ライフサイエンスコーパス: genital

1 red in sun-protected areas, specifically the genitals.

2 id not detect any cortical representation of genitals [7-9].

3 l cell (ESC) proliferation ex vivo, and that genital administration of an IL-4-expressing adenoviral

4 Genital and anal specimens were available for 1348 MSW p

5 Three-site genital and extragenital screening for Mycoplasma genita

6 as lymph node metastasis, new melanomas, and genital and oral mucosal SCCs.

7 We obtained plasma specimens, genital and rectal fluids, and tissue samples (rectal, c

8 ate in mucosal tissues, including the female genital and respiratory tract.

9 vitro activity against HD strains from both genital and skin ulcers.

10 e of adverse events (AEs), hypoglycemia, and genital and urinary infections were also similar to plac

11 t an increase in total AEs, hypoglycemia, or genital and urinary infections.

12 lesions of thick scaly skin on the face and genitals and thickened, red, and scaly skin on the hands

13 tently reported risk indicators for the male genital anomalies cryptorchidism and hypospadias are pre

14 etween low placental weight and risk of both genital anomalies.

15 We have elicited local genital antigen-specific immune responses after topical

16 Studies in humans debate whether genitals are represented displaced below the foot of the

17 ding interest, the neural representations of genitals are still poorly understood [6].

18 Genitals are unique body parts in that they show sexual

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

20 omen, we found that individuals with diverse genital bacterial communities dominated by anaerobes oth

21 Genital C. trachomatis strains can counter tryptophan li

22 mples were tested for the presence of female genital cancer by comparing interleukin 6 concentration

23 cer (HR, 2.77; 95% CI, 1.29-5.96) and female genital cancers (HR, 3.43; 95% CI, 1.44-8.19).

24 risk bacteria increased numbers of activated genital CD4(+) T cells in a murine model.

25 promises TFV and TAF protection in blood and genital CD4+ T cells and suggests that MPA may decrease

26 In contrast, with genital CD4+ T cells, MPA suppressed TAF inhibition of H

27 osphate (TFV-DP) concentrations in blood and genital CD4+ T cells.

28 cooperates with antibody to protect against genital chlamydia and establish neutrophils as a key eff

29 Health Clinic (eSHC), in which patients with genital chlamydia are diagnosed and medically managed vi

30 tions involved in humoral protection against genital chlamydia infection is crucial to development of

31 Genital Chlamydia trachomatis infections in women typica

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

33 involvement is a rare, self-limiting, benign genital condition.

34 Several genital conditions that increase HIV risk are more preva

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

36 the idea that this protrusion corresponds to genital cortex, we observed a size increase of this prot

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

38 ephropathy, blastoma, gonadal dysgenesis and genital discordance.

39 rial for Women who experienced primary HSV-2 genital disease and compared them with sequences of viru

40 e screening test for the diagnosis of female genital diseases using a dual-material collection device

41 portant role in the detection of many female genital diseases, but the lack of suitable collection de

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

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

44 Genital exfoliated cells were collected and genotyped fo

45 Genitals feature prominently in the oldest pieces of fig

46 INTERPRETATION: Recurrence of female genital fistula and adverse pregnancy-related maternal a

47 Female genital fistula is a devastating maternal complication o

48 Genital fluid specimens were collected every other month

49 dinal medical care of survivors and accurate genital fluid testing for Ebola.

50 me time, evidence that the virus persists in genital fluids and can be sexually transmitted, along wi

51 hat prominently control rectal, bladder, and genital functions.

52 930), trichomoniasis (1 study; n = 779), and genital herpes (1 study; n = 779).

53 In a cohort of patients with genital herpes and healthy controls, the minor G allele

54 Using a mouse model of genital herpes infection, we demonstrate that both antib

55 latform against primary and secondary female genital herpes infections.

56 Importance: Genital herpes is a prevalent sexually transmitted infec

57 sions and Relevance: Serologic screening for genital herpes is associated with a high rate of false-p

58 screening, harms of screening, reduction in genital herpes outbreaks.

59 We evaluated a genital herpes prophylactic vaccine containing herpes si

60 Importance: Genital herpes simplex virus (HSV) infection is a preval

61 Genital herpes simplex virus type 2 (HSV-2) infection ca

62 Serologic screening for genital herpes was associated with psychosocial harms, i

63 for bacterial vaginosis, trichomoniasis, and genital herpes was performed in a high-prevalence popula

64 Persons with genital herpes were randomized into 3 dose cohorts to re

65 e human pathogens that can cause cold sores, genital herpes, and blindness.

