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1 nd identify potential therapies for critical pertussis.
2 the possibility of host-targeted therapy for pertussis.
3       Preterm infants are most vulnerable to pertussis.
4 nated mothers required intubation or died of pertussis.
5      Infants are at greatest risk for severe pertussis.
6 nization (WHO) clinical case definitions for pertussis.
7 with cough illness that is not recognized as pertussis.
8 t protect against transmission of Bordetella pertussis.
9 ccination during pregnancy to prevent infant pertussis.
10  memory induced by natural infection with B. pertussis.
11 and Prevention case definition of "definite" pertussis.
12 f 10 infant cases qualified as having severe pertussis.
13 or reducing the morbidity and mortality from pertussis.
14 athology that promotes mortality in critical pertussis.
15  in adaptive immunological memory against B. pertussis.
16 lence of the whooping cough agent Bordetella pertussis.
17 tion requires growing large quantities of B. pertussis.
18 icient and those with pertactin-producing B. pertussis.
19                      We have used Bordetella pertussis, a common neonatal respiratory tract infection
20          In response to low temperatures, B. pertussis adapted its fatty acid composition and membran
21                                           B. pertussis also requires a relatively expensive growth me
22 ermine the incidence of severe and nonsevere pertussis among a population of Zambian infants.
23 cal factor in establishing infection with B. pertussis and acts by specifically inhibiting the respon
24 ces in low-temperature adaptation between B. pertussis and B. bronchiseptica may result from selectiv
25 ely related respiratory pathogens Bordetella pertussis and Bordetella bronchiseptica Although B. pert
26 d that Bordetella bronchiseptica, Bordetella pertussis and Bordetella parapertussis have the recyclin
27  a previous report on the effect of adding a pertussis and diphtheria component to the tetanus vaccin
28 nce to support maternal immunisation against pertussis and influenza is rapidly accumulating, importa
29 raction that is central to infection with B. pertussis and other Bordetella species.
30 panded in the lungs during infection with B. pertussis and proliferated rapidly after rechallenge of
31 n the lungs of mice during infection with B. pertussis and significantly expanded through local proli
32 l virus, sepsis-induced respiratory failure, pertussis, and "other"; and preextracorporeal membrane o
33 rategy, and is currently limited to tetanus, pertussis, and influenza vaccines.
34  streptococcus, respiratory syncytial virus, pertussis, and influenza.
35 in Bordetella pertussis, the causal agent of pertussis, and related organisms, including the broad ho
36 ced diphtheria toxoid, and reduced acellular pertussis; and human papillomavirus vaccines) in additio
37                                    Levels of pertussis antibodies in all group B siblings at birth we
38 during 2008-2014 on the kinetics of maternal pertussis antibodies in unvaccinated women and their inf
39  increases in the prevalence of undetectable pertussis antibodies were found at 10 years after high c
40  vaccine containing diphtheria, tetanus, and pertussis antigens (DTP3) was >/=90% in 14 countries in
41                                For acellular pertussis antigens, 2-fold higher maternal antibody was
42              A maternal monovalent acellular pertussis (aP) vaccine, in development, could prevent ma
43 cohort vaccinated exclusively with acellular pertussis (aP) vaccine.
44       Maternal vaccination with an acellular pertussis (aP)-containing vaccine is a recommended strat
45 tussis (whooping cough) caused by Bordetella pertussis are on the rise, and understanding factors tha
46 e age, and vaccines to prevent influenza and pertussis are recommended during pregnancy.
47                             Risk factors and pertussis-associated clinical findings were identified.
48 ence and clinical presentation of Bordetella pertussis-associated hospitalization in perinatal HIV-ex
49                             Only 16 (38%) B. pertussis-associated hospitalizations fulfilled the Cent
50 tegy in a setting such us ours to prevent B. pertussis-associated illness in women and their young in
51                             Ten PCR-positive pertussis-associated illnesses were detected in HIV-infe
52 at 27-36 weeks gestation had a lower risk of pertussis at <8 weeks of age than infants born to women
53  months to 6 years of age and diagnosed with pertussis between 2011 and 2013.
54 ed role in protective immunity to Bordetella pertussis, but this evidence is based largely on periphe
55 he time of illness visits were tested for B. pertussis by polymerase chain reaction (PCR).
