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1 macaques have a cyclical pattern of changing cervicovaginal Ab and immunoglobulin levels that is simi
2 S) in utero develop abnormalities, including cervicovaginal adenosis that can lead to cancer.
3                     Five hundred consecutive cervicovaginal and anorectal specimens submitted for GBS
4 ted atazanavir (ATV) underwent serial paired cervicovaginal and plasma sampling for antiretroviral co
5 p cultures of human tonsils, lymph nodes and cervicovaginal and rectosigmoid tissues, including proto
6  screened for cervicovaginal HSV-2 DNA, GUD, cervicovaginal and systemic HIV-1 RNA, and reproductive
7 collected daily genital swabs of the vulvar, cervicovaginal, and perianal areas for HSV culture, main
8                                  Humoral and cervicovaginal antibodies reacting to MgpB were induced
9 different HPV serotypes induced 10-fold more cervicovaginal antigen-specific CD8+ T cells than primin
10                                              Cervicovaginal bacteria modulate genital inflammation; h
11 virions initially bind preferentially to the cervicovaginal basement membrane (BM) at sites of trauma
12 atforms for inducing durable intraepithelial cervicovaginal CD8+ T cell responses by promoting local
13 ectively, were cloned and characterized from cervicovaginal cells by use of an overlapping PCR method
14                                   Exfoliated cervicovaginal cells from 19 of 54 animals tested positi
15 ages of HPV16 were cloned and sequenced from cervicovaginal cells.
16            Using a recently developed murine cervicovaginal challenge model, we evaluated the importa
17 to gonococcal infection in a murine model of cervicovaginal colonization and identified MisR-regulate
18 ssue drug exposure through modulation of the cervicovaginal, colorectal, or immune cell transporters.
19 cases, the frequency of this response in the cervicovaginal compartment far exceeded the frequency in
20                                              Cervicovaginal cytokine concentrations did not differ be
21  well as results from in vitro activation of cervicovaginal epithelial cells and U1/HIV promonocytic
22                                However, some cervicovaginal epithelial cells failed to express p63, r
23 bitory effect of DES was transient, and most cervicovaginal epithelial cells recovered expression of
24  and that conditioned medium from GC-exposed cervicovaginal epithelial cells with elevated levels of
25         Here we report interactions of human cervicovaginal epithelial cells with the most abundant c
26                            In p63(-/-) mice, cervicovaginal epithelium differentiated into uterine ep
27 epithelium of the progesterone group and the cervicovaginal epithelium of the combination group.
28 tal day 1 to 5 inhibited induction of p63 in cervicovaginal epithelium via epithelial ERalpha.
29 ar cell-associated blood HIV-1 DNA load, and cervicovaginal fluid (CVF) HIV-1 DNA load were determine
30        Anti-MVA IgG and IgA were detected in cervicovaginal fluid after a second vaccine dose.
31    Appropriate clinical sampling devices for cervicovaginal fluid collection would help physicians de
32 ed to develop an effective device to collect cervicovaginal fluid from women with symptoms of endomet
33                                              Cervicovaginal fluid plays an important role in the dete
34               The estimated median volume of cervicovaginal fluid was 0.51 ml (interquartile range, 0
35 llected for measuring the HIV-1 RNA level in cervicovaginal fluid, phosphate-buffered saline containi
36 ion stimulated by HLA antigens in seminal or cervicovaginal fluid.
37  inner cotton portion was designed to absorb cervicovaginal fluid.
38 ssfully used the developed device to collect cervicovaginal fluid.
39           ADCC antibodies are present in the cervicovaginal fluids, which indicates that this form of
40 ells, isolated immune cells, and analyses of cervicovaginal fluids.
