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1 ction and excretion during murine chlamydial genital infection.
2 solate lacked virulence in a murine model of genital infection.
3  properties, in a murine model of chlamydial genital infection.
4 erent time points throughout the course of a genital infection.
5 rotective immunity against murine chlamydial genital infection.
6 as tested by use of a murine model of female genital infection.
7 y slightly delayed resolution of the primary genital infection.
8 2 gB2 and gD2 in response to recurrent HSV-2 genital infection.
9 echanisms associated with protection against genital infection.
10 oduce protective immunity against chlamydial genital infection.
11 pregulation and OPTN expression during HSV-2 genital infection.
12  to 97% of latent HSV DNA in mouse models of genital infection.
13 ss of age, are an important reservoir of HPV genital infection.
14 and CCR5-dependent migration observed during genital infection.
15 t Sigmodon hispidus model of HSV-2 and HSV-1 genital infection.
16 ot required for controlling chlamydial lower genital infection.
17 erity of oviduct pathology upon C. muridarum genital infection.
18  the host response in immunity to chlamydial genital infection.
19 response in the male urethra to a chlamydial genital infection.
20  influx or normal resolution of C. muridarum genital infection.
21 r to what has been found in rodent models of genital infection.
22 t trichomonal, gonococcal, and/or chlamydial genital infection.
23 f trichomonal, gonococcal, and/or chlamydial genital infection.
24 accine by using a murine model of chlamydial genital infection.
25 s of IL-1beta expression during a chlamydial genital infection.
26  chlamydial developmental cycle in an actual genital infection.
27 mplex virus type 1 (HSV-1) or type 2 (HSV-2) genital infection.
28 ount >10,000, or gonococcal/chlamydial lower genital infection.
29 llowing the resolution of primary chlamydial genital infection.
30 umoral immune responses during uncomplicated genital infections.
31  correlated with the occurrence of antenatal genital infections.
32 and potentially more difficult to treat than genital infections.
33 rproliferation of primary HSV type 2 (HSV-2) genital infections.
34 dial gastrointestinal infection than against genital infections.
35 ar human pathogen responsible for ocular and genital infections.
36 ccur in the absence of detectable viremia or genital infections.
37 ry effective vaccine against respiratory and genital infections.
38 gainst a variety of enteric, respiratory, or genital infections.
39            Of the 328 participants who had a genital infection, 151 (98%) of 154 in the ceftriaxone g
40 ns of patients with confirmed C. trachomatis genital infection: 40 women with pelvic inflammatory dis
41 pisodes (56.6% vs. 51.8%), events suggesting genital infection (9.0% vs. 2.5%), and events suggesting
42 erval: 0.42, 1.38) nor gonococcal/chlamydial genital infection (adjusted hazard ratio = 1.16, 95% con
43 ity against reinfection develops after human genital infection, although it appears, at best, to be p
44 e is known about the concurrence of oral and genital infection among healthy individuals.
45  development of PID or gonococcal/chlamydial genital infection among predominantly young, African-Ame
46 this study, we assessed the risk of incident genital infection and 6-month persistent genital infecti
47                    This study shows that SIV genital infection and disease course are enhanced by sub
48 t viral vaccines in protection against HSV-2 genital infection and disease.
49                                              Genital infection and hypotension were significantly mor
50 le of these cells in resolution of a primary genital infection and in protection of HSV-immune animal
51 acterize the influence of IRF3 on chlamydial genital infection and its relationship to IFN-beta expre
52  our understanding of immunity to chlamydial genital infection and may provide important insight into
53 lication-defective HSV vaccine against HSV-2 genital infection and that B7-1 and B7-2 induce immune r
54        Here we review immunity to chlamydial genital infection and vaccine development using the C. m
55 ment with SGLT2i showed an increased risk of genital infections and DKA and a reduced AKI risk compar
56  modified MACE and HHF, an increased risk of genital infections and DKA, and a lower risk of AKI, reg
57 and developing protective strategies against genital infections and gynecological cancers.
58 implemented to control Chlamydia trachomatis genital infections and their complications have shown in
59 gout, as well as a positive control outcome (genital infection) and negative control outcomes (osteoa
60 and might increase risk of urinary tract and genital infection, and excessive inhibition of SGLT1 can
61 e of FLG mutations on the risk of AD flares, genital infections, and postpartum problems related to p
62  Joint Infections, Urinary Tract Infections, Genital Infections, and Skin and Soft Tissue Infections;
63  Joint Infections, Urinary Tract Infections, Genital Infections, and Skin and Soft Tissue Infections;
64 he pathologic consequences of C. trachomatis genital infection are well-established, the mechanism(s)
65 tential risks of Fournier gangrene, a severe genital infection associated with SGLT2I use.
