ライフサイエンスコーパス: genital

1 concordant CIS-CIS RRs were 2.74 for female genital, 1.77 for cervical and 2.29 for SCC skin CISs.

2 hat are characterized by orofacial, skin and genital abnormalities result when this axis goes awry.

3 choanae, Retardation of growth/development, Genital abnormalities, and Ear anomalies) syndrome, in w

4 sed on gender role or expression rather than genital anatomy.

5 fectiveness of HPV-16/18 vaccination against genital and anal infections.

6 Risk for these genital and anal SPCs are high and a follow-up plan shou

7 anogenital (cervical, other female and male genital and anal) and skin squamous cell CIS; additional

8 F3B1 mutations occur more commonly in female genital and anorectal melanomas and CTNNB1 mutations imp

9 HIV transmission via genital and colorectal mucosa are the most common routes

10 rium that can be associated with a number of genital and extragenital conditions.

11 Three-site genital and extragenital screening for Mycoplasma genita

12 e retention, as well as the concentration of genital and intestinal cytokines.

13 cell (DC) subsets are abundantly present in genital and intestinal mucosal tissue and are among the

14 A striking difference between genital and ocular clinical isolates of Chlamydia tracho

15 maviruses (HPVs) are causative agents in ano-genital and oropharyngeal cancers.

16 EP, WT HIV-1 dissemination was delayed until genital and plasma RPV concentrations waned.

17 IV-1 dissemination in infected animals until genital and plasma RPV concentrations waned.

18 C/FTC/TAF led to rapid decay of HIV-1 RNA in genital and rectal fluids.

19 However, the relationship between genital and subjective arousal might not be relevant to

20 esults showed that bisexual-identified men's genital and subjective arousal patterns were more bisexu

21 Additionally, liver, spleen, genital, and brain imidacloprid concentrations were dete

22 ility, epilepsy, ptosis, hypothyroidism, and genital anomalies, we uncovered bi-allelic variants in U

23 ts, Duane anomaly), and ocular, cardiac, and genital anomalies.

24 inal vesicles may accompany other urinary or genital anomalies.

25 ant association between use of powder in the genital area and incident ovarian cancer.

26 he relationship between use of powder in the genital area and ovarian cancer is not established.

27 ssociation between ever use of powder in the genital area and ovarian cancer risk among women with a

28 ssociation between ever use of powder in the genital area and self-reported incident ovarian cancer.

29 and frequent (>=1/week) use of powder in the genital area.

30 with 38% self-reporting use of powder in the genital area.

31 l arousal in women comprises two components: genital arousal and subjective arousal.

32 For some women, genital arousal enhances subjective arousal; for others,

33 arousal, and only some women with decreased genital arousal have low subjective arousal.

34 Genital arousal is characterized by genital vasocongesti

35 eport sexual arousal problems have decreased genital arousal, and only some women with decreased geni

36 Patterns of physiological (genital) arousal to male and female erotic stimuli can p

37 Our results suggest that highly prevalent genital bacteria increase HIV risk by inducing mucosal H

38 nt basal cell carcinoma of the skin and male genital cancer were associated with significantly increa

39 The results showed that these genital cancers might run in families and as SPCs are as

40 BV treatment reduced genital CD4+ T-cell HIV susceptibility and IL-1 levels,

41 -pull-amplify approach elicited systemic and genital CD8(+) T cell responses against high-risk human

42 mportance of local Ag presentation to elicit genital CD8(+) T(RM) provides a rationale to develop nov

43 rentiation of cognate CD8(+) T(RM) Secondary genital CD8(+) T(RM) were induced in the absence of CD4(

44 Genital cell remodeling by HIV includes downregulating T

45 Following a genital challenge (as determined by number of mice with

46 CD8-mediated protection to a vaccinia virus genital challenge.

47 cillus iners substantially increased several genital chemokines associated with HIV acquisition, incl

48 IL-1 levels, but dramatically increased the genital chemokines that may enhance HIV susceptibility;

49 e incidence, and to date no vaccines against genital chlamydia have been tested in clinical trials.