66 simplex virus 1 (HSV-1), a leading cause of genital herpes, infects oral or genital mucosal epitheli

67 Using a mouse model of genital herpes, we found that HSV-1-infection-associated

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

69 rce (USPSTF) recommendation on screening for genital herpes.

70 persons without past or current symptoms of genital herpes; studies evaluating accuracy and harms of

71 x virus (HSV) were independent predictors of genital HIV RNA shedding after adjusting for plasma HIV

72 ated with a reduction in subsequent incident genital HPV 6, 11, and 16 infections.

73 on models identified factors associated with genital HPV detection.

74 Genital HPV genotypes were detected using Roche Linear A

75 ed HPV antibodies protect against subsequent genital HPV infection (ie, natural immunity).

76 Concordance of oral and genital HPV infection among men is unknown.

77 The prevalence of genital HPV infection and the HPV vaccination coverage r

78 To estimate the prevalence of genital HPV infection and the HPV vaccination rate in th

79 us (HPV) infection following a type-specific genital HPV infection for the 9-valent vaccine HPV types

80 )-associated disease, prospective studies of genital HPV infection in this population are scarce.

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

82 The overall genital HPV infection prevalence appears to be widesprea

83 The overall genital HPV infection prevalence was 45.2% (95% CI, 41.3

84 ral HPV prevalence among men with concurrent genital HPV infection was 4-fold greater (19.3%) than am

85 the United States, the overall prevalence of genital HPV infection was 45.2% (95% CI, 41.3%-49.3%).

86 tion, as well as the concordance of oral and genital HPV infection, among U.S. men and women.

87 MSW with prior genital HPV infections had a higher risk of a subsequent

88 of US males aged 14-59 years have detectable genital HPV infections.

89 rker (Y chromosome DNA) were associated with genital HPV partner concordance and estimated the fracti

90 ated with infection by higher numbers of all genital HPV types (relative risk ratio, 1.26; 95% confid

91 Genital HPV was assessed in 725 concordant HIV-negative

92 ends against routine serologic screening for genital HSV infection in asymptomatic adolescents and ad

93 eigh the benefits of serologic screening for genital HSV infection in asymptomatic adolescents and ad

94 c screening and preventive interventions for genital HSV infection in asymptomatic adults and adolesc

95 at doses of 30 microg and 100 microg reduced genital HSV shedding and lesion rates.

96 We evaluated the frequency of genital HSV shedding in HIV-seropositive and HIV-seroneg

97 The primary end point was within-participant genital HSV shedding while receiving pritelivir compared

98 High rates of genital HSV-1 infection and moderate HSV-2 prevalence me

99 atment rescued mice from lethality following genital HSV-1 infection.

100 ents for CD8 TRM cells in protection against genital HSV-2 infection and identify the population of A

101 e and pull' method confer protection against genital HSV-2 infection, and that IFN-gamma produced by

102 telivir with valacyclovir for suppression of genital HSV-2 infection.

103 Healthy adults with 4 to 9 annual genital HSV-2 recurrences were eligible.

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

105 ance: Among adults with frequently recurring genital HSV-2, the use of pritelivir compared with valac

106 Genital human immunodeficiency virus (HIV) RNA shedding

107 termined the prevalence and risk factors for genital human papillomavirus (HPV) detection among men w

108 nationally representative prevalence data on genital human papillomavirus (HPV) in males in the Unite

109 the association between vaginal douching and genital human papillomavirus (HPV) infection have found

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

111 characterized by mesomelic limb shortening, genital hypoplasia, and distinctive facial features.

112 Genital immune activation is suspected to modulate local

113 on with penile HIV shedding, suggesting that genital immune activation may increase the risk of sexua

114 obicide, is an effective suppressor of HSV-2 genital infection in female BALB/c mice.

115 Using the Chlamydia muridarum genital infection model of mice, which replicates many f

116 ing hazard ratios (HRs) among men with prior genital infection, compared with men with no prior genit

117 l infection, compared with men with no prior genital infection, in individual HPV type and grouped HP

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

119 mplex virus type 1 (HSV-1) or type 2 (HSV-2) genital infection.