66 levels, except for a more pronounced risk of genital infections associated with SGLT2i for HbA1c leve
67 mpagliflozin, there was an increased rate of genital infection but no increase in other adverse event
68 2 inhibitor initiators showed higher risk of genital infection, but no altered risk of osteoarthritis
69           Our results thus newly reveal that genital infection by an obligate intracellular bacterium
70 herefore, it is possible that women cured of genital infection by antibiotics remain infected in the
71 FI) represents 36% of female infertility and genital infection by Chlamydia trachomatis (C. trachomat
72                                              Genital infection by herpes simplex virus (HSV)-2 offers
73 mmunity is crucial for resistance of mice to genital infection by the obligate intracellular bacteriu
74 HPV) may affect risks of subsequent incident genital infections by HPV 6, 11, 16, or 18 in men.
75                                    In women, genital infection can cause endometritis and pelvic infl
76                                    Ascending genital infections cause inflammation of fallopian tubes
77  protection against the life-long, recurrent genital infections caused by HSV-2 have failed.
78 oteases, the caspases, during C. trachomatis genital infection causes the disruption of key fertility
79 bit delayed clearance of Chlamydia muridarum genital infection compared to wild-type (WT) mice.
80 ing hazard ratios (HRs) among men with prior genital infection, compared with men with no prior genit
81  low-level Chlamydia psittaci and C. pecorum genital infection detected in virgin heifers suggests pr
82 outcomes were hypovolemia, fractures, falls, genital infections, diabetic ketoacidosis (DKA), acute k
83      Aside from an increased risk of mycotic genital infections, empagliflozin-treated patients had f
84 s are being used to help differentiate lower genital infection from upper genital disorder.
85 n individual analyses, men with prior HPV 16 genital infections had a significantly higher risk of su
86  antibiotic intervention of human chlamydial genital infection has a similar effect on protective imm
87  rechallenge in a murine model of chlamydial genital infection has been achieved only by infection or
88             The murine model of C. muridarum genital infection has been extremely useful for identifi
89 tic evaluation of HSV viremia during primary genital infection has not been performed previously.
90 um and Chlamydia trachomatis mouse models of genital infection have been used to study chlamydial imm
91 homatis (CT) and Neisseria gonorrhoeae (NG), genital infections have classically been the focus for r
92                     SGLT-2 inhibitors caused genital infection (high certainty), whereas GLP-1 recept
93  dapagliflozin initiators had lower risks of genital infections (HR, 0.92; 95% CI, 0.89-0.95) and DKA
94 canagliflozin initiators had a lower risk of genital infections (HR, 0.94; 95% CI, 0.91-0.97) but a h
95 obicide, is an effective suppressor of HSV-2 genital infection in female BALB/c mice.
96 solution of primary and secondary chlamydial genital infection in immunoglobulin A (IgA)-deficient (I
97 he course and outcome of Chlamydia muridarum genital infection in mice genetically deficient in the r
98 s essential for the resolution of chlamydial genital infection in mice.
99 linicians should note the increased risk for genital infection in patients receiving SGLT2 inhibitors
100  known about the host response to chlamydial genital infection in the male, particularly about the na
101 oviduct pathology during Chlamydia muridarum genital infection in the mouse model.
102   A major problem in the study of chlamydial genital infections in animal models has been the use of
103        The majority of Chlamydia trachomatis genital infections in humans are asymptomatic and withou
104 s is a bacterial pathogen causing ocular and genital infections in humans.
105 r mechanistic models to longitudinal data on genital infections in unvaccinated men.
106 l infection, compared with men with no prior genital infection, in individual HPV type and grouped HP
107                                       Murine genital infection induced with the mouse pneumonitis bio
108 pigs acquired via sexual contact to those of genital infections induced artificially with known quant
109             Nine of 217 patients (4.1%) with genital infection/inflammation had objective ReA feature
110                                              Genital infection/inflammation was asymptomatic in 78% o
111                        Chlamydia trachomatis genital infection is a worldwide public health problem,
112 the prevalence of human papillomavirus (HPV) genital infection is similarly high in males and females
113 nd disease severity of Chlamydia trachomatis genital infection is whether more prevalent strains or s
114 ution of herpes simplex virus type 2 (HSV-2) genital infections is not fully understood.
115 sponse associated with Chlamydia trachomatis genital infections is thought to be initiated by the rel
116 le of inflammasome components during in vivo genital infection, mice lacking NLRP3, NLRC4, and ASC we
117                Using the Chlamydia muridarum genital infection model of mice, which replicates many f
118 n-specific harms, SGLT-2 inhibitors increase genital infections (odds ratio (OR) 3.29 (95% CI 2.88 to
119            Our results indicate that primary genital infection of mice with murine C. trachomatis ind
120 dant stress, were elevated during chlamydial genital infection of mice.
