ライフサイエンスコーパス: carditis

1 cterial thrombotic endocarditis or infective carditis.

2 ion with the spirochete results in increased carditis.

3 rial burdens in the heart and increased Lyme carditis.

4 he accumulation of leukocytes in murine Lyme carditis.

5 nd followed the development of arthritis and carditis.

6 ry sequelae, such as Lyme arthritis and Lyme carditis.

7 s in the heart, including the development of carditis.

8 i can result in development of arthritis and carditis.

9 ot abrogate development of Lyme arthritis or carditis.

10 r, it resulted in increased severity of Lyme carditis.

11 ole in the development of Lyme arthritis and carditis.

12 sis, and Sir David Dundas on acute rheumatic carditis.

13 th B cells and T cells but have no effect on carditis.

14 the subsequent development of arthritis and carditis.

15 s of the BNT162b2 vaccine had higher odds of carditis (adjusted odds ratio [OR], 3.57 [CI, 1.93 to 6.

16 Case reports of carditis after BNT162b2 vaccination are accruing worldwi

17 not CD11b-/- mice, developed aggravated Lyme carditis after exposure to B. burgdorferi.

18 to cardiac myosin were similar in rheumatic carditis among a small sample of worldwide populations,

19 cells can promote resolution of murine Lyme carditis and are the first demonstration of a beneficial

20 Antisera to Arp or DbpA induced both carditis and arthritis remission but did not significant

21 Carditis and arthritis was determined by blinded histopa

22 age ankle diameter and histologic scores for carditis and arthritis were significantly higher after 2

23 ve T cells and B cells induced resolution of carditis and arthritis, 3) infected mice reconstituted w

24 elia burgdorferi results in the remission of carditis and arthritis, as well as global reduction of s

25 Infected MyD88(-/-) mice developed carditis and arthritis, similar to the disease in wild-t

26 culation, immunocompetent mice resolved both carditis and arthritis, whereas foci of myocarditis and

27 matory infiltrates during Lyme arthritis and carditis and demonstrate the coexistence of multiple mac

28 the evidence basis for defining subclinical carditis and including it as a major criterion of the Jo

29 nflammatory heart diseases such as rheumatic carditis and myocarditis.

30 be critical for resolution of arthritis and carditis and that protective antibodies are generated du

31 pressed at the lesional level in murine Lyme carditis and to demonstrate a Th1 pattern of cytokine ex

32 cted course of arthritis, a low incidence of carditis, and absence of other major manifestations of a

33 acute rheumatic fever recurrence, changes in carditis, and correlates of mortality after acute rheuma

34 The findings of cardiac mucosa, carditis, and intestinal metaplasia in an endoscopically

35 blood lymphocytes of patients with rheumatic carditis, and mAb 10.2.5, produced from a tonsil, were c

36 to test the hypothesis that cardiac mucosa, carditis, and specialized intestinal metaplasia at an en

37 for C3H mice but did not cause arthritis or carditis, and spirochetes were at low levels or absent i

38 Anemia, thrombocytopenia, hepatitis, carditis, and splenomegaly were noted in all mice during

39 The development of arthritis and carditis, and the resolution of arthritis, were similar

40 Development of Lyme carditis appeared to be independent of modulation by IL-

41 dy-mediated inflammatory arthritis, valvular carditis arises in part because of Fc receptor-mediated

42 Doppler echocardiography in the diagnosis of carditis as a major manifestation of acute rheumatic fev

43 bsolute risk, there is an increased risk for carditis associated with BNT162b2 vaccination.

44 Most decedents already had chronic carditis at initial acute rheumatic fever diagnosis, sug

45 Incident diagnosis of carditis based on the International Classification of Di

46 alysis revealed no change in the severity of carditis between wild-type and IFNgamma-deficient mice a

47 rate ameliorates the severity of murine Lyme carditis by at least two mechanisms.

48 position of inflammatory infiltrates in Lyme carditis by promoting the accumulation of leukocytes ass

49 mportance of monitoring for possible adverse carditis cases when prescribing these drugs.

50 that cross-reactive antibodies in rheumatic carditis cause injury at the endothelium and underlying

51 Fatal Lyme carditis caused by the spirochete Borrelia burgdorferi r

52 yosin, there is no unifying hypothesis about carditis caused globally by many different serotypes.

53 beta2 integrin chain develop aggravated Lyme carditis, compared to that developed by wild-type (WT) m

54 ned disease conditions such as arthritis and carditis differed in severity in mice infected solely wi

55 ntrolling the development of aggravated Lyme carditis, disease induction was analyzed in CD11a-/-, CD

56 inflammation in cardiac epithelium (gastric carditis) have yielded contradictory results, perhaps be

57 Moderate-to-severe carditis (hazard ratio 12.7 [95% CI 3.9-40.9]) and prolo

58 1.02-2.70), and rheumatic fever or rheumatic carditis (HR, 1.75; 95% CI, 1.06-2.89).

59 ercent, aseptic meningitis in 2 percent, and carditis in 0.5 percent.

60 An analysis of rheumatic carditis in a Pacific Islander family confirmed the pres

61 ut was no longer able to cause arthritis and carditis in C3H mice.

62 suggest that the increased severity of Lyme carditis in CD18 hypomorph mice is caused by deficiency

63 rdiac myosin in the development of rheumatic carditis in humans.

64 blockade both prevented and treated valvular carditis in K/B.g7 mice.