56                       In infants, Bordetella pertussis can cause severe disease, manifested as pronou
57                       Maternal antibodies to pertussis can hamper infant immune responses to pertussi
58 We conducted a case-control evaluation among pertussis cases <2 months old with cough onset between 1
59                                              Pertussis cases aged <2 months with onset between 1 Janu
60 Extended, retrospective analysis of reported pertussis cases between January 1, 1990, and December 31
61 g kindergarten in 2011 and 2012 and reported pertussis cases in 2012 for children in age groups 5 yea
62 and 11 statistically significant clusters of pertussis cases in children and adolescents were identif
63     Because of increased numbers of recorded pertussis cases in the United States, this study sought
64                                     Of 26259 pertussis cases reported in children (aged <18 years), 2
65   We analyzed data on probable and confirmed pertussis cases reported through Enhanced Pertussis Surv
66                              In 2012, >48000 pertussis cases were reported in the United States.
67 t pertussis vaccination does not prevent all pertussis cases.
68 l terms, currently there is no evidence that pertussis causes a significant burden of disease in youn
69                  In the postneonatal period, pertussis causes a small fraction of hospitalized pneumo
70 er of DAP-type peptidoglycan from Bordetella pertussis, causes cytopathology in the respiratory epith
71                            Six of 17 (35.3%) pertussis-confirmed cases in infants <2 months of age we
72 overage in three doses of diphtheria tetanus pertussis containing vaccine between 2013 and 2015.
73  they received a priming series of acellular pertussis containing vaccines.
74 ovement in third dose of diphtheria- tetanus-pertussis-containing vaccine (DTP3) coverage in polio hi
75              Despite all countries including pertussis-containing vaccines in their routine childhood
76 in low- and middle-income countries (LMICs), pertussis continues to cause deaths in the youngest infa
77 ough the Expanded Programme on Immunization, pertussis continues to circulate globally.
78                An exploratory analysis of B. pertussis culture was performed on induced sputum specim
79                                        In B. pertussis, deletion of the rseA gene results in high tra
80 ), and induced sputum, have been used for B. pertussis detection, although there is limited head-to-h
81 re admitted to hospital within 21 days of B. pertussis detection, whereas none of the 20 cases >/=2 m
82 an primates that BPZE1 protects against both pertussis disease and B. pertussis infection.
83 ed knowledge gaps with respect to the infant pertussis disease burden in LMICs, and discussed propose
84                There are limited data on the pertussis disease burden in this age group from low- and
85  country, we identified a moderate burden of pertussis disease in early infancy in Pakistan.
86 ibed following diphtheria-tetanus-whole cell pertussis (DTP) vaccination.
87 ived 1 dose of Diphtheria Tetanus whole cell Pertussis (DTwP).
88              With a continuing resurgence in pertussis, efforts should focus on maximizing Tdap uptak
89  the late 2000s, when an increased burden of pertussis emerged among children 1 to 10 years old, resu
90                                           B. pertussis encodes many uncharacterized transcription fac
91 n clinical isolates from a recent California pertussis epidemic.
92                    Few data exist describing pertussis epidemiology among infants and children in low
93 o effective therapies for treating fulminant pertussis exist.
94 tely 0.1% of children who were infected with pertussis experienced a clinically significant second ep
95 unity to the respiratory pathogen Bordetella pertussis gammadelta T cells, predominantly Vgamma4(-)ga
96                            Unfortunately, B. pertussis has relatively slow growth in culture, with lo
97 es: polio, pentavalent (diphtheria, tetanus, pertussis, hepatitis B virus, and Haemophilus influenzae
98 h covers diphtheria, tetanus, and whole-cell pertussis; hepatitis B; and Haemophilus influenzae type
99  and their infants to evaluate the burden of pertussis illness in a black-African community.
100       The success of tetanus, influenza, and pertussis immunisation during pregnancy has led to consi
101 universal tetanus, diphtheria, and acellular pertussis immunisation during pregnancy.
102                                     Maternal pertussis immunization has been proposed as an effective
103 t prospective surveillance studies of infant pertussis in a developing country, we identified a moder
104                              Isolation of B. pertussis in adults is difficult, resulting in a delayed
105 ies had geographic clusters of high rates of pertussis in children ages 10 to 14 years old, consisten
106 s gestation was more effective at preventing pertussis in infant than vaccination during the second t
107 an postpartum Tdap vaccination at preventing pertussis in infants <8 weeks of age .
