ライフサイエンスコーパス: genital ulcer

1 of CD14(+) cells expressing CCR5 within the genital ulcer.

2 both secondary bacterial skin infections and genital ulcers.

3 ed sexually and can cause recurrent, painful genital ulcers.

4 by Haemophilus ducreyi in the production of genital ulcers.

5 eptive digital-anal contact, anal warts, and genital ulcers.

6 ion of HSV, H. ducreyi, and T. pallidum from genital ulcers.

7 ficant worldwide pathogen, causing recurrent genital ulcers.

8 sidered in women presenting with acute-onset genital ulcers.

9 1 acquisition and secondary was incidence of genital ulcers.

10 5 and CXCR4) by monocytic cells within human genital ulcers.

11 ins, and other bacteria known to superinfect genital ulcers.

12 esting for HSV when evaluating patients with genital ulcers.

13 49 years old worldwide and causing recurrent genital ulcers.

14 tologic lesions included oral ulcers (100%), genital ulcers (62%), erythema nodosum (46%), and papulo

15 is shed episodically, leading to occasional genital ulcers and efficient transmission.

16 The strong association between genital ulcers and HIV infection in this population high

17 syndromic management will improve healing of genital ulcers and may potentially reduce HIV transmissi

18 How Haemophilus ducreyi, which causes genital ulcers and regional lymphadenitis, interacts wit

19 disease characterized by recurrent oral and genital ulcers and significant organ involvement.

20 To determine the etiology of genital ulcers and to assess the prevalence of human imm

21 ariety of serum specimens from patients with genital ulcers and urethritis and from healthy blood don

22 The annual incidences of genital ulcers and urethritis were 4.2% and 15.5%, respe

23 djustments for other host factors (age, sex, genital ulcer, and index partner's virus load) known to

24 smission (male-to-female or female-to-male), genital ulcers, and carriage of the putative ligand (HLA

25 sexually transmitted infections resulting in genital ulcers, and endemic infectious diseases (e.g., m

26 Syphilitic genital ulcers are cofactors for the bidirectional trans

27 identified unprotected sex with a CSW and a genital ulcer as independent risk factors associated wit

28 erformance of our HD PCR relative to Allplex Genital Ulcer assay (Seegene Inc) using the Cohen's kapp

29 The presence of an active genital ulcer at the time of screening was found in 46 (

30 ve risk 0.53 [0.46-0.62]) and HSV-2 positive genital ulcers by 63% (0.37 [0.31-0.45]) in the aciclovi

31 <0.001) and the occurrence of HSV-2-positive genital ulcers by 73% (risk ratio, 0.27; 95% CI, 0.20 to

32 IV-1 virions can consistently be detected in genital ulcers caused by HSV-2, which suggests that geni

33 We evaluated genital ulcer disease (GUD) and HSV-2-associated GUD at

34 higher virus set point, and the presence of genital ulcer disease (GUD) during the early phase of HI

35 es simplex virus type 2 (HSV-2) shedding and genital ulcer disease (GUD) has not been evaluated.

36 dard laboratory methods for the diagnosis of genital ulcer disease (GUD) in 105 patients; 36% were hu

37 d with cervicovaginal HSV-2 DNA shedding and genital ulcer disease (GUD) in a cohort of women living

38 Viremia was increased with genital ulcer disease (GUD) in both subjects with incide

39 Monocytes recruited to genital ulcer disease (GUD) sites express increased leve

40 ltaneously detects the three major causes of genital ulcer disease (GUD), Haemophilus ducreyi, Trepon

41 uman immunodeficiency virus (HIV) infection, genital ulcer disease (GUD), penile epithelial trauma, m

42 tive men with urethritis and with or without genital ulcer disease (GUD).

43 roid has dramatically declined as a cause of genital ulcer disease (GUD).

44 ; 95% confidence interval [CI], 1.9-8.3) and genital ulcer disease (HRR=2.5; 95% CI, 1.1-5.3).

45 pecimens obtained from 163 patients (96 with genital ulcer disease [GUD]).

46 ates for genital-tract infections (syphilis, genital ulcer disease [GUD], Neisseria gonorrhoeae infec

47 asma HIV-1 RNA levels among, and presence of genital ulcer disease among HIV-1-infected partners and

48 irus type 2, human papillomavirus (HPV), and genital ulcer disease among men, and it reduces HPV, gen

49 HSV-2 infection is a common cause of genital ulcer disease and a significant public health co

50 uld have additional benefits beyond reducing genital ulcer disease and HSV-associated HIV transmissio

51 herpes simplex virus (HSV) type 2-associated genital ulcer disease and lesional HSV shedding.

52 Among 40 consecutive patients with genital ulcer disease and with sufficient sample for bot

53 vir had a smaller effect on the frequency of genital ulcer disease as well as a smaller effect on the

54 chancroid, a sexually transmitted cutaneous genital ulcer disease associated with increased heterose

55 Measuring incidence density in the genital ulcer disease cases directly gave the highest es

56 reening), and a cohort study of seronegative genital ulcer disease cases were compared.

57 us lesions of the human sexually transmitted genital ulcer disease chancroid are characterized by the

58 i, a Gram-negative bacterium that causes the genital ulcer disease chancroid, activates inflammasomes

59 philus ducreyi, the etiological agent of the genital ulcer disease chancroid, binds extracellular mat

60 etiologic agent of the sexually transmitted genital ulcer disease chancroid, has been shown to assoc

61 Haemophilus ducreyi, which causes the genital ulcer disease chancroid, requires high basal lev

62 i is a hemin-requiring bacterium causing the genital ulcer disease chancroid.