65 s hypothesis, we examined the course of Lyme carditis in mice selectively deficient in B cells or alp

66 Arthritis and carditis in mice that had immunizing infections with B.

67 t may be important in the resolution of Lyme carditis in mice.

68 R2 on the development and resolution of Lyme carditis in resistant (C57BL/6J [B6]) and sensitive (C3H

69 he development and severity of arthritis and carditis in the C3H IL-17RA(-/-) mice were similar to wh

70 he controversy regarding the role of gastric carditis in the development of metaplasia and neoplasia

71 degree conduction block associated with Lyme carditis in the United States.

72 The enhancement of Lyme carditis in these mice is characterized by increased mac

73 Lyme carditis is an uncommon manifestation of Lyme disease th

74 The cardiac infiltrate seen in murine Lyme carditis is composed predominantly of macrophages, but s

75 hird-degree heart block associated with Lyme carditis is essential to providing prompt and appropriat

76 can be recurrent or prolonged, whereas Lyme carditis is mostly nonrecurring.

77 A prominent difference between arthritis and carditis is the differential representation of phagocyte

78 PSReA have been reported to have late onset carditis, it is judicious to recommend that patients wit

79 The diagnosis of Lyme carditis (LC), an early disseminated manifestation of Ly

80 he pathogenic antibody response in rheumatic carditis may reflect the conversion of a T-cell-independ

81 ease in certain hosts, such as arthritis and carditis, may be autoimmunity mediated due to molecular

82 This can be followed by symptoms such as carditis, neuritis, meningitis, or arthritis if not trea

83 B. burgdorferi infection can lead to Lyme carditis, neurologic complications, and arthritis becaus

84 e sudden cardiac deaths associated with Lyme carditis occurred from late summer to fall, ages ranged

85 s resolution without affecting the status of carditis or influencing the status of infection, includi

86 as assessed by the genesis of arthritis and carditis or long-term persistence of pathogens in mice o

87 In LD patients with neuroborreliosis, carditis, or arthritis (n = 75), sensitivity was compara

88 GlcNAc/anti-myosin mAb 3.B6 from a rheumatic carditis patient was cytotoxic for human endothelial cel

89 king a subset of MAbs derived from rheumatic carditis patients that bind both myosin and streptococca

90 Incidence of carditis per 100 000 doses of CoronaVac and BNT162b2 adm

91 matic fever recurrence, tabulated changes in carditis, performed Kaplan-Meier survival analyses, and

92 Among 131 (84%) of 156 survivors, one had carditis progression by echo.

93 Carditis regressed in immunocompetent mice and those lac

94 Our results show that carditis regresses in B-cell-deficient B10.A(k) mice but

95 cell-mediated immunity may be important for carditis regression.

96 ted alphabeta T-cell-deficient mice promoted carditis resolution.

97 of IL-10 during infection of arthritis- and carditis-susceptible C3H mice.

98 phages comprise the principal immune cell in carditis, T-cell responses that augment cell-mediated im

99 ts that cardiac myosin epitopes in rheumatic carditis target the S2 region of cardiac myosin and are

100 orreliosis is characterized by arthritis and carditis that are most severe at 2 to 3 wk, then regress

101 eliably produces an infectious arthritis and carditis that peak around 3 weeks postinfection and then

102 burgdorferi, results in acute arthritis and carditis that regress as a result of B. burgdorferi-spec

103 sent in autoimmune myocarditis and rheumatic carditis, the purpose of the current study was to determ

104 T cells modulate the severity of murine Lyme carditis through the action of IFN-gamma, which appears

105 ed infections and with ongoing arthritis and carditis, treatment selectively induced arthritis resolu

106 however, in the developing world, rheumatic carditis, Trypanosoma cruzi, and bacterial infections su

107 velopment of experimental Lyme arthritis and carditis via CXCR2-mediated recruitment of neutrophils i

108 The presence of cardiac epithelium and carditis was associated with deterioration of lower esop

109 In contrast, the resolution of carditis was delayed in CIITA-deficient animals compared

110 Murine Lyme carditis was not affected by either IL-11 or IL-11 antib

111 Development of disease (arthritis and carditis) was attenuated only in the early stage of infe

112 k between infections with GAS and autoimmune carditis, we studied the proliferative responses of PBMC

113 To investigate cardiac injury in borrelia carditis, we used antibody-deficient mice persistently i

114 s of BBA57 in transmission, joint arthritis, carditis, weakening immune responses, and regulating oth

115 c human T cell clones derived from rheumatic carditis were cross-reactive with human cardiac myosin,

116 i spirochetes that do not cause arthritis or carditis were developed and used to investigate Lyme dis

117 The anti-myosin mAbs from rheumatic carditis were found to react with specific peptides from

118 aged 12 years or older first diagnosed with carditis were selected as case patients.

119 All other hospitalized patients without carditis were treated as control participants.

120 itis occurred more commonly in patients with carditis whose sphincter, on manometry, was structurally

121 role of IFNgamma in the development of Lyme carditis, wild-type and IFNgamma-deficient C57BL/6 mice

122 No association between CoronaVac and carditis with a magnitude similar to that for BNT162b2 w

123 tic heart disease, acute rheumatic fever, or carditis with acute rheumatic fever (primary outcomes) w

124 are similar among populations with rheumatic carditis worldwide, regardless of the infecting group A