50 Genital chlamydia infection in women causes complication

51 Human genital Chlamydia infection is a major public health con

52 nt contributions of caspase-1 and -11 during genital Chlamydia infection.

53 ay in chlamydial spreading caused by FTY720, genital Chlamydia is able to both spread to the gastroin

54 Thus, genital Chlamydia is able to launch a 2nd wave of spread

55 ontributes to oviduct pathology during mouse genital Chlamydia muridarum infection.

56 Since genital Chlamydia spreading to the gastrointestinal trac

57 nal microbiota in a cohort of 149 women with genital Chlamydia trachomatis infection at baseline who

58 Genital Chlamydia trachomatis infections in women typica

59 The reproductive system complications of genital chlamydial infection include fallopian tube fibr

60 and tubal factor infertility resulting from genital chlamydial infection.

61 Interview with Patricia Brennan, who studies genital co-evolution and sexual conflict in vertebrates

62 at the HIV RNA populations emerging from the genital compartment after ART interruption might not be

63 Future research should evaluate whether the genital compartment might contribute to viral rebound in

64 Future research should evaluate whether the genital compartment might contribute to viral rebound in

65 The genital concentration of CCL2 was the best marker to dis

66 n to stabilised paired flight and subsequent genital contact.

67 To study the evolution of genital cortex we flattened cortical hemispheres and ass

68 ress this issue by a comparative analysis of genital cortex.

69 l from those who are not mentally aroused by genital cues.

70 ed any dose of study drug and had a positive genital culture for N gonorrhoeae at baseline.

71 With female genital cutting as a motivating example, we develop empi

72 after 1 month; secondary endpoints included genital cytokine/chemokine levels, cervical immune cell

73 osum, axon pathfinding, cardiac, ocular, and genital defects).

74 smoking in utero was associated with earlier genital development (Tanner 2, -1.3 months, 95% confiden

75 lopment not requiring steroids, whereas male genital development required testicular testosterone plu

76 Tanner stages 2 to 5 for pubic hair, breast, genital development, and a combined puberty indicator.

77 rize sites of DNA methylation that influence genital development.

78 tal skin, thereby facilitating male external genital differentiation.

79 Additionally, IL-36gamma(-/-) mice develop genital disease more rapidly, have significantly reduced

80 igen-specific B cells were detected in local genital draining lymph nodes.

81 Emerging evidence shows that genital dysbiosis and/or specific bacteria might have an

82 induced inflammatory cytokine production by genital epithelial cells and produced D-lactate.

83 TAF accumulated inside genital epithelial cells as TFV-DP, the active drug form

84 nhancing the translocation of HIV across the genital epithelium.

85 dual therapy had no detectable HIV in their genital fluid, versus 14/15 (93%) under triple therapy (

86 d its association with decay of HIV-1 RNA in genital fluids and the rectum have not yet been addresse

87 ncreased HIV-RNA and/or -DNA shedding in the genital fluids of people who maintained undetectable pla

88 of participants who had no detectable HIV in genital fluids, both according to each strategy and then

89 years or older with uncomplicated untreated genital gonorrhoea at two sites in Australia and one sit

90 e mechanisms of protection against recurrent genital herpes and promote the tegument RR2 protein as a

91 T(RM) cells in protection against recurrent genital herpes and promotes the RR2-based subunit therap

92 Herpes simplex virus 2 (HSV2) causes genital herpes in >400 million persons worldwide.

93 Here, using genital herpes infection in mice, we show that primary i

94 aginal mucosa and provide protection against genital herpes infection in mice.

95 tablished, these cells protect hosts against genital herpes infection.

96 peutic mucosal vaccines.IMPORTANCE Recurrent genital herpes is one of the most common sexually transm

97 both the severity and frequency of recurrent genital herpes lesions.

98 e mechanisms of protection against recurrent genital herpes remain to be fully elucidated.

99 , eliminating or at least reducing recurrent genital herpes remains a challenge.

100 both the severity and frequency of recurrent genital herpes sores.

