ライフサイエンスコーパス: booster

1 em frequencies before and after the 11-month booster.

2 -level therapists with a follow-up telephone booster.

3 ailure based on its activity as a cyclic AMP booster.

4 included five weekly sessions and a 1-month booster.

5 n time since infant priming and receipt of a booster.

6 accine and in 100% of participants after the booster.

7 y series, at 8 months of age, and before the booster.

8 rotection between the primary series and the booster.

9 delivered as a 3-dose primary series with no booster.

10 ccine and then 1 wk, 1 mo, and 1 y after the booster.

11 0002) in spleen were fewer than after saline booster.

12 ses of HBV vaccine were given an HBV vaccine booster.

13 imary course of MenACWY and after a 12-month booster.

14 s of anti-HBs measurements 30 days after the booster.

15 ading to the discovery of potent ethionamide boosters.

16 nC-CRM(197) (P = .0286) or saline (P = .001) boosters.

17 Thus, we need improved vaccines and boosters.

18 city, often necessitating multiple doses and boosters.

19 -cell vaccines in a primary schedule without boosters.

20 g (11 core, 2 optional sessions; 2 telephone boosters; 2 home visits) provided specific strategies to

21 After the booster, 93.1%-100% of participants achieved MN titers o

22 bset of 47 children who had received a JE-CV booster after an inactivated JE vaccine primary immuniza

23 After an in vivo booster Ag challenge, the ratio of Ag-reactive T cells t

24 pollen season was significantly lower in the booster AIT group (Delta=38.4%, P<.01).

25 Twice as many patients in the booster AIT group as in the control group reported havin

26 effects of a preseasonal, ultra-short-course booster AIT on clinical outcome parameters.

27 Booster AIT using tyrosine-absorbed allergoids containin

28 tients received one preseasonal short-course booster AIT using tyrosine-absorbed grass pollen allergo

29 The booster AIT was generally well tolerated, with only two

30 showed significant differences favouring the booster AIT.

31 HCWs) vaccinated as adults and response to a booster among those without protective levels of antibod

32 Twelve hours after the MenC-PS booster, an increased frequency of apoptotic (AnnexinV(+

33 s with inadequate anti-HBs levels received a booster and 32 (94%) developed levels >12 mIU/mL within

34 HCWs with anti-HBs <12 mIU/mL were offered a booster and levels were measured 1, 7, and 21 days after

35 y room and had likely received a vaccination booster, and a total of 202 children showed higher vacci

36 composition, multishot regimen, recommended boosters, and potential for adverse reactions.

37 We aimed to compare the post-booster antibody response in UK infants given a reduced

38 % CI, 1.24-3.05) and for ritonavir used as a booster (aOR, 1.56; 95% CI, 1.11-2.20).

39 m, we report on infant immune responses to a booster aP vaccine dose in this randomized controlled cl

40 series of aP vaccines, was resolved with the booster aP vaccine dose.

41 rsion rates were significantly higher in the booster arm for the per-protocol population (53.8% vs 37

42 0 months and will be given (trial ongoing) a booster at 12 months (group 3), and 198 were given place

43 e at 0 months, or one dose at 0 months and a booster at 12 months) or placebo.

44 of WT JE strains at baseline, then after the booster at 28 days and 6 months in all subjects present

45 Receiving a booster at age 10-14 years decreased HBsAg seroprevalenc

46 was to investigate if a two-dose prime with booster at age 9 months compared with a three-dose prime

47 Use of a 2+1 PCV schedule with booster at age 9 months in a resource-poor setting impro

48 phtheria, acellular pertussis (Tdap) vaccine booster between 2 consecutive pregnancies is investigate

49 Booster biocides have been widely applied to ships and o

50 tive to controlling contamination of fish by booster biocides, with low consumption of biodegradable

51 ed by postnatal nonmyeloablative same donor "booster" bone marrow (BM) transplants in murine models o

52 tudy is the first to demonstrate that NAD(+) boosters can also directly affect skeletal muscle mitoch

53 ention arm attended 11 one-hour weekly and 2 booster classroom sessions of an intervention based on c

54 sisted of 4 weekly clinic appointments and 1 booster clinic at month 6, where multidisciplinary profe

55 ational interviewing with a 20- to 30-minute booster conducted by master's-level counselors.

56 , right ventricular free wall strain, and LA booster, conduit, and reservoir strains.

57 on, MMR booster vaccination compared with no booster did not result in worse JIA disease activity and

58 nsitional care including early follow-up and booster discharge instructions.

59 ubsequent cohorts, and one cohort received a booster dose after 1 year.

