ライフサイエンスコーパス: vaginal infection

1 cine for efficacy in a BALB/c mouse model of vaginal infection.

2 rm birth rates in a mouse model of ascending vaginal infection.

3 n of TAF and emtricitabine (FTC) can prevent vaginal infection.

4 se rendered recipients more resistant to HSV vaginal infection.

5 the sensors are also minimally induced after vaginal infection.

6 protect against disseminated candidiasis and vaginal infection.

7 imental disseminated candidiasis and Candida vaginal infection.

8 l concentration of oxytetracycline following vaginal infection.

9 ibodies, can help the host to resist Candida vaginal infection.

10 possible source of initial cell contact for vaginal infection.

11 acterial vaginosis (BV) is a common cause of vaginal infection.

12 PTB can be associated with ascending vaginal infection.

13 cacy of a novel regimen to prevent recurrent vaginal infections.

14 ileged eye, however, may differ from skin or vaginal infections.

15 in prevention of diseases that develop from vaginal infections.

16 ually transmitted infections and symptomatic vaginal infections.

17 ion during primary and secondary C. albicans vaginal infections.

18 en observed in experimental Candida albicans vaginal infections.

19 protection or immunopathology during oral or vaginal infections.

20 c factors controlling the immune response to vaginal infections.

21 rtain intestinal and, possibly, treatment of vaginal infections.

22 y lactobacilli have decreased acquisition of vaginal infections.

23 ral treatment administered monthly to reduce vaginal infections among Kenyan women at risk for HIV-1

24 significantly reduced the clinical signs of vaginal infection and effectively decreased animal morta

25 sure to prevent dissemination of HIV-1 after vaginal infection and low-frequency resistance mutations

26 en in vivo in mouse models of N. gonorrhoeae vaginal infection and methicillin-resistant S. aureus sk

27 11,392 women who enrolled in the multicenter Vaginal Infections and Prematurity Study (1984-1989) at

28 he PRA1 gene is strongly up-regulated during vaginal infections and that its expression positively co

29 s play a role in limiting and clearing HSV-2 vaginal infections and that they are, in association wit

30 ch higher for paint applications, influenza, vaginal infections, and ultrasound (reaching, e.g., 4-6)

31 innate resistance by neutrophils against the vaginal infection appear negligible, significant in vitr

32 nt experimental rodent models of C. albicans vaginal infection are used for many applications, the ro

33 Vaginal infections are common and have been associated w

34 Vaginal infections are common, frequently recur, and may

35 w these marked differences in the biology of vaginal infection between these otherwise genetically si

36 Ab B6.1 also protected against C. tropicalis vaginal infection, but MAb B6 did not.

37 tions were significantly less susceptible to vaginal infection by C. glabrata, suggesting a potential

38 nt a dominant host defense mechanism against vaginal infections by Candida albicans.

39 uent contact with HSV-specific T cells after vaginal infection compared with epicutaneous infection.

40 In 394 vaginal infections, cure was 93.5% (95% CI, 90.1%-96.1%;

41 or kidney infections (UTIs) and cervical or vaginal infections (CVIs) during pregnancy, as well as o

42 eudoestrus that were given MAb C3.1 prior to vaginal infection developed fewer vaginal Candida CFU th

43 terval (CI) 1.2-4.0), medical treatments for vaginal infection during pregnancy (OR = 2.4, 95% CI 1.2

44 ficantly elevated odds ratios were noted for vaginal infections during pregnancy (odds ratio (OR) = 2

45 d for the ability to protect against Candida vaginal infection, established by intravaginal (i.vg.) i

46 including breast and gynecological cancers, vaginal infections, fertility, pregnancy and post-menopa

47 f delivery about pregnancy events, including vaginal infections, genital herpes, urinary tract infect

48 sotype of the MAb modulates the outcome of a vaginal infection in a murine model.

49 Bacterial vaginosis (BV) is the most common vaginal infection in reproductive women, which is charac

50 der estrogen-treated conditions, resulted in vaginal infection in rhesus, but not pig-tailed, macaque

51 titative analysis in response to C. albicans vaginal infection in the presence of hormones.Our data s

52 egative women 18-45 years old with 1 or more vaginal infections, including bacterial vaginosis (BV),

53 n conclusion, susceptibility to a chlamydial vaginal infection is dependent on the age of the mice, w

54 vaginal candidiasis are prominent causes of vaginal infections, leading to discomfort and negative p

55 Women without evidence of vaginal infection may exhibit transient changes in their

56 progesterone mediates susceptibility to ZIKV vaginal infection may provide insights into host mechani

57 progesterone mediates susceptibility to ZIKV vaginal infection may provide insights into host mechani

58 Using a vaginal infection model in complement-intact guinea pigs

59 acy against Neisseria gonorrhoeae in a mouse vaginal infection model.

60 orrect in the clinically relevant guinea pig vaginal infection model.

61 DMPA treatment is a key component of mouse vaginal infection models for herpes simplex virus and Ch

62 ne state, which is a common feature of mouse vaginal infection models for other pathogens, through me

63 However, the subcutaneous group resolved the vaginal infection more slowly, with 60% (6 of 10 mice) o

64 ently, biofilms have also been implicated in vaginal infections, notably bacterial vaginosis (BV) and

65 bitor (NNRTI) MIV-150 in carrageenan reduced vaginal infection of macaques with simian immunodeficien

66 Notably, vaginal infection of pregnant dams during early pregnanc

67 To assess the effect of treatment of vaginal infections on vaginal shedding of cell-free huma

68 of vaginal T cells occurred during a primary vaginal infection or during a secondary vaginal infectio

69 stered dose appears to impact SHIV(SF162P3N) vaginal infection outcome in an unexpected manner.

70 om the United States and Kenya with a recent vaginal infection received intravaginal metronidazole 75

71 ers significantly greater protection against vaginal infection than seen in unvaccinated mice (P < .0

72 iii) the partial protection from a secondary vaginal infection under pseudoestrus conditions.

73 ilar, but not identical, fashions and caused vaginal infection; (vi) different switch phenotypes of t

74 Vaginal infection was also more efficient in P2X7R-defic

75 riodic presumptive treatment (PPT) to reduce vaginal infections, we observed a significant reduction

76 riodic presumptive treatment (PPT) to reduce vaginal infections were analyzed to assess the effect of

77 roup (19 [23%] vs three [4%], p=0.0005), but vaginal infections were less common (one [1%] vs eight [

78 mary vaginal infection or during a secondary vaginal infection where partial protection was observed.

79 Thus humanized mouse models of HIV vaginal infection will allow the study of the mechanisms

80 ct a substantial proportion of macaques from vaginal infection with a CCR5-using virus (SHIV-162P3).

81 Kinetic analyses of vaginal infection with C. albicans in C57BL/6 mice demon

82 ory lymphocyte clusters within the FRT after vaginal infection with Chlamydia Despite robust establis

83 mounted effective immune responses following vaginal infection with Chlamydia trachomatis.

84 Vaginal infection with either HSV-1 or HSV-2 was blocked

85 ns of macaque CCR5 could prevent or suppress vaginal infection with highly virulent SIVmac251.

86 When challenged by vaginal infection with HSV-2, the DNA-immunized animals

87 Vaginal infection with the mouse pneumonitis agent of Ch

88 A Th1-type response develops following vaginal infection with the mouse pneumonitis biovar of C

89 Murine vaginal infection with the obligate intracellular bacter

90 Women with bacterial vaginosis have complex vaginal infections with many newly recognized species, i