101 le candidate Ag to be incorporated in future genital herpes therapeutic mucosal vaccines.IMPORTANCE R

102 ficacy, in the guinea pig model of recurrent genital herpes, of subunit vaccine candidates that were

103 ficacy, in the guinea pig model of recurrent genital herpes, of subunit vaccine candidates that were

104 ced significant protection against recurrent genital herpes.

105 e for a role for IFI16 in protection against genital herpes.

106 to explore relationships between changes in genital hiatus (GH) and development of pelvic organ prol

107 in HIV-uninfected Sm+ Ugandan adult women on genital HIV susceptibility and mucosal and systemic immu

108 nterview and provided biological samples for genital HPV analysis.

109 AFs or age-standardized rates (ASRs) of OPC, genital HPV in healthy women, or tobacco use.

110 refore, we aim to evaluate the prevalence of genital HPV infection among adolescents and young adults

111 ver, the population prevalence data for male genital HPV infection is not well known, while the HPV v

112 dence) of at least one HPV-related endpoint (genital HPV infections, anogenital wart diagnoses, or hi

113 f virus shedding using a guinea pig model of genital HSV-2 infection that recapitulates the shedding

114 Compared with baseline, genital HSV-2 shedding rates immediately after dosing we

115 hould be counseled to recognize the signs of genital human papillomavirus infection.

116 Genital IFN-alpha2a levels are also elevated post-treatm

117 c and mucosal immune activation and elevated genital IL-1alpha levels.

118 innate immune genes was confirmed in an ano-genital immortalized keratinocyte cell line, N/Tert-1.

119 Genital immune activation is suspected to modulate local

120 mpact of oral metronidazole treatment on the genital immune parameters of HIV acquisition risks in Ke

121 Genital immunology is a key determinant of human immunod

122 In the mouse model of genital infection using Chlamydia muridarum, IL-1R signa

123 Pooled prevalence of current genital infection was 3.0% (95% CI 2.3-3.8) in general p

124 Genital infection with herpes simplex virus type 2 (HSV-

125 greater female-to-male (F-M) transmission of genital infection with human papillomavirus (HPV) relati

126 Of the 328 participants who had a genital infection, 151 (98%) of 154 in the ceftriaxone g

127 otentially useful for patients with isolated genital infection, or for patients who are allergic or i

128 Using the Chlamydia muridarum model of genital infection, we demonstrate a protective role for

129 s is a bacterial pathogen causing ocular and genital infections in humans.

130 The proportion of patients with genital infections was greater with empagliflozin than p

131 nalyses and remained independent of elevated genital inflammation and bacterial vaginosis.

132 Bacterial vaginosis (BV) causes genital inflammation and increased HIV acquisition risk.

133 s, one of which was characterized by extreme genital inflammation and persistent bacterial vaginosis

134 his BVAB1-dominated subtype may have chronic genital inflammation due to persistent BV, which may pla

135 ients with features of the CVM, such as high genital inflammation, elevated vaginal pH and dysbiotic

136 ease the HIV risk, although their effects on genital inflammation, particularly HIV-susceptible T-hel

137 increase HIV risk, although their effects on genital inflammation, particularly HIV-susceptible Th17

138 which varied in levels of cancer biomarkers, genital inflammation, vaginal pH and VMB composition.

139 correlated to other biomarkers and linked to genital inflammation.

140 ), one of which was strongly associated with genital inflammation.

141 tory taxa, while CCVR use is associated with genital inflammation.

142 d gram-negative taxa correlated with reduced genital interleukin (IL)-1alpha/beta.

143 To maximize both systemic and genital intraepithelial CD8(+) T cells against vaccine A

144 to some extent, by Lactobacillus iners, the genital Lactobacillus spp. that predominates in African,

145 Recurrent HSV genital lesions are thought to arise from reactivated la

146 humans due to its ability to cause oral and genital lesions, ocular disease, and encephalitis.

147 viral shedding that develops into recurrent genital lesions.

148 ssue sarcoma; ovarian; bladder; other female genital; leukaemia; and head and neck cancer.