60 esponses were significantly increased upon a booster dose and remained at high levels even after thre

61 The duration of protection and need for a booster dose are unknown.

62 n 2006, given at 2 and 4 months of age and a booster dose at 13 months (2 + 1 schedule).

63 nt (TV005), and to evaluate the benefit of a booster dose at 6 months.

64 s (earlier than currently recommended) and a booster dose at 9-12 months of age.

65 -4); or at ages 2 and 4 months (2-4), with a booster dose at age 11.5 months.

66 ages 2 months, 4 months, and 6 months, and a booster dose at age 12 months.

67 every pregnancy was combined with a toddler booster dose at age 18 months; incidence was reduced to

68 ermine if effective control persists or if a booster dose becomes necessary as has been the case in i

69 ant differences in antibody levels after the booster dose for almost all serotypes.

70 Interestingly, a booster dose further enhances the immune responses, a fe

71 dose primary series of Hib vaccine without a booster dose has resulted in a significant and sustained

72 f conjugate Hib vaccine in infancy without a booster dose in Kenya.

73 -term immune responses induced after a JE-CV booster dose in toddlers were able to neutralize WT viru

74 trol persists, these findings suggest that a booster dose is not currently required in Kenya.

75 A 3-dose PCV13 regimen followed by a booster dose may be required to protect against pneumoco

76 t PCV13-included serotypes 1 month after the booster dose measured by multiplex immunoassay.

77 We hypothesized that a booster dose might increase it.

78 nd those primed with JE-MB received a single booster dose of (group 3) JE-MB or (group 4) JE-VC.

79 We then assessed the effect of adding a booster dose of a modified vaccinia Ankara (MVA) strain,

80 enicity and reactogenicity of a heterologous booster dose of A/turkey/Turkey/1/2005(H5N1)-AS03B (AS03

81 se priming regimen of the DNA vaccine with a booster dose of an adenovirus type 5 (Ad5)-vectored vacc

82 A booster dose of HB vaccination was administered to 1974

83 es were 91% and 91%, and 98% and 95% after a booster dose of JE-MB or JE-VC, respectively.

84 A booster dose of MenB-4C may be needed to maintain protec

85 e Ab levels nor the capacity to respond to a booster dose of MenC Ag.

86 ccine compared with the B-cell response to a booster dose of rabies vaccine given to previously immun

87 Those with levels <10 mIU/mL received 1 booster dose of recombinant hepatitis B vaccine 2-4 week

88 year-olds, similar to those expected after a booster dose of TT.

89 individuals aged >/= 70 years who received a booster dose of ZV were compared to responses of 100 par

90 Bs level >/=10 mIU/mL at 30 years and an 88% booster dose response, we estimate that >/=90% of partic

91 ccal serogroup B vaccines and the need for a booster dose to sustain individual protection against in

92 A booster dose was administered to 164 persons, and 77% re

93 Response to a booster dose was positively correlated with younger age,

94 The immunogenicity of the booster dose was strongly associated with immunogenicity

95 for follow-up, 75 of 85 (88%) responded to a booster dose with an anti-HBs level >/=10 mIU/mL at 30 d

96 variations in PCV uptake (and receipt of the booster dose) might influence the effectiveness of PCVs

97 PCV10 vaccination, both before and after the booster dose, for all 4 shared serotypes except for sero

98 L at 22 years and those who responded to the booster dose, protection was demonstrated in 87% of the

99 on of RTS,S/AS01 efficacy, with or without a booster dose, providing a valuable surrogate of effectiv

100 One month after the booster dose, significantly lower antibody titers were m

101 e primary outcome, GMCs at 1 month after the booster dose, was not significantly different between sc

102 rime" recipients for rapid protection with a booster dose, years later, of a vaccine then manufacture

103 e long-lived, rising to 30% (28-32%) after a booster dose.

104 er 2 years, subsets in each group received a booster dose.

105 ter RTS,S/AS01 vaccination with or without a booster dose.

106 rences between schedules persisted until the booster dose.

107 orts from high-income countries giving a PCV booster dose.

108 ted for >/= 10 years and was enhanced by the booster dose.

109 Four participants did not receive a booster dose; 67 of 75 study vaccine recipients were fol

110 the VZV antibody response at 6 weeks in the booster-dose group, compared with the age-matched first-

111 her at baseline and after vaccination in the booster-dose group, compared with the first-dose group,

112 Booster doses are not needed.

113 Booster doses are not needed.

114 been found to wane after vaccination, these booster doses can serve to more fully protect adolescent

115 aken together, these data indicate that oral booster doses effectively elicit protective immune respo

116 inistration in early versus later age and of booster doses for elderly individuals at an appropriate

117 In many countries, Hib vaccine booster doses have been implemented after infant immuniz

118 and adolescent vaccinations and the need for booster doses in older adolescents.