120 nalyses showed consistent increased risks of genital infections (regulatory submissions 4.75 [4.00-5.

121 HPV) may affect risks of subsequent incident genital infections by HPV 6, 11, 16, or 18 in men.

122 protection against the life-long, recurrent genital infections caused by HSV-2 have failed.

123 n individual analyses, men with prior HPV 16 genital infections had a significantly higher risk of su

124 r mechanistic models to longitudinal data on genital infections in unvaccinated men.

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

126 e of FLG mutations on the risk of AD flares, genital infections, and postpartum problems related to p

127 Aside from an increased risk of mycotic genital infections, empagliflozin-treated patients had f

128 We evaluated whether genital inflammation affects the selection of the transm

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

130 Genital inflammation associated with sexually transmitte

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

132 th African women, we found that preinfection genital inflammation facilitates transmission of less in

133 Genital inflammation is a key determinant of human immun

134 , sperm present on a vaginal swab wet mount, genital inflammation of either partner, genital ulcerati

135 at an increased risk of HIV acquisition, and genital inflammation or the vaginal microbiome may contr

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

137 raception were significantly associated with genital inflammation.

138 Cervicovaginal bacteria modulate genital inflammation; however, their role in HIV suscept

139 ng (RR, 1.7 [95% CI, 1.1-2.7]; P = .01), and genital lesions (RR, 2.1 [95% CI, 1.2-3.4]; P = .005), c

140 f HSV in positive swabs and the frequency of genital lesions and shedding episodes.

141 wice daily for HSV-2 detection and monitored genital lesions for 28-day periods at baseline and at in

142 ex viruses (HSV) cause painful cold sores or genital lesions in many people; less often, they affect

143 Genital lesions were present on 1.9% of days in the prit

144 Genital lesions were reported on 749 of 3875 days (19%),

145 f people worldwide, causing painful oral and genital lesions, in addition to a multitude of more seve

146 hat vaccine-elicited immune responses in the genital lymph nodes could help prevent infection after p

147 te of virus replication had shifted from the genital lymph nodes to the gut.

148 liced SIV RNA levels were the highest in the genital lymph nodes, indicating that this is the site wh

149 In conclusion, we found higher risks of both genital malformations in boys born with a low placental

150 Genital maps indicate a deep homology of penis and clito

151 This suggests that the genital microbiota and HSV-2 infection may influence HIV

152 Therefore, we assessed the impact of the genital microbiota on mucosal immunology in ACB women an

153 ike other routes, ZIKV replicates within the genital mucosa even in wild-type (WT) mice.

154 CD1d and HIV receptors resided in the female genital mucosa, a site where HIV-1 transmission occurs.

155 calized recurrent infections in the skin and genital mucosa.

156 ing cause of genital herpes, infects oral or genital mucosal epithelial cells before infecting the pe

157 icovaginal HIV-neutralizing IgA responses in genital mucosal secretions of HIV-exposed women, which i

158 on urine, biopsy, cervicovaginal lavage, and genital mucosal surface specimens.

159 Amasanti and colleagues consider female genital mutilation in the UK, how overly intrusive effor

160 toire that predictably involves cannibalism, genital mutilation, male preference for teneral females,

161 ibalism, opportunistic mating, mate-binding, genital mutilation, plugging, and emasculation.

162 Genital mycoplasmas, which can be vertically transmitted

163 Genital mycotic infections were increased with SGLT-2 in

164 Cortical genital neurons showed unusual multi-body-part responses

165 Specifically, genital neurons were co-activated by distant body region

166 analyzed data of 263 women with at least one genital or anorectal sexually transmitted infection from

167 t, ear, craniofacial nerves and skeleton and genital organs.

168 ult in severe bladder, kidney, ureteral, and genital pathologies.