108 ve than postpartum vaccination at preventing pertussis in infants <8 weeks of age.
109 ed as a means to reduce the burden of infant pertussis in low- and middle-income countries (LMICs), b
110     Evidence suggests that the resurgence of pertussis in many industrialized countries may result fr
111 ective strategy in reducing the incidence of pertussis in neonates prior to the onset of the primary
112  still associated with an increased risk for pertussis in some populations.
113 red for persistence of the human pathogen B. pertussis in the murine LRT and we provide evidence that
114 produced IL-17 in response to heat-killed B. pertussis in the presence of APC.
115 rize the available evidence of the burden of pertussis in the region, given historical data, and desc
116 vidence of ongoing circulation of Bordetella pertussis in the region.
117 g immunity may have had on the resurgence of pertussis in the United States at the community level.
118 zymatic activity inhibits phagocytosis of B. pertussis in vitro.
119                                The source of pertussis in young infants is most often a family member
120                                   In typical pertussis in young infants, the child will appear decept
121 uced responses to booster doses of acellular pertussis, inactivated polio, and diphtheria vaccines at
122 theria vaccine (diphtheria-tetanus-acellular pertussis-inactivated poliovirus/Haemophilus influenzae
123 demic pertussis since the lowest point in US pertussis incidence (after January 1, 1977), and for stu
124 onths, antenatal immunization reduced annual pertussis incidence by 60%, from 780 per 100,000 firstbo
125                    Reductions in symptomatic pertussis incidence by age group, increases in wP vaccin
126                                       Rising pertussis incidence has prompted a number of countries t
127 e effectiveness of this strategy in reducing pertussis incidence in infants.
128 rtussis vaccination schedule and fit to 2012 pertussis incidence.
129 unity to B. pertussis Natural immunity to B. pertussis induced by infection is considered long lastin
130 ctive cohort study design evaluating whether pertussis-infected infants born in 2011-2015 whose mothe
131                   The case fatality ratio of pertussis-infected pneumonia cases 1-5 months of age was
132     We conducted a population-based study of pertussis infection and reinfection during a 5-year peri
133                           Recurrent cases of pertussis infection are extremely rare.
134 ia of respiratory illness were tested for B. pertussis infection by PCR on paired NPSs and NPAs; or p
135 eded to understand the immune response to B. pertussis infection in children vaccinated with aP vacci
136 rtactin-deficient and pertactin-producing B. pertussis infection in infants and describe correspondin
137 d children with >/=2 episodes of symptomatic pertussis infection that met the case definition were in
138 ious study used a murine model of Bordetella pertussis infection to demonstrate that treatment with t
139 ds and aP vaccine at the time of their first pertussis infection, 1 (4%) had received 1 dose, and 5 (
140 he circulation, significantly exacerbated B. pertussis infection.
141 otects against both pertussis disease and B. pertussis infection.
142 s of immunity against subsequent symptomatic pertussis infection.
143  impaired their innate immune response to B. pertussis infection.
144 mmune response and restored resistance to B. pertussis infection.
145  suppress innate immune responses against B. pertussis infection.
146 rtactin-producing and pertactin-deficient B. pertussis infections.
147                                   Bordetella pertussis is a human pathogen that can infect the respir
148 ression among Bordetella species and that B. pertussis is capable of expressing a full range of T3SS-
149 is study, a neonatal mouse model of critical pertussis is characterized, and a central role for pertu
150                                              Pertussis is circulating freely among this population of
151       The Gram-negative bacterium Bordetella pertussis is the causative agent of whooping cough, a se
152            Natural infection with Bordetella pertussis is thought to result in 4-20 years of immunity
153 ed by the obligate human pathogen Bordetella pertussis is undergoing a worldwide resurgence.