119 The possibility of earlier or more numerous booster doses of acellular pertussis vaccine either as p

120 dy was still evident in reduced responses to booster doses of acellular pertussis, inactivated polio,

121 ins are sustained or attenuated, and whether booster doses of the intervention are needed to maintain

122 Booster doses were provided for those with loss of prote

123 nding NYVAC-C-KC vectors (weeks 0 and 4) and booster doses with NYVAC-C-KC vectors plus the clade C H

124 gies such as different age-spacings, further booster doses, and cocooning.

125 and remained at high levels even after three booster doses.

126 antiflagellin IgG levels increased following booster doses.

127 econdary humoral immune responses to tetanus booster during treatment were reduced, but antibody tite

128 The intervention group received booster education every visit by viewing a 15-minute edu

129 ysaccharides at 4-8 weeks, consistent with a booster effect.

130 2 MOG-specific transgenic mice, and repeated boosters facilitated generation of activated CD44(high)

131 The use of PPV as a booster following PCV causes early increases in antibody

132 o employ it as a direct and universal signal booster for loop mediated isothermal reaction (LAMP).

133 tly higher in those who had received the MVA booster (geometric mean titer, 1750; P<0.001).

134 At month 13, post-booster, GMCs were equivalent between schedules for sero

135 o receive 1 dose (control group) or 2 doses (booster group) of the influenza vaccine 5 weeks apart.

136 seroprotection at 10 weeks was higher in the booster group: 54% vs 43.2% for A(H1N1)pdm; 56.9% vs 45.

137 brief intervention with attempted telephone booster had no effect on drug use in patients seen in sa

138 l children following infant (with or without booster) Hib vaccination.

139 es were available for analysis 1 month after booster immunisation versus 86 in group 2.

140 both Vaccine-NP and IAV groups following the booster immunisation.

141 Booster immunisations were given at weeks 16 and 18.

142 After booster immunisations, most of the immune responses show

143 modified vaccinia virus Ankara (MVA) ME-TRAP booster immunization 8 weeks later (n = 26).

144 alized LeTx in vitro 78 days after the final booster immunization and protected the mice from in vivo

145 mmunization with G14D-CCV and at 3 d after a booster immunization as compared with control fish only

146 After booster immunization in a rabbit, we find that the antig

147 Also, in contrast with GBS-III, booster immunization of MenC-primed mice with isolated M

148 to other H5 antigen vaccines, it required a booster immunization to prime protective immune response

149 nd whether augmented IgG responses following booster immunization were also dependent on CD4(+) T cel

150 )ICOS(+) cTfh subset clonally expanded after booster immunization whose frequencies correlated with v

151 A subset of participants received a booster immunization with an A/Indonesia(H5N1) vaccine a

152 ugmented PS-specific IgG response similar to booster immunization with intact MenC.

153 enhance PS-specific IgG responses following booster immunization with their encapsulated isogenic pa

154 ristics, including the ability to respond to booster immunization within days of initial priming.

155 tly, cross-primed CD8 T cells can respond to booster immunization within days of the initial immuniza

156 various B cell populations, the response to booster immunization, and the generation of plasma cells

157 Activated MBCs were also induced by TT booster immunization, indicating that the expansion of t

158 rition of memory CD8 T cells was reversed by booster immunization, which restored protection.

159 d) were taken before and 28 days after PCV13 booster immunization.

160 CD8(+) T cell anamnestic response following booster immunization.

161 tivector antibodies did not interfere with a booster immunization.

162 obulin diversity, and cannot be corrected by booster immunization.

163 for the improved survival that results from booster immunization.

164 mediate the enhanced protection conferred by booster immunization.

165 accharide (PS)-specific IgG titers following booster immunization.

166 cells for augmented IgG responses following booster immunization.

167 ugmented PS-specific IgG responses following booster immunization.

168 These data suggest that regular booster immunizations may be required to sustain protect

169 TM expansion in the presence of TE, enabling booster immunizations to bypass TE-mediated negative fee

170 This allows booster immunizations to rapidly expand CD8(+) central m

171 Our results show that heterologous booster immunizations with the chimpanzee-derived Ad vec

172 again 1 week, 1 month, and 1 year after the booster in 250 healthy children aged 6-12 years in an op

173 followed by a modified vaccinia virus Ankara booster induces exceptionally high frequency T-cell resp

174 tered IM in 8 subjects/DL, with an identical booster injection 28 days later and 1-year follow-up.