169 trachomatis infection of mice also causes no genital pathology, but unlike women, does not generate C

170 versity communities strongly correlated with genital pro-inflammatory cytokine concentrations in both

171 ct of DMPA and intravaginal practices on the genital proteome and microbiome to gain mechanistic insi

172 This relative size of the genital protrusion co-varied with relative testicle size

173 served a sexual monomorphism of the putative genital protrusion in all species, similar to previous o

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

175 Genital replication of CMV and EBV was the most common a

176 e wondered what a high-resolution mapping of genital representations might tell us about the sexual d

177 Genital representations were somatotopic and bilaterally

178 We identified genital responses in rat somatosensory cortex in a regio

179 Genital responses were more common in males than in fema

180 as deleted before sex determination and most genital ridge somatic cells differentiated into steroido

181 We tested baseline genital samples for Y chromosome DNA and HPV DNA using p

182 tection of human papillomavirus (HPV) DNA in genital samples may not always represent true infections

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

184 lates from the plasma, and in some instances genital secretions, of eight HIV-1 donor and recipient p

185 Studies of subjective and genital sexual arousal in monosexual (i.e. heterosexual

186 Species differed in external genital sexual dimorphism, but we observed a sexual mono

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

188 HSV) helicase-primase inhibitor that reduced genital shedding and lesions.

189 an association between M. genitalium and HIV genital shedding and the high prevalence and persistence

190 The proportion of visits with genital shedding decreased with time since ART initiatio

191 Predictors of genital shedding were HIV disease stage, antiretroviral

192 d to compare the magnitude and prevalence of genital shedding, respectively, by time since ART initia

193 L and 23.6% of visits with detectable VL had genital shedding.

194 Mammalian external genitals show sexual dimorphism [1, 2] and can change si

195 a-HPV types included HPV-38 (beta-2) in both genital skin (32.2%) and eyebrow hairs (16.1%), HPV-12 (

196 Any beta-HPV was most prevalent in genital skin (81.6%), followed by forearm skin (64.4%),

197 man HSV-2 reactivation in situ in sequential genital skin biopsy specimens obtained from HSV-2-seropo

198 provided eyebrow hairs, forearm skin swabs, genital skin swabs, oral rinse samples, and anal swabs.

199 1.0%) across the 3 keratinized tissue sites (genital skin, eyebrow hairs, forearm skin) than across t

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

201 We genotyped pairs of genital specimens from 459 people; 213 (46%) were men, t

202 tions, we analyzed HSV-2 strains detected in genital swab specimens from trial participants who were

203 Participants obtained genital swab specimens twice daily for HSV-2 detection a

204 swabs and/or GWs preceded by a viable normal genital swab were analyzed.

205 3 variants detection in GW and the preceding genital swab.

206 ughout treatment, the participants collected genital swabs 4 times daily for testing by HSV polymeras

207 n Men (HIM) Study participants who had HPV-6 genital swabs and/or GWs preceded by a viable normal gen

208 Using over 150 genital swabs from North and South America and Africa, w

209 variants prevalence was increased in GWs and genital swabs of cases compared to controls.

210 HPV-6 B1 variants are more prevalent in genital swabs that precede GW development, and confer an

211 Now, genital swellings have been found in tuatara embryos, ar

212 y promoted durable regression of established genital TC-1 tumors.

213 of CD4(+) and CD8(+) T cells that persist in genital tissue for extended periods.

214 ity elicited by Chlamydia infection of human genital tissue may analogously promote repair processes

215 he C. muridarum organisms spreading from the genital to the GI tracts were detected in different mous

216 The female genital tract (FGT) microbiome may affect vaginal pH and

217 The female genital tract (FGT) provides a means of entry to pathoge

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

219 C) remains the most common malignancy of the genital tract among women in developed countries.

220 ve dosing strategies to protect lower female genital tract and colorectal tissues.

221 homatis is also attenuated in both the mouse genital tract and nonhuman primate ocular tissue.

222 We utilized a murine genital tract carriage model to demonstrate that M1 and

223 al infection, compared with those with upper genital tract chlamydial infection (13.8% vs 9.5%; P =04

224 l responses was detected in women with lower genital tract chlamydial infection, compared with those

225 t effectors in the innate defence of the uro-genital tract creates new translational possibilities fo

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

227 athogen responsible for both male and female genital tract disease.

228 sh a successful infection in the mouse lower genital tract following an intravaginal inoculation.

229 Viable M. genitalium persisted in the lower genital tract for 8 weeks in three animals, 4 weeks in t

230 chomatis strain (L2-5) survived in the lower genital tract for more than 3 weeks.