149 ted splenocytes, intestinal lymphocytes, and genital lymphocytes as well as serum and intestinal lumi

150 st that couples-level joint consideration of genital microbiome and STI or related outcomes could lea

151 lateralized behavior may have coevolved with genital morphology, we quantified the shape of female an

152 fic effector T cells from circulation to the genital mucosa via topical vaginal application of chemok

153 chomatis targets epithelial cells lining the genital mucosa.

154 ficacy of DC-based vaccination to the female genital mucosa.

155 d induce homing to the intestinal and female genital mucosae.

156 immediate events following viral exposure at genital mucosal sites that lead to selection of specific

157 t are not fully characterized, especially in genital mucosal tissues (the main HIV-1 entry portal on

158 experienced by women having undergone female genital mutilation/cutting (FGM/C) are a source of growi

159 inhibitors include euglycemic ketoacidosis, genital mycotic infections, and volume depletion.

160 Diarrhea, genital mycotic infections, volume depletion, and diabet

161 e proportion of patients with eradication of genital N gonorrhoeae based on culture at test of cure,

162 f quantification, HIV RNA can be detected in genital or rectal secretions, termed discordant shedding

163 We extracted all measures of current (genital or rectal), recent, and ever infection with C tr

164 the genitals were negatively correlated with genital organ weight and, 5) behavioral observations ind

165 ng evolutionary change in the size of a male genital organ, which will help to better understand not

166 from the genital tract in ~4 weeks, but the genital organisms can spread to the gastrointestinal tra

167 underlying evolutionary differences in male genital organs and organ size more generally.

168 gous KO mice were infertile, due to abnormal genital organs.

169 We found that this genital outgrowth forms through extreme increases in epi

170 The genital pathogen Chlamydia is known to colonize the gast

171 that gastrointestinal Chlamydia may promote genital pathology via an indirect mechanism.

172 ion if they had a diagnosis of uncomplicated genital, pharyngeal, or rectal gonorrhoea.

173 The relative size of the putative genital protrusion varied more than 3-fold between speci

174 atients with limited skin disease, including genital psoriasis and psoriatic arthritis patients, also

175 cers were too small to be detected.Keywords: Genital/Reproductive, UltrasoundSupplemental material is

176 comitant strong systemic and intraepithelial genital-resident CD8(+) T cell responses.

177 bility that is restricted to PGCs within the genital ridge during a narrow temporal window.

178 nous PGCs migrate through circulation to the genital ridge.

179 al [CI], 6.3-21.9%) of HPV DNA detections in genital samples were attributable to vaginal sex in the

180 Questionnaires and genital samples were collected at 0 and 4 months.

181 Effective future control of female genital schistosomiasis (FGS) requires an integrated and

182 ers need to differentiate the women for whom genital sensations have a critical role in their subject

183 g equations was used to assess predictors of genital shedding among women with undetectable plasma vi

184 Exploring viral genital shedding during LDRs is crucial to ensure their

185 We found HSV genital shedding rates were positively correlated with H

186 Predictors of genital shedding were HIV disease stage, antiretroviral

187 al function is influenced by discomfort over genital size which leads to seek surgical and non-surgic

188 erone plus dihydrotestosterone (DHT) made in genital skin according to a "classic" pathway.

189 slocation of the androgen receptor in female genital skin primary cultures.

190 rogen receptor expression in male and female genital skin using immunohistochemistry and demonstrated

191 res of human fetal organs (adrenals, gonads, genital skin) from the major period of sexual differenti

192 activation to 5alpha-dihydrotestosterone in genital skin, thereby facilitating male external genital

193 e-to-female HIV-1 transmission and blood and genital specimens collected near the time of transmissio

194 on Study) in the US, Africa, and Peru with 2 genital specimens each containing >/=105 copies herpes s

195 Male genital structures are among the most rapidly evolving m

196 We pooled genital sub-studies from 2 clinical trials in this area.

197 These results suggest that HIV remodels genital T cells to prolong viability and promote viral d

198 %); however, solid cancers (renal, sarcomas, genital, thyroid) were seen.