175 e additionally block-randomised to receive a booster injection on either day 28 or day 90 after the f

176 The second (booster) injection of MVA85A or placebo was given 6-12 m

177 Additional booster injections are required to augment the antibody

178 T cell expansion measured during subsequent booster injections over at least 100days.

179 tered on weeks 0, 6, and 12, followed by two booster inoculations with vesicular stomatitis virus (VS

180 immune factors, being the most potent immune booster known to science.

181 Two Apa-boosters markedly improved waning BCG-immunity and signi

182 At least 95% of primary and booster MenACWY recipients achieved hSBA titers >or=1:4

183 We show that booster modified vaccinia virus Ankara immunization indu

184 ing MenC conjugate vaccine priming, before a booster of a combined Haemophilus influenzae type b-MenC

185 ecific memory B cells were measured before a booster of a Hib-serogroup C meningococcal (MenC) conjug

186 on dendritic cells (DCs) is well known as a booster of immune responses.

187 type II collagen (CII) in CFA followed by a booster on day 21, which consisted of CII in IFA.

188 We assessed the effects of a PS booster on immune responses, frequency, and survival of

189 er scale and confirmed as potent ethionamide boosters on M. tuberculosis -infected macrophages.

190 in vitro/ex vivo evaluations of ethionamide boosters on the targeted protein EthR and on the human p

191 Blood was collected before the 11-month booster or 7-9 days afterward.

192 en 24 h before virus exposure, followed by a booster postexposure dose.

193 in BCG-primed mice and investigated its BCG-booster potential.

194 randomly assigned to a two-session (plus two boosters) presurgical stress management intervention (SM

195 In support of the Nigeria Malaria Booster Program we assessed PMV practices in three Senat

196 uction of catch-up (2003) and routine (2006) booster programmes for young children.

197 After MenC-PS booster, proliferating (BrdU(+)) MenC-PS-specific naive

198 h analysis of atrial reservoir, conduit, and booster pump function trails in that regard, the gap is

199 ed with decreased LA reservoir, conduit, and booster pump functions.

200 ated with reduced LA conduit, reservoir, and booster pump LA function.

201 reservoir strain, LA conduit strain, and LA booster pump strain were quantified.

202 Compared to saline, MenC-PS booster reduced BrdU(+) IgG(+) MenC-PS-specific B cells

203 n with HIV molecules showed that CE+gag pDNA booster regimen further expanded the breadth of HIV CE r

204 Following p27CE pDNA priming, two booster regimens, gag pDNA or codelivery of p27CE+gag pD

205 Higher baseline and post-Hib-MenC booster responses (anti-PRP IgG and memory B cells) were

206 P or NANP conjugates induced antibodies with booster responses and were positive by the sporozoite im

207 enic and induce measurable IgG, PC, and Bmem booster responses at 11 months.

208 V induced multiple IgG subclasses and strong booster responses in all ages.

209 for nine of the 13 serotypes in PCV13, post-booster responses in infants primed with a single dose a

210 i, did not inhibit augmented PS-specific IgG booster responses of mice primed with heat-killed cells.

211 vaccination, there were robust memory B cell booster responses that, unlike Ab levels, were not depen

212 te that memory for augmented PS-specific IgG booster responses to Gram-negative and Gram-positive bac

213 Especially notable is the inability of booster schedules to alleviate resurgence when vaccines

214 e that the ultimate effectiveness of vaccine booster schedules will likely depend on correctly pinpoi

215 r motorcyclists and bicyclists, car seat and booster seat use for child motor vehicle passengers, spe

216 iveness of CBP may be enhanced by additional booster sessions and concomitant treatment of parental d

217 drop-in classes versus home practice and PT booster sessions versus home practice.

218 ith a positive response were given 3 monthly booster sessions.

219 y individual sessions with a therapist and 2 booster sessions.

220 Our results also suggest that an adolescence booster should be considered in individuals born to HBsA

221 We demonstrated that the MenC-PS booster significantly reduced the frequency of newly act

222 "leakiness." For scenarios I-IV, successful booster strategies were identified and varied considerab

223 In SOTR, a booster strategy 5 weeks after standard influenza vaccin

224 ssays, was poor despite the observation that boosters successfully reinduced protective levels of HBs

225 t intervention (SM), a two-session (plus two boosters) supportive attention group (SA), or a standard

226 ad significantly greater immunogenicity post-booster than those given the 2 + 1 schedule for serotype

227 nthracis in the wet season and can partially booster their immunity to B. anthracis.

228 such as structured treatment interruptions, booster therapies and induction-maintenance therapies.

229 d on time in a 3-dose primary series without booster to a high proportion of eligible children and th

230 the PWFA scheme very attractive as an energy booster to an electron-positron collider.