41                                      Rather, cervicovaginal HA plays an unanticipated important role
42             They are active ex vivo in human cervicovaginal histocultures infected by HSV-2 and in vi
43 clovir had little impact on (1) detection of cervicovaginal HIV-1 RNA (risk ratio [RR], 0.96; 95% con
44                                              Cervicovaginal HIV-1 RNA and herpes simplex virus type 2
45 0.8-1.2) at day 7 of treatment, (2) the mean cervicovaginal HIV-1 RNA load (-0.06 log(10) copies/mL;
46                        Here, we evaluate for cervicovaginal HIV-neutralizing IgA responses in genital
47  16 IgA was associated with sexual behavior, cervicovaginal HPV 16 DNA, and cytological abnormalities
48 women, previously tested for the presence of cervicovaginal HPV DNA, were analyzed.
49 evels (continuous and categorical forms) and cervicovaginal HPV infection (due to high-risk HPV or va
50  have been shown to be at increased risk for cervicovaginal HPV infection and CIN, and cervical cance
51 total of 2353 sexually active women for whom cervicovaginal HPV infection status and serum 25-hydroxy
52 clinical serum samples from women with known cervicovaginal HPV infection status.
53                                              Cervicovaginal HPV prevalence is associated with less-th
54 e most sensitive method for the detection of cervicovaginal HPV.
55     The seroprevalences of IgG in women with cervicovaginal HPV16, HPV16-related types, and other HPV
56 nal HIV-1 RNA (RR, 0.70; 95% CI, 0.4-1.2) or cervicovaginal HSV-2 DNA (RR, 0.69; 95% CI, 0.4-1.3), ha
57 c therapy for herpes reduced the quantity of cervicovaginal HSV-2 DNA and slightly improved ulcer hea
58  study was to assess factors associated with cervicovaginal HSV-2 DNA shedding and genital ulcer dise
59                                              Cervicovaginal HSV-2 DNA was detected in 42% of women (9
60               Participants were screened for cervicovaginal HSV-2 DNA, GUD, cervicovaginal and system
61 RT is strongly associated with a decrease in cervicovaginal HSV-2 shedding, and the impact was sustai
62 ious diseases; however, its association with cervicovaginal human papillomavirus (HPV) infection has
63                             Risk factors for cervicovaginal human papillomavirus (HPV) infection were
64  submicromolar range in ex vivo lymphoid and cervicovaginal human tissues and at 3-12 micromol/L in C
65                                 We evaluated cervicovaginal IgA in Partners PrEP Study participants u
66         The relationship between vaccine and cervicovaginal IgG achieved significance (odds ratio [OR
67 y concentration required for protection from cervicovaginal infection is comparable to that required
68 e report the development of a mouse model of cervicovaginal infection with HPV16 that recapitulates t
69 ciation was lost after adjustment for HPV 16 cervicovaginal infection.
70 oncomitant lower genital-tract infections on cervicovaginal inflammatory cells was assessed in 967 wo
71  age, and race have an independent effect on cervicovaginal inflammatory cells.
72 votella bivia) were strongly associated with cervicovaginal inflammatory cytokines, but not with alte
73 helium to be columnar (uterine) or squamous (cervicovaginal) is determined by mesenchymal induction d
74 , respiratory syncytial virus (RSV) M/M2, in cervicovaginal keratinocytes.
75           Twenty-four couples were enrolled; cervicovaginal lavage (CVL) and tissue were collected 2
76 ducted to analyze the presence of HCV RNA in cervicovaginal lavage (CVL) fluid from 71 women (58 HCV/
77 ty (CMI) was evaluated for the first time in cervicovaginal lavage (CVL) fluid from RVVC patients.
78 sence of a heat-stable soluble factor in the cervicovaginal lavage (CVL) fluid of both HIV-infected a
79                                              Cervicovaginal lavage (CVL) fluid was evaluated for tota
80 ory cytokine concentrations were measured in cervicovaginal lavage (CVL) from 49 women 6, 17, 30, and
81 igned to determine the antiviral activity in cervicovaginal lavage (CVL) samples collected after intr
82 tic cells secreted TNF- alpha in response to cervicovaginal lavage (CVL) samples from women with BV.
83 ng into the genital tract, paired plasma and cervicovaginal lavage (CVL) samples were obtained from 1
84                                              Cervicovaginal lavage (CVL) samples were obtained from 2
85 nerella vaginalis, and Mycoplasma hominis in cervicovaginal lavage (CVL) samples were quantified by p
86 he Women's Interagency HIV Study contributed cervicovaginal lavage (CVL) samples.