199 quacy of drug dosing in the VR and measuring genital tissue drug concentrations to develop more preci

200 ine model to study the immunobiology of male genital tissue in the context of transplantation and dev

201 highlight the importance of assessing intact genital tissue samples to gain insights into HIV suscept

202 Higher HIV RNA molecular diversity in the genital tract (compared to that in blood plasma) and evi

203 centrations of antiretrovirals in the female genital tract (FGT) are critical for suppression of vira

204 Female genital tract (FGT) inflammation increases HIV infection

205 Dysbiosis in the female genital tract (FGT) is characterized by the overgrowth o

206 ized HIV-1 diversity in the blood and female genital tract (FGT) within 2 weeks after detection of in

207 y of tenofovir alafenamide (TAF) in the male genital tract (MGT) and the semen quality of individuals

208 symptomatic and do not cause permanent upper genital tract (UGT) damage.

209 while the chlamydial mutant infection in the genital tract alone was unable to induce any significant

210 e attenuated in inducing hydrosalpinx in the genital tract also reduce their colonization in the gast

211 te of infection, GAS can colonize the female genital tract and cause severe diseases, such as puerper

212 impaired in ability to colonize the primate genital tract and cause uterine wall pathologic findings

213 obiomial composition higher up in the female genital tract and in the fallopian tubes (the site of or

214 ated, but not naive, CD8(+) T cells into the genital tract and induced in situ proliferation and diff

215 show that viral populations within the male genital tract are defined by factors beyond transient in

216 Our study highlights the male genital tract as a local source of HIV that can be rever

217 lts in higher bacterial burdens in the upper genital tract at earlier time points, correlating with l

218 nable chlamydial evasion of the female lower genital tract barrier during sexual transmission.

219 to study the HIV-1 population in the female genital tract before virus is detectable in the bloodstr

220 hlamydia trachomatis infection of the female genital tract can lead to irreversible fallopian tube sc

221 Time to NAAT clearance of rectal and genital tract CT was similar, and intermittent rectal CT

222 herpes simplex virus-2 (HSV-2) in the human genital tract despite low CD8+ and CD4+ tissue-resident

223 women infected with chlamydiae develop upper genital tract disease, but the reason(s) for this remain

224 ttle HIV-1 diversity in the blood and female genital tract during the first 2 weeks after virus was d

225 te a role for TLR3 signaling in limiting the genital tract fibrosis, scarring, and chronic inflammati

226 Hormonal contraceptives may increase genital tract HIV viral load (gVL) and sexual transmissi

227 ressed predominantly by luminal cells of the genital tract in response to infection, and low levels o

228 l, chlamydial organisms are cleared from the genital tract in ~4 weeks, but the genital organisms can

229 nstrated significant attenuation in a murine genital tract infection model.

230 6J mice are susceptible to a transient lower genital tract infection with MmuPV1 mouse papillomavirus

231 The T-cell response to chlamydia genital tract infections in humans and mice is unusual b

232 r immunopathology during Chlamydia muridarum genital tract infections.

233 We conclude that the male genital tract is a site where virus can be brought in fr

234 Elevated inflammation in the female genital tract is associated with increased HIV risk.

235 can productively infect mice when the lower genital tract is bypassed and bacteria are deposited dir

236 ibute to interaction with the primate female genital tract is limited by the lack of relevant animal

237 l Chlamydia failed to directly spread to the genital tract lumen, suggesting that gastrointestinal Ch

238 se may influence HIV risk through changes in genital tract microbiota and inflammatory cytokines.

239 olonization site from the oral cavity to the genital tract of a human or humanoid and had to evolve m

240 -positive bacterium that colonizes the lower genital tract of approximately 18% of women globally as

241 ive morbidities after ascending to the upper genital tract of women, and repeated infection can lead

242 The genital tract pathogen Chlamydia trachomatis is frequent

243 Although Chlamydia trachomatis is a human genital tract pathogen, chlamydial organisms have freque

244 hlamydial replication and possibly increased genital tract pathogenesis during human infection.