121                                              Genital infection of rats with Mycoplasma pulmonis cause
122 cellular pathogen responsible for ocular and genital infections of significant public health importan
123                                Nongonococcal genital infections, often asymptomatic, can trigger a re
124 erpes simplex virus type 2 (HSV-2) and other genital infections on human immunodeficiency virus type
125 otentially useful for patients with isolated genital infection, or for patients who are allergic or i
126 tures, lower limb amputations, ketoacidosis, genital infections, or symptomatic hypovolaemia, althoug
127 ne approach for preventing a chronic, latent genital infection rather than an acute respiratory infec
128 revalent, asymptomatic Chlamydia trachomatis genital infection reduces reproductive sequelae in infec
129 nalyses showed consistent increased risks of genital infections (regulatory submissions 4.75 [4.00-5.
130 er; however, we propose that women, cured of genital infection, remain at risk for autoinoculation fr
131 bserved in women after Chlamydia trachomatis genital infection result from ascension of the bacteria
132 ition, SGLT2 inhibitors doubled the risk for genital infections (RR, 2.69 [CI, 1.61 to 4.52]; high ce
133 oral HPV infection was higher among men with genital infection than among uninfected men (11.4% vs. 5
134                Bacterial vaginosis (BV) is a genital infection that frequently presents in women infe
135 OS2(-/-)) mice resolve Chlamydia trachomatis genital infection, the production of reactive nitrogen s
136 est that type I IFNs exacerbate C. muridarum genital infection through an inhibition of the chlamydia
137 , particularly isolates from respiratory and genital infections to form biofilm, compared with typabl
138                        In the mouse model of genital infection using Chlamydia muridarum, IL-1R signa
139 ia trachomatis in an in vitro model of human genital infection using the intracellular iron-chelating
140                                           In genital infection, viral DNA reached SC and DRG simultan
141                 Pooled prevalence of current genital infection was 3.0% (95% CI 2.3-3.8) in general p
142 ately preceding PID or gonococcal/chlamydial genital infection was not different between women who de
143              The proportion of patients with genital infections was greater with empagliflozin than p
144 r 1998, an outbreak of Chlamydia trachomatis genital infections was reported among 18 residents of a
145       Using the Chlamydia muridarum model of genital infection, we demonstrate a protective role for
146 ole of type I IFNs during in vivo chlamydial genital infection, we examined the course and outcome of
147 inoculating dose of C. muridarum modulates a genital infection, we measured innate and adaptive cell
148 ith possible or proven Chlamydia trachomatis genital infection were screened for symptoms of ReA.
149 en douching and PID or gonococcal/chlamydial genital infections were assessed by proportional hazards
150 m women with gonococcal cervicitis and other genital infections were examined.
151 s, symptoms, and other reports suggestive of genital infections were more frequent in the dapaglifloz
152                         Although urinary and genital infections were more frequently reported in the
153                              HSV-2 and other genital infections were the most important risk factors
154                                   Unlike the genital infection where CD8(+) T cells are primed, yet f
155 ment of a highly efficacious vaccine against genital infection will depend on the generation of a liv
156 (+) T cells, allowing for protection against genital infection with C. trachomatis.
157 es draining the genital tract in response to genital infection with C. trachomatis.
158                                              Genital infection with Chlamydia trachomatis results in
159 A-A*0201 transgenic mice following ocular or genital infection with either HSV-1 or HSV-2.
160                                              Genital infection with herpes simplex virus 2 (HSV-2) is
161                                              Genital infection with herpes simplex virus type 2 (HSV-
162 ent genital infection and 6-month persistent genital infection with HPV16 in relation to baseline ser
163 cing establishment of latent infection after genital infection with HSV-2.
164 greater female-to-male (F-M) transmission of genital infection with human papillomavirus (HPV) relati
165                                              Genital infection with human papillomavirus (HPV), as de
166 al studies from sub-Saharan Africa show that genital infection with Schistosoma haematobium [correcte
167 w cytometry the mononuclear cell response to genital infection with the agent of guinea pig inclusion
168 ular adhesion molecule type 1 (ICAM-1) after genital infection with the C. trachomatis agent of mouse
169                                              Genital infection with the inflammation- and caspase-ind
170                      Following resolution of genital infection with the mouse pneumonitis (MoPn) biov
171    The molecular mechanisms of resistance to genital infection with the mouse pneumonitis (MoPn) stra
172 d chlamydial vaccine or repeated abbreviated genital infection with virulent chlamydiae promotes anam
173 abdominal pain are frequent complications of genital infections with Chlamydia trachomatis.
174                                              Genital infections with human papillomavirus (HPV) are i
175 rms were largely specific to drug class (eg, genital infections with SGLT-2 inhibitors, severe gastro
176  1 (Th1) response is essential for resolving genital infections with the mouse pneumonitis biovar of

 
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