63 etiologic agent of the sexually transmitted genital ulcer disease chancroid.

64 tive obligate human pathogen that causes the genital ulcer disease chancroid.

65 Genital ulcer disease has been epidemiologically linked

66 eyi causes chancroid, a sexually transmitted genital ulcer disease implicated in increased heterosexu

67 on an increasingly important role in causing genital ulcer disease in addition to being the primary n

68 ed diseases and are the most common cause of genital ulcer disease in the United States.

69 Haemophilus ducreyi causes chancroid, a genital ulcer disease that facilitates the transmission

70 c agent of chancroid, a sexually transmitted genital ulcer disease that facilitates the transmission

71 es simplex virus is the most common cause of genital ulcer disease worldwide.

72 on, and only at the STI clinic were marital, genital ulcer disease, and HIV-infection status associat

73 Sexually transmitted diseases, genital ulcer disease, and progesterone therapy increase

74 h and without sexually transmitted diseases, genital ulcer disease, and progesterone-predominant cond

75 d with increased risk of HIV-1 infection and genital ulcer disease, and these effects remained after

76 s who had an AIDS-defining illness or active genital ulcer disease, and those that were taking antire

77 - and late-stage infection, higher HIV load, genital ulcer disease, and younger age of the index part

78 ulcer disease among men, and it reduces HPV, genital ulcer disease, bacterial vaginosis, and trichomo

79 eople by reducing the prevalence of herpetic genital ulcer disease, but could also have an additional

80 to assess the possible benefits of treating genital ulcer disease, chorioamnionitis, mastitis, and m

81 ducreyi, the etiologic agent of chancroid, a genital ulcer disease, produces a cell-associated hemoly

82 Transmission of HIV was associated with genital ulcer disease, syphilis, and vaginal or penile d

83 In multivariate models, vulvitis, genital ulcer disease, vaginal discharge, and Candida va

84 Haemophilus ducreyi causes chancroid, a genital ulcer disease.

85 uction contributing to the pathogenesis of a genital ulcer disease.

86 creyi is the etiologic agent of chancroid, a genital ulcer disease.

87 c agent of chancroid, a sexually transmitted genital ulcer disease.

88 HSV-2) infection is the most common cause of genital ulcer disease.

89 mples from patients with chancroid and other genital ulcer diseases and from normal subjects containe

90 ubjects and patients with chancroid or other genital ulcer diseases contained antibodies to purified

91 emophilus ducreyi, is one of the most common genital ulcer diseases in developing countries.

92 ter and a 73% reduction in the occurrence of genital ulcers due to HSV-2.

93 or seroconversion during follow-up, reported genital ulcer, history of STD, and number of sex partner

94 l vaginosis (HR, 2.1), and the occurrence of genital ulcers (HR, 2.7).

95 In addition to recurrent genital ulcers, HSV-2 causes neonatal herpes, and it is

96 r vaginal discharge, urethral discharge, and genital ulcer in sub-Saharan Africa (SSA).

97 eased the incidence of extrapulmonary TB and genital ulcers in HIV-negative patients.

98 used PCR assays to determine the etiology of genital ulcers in patients presenting to a sexually tran

99 3 times daily) was conducted among men with genital ulcers in South Africa.

100 ulation highlights the urgency of preventing genital ulcers in the southern United States.

101 easured the microbial community structure of genital ulcers in women.

102 mplicating interpretation of the role of the genital ulcer itself in the infectiousness of HIV.

103 ood of early HIV infection the most included genital ulcers (LR, 5.4; 95% CI, 2.5-12), weight loss (L

104 V-2 infection are needed, particularly since genital ulcers may facilitate the transmission of the hu

105 virus 2 (HSV-2) is the most common cause of genital ulcers, no study has systematically evaluated th

106 Incidence of genital ulcers on examination was reduced by 47% (relati

107 Genital ulcer or whole blood specimens from patients wit

108 V disease stage, antiretroviral regimen, and genital ulcers or cervical tenderness.

109 scores indicating worse pain), the number of genital ulcers, overall disease activity, and quality of

110 iral load correlates with the development of genital ulcers, shedding also commonly occurs even when

111 lent in some US cities and that persons with genital ulcers should be a focus of HIV prevention activ

112 In Madagascar, primary care of genital ulcers should include syndromic treatment for sy

113 virus (HSV) type 2, the most common cause of genital ulcers, should be evaluated as a strategy for HI

114 We tested 112 genital ulcer specimens by the polA PCR, obtaining a sen

115 V DNA were detected in 56, 15, and 13% of 39 genital ulcer specimens, respectively, and H. ducreyi DN

116 oligonucleotides in a microwell format, 298 genital ulcer swab specimens collected in New Orleans du

117 lso had reduced risks of HSV-2 infection and genital ulcer syndrome in the past 12 months compared wi

118 eria and viruses, including those that cause genital ulcers, tested negative.

119 n agent-based mathematical model of an HSV-2 genital ulcer to integrate mechanistic observations of T

120 partners, herpes simplex virus 2 infection, genital ulcers, Trichomonas vaginalis, vaginitis or cerv

121 In 1994, an apparent outbreak of atypical genital ulcers was noted by clinicians at the sexually t

122 % [95% CI: 15.4% to 30.3%], n = 48); and for genital ulcer were herpes simplex virus type 2 (HSV-2) (

123 ana and the Central African Republic who had genital ulcers were enrolled in a randomized, double-bli

124 variation was substantial, particularly for genital ulcer where HSV-2 replaced chancroid as the prim

125 Genital herpes is the main cause of genital ulcers worldwide; the prevalence of herpes simpl