231 e host defense mechanisms protect the female genital tract from pathogens, but the impact of sexual i

232 Infections of the lower genital tract in heterozygous (immunocompetent) mice of

233 However, the mechanisms of GAS genital tract infection are not well understood.

234 uide investigation, an experimental model of genital tract infection has been developed in female mic

235 Chlamydia trachomatis genital tract infection is a major cause of female repro

236 Lower genital tract infections caused by both sexually and not

237 and treatment of HIV-related conditions and genital tract infections may decrease the risk of HIV-1

238 birth, yet the attributable risk for female genital tract infections remains to be defined.

239 cted with these strains developed productive genital tract infections.

240 ermatozoa are exposed in the male and female genital tract influence CatSper activation via modulatio

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

242 cell-mediated immune (CMI) responses in the genital tract mucosa.

243 tial role for gastrointestinal chlamydiae in genital tract pathogenicity.

244 es, carrying the potential for postinfection genital tract sequelae.

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

246 t with chlamydial pathogenicity in the upper genital tract suggests a potential role for gastrointest

247 k (85%) was required to protect lower female genital tract tissue from HIV, while adherence to 2 of 7

248 ecruitment of an effector cell population to genital tract tissue.

249 activation of an effector cell population in genital tract tissues by CD4(+) T cells.

250 ells in vivo independently of proximal upper genital tract tissues.

251 r Chlamydia muridarum dissemination from the genital tract to the gastrointestinal (GI) tract.

252 wn that Chlamydia muridarum spreads from the genital tract to the gastrointestinal tract potentially

253 pathogenesis, readily spreads from the mouse genital tract to the gastrointestinal tract, establishin

254 In men, pathogens can also spread to the genital tract via the continuous ductal system, elicitin

255 F-dependent chlamydial survival in the lower genital tract was confirmed in multiple strains of mice.

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

257 organisms were cleared from the mouse lower genital tract within a few days, while a CPAF-sufficient

258 ased into semen by various cells of the male genital tract, as well as by infected monocytes and lymp

259 lture and are cleared faster from the murine genital tract, highlighting the importance of CpoS for C

260 Multiple viruses coinfect the male genital tract, influencing each other's replication and

261 athogenicity with ascending infection in the genital tract, since attenuated C. muridarum spread sign

262 0 times higher than that in the lower female genital tract, whereas concentrations of endogenous nucl

263 with diverse roles in function of the female genital tract.

264 is the most common malignancy of the female genital tract.

265 th its attenuated pathogenicity in the upper genital tract.

266 nal tract and its pathogenicity in the upper genital tract.

267 s of proinflammatory immune mediators in the genital tract.

268 were directly delivered into the mouse upper genital tract.

269 L-1beta, and IL-17A production in the female genital tract.

270 isk and the immune environment in the female genital tract.

271 ing host-pathogen interactions in the female genital tract.

272 nfluence pathology and immunity in the upper genital tract.

273 ses at barrier tissues, including the female genital tract.

274 y correlated with pathogenicity in the upper genital tract.

275 muridarum cannot directly autoinoculate the genital tract.

276 ined robust ascending infection of the upper genital tract.

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

278 contribute to its pathogenicity in the upper genital tract.

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

280 pathogenesis is clearly demonstrated in the genital tracts of mice infected with Chlamydia muridarum

281 am-positive bacteria that colonize the lower genital tracts of women and are frequently associated wi

282 g C. trachomatis survival in the mouse lower genital tracts.

283 ning natural HPV immunity against subsequent genital type-specific HPV infection in female and male s

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

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

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

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

288 unt, genital inflammation of either partner, genital ulceration of the man, and first follow-up inter

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

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

291 49 years old worldwide and causing recurrent genital ulcers.

292 In addition, regressing genital viral warts also harbored high G-to-A or C-to-T

293 A common cause of female genital virilization is congenital adrenal hyperplasia (

294 e etiological agents of approximately 90% of genital warts (GWs).

295 n papillomavirus (HPV)-related cutaneous and genital warts and anogenital (pre)cancer.

296 heat treatment correlated with regression of genital warts in a subset of patients, including at dist

297 6/11/16/18 infection, approximately 90% for genital warts, approximately 45% for low-grade cytologic

298 uman papilloma virus cervical cell lines and genital warts.

299 carcinomas develop primarily on the face and genitals, without other features characteristic of basal

300 need of evaluating antiretroviral effects on genital wound healing in future clinical trials.