154 ussis (whooping cough), caused by Bordetella pertussis, is resurging in the United States and worldwi
155 ged with a high dose of a highly virulent B. pertussis isolate, they were fully protected against dis
156    Molecular characterization of archived B. pertussis isolates (collected January 2007 to March 2014
157                               Sixty of 72 B. pertussis isolates were viable for analysis.
158                                   Bordetella pertussis isolation by culture has low detection sensiti
159               A study of an Escherichia coli pertussis-like toxin demonstrates that this protein acts
160 al chemoselectivity, suggesting this E. coli pertussis-like toxin may serve as a unique tool to study
161 n spread to other bodily locations) encode a pertussis-like toxin that inhibits mammalian cell growth
162                                              Pertussis-like toxins are secreted as disulfide-bonded h
163                                              Pertussis-like toxins are secreted by several bacterial
164 toxin in whooping cough is well-established, pertussis-like toxins produced by other bacteria are les
165 lecular mechanism underpinning activation of pertussis-like toxins, and we also identified difference
166 mpared with B. bronchiseptica Remarkably, B. pertussis maintained the production of virulence factors
167 vaccines (tetanus, diphtheria, and acellular pertussis, measles and rubella, or measles, mumps, and r
168 IgG levels specific for diphtheria, tetanus, pertussis, measles, rubella, and Haemophilus influenzae
169 ults indicate a role for S1P signaling in B. pertussis-mediated pathology and highlight the possibili
170 ropose that the reduced plasticity of the B. pertussis membranes ensures sustained production of viru
171 ated flux balance analysis-based model of B. pertussis metabolism.
172                                              Pertussis MI programs have proven effective in reducing
173 strategies to assess the potential impact of pertussis MI.
174                  In response to increases in pertussis morbidity and mortality among young infants, s
175 ams have proven effective in reducing infant pertussis mortality in high-income countries using tetan
176 We systematically reviewed studies reporting pertussis mortality rates (PMRs) per million population,
177                          We estimated infant pertussis mortality rates at which maternal vaccination
178 y sensitivity analyses identified the infant pertussis mortality rates required to make maternal immu
179 untry, at a vaccine price of $4/dose, infant pertussis mortality would need to be 0.043 per 1000 to c
180  respiratory CD4 TRM cells in immunity to B. pertussis Natural immunity to B. pertussis induced by in
181  with respect to infants at greatest risk of pertussis, needs to be further evaluated.
182                                Compared with pertussis-negative African cases in this age group, pert
183               Most severe and fatal cases of pertussis occur in infants <8 weeks of age, before initi
184                                              Pertussis, or whooping cough, caused by the obligate hum
185                          Among 32 reports of pertussis outbreaks, which included 10,609 individuals f
186 been factors contributing to community-level pertussis outbreaks.
187  be a valuable tool to investigate causes of pertussis pathogenesis and identify potential therapies
188                                   Among 9801 pertussis patients aged >/=3 months, 77.6% were AAV.
189  and complications are less common among AAV pertussis patients, demonstrating that the positive impa
190                      Biofilm formation by B. pertussis plays an important role in pathogenesis.
191 is-negative African cases in this age group, pertussis-positive cases were younger, more likely to vo
192 ls from the lungs of mice reinfected with B. pertussis produced significantly more IL-17 than gammade
193 ); and (3) with the addition of an antenatal pertussis program.
194 VirB/VirD4, E. coli R388 Trw, and Bordetella pertussis Ptl systems support conjugative DNA transfer i
195                                              Pertussis rates were comparable among all other age grou
196 Infants aged <1 year are at highest risk for pertussis-related morbidity and mortality.
197                                              Pertussis remains a cause of morbidity and mortality amo
198                                 Diagnosis of pertussis remains a challenge, and consequently research
199 is and Bordetella bronchiseptica Although B. pertussis represents a pathogen strictly adapted to the
200 results indicate that the blunting of infant pertussis responses induced by maternal immunization, me
201 dap vaccine during pregnancy had less severe pertussis, resulting in a lower risk of hospitalization
202                                     Although pertussis resurgence has been attributed to waning immun
203  (HIV) modestly increased the risk of infant pertussis (risk ratio, 1.8 [95% CI, .5-6.9]).