87 pothesis-generating study, 17 women provided cervicovaginal lavage (CVL) specimens at baseline (all h
88 irus (CMV) was studied in blood, saliva, and cervicovaginal lavage (CVL) specimens from 33 HIV-1-infe
89 Abbott RealTime HIV-1 assay using plasma and cervicovaginal lavage (CVL) specimens.
90 formalin-fixed-tissue specimens collected by cervicovaginal lavage (CVL) within 90 days of each other
91                                              Cervicovaginal lavage and plasma from 122 HIV-uninfected
92 ysis of 16S ribosomal RNA gene sequencing of cervicovaginal lavage clustered each participant visit i
93 in plasma, female reproductive tract tissue, cervicovaginal lavage fluid and its intracellular metabo
94  and innate resistance) was also detected in cervicovaginal lavage fluid from both species.
95 rrent quantified HIV-1 RNA concentrations in cervicovaginal lavage fluid in 301 women infected with t
96                                      Testing cervicovaginal lavage fluids for >40 HPV genotypes using
97 p160-specific IgA responses were detected in cervicovaginal lavage fluids in 6 of 13 HEPS CSWs but 0
98 nd prevalence of human papillomavirus DNA in cervicovaginal lavage fluids were all >50% and were 2-30
99  endocervical swabs were more sensitive than cervicovaginal lavage for HIV-1 RNA detection by PCR but
100 d in the plasma of 2 women and in at least 1 cervicovaginal lavage sample from all 6 women.
101                                              Cervicovaginal lavage samples (n = 19) were collected, c
102 s and proviral DNA in cervical, vaginal, and cervicovaginal lavage samples by polymerase chain reacti
103 + (GP+-PCR), for the detection of HPV DNA in cervicovaginal lavage samples from 208 women.
104 nerella vaginalis, and Mycoplasma hominis in cervicovaginal lavage samples were quantified by PCR.
105                         In an analysis of 95 cervicovaginal lavage samples, we found that 12 (12.6%)
106 ens from endocervical canal wick and most in cervicovaginal lavage samples.
107 5) ng/mL)] and ex vivo antiviral activity of cervicovaginal lavage samples.
108                                              Cervicovaginal lavage sequencing (n = 109) resulted in a
109 ty-two cytokines were measured by Luminex in cervicovaginal lavage specimens at enrollment.
110 al neoplasia grade 3 and cancer (CIN3+) with cervicovaginal lavage specimens collected at enrollment
111                                              Cervicovaginal lavage specimens from enrollment were tes
112 NA testing were conducted annually in serial cervicovaginal lavage specimens obtained over 8-10 years
113 land (of whom 184 were HIV+), provided 1,426 cervicovaginal lavage specimens tested for HPV DNA by a
114                                    Antenatal cervicovaginal lavage specimens were assessed for HIV-1
115                                              Cervicovaginal lavage specimens were collected from each
116                                         When cervicovaginal lavage specimens, the reverse line-blot a
117 09/11 system was evaluated with a set of 262 cervicovaginal lavage specimens.
118  were used to characterize HPV-16-containing cervicovaginal lavage specimens.
119 w ProTalpha variants from CD8(+) T cells and cervicovaginal lavage with potent anti-HIV-1 activity.
120   Schistosoma PCR was done on urine, biopsy, cervicovaginal lavage, and genital mucosal surface speci
121                                    Gingival, cervicovaginal lavage, and plasma specimens were collect
122  wicks should be considered as an adjunct to cervicovaginal lavage, to improve the sensitivity and pr
123 py and tests for human papillomavirus DNA in cervicovaginal lavage-for a median follow-up of 3.2 year
124 shes and from the ectocervix and vagina with cervicovaginal lavage.
