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1 as infiltrating lymphocytes were seen in the endocervix.
2 lations in the transition zone and adjoining endocervix.
3 the response to acute infection in the human endocervix.
4 positing Chlamydia muridarum directly on the endocervix.
5 tween the lower uterine corpus and the upper endocervix.
6 rachomatis and N. gonorrhoeae, respectively, endocervix, 65 and 40%; urine, 72 and 24%; and vagina, 8
8 erized a human genital mucosa explant model (endocervix and ectocervix/vagina) to mimic genital herpe
9 e normally simple columnar epithelium of the endocervix and uterine cavity were monitored by keratin
10 and in women, cells from the ectocervix and endocervix are among the first host cells encountered by
11 s and fibroblasts from the endometrium (EM), endocervix (CX) and ectocervix (ECX) significantly delay
12 inct epithelial cell lines from normal human endocervix, ectocervix, and vagina to characterize gonoc
13 the RT (Fallopian tube, uterine endometrium, endocervix, ectocervix, and vaginal mucosa) and temporal
14 opian tube, but variably expressed by normal endocervix, endometrium, and fallopian tube (60, 64, and
16 ed from normal human vagina, ectocervix, and endocervix expressed mRNA for TLR1, -2, -3, -5, and -6.
18 l to initiate a synchronous infection in the endocervix in the first 24 h to evaluate the sequential
20 a higher level of acute inflammation in the endocervix, oviduct, and mesosalpingeal tissues than in
21 sult from ascension of the bacteria from the endocervix to the oviduct, where an overly aggressive in
22 genital tract disease that ascended from the endocervix to the uterine horns, oviducts, and ovaries i
23 epithelial layers of the vagina, ectocervix, endocervix, uterus, and fallopian tubes in the female re
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