231 able but require multiple doses and frequent boosters to induce and maintain immunity.

232 6 h each (18 h in total) on AIMS and a 1.5 h booster training session at the clinic (two to three nur

233 Responders received 3 monthly booster treatment sessions and were reassessed at 3 and

234 olus subcutaneous (sc) injection followed by booster treatments given 24 and 48h later.

235 In countries with no pertussis booster until school age, continued monitoring of protec

236 ion (BMI) (n = 203), or BMI plus a telephone booster using personalized feedback or BMI + B (n = 193)

237 n motivational interviewing with a telephone booster using personalized feedback were most effective

238 a history of previous TBE vaccinations were booster vaccinated with TBE and influenza vaccine and co

239 tients were randomly assigned to receive MMR booster vaccination (n=68) or no vaccination (control gr

240 fficient immune response upon primary and/or booster vaccination and affects 1-10% of vaccinees.

241 Here, we introduce an in vitro booster vaccination approach that relies on antigen-depe

242 predictors of long-term immunity around the booster vaccination at 11 months of age.

243 Effector T cells (TEFF) are a barrier to booster vaccination because they can rapidly kill Ag-bea

244 ever, effector T cells (TE) are a barrier to booster vaccination because they can rapidly kill antige

245 -adjuvanted vaccine followed by heterologous booster vaccination boosted immune responses to the homo

246 who had undergone primary immunization, MMR booster vaccination compared with no booster did not res

247 long-term protection against hepatitis B and booster vaccination does not appear to be necessary in H

248 ence of antibodies after acellular pertussis booster vaccination during adolescence.

249 However, the CE+gag pDNA booster vaccination elicited significantly broader CE ep

250 ved protection against tuberculosis by viral booster vaccination in a natural target species and has

251 nd persistence of antibodies after pertussis booster vaccination in adolescents.

252 ed vaccinia virus Ankara (MVA) followed by a booster vaccination is sufficient to protect against an

253 ificant proportion of them do not respond to booster vaccination or demonstrate memory despite receiv

254 ens comprising CE pDNA prime and CE+gag pDNA booster vaccination significantly increased cytotoxic T

255 ission model, we searched for cost-effective booster vaccination strategies using a genetic algorithm

256 Here we report that after booster vaccination there was a rapid and robust influen

257 Booster vaccination to achieve protective HBV immunity o

258 Appropriate timing of booster vaccination was also critical, as a tight boosti

259 Booster vaccination with a subunit vaccine (Ag85B-ESAT-6

260 em for either natural exposure or subsequent booster vaccination with either conjugate or polysacchar

261 1 month after priming vaccine doses, before booster vaccination, and 1 month after booster vaccine d

262 els were assessed for 6 months following the booster vaccination.

263 or repertoires following tetanus toxoid (TT) booster vaccination.

264 isted in all children 6 months following the booster vaccination.

265 ey/Turkey/1/2005(H5N1) 10 days following the booster vaccination.

266 followed up at 3, 5, and 10 years after this booster vaccination.

267 ia for >/=30 years without requiring further booster vaccination.

268 nuclear cell samples after their primary and booster vaccination.

269 it may no longer be necessary to administer booster vaccinations every 10 years and that the current

270 thylcellulose for eight courses, followed by booster vaccinations every 6 weeks.

271 Thus, our results indicate that booster vaccinations impact antitumor immunity to differ

272 Adolescent pertussis ("Tdap") booster vaccinations were more effective against B. pert

273 Thus, booster vaccinations with agonistic costimulatory antibo

274 vaccinia-NY-ESO-1 (rV-NY-ESO-1), followed by booster vaccinations with recombinant fowlpox-NY-ESO-1 (

275 nti-HBs serum titers, the potential role for booster vaccinations, and antiviral prophylaxis prior to

276 many countries have nevertheless recommended booster vaccinations, the timing and number of which var

277 dequate immune responses were elicited after booster vaccinations.

278 Pertussis booster vaccine (Tdap) recommendations assume that pertu

279 efore booster vaccination, and 1 month after booster vaccine doses.

280 The rapid and robust response to a booster vaccine suggests a long-lasting amnestic respons

281 Tetanus booster vaccine, pneumococcal vaccine, and intracutaneou

282 rensis immunoprotective antigen IglC) as the booster vaccine.

283 iven one intramuscular dose (0.5 mL) of H5N1 booster vaccine.

284 uencies and Ab at baseline and following the booster vaccine.

285 different H5N1 antigen using low-dose Anhui (booster) vaccine.

286 Of note, the candidate booster vaccines currently under clinical development ha

287 antigