ライフサイエンスコーパス: abscess formation

1 staphylococcal virulence in mouse models of abscess formation.

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

3 l proliferation and modulating the course of 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 ge volume of gas collection without signs of abscess formation.

9 in mice with varying susceptibility to liver abscess formation.

10 e transcriptase inhibitors (NRTIs) influence abscess formation.

11 art by enhancing neutrophil accumulation and abscess formation.

12 ing bacterial bloodstream infection to drive abscess formation.

13 LR4 (Toll-like receptor 4), are resistant to abscess formation.

14 ral sequential bacterial dacryoadenitis with abscess formation.

15 positively correlates with the frequency of abscess formation.

16 nfluences Ab responses to infection and skin abscess formation.

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

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

19 utaneous nodules that can progress to dermal abscess formation.

20 outcome was the incidence of intra-abdominal abscess formation.

21 equired for staphylococcal dissemination and abscess formation.

22 val in oxygenated tissues prior to anaerobic abscess formation.

23 teomyelitis, septic arthritis and metastatic abscess formation.

24 ed vaccine protection against staphylococcal abscess formation.

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

26 ins most commonly cause skin infections with abscess formation.

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

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

29 of epithelial cell, and murine subcutaneous abscess formation.

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

31 e concurrent infection elsewhere or possible abscess formation.

32 licits chronic infection, resulting in brain abscess formation.

33 onance imaging technology to visualize brain abscess formation.

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

35 modulated the development of intraabdominal abscess formation.

36 This zwitterionic motif is essential for abscess formation.

37 ]), including ulceration (2 of 12 [17%]) and abscess formation (1 of 12 [8%]).

38 mation of renal abscesses but decreased skin abscess formation alongside diminished dermonecrosis.

39 vealed that TLR4 mediates a tradeoff between abscess formation and bacterial clearance.

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

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

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

43 nucleotide biosynthetic operon that promoted abscess formation and colonization, respectively, thereb

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

45 ly essential for surviving tobacco exposure, abscess formation and epithelial invasion was also deter

46 Abscess formation and full-thickness esophageal wall dis

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

48 neficial effect of omentoplasty on presacral abscess formation and perineal wound healing after APR,

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

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

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

52 ysteine concentration significantly enhanced abscess formation and size.

53 r findings define hallmarks of E. coli liver abscess formation and suggest that hyperactivation of th

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

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

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

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

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

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

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

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

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

63 sting that the immune pathways that regulate abscess formation are induced within hours.

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

65 liver resulted in histopathological signs of abscess formation as early as 24 h post-infection.

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

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

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

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

70 Abscess formation associated with intra-abdominal sepsis

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

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

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

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

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

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

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

78 We provide evidence that NRTIs inhibit abscess formation by preventing the tissue necrosis that

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

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

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

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

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

84 ionally essential in multiple environments - abscess formation; epithelial colonization; and cigarett

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

86 E for intestinal wall thickening, stricture, abscess formation, fibrofatty proliferation, and fat ede

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 replication is a key mechanism underpinning abscess formation in hvKp infections.

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

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

111 inase (dCK), mitigates Staphylococcus aureus abscess formation in organ tissues upon invasive bloodst

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

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

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

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

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

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

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

119 cantly associated with the risk of presacral abscess formation in the overall population (RR 1.11; 95

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

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

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

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

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

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

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

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

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

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

130 Abscess formation is not unique to staphylococcal infect

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

132 tely following E. coli inoculation prevented abscess formation, leading to a concomitant 100,000-fold

133 vestigation, to study the pathophysiology of abscess formation, mice were intravenously infected with

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

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

136 1; P = .01) and no differences in fistula or abscess formation or in pouch failure.

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

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

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

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

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

142 The high efficacy of NRTIs in preventing abscess formation suggests that the consequences of reve

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

144 Clinical presentation can vary from abscess formation to pneumonia and sepsis.

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

146 oculation of the organisms and after corneal abscess formation was confirmed.

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

148 Intra-abdominal abscess formation was more common following laparoscopic

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

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

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

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

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

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

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

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

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

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

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

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

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