204 hooping cough causative bacterium Bordetella pertussis Secreted as soluble protein, it targets myeloi
205 clinically significant illness, or of severe pertussis (seizure, encephalopathy, pneumonia, and/or ho
206 after January 1, 2000), endemic and epidemic pertussis since the lowest point in US pertussis inciden
207                  These CD4 TRM cells were B. pertussis specific and secreted IL-17 or IL-17 and IFN-g
208                                   Bordetella pertussis strains lacking expression of pertactin, a bac
209 ed pertussis cases reported through Enhanced Pertussis Surveillance (Emerging Infections Program Netw
210                                      Serious pertussis symptoms and complications are less common amo
211 receive a tetanus, diphtheria, and acellular pertussis (Tdap) vaccine at 27-36 weeks gestation during
212 o receive tetanus, diphtheria, and acellular pertussis (Tdap) vaccine at the start of the third trime
213 ct a maternal tetanus, diphtheria, acellular pertussis (Tdap) vaccine booster between 2 consecutive p
214 countries using tetanus-diphtheria-acellular pertussis (Tdap) vaccines in their maternal and infant p
215 trative coverage with 3rd dose of diphtheria-pertussis-tetanus vaccine in the 107 high-risk LGAs impr
216 e "master virulence regulator" in Bordetella pertussis, the causal agent of pertussis, and related or
217                                   Bordetella pertussis, the causative agent of whooping cough, secret
218 nt nasopharyngeal colonization by Bordetella pertussis, the principal causative agent of whooping cou
219 has low detection sensitivity for diagnosing pertussis; the diagnosis is confirmed by measuring serum
220                     By comparing parental B. pertussis to an rseA gene deletion mutant (PM18), we sou
221 morbidity and mortality caused by Bordetella pertussis To better inform such interventions, we conduc
222 A-produced signaling of cAMP thus enables B. pertussis to evade the key innate host defense mechanism
223 a may result from selective adaptation of B. pertussis to the human host.
224  during each pregnancy to reduce the risk of pertussis to their infants.
225 agnosis is confirmed by measuring serum anti-pertussis toxin (anti-PT) or anti-filamentous hemaggluti
226                            B. pertussis uses pertussis toxin (PT) and adenylate cyclase toxin (ACT) t
227 MCs) of cord blood antibodies to recombinant pertussis toxin (PT) and filamentous hemagglutinin (FHA)
228 sis is characterized, and a central role for pertussis toxin (PT) is described.
229 1143-induced AA contraction was sensitive to pertussis toxin (PTX), the LPA1&3 antagonist Ki16425, an
230       We found that following EAE induction, pertussis toxin administration leads to IL-1 receptor ty
231 ntrast, inhibition of Galphai signaling with pertussis toxin affects speed but not the intermittent m
232 cs, and this reversal effect is inhibited by pertussis toxin and by genetic deletion of alpha-gustduc
233  propose that it is the systemic activity of pertussis toxin and not pulmonary pathology that promote
234       However, the increase was inhibited by pertussis toxin as well as by wortmannin but not by AG14
235                         Although the role of pertussis toxin in whooping cough is well-established, p
236 coupled receptors, the effects of AAL-R were pertussis toxin insensitive in our model.
237 bitors of cAMP/PKA signaling, insensitive to pertussis toxin or beta-arrestin knock-out, and mimicked
238 ylcholine, after G-protein inactivation with pertussis toxin or in myocytes from M2- or M1/3-muscarin
239 RHGEF1, and DOCK2 is completely inhibited by pertussis toxin pretreatment, thus suggesting different
240                       Surprisingly, although pertussis toxin targets a cysteine residue within the al
241 nal vaccination results in higher birth anti-pertussis toxin titers in preterm neonates.
242                Treatment of fibroblasts with pertussis toxin, an inhibitor of Galphai-coupled recepto
243 was also observed in neurons pretreated with pertussis toxin, an uncoupler of G proteins and MOR.
244  CB1R antagonist rimonabant and Gi uncoupler pertussis toxin, and absent in Cnr1(-/-) RGCs.
245                        Levels of antibody to pertussis toxin, antibody to filamentous hemagglutinin,
246 nist-induced rosette formation is blocked by pertussis toxin, dependent on PI3K activity and accompan
247 obulin (Ig) G specific for diphtheria toxin, pertussis toxin, filamentous hemagglutinin and pertactin
248 ect of MQC was reversed by pretreatment with pertussis toxin, indicating that FFA3 acts via the Gi/o
249       This inhibition is slowly established, pertussis toxin-insensitive, partially reversed within t
250              Despite the fact that S1PRs are pertussis toxin-sensitive G protein-coupled receptors, t
251 rom IL-17-activated PCs, but not ECs, induce pertussis toxin-sensitive neutrophil polarization, likel
252                         We reveal a role for pertussis toxin-sensitive signaling for TRM cell dendrit
253 ade that was sensitive to ERK inhibitors and pertussis toxin.
