscess formation without associated leak were higher in

132 e, immunization with the CRD inhibited liver-abscess formation, yet in humans, a naturally acquired i