125   HSV-2 DNA and HIV-1 RNA were quantified in cervicovaginal lavage.
126 t lifestyle and sexual behavior and obtained cervicovaginal-lavage samples for the detection of HPV D
127 y, and inflammatory cells were quantified in cervicovaginal lavages (CVLs) of 24 women enrolled in th
128                                              Cervicovaginal lavages collected from 19,512 women atten
129 L-10 were measured prior to HIV infection in cervicovaginal lavages from 58 HIV seroconverters and 58
130  tryptophan, indole, and IFN-gamma levels in cervicovaginal lavages from women with either naturally
131  [RLU/PC]) using Hybrid Capture 2 testing of cervicovaginal lavages obtained at enrolment.
132 munoglobulins G and A and some antibodies in cervicovaginal lavages varied with the stages of the men
133 ADCC mediated by antibodies present in sera, cervicovaginal lavages, and breast milk from HIV-1-infec
134 blot analysis, secreted HD-5 was detected in cervicovaginal lavages, with the highest concentrations
135 [P=.01]) but was weakened by the presence of cervicovaginal leukocytes.
136                                              Cervicovaginal mesenchyme induced p63 in Mullerian duct
137    These studies suggest that members of the cervicovaginal microbiome can modify N. gonorrhoeae, whi
138        Increasing evidence suggests that the cervicovaginal microbiota (CVM) plays an important role
139      Our study proposes a mechanism by which cervicovaginal microbiota impact genital inflammation an
140                                          The cervicovaginal microbiota of 51 participants were compos
141                  We molecularly assessed the cervicovaginal microbiota over time in human immunodefic
142 is consistent with hypotheses that the local cervicovaginal milieu plays a role in susceptibility to
143 ed CD8+ T cell responses in the female mouse cervicovaginal mucosa after intravaginal immunization wi
144 duction of innate antiviral responses in the cervicovaginal mucosa by topical application of TLR agon
145                                   The intact cervicovaginal mucosa is a relative barrier to the sexua
146 nd other antiviral effector molecules in the cervicovaginal mucosa of treated animals.
147      Soluble factors from CD8(+) T cells and cervicovaginal mucosa of women are recognized as importa
148  the primed CD8+ T cells proliferated in the cervicovaginal mucosa upon HPV intravaginal boost.
149 ts for SIV were in the lamina propria of the cervicovaginal mucosa, immediately subjacent to the epit
150 ss the HIV-1 coreceptor CCR5 in normal human cervicovaginal mucosa, whereas all three cell types expr
151 d proinflammatory cytokine expression in the cervicovaginal mucosa.
152 after a single atraumatic application to the cervicovaginal mucosa.
153 fibers (pore sizes) in fresh undiluted human cervicovaginal mucus (CVM) obtained from volunteers with
154                   Here, we report that human cervicovaginal mucus (CVM), obtained from donors with no
155 tibodies (Ab) can trap individual virions in cervicovaginal mucus (CVM), thereby reducing infection i
156                     In fresh undiluted human cervicovaginal mucus (CVM), which has a bulk viscosity a
157 coelastic human mucus, such as non-ovulatory cervicovaginal mucus, at a significant rate.
158 (PLGA) nanoparticles rapidly penetrate human cervicovaginal mucus, whereas PLGA nanoparticles coated
159 urface chemistries in samples of fresh human cervicovaginal mucus.
160 he transport of nanoparticles in fresh human cervicovaginal mucus.
161                      We have developed human cervicovaginal organ culture systems to examine the init
162                                              Cervicovaginal:plasma antiretroviral concentration ratio
163 sterdam, the Netherlands, and analyzed their cervicovaginal samples and clinical data.
164 tration and viscoelastic properties of these cervicovaginal samples are similar to those in many othe
165 ith suppressed plasma virus loads, blood and cervicovaginal samples collected twice weekly for 3 week
166 ction by cervical cytology and self-obtained cervicovaginal samples for up to 27 months, and for vacc
167                                All underwent cervicovaginal sampling and Pap testing at regular inter
168                           Subjects underwent cervicovaginal sampling and Pap testing on day 1 and the
169 l collection device and medium were used for cervicovaginal sampling.
170 nce of human immunodeficiency virus (HIV) in cervicovaginal secretions (CVS) may be a risk factor for
171 ted with human CD4+ cells that are shed into cervicovaginal secretions (CVS).