245 mechanisms associated with Chlamydia-induced genital tract pathogenesis in humans, we used CRISPR gen

246 This correlated with the increased genital tract pathology observed in mice infected at ZT3

247 mydia might induce the second hit to promote genital tract pathology, and we are now providing experi

248 us cause of tubal infertility, induces upper genital tract pathology, such as hydrosalpinx, which can

249 Both mutants are attenuated in inducing genital tract pathology.

250 inal Chlamydia in promoting pathology in the genital tract possibly via an indirect mechanism.

251 Single viral templates from blood plasma and genital tract RNA and DNA were sequenced across HIV-1 en

252 Recovery of viable M. genitalium from lower genital tract specimens was improved by diluting the spe

253 ine Chlamydia readily spreads from the mouse genital tract to the gastrointestinal tract while induci

254 hanisms by which GBS traffics from the lower genital tract to vulnerable host niches are not well und

255 re genetically similar to both the blood and genital tract variants of their male partners, indicatin

256 und in blood are likely to also protect from genital tract variants.

257 cteria are deposited directly into the upper genital tract via transcervical inoculation.

258 The plasmid-encoded pGP3, a genital tract virulence factor, is essential for Chlamyd

259 ose that chlamydial chromosomal-gene-encoded genital tract virulence factors may be essential for Chl

260 erting female partners found that the males' genital tract viruses were rarely distinct from the bloo

261 responses were induced in the lungs and the genital tract with the optimized GC-coated LPN adjuvant

262 We studied HIV-1 reactivation in the female genital tract, a dynamic anatomical target for HIV-1 inf

263 te or chronic inflammation of the urinary or genital tract, abdominal pain, abdominal mass, obstructi

264 8, paralleling their infection course in the genital tract, but persisted in the large intestine for

265 In the genital tract, deficiency in pGP3 significantly reduced

266 rrelated with its pathogenicity in the upper genital tract, we evaluated the effect of FTY720 on chla

267 ed increased chlamydial burdens in the upper genital tract, which correlated with increased CD4 T cel

268 We studied HIV-1 reactivation in the female genital tract, which is often the portal of HIV-1 entry

269 partners, indicating a lack of evidence for genital tract-specific lineages.

270 vation for antigonococcal Ab function in the genital tract.

271 rachomatis when it is deposited in the lower genital tract.

272 scriptional responses in cells that line the genital tract.

273 such viruses were also detected in the donor genital tract.

274 nfluence pathology and immunity in the upper genital tract.

275 on in the gastrointestinal tract than in the genital tract.

276 and maintain its pathogenicity in the upper genital tract.

277 itis on the HIV-1 population within the male genital tract.

278 the microbiological environment in the lower genital tract.

279 HIV replication as the cause of DS from the genital tract.

280 rucial for GAS fitness in the female primate genital tract.

281 nly colonizes the lower gastrointestinal and genital tracts and, during pregnancy, neonates are at ri

282 hich can cause fibrotic pathology in women's genital tracts, is also frequently detected in the gastr

283 y lead to fibrotic blockage in women's upper genital tracts, resulting in tubal infertility.

284 es systemic viral dissemination after female genital transmission.

285 dal tissues, leading to DHT formation at the genital tubercle.

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

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

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

289 both secondary bacterial skin infections and genital ulcers.

290 In mammals, genitals undergo major changes in puberty.

291 Genital arousal is characterized by genital vasocongestion and other physiological changes t

292 1), the genetic characteristics of blood and genital viruses from males were compared to those of the

293 Using multiple assays, the blood and genital viruses were consistently found to be compartmen

294 Genital wart (GW) incidence is high among men.

295 e nationwide, real-world data on the risk of genital warts (GWs) after <3 vaccine doses.

296 Approximately 90% of genital warts are caused by human papillomavirus (HPV) t

297 qHPV was 1.0/100PY (95% CI, 0.3-2.6) and of genital warts was 1.0/100PY (95% CI, 0.3-2.5).

298 onfidence interval [CI], 1.1-4.1), and IR of genital warts was 2.3/100PY (95% CI, 1.2-4.1).

299 l neoplasia of grade 2 or higher [CIN2+], or genital warts).

300 uded rates of abnormal cervical cytology and genital warts.

301 , 4) adult female imidacloprid levels in the genitals were negatively correlated with genital organ w