254  activity was elevated expressed very little pertussis toxin.
255 lar signal-regulated kinases (ERK) 1/2 or by pertussis toxin.
256  with 11% lower postvaccination antibody for pertussis toxoid (GMR, 0.89; 95% CI, 0.87-0.90) and fila
257                        Mathematical model of pertussis transmission fit to US incidence data in a sim
258 etween neonatal mice, the first report of B. pertussis transmission in mice.
259                                 We simulated pertussis transmission within an individual-based model
260                                           B. pertussis uses pertussis toxin (PT) and adenylate cyclas
261  of Tdap (tetanus, diphtheria, and acellular pertussis)-vaccinated pregnant women and 37 infants of w
262 sed on studies in unvaccinated or whole-cell pertussis-vaccinated children.
263 esponding directly to the aging of acellular pertussis-vaccinated cohorts.
264 occurred in vaccinated persons, showing that pertussis vaccination does not prevent all pertussis cas
265 s, demonstrating that the positive impact of pertussis vaccination extends beyond decreasing risk of
266                                    Antenatal pertussis vaccination is being considered as a means to
267                                     However, pertussis vaccination may have an impact on disease seve
268 to 9 age groups corresponding to the current pertussis vaccination schedule and fit to 2012 pertussis
269 anus, reduced-dose diphtheria, and acellular pertussis vaccine (Tdap) could be an effective way of mi
270 netics of antibody responses to an acellular pertussis vaccine by a genome-wide association study in
271 east 3 doses of diphtheria-tetanus-acellular pertussis vaccine by the end of 15 months of age.
272 tive potential of the novel, live attenuated pertussis vaccine candidate BPZE1.
273 analysis of published studies that evaluated pertussis vaccine efficacy or effectiveness within 3 yea
274           We calculated the effectiveness of pertussis vaccine in preventing parapertussis among Oreg
275                                              Pertussis vaccine may induce cross-immunity.
276                       Blunting of the infant pertussis vaccine response was detected in group B sibli
277 eks of age, before initiation of the primary pertussis vaccine series.
278 id, reduced diphtheria toxoid, and acellular pertussis vaccine).
279                    Dengue, tuberculosis, and pertussis vaccine-specific CD4(+) T cells were readily d
280 diphtheria and tetanus toxoids and acellular pertussis vaccine.
281 id, reduced diphtheria toxoid, and acellular pertussis) vaccine was recommended for women during each
282 having received an age-appropriate number of pertussis vaccines (AAV) (for persons aged >/=3 months)
283 nly (three doses of diphtheria, tetanus, and pertussis vaccines [DTP3] commencing in 1985, 1995, or 2
284 nd ethically preferred until next-generation pertussis vaccines become available.
285 lysis of the short-term protective effect of pertussis vaccines limited to formulations currently on
286                            Current acellular pertussis vaccines may not protect against transmission
287  antenatal care programs to deliver maternal pertussis vaccines, particularly with respect to infants
288 tussis can hamper infant immune responses to pertussis vaccines.
289 s after high childhood coverage of acellular pertussis vaccines.
290 reventing hospitalization among infants with pertussis was 72% (95% confidence interval [CI], 49%-85%
291        Enhanced innate immune response to B. pertussis was characterized by increased production of p
292                                   Bordetella pertussis was detected in 53 of 4200 (1.3%) cases and 11
293 (95% confidence interval, 4.2%-26.8%; 5/40); pertussis was identified in 3.7% of 137 in-hospital deat
294   We encountered an adult patient in whom B. pertussis was isolated by culture who previously receive
295                                     Cases of pertussis (whooping cough) caused by Bordetella pertussi
296                                              Pertussis (whooping cough), caused by Bordetella pertuss
297                                 Infants with pertussis whose mothers received Tdap during pregnancy h
298 fy all children with 2 reported incidents of pertussis with symptom onset between 1 January 2010 and
299 d a clinically significant second episode of pertussis within 4 years.
300                              Transmission of pertussis within this population was simulated to captur

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