172                                              Cervicovaginal secretions and endocervical cells were co
173 nuclear cells and SIV-specific antibodies in cervicovaginal secretions at the time of challenge was a
174             These findings are evidence that cervicovaginal secretions contribute to innate resistanc
175                                              Cervicovaginal secretions from 86 Kenyan women, includin
176 rving the innate antiviral activity found in cervicovaginal secretions is critical.
177 specific antibodies were not detected in the cervicovaginal secretions of 10 STV monkeys examined.
178 ections have levels of sialidases present in cervicovaginal secretions that can result in desialylati
179 e cervix and assays for fetal fibronectin in cervicovaginal secretions, also had low sensitivity and
180 ysis of molecular and cellular components in cervicovaginal secretions, as well as results from in vi
181 ular, as well as other bodily fluids such as cervicovaginal secretions, could increase oral transmiss
182 IgA and IgG Abs in mucosal secretions (e.g., cervicovaginal secretions, rectal washes, and saliva) an
183 eutralizing antibodies also were observed in cervicovaginal secretions.
184                                              Cervicovaginal shedding was detected in 8 (4.4%) CMV-pos
185                                    Depressed cervicovaginal SLPI levels have been correlated with bot
186 ews; physical examination; blood, urine, and cervicovaginal specimen collection and repository; labor
187                                     For both cervicovaginal specimens (clinician collected and self-c
188 tween clinician-collected and self-collected cervicovaginal specimens (P > 0.01 for all comparisons).
189 zed HPV DNA types detected in self-collected cervicovaginal specimens and demographic, sexual behavio
190 ecovered throughout the 8-week experiment in cervicovaginal specimens and up to 2 weeks postinfection
191 ssays by each method were performed with 596 cervicovaginal specimens collected from participants in
192 d HSV-2 present in more than 60,000 clinical cervicovaginal specimens derived from samples originatin
193                          Thus, use of HC2 on cervicovaginal specimens for screening could result in f
194 eptible leukocytes on female genital mucosa, cervicovaginal specimens from 32 HIV-negative STD clinic
195                Using data and self-collected cervicovaginal specimens from 4150 females, 14-59 years
196  of carcinogenic human papillomavirus DNA in cervicovaginal specimens self-collected using a novel de
197 cervicovaginal specimens, and self-collected cervicovaginal specimens taken at home.
198 cted cervical specimens, clinician-collected cervicovaginal specimens, and self-collected cervicovagi
199              Thirty-eight women provided 275 cervicovaginal specimens.
200  determined by the Linear Array HPV Assay in cervicovaginal swab samples from females aged 14-59 year
201  females aged 14-59 years who self-collected cervicovaginal swab specimens.
202 dida species-specific PCR tests performed on cervicovaginal swabs over a 4-year period demonstrated c
203                                              Cervicovaginal swabs, which were used to measure bacteri
204  CCR5 expression, and cytokine production of cervicovaginal T cells in up to 16 donors.
205                                      Using a cervicovaginal tissue culture system, we found that expr
206 cells and macrophages in vitro, in polarized cervicovaginal tissue explants, and in the female genita
207 by examining mononuclear cells obtained from cervicovaginal tissue, the mechanisms whereby HIV type 1
208 integration in organotypic cultures of human cervicovaginal tissue.
209            We documented robust responses in cervicovaginal tissues and uterus, but only several days
210 osal barrier greatly limits the infection of cervicovaginal tissues, and thus the initial founder pop
211 els of GBS interaction with the human female cervicovaginal tract using human vaginal and cervical ep
212 ces of the respiratory, gastrointestinal and cervicovaginal tracts to efficiently reach the underlyin
213 mucosal surfaces of the gastrointestinal and cervicovaginal tracts, both of which are normally coated
214 ls of viral entry in the gastrointestinal or cervicovaginal tracts.
215 y switch for Mullerian duct epithelium to be cervicovaginal versus uterine.
216         Intravaginal HPV prime/boost reduced cervicovaginal viral titers 1,000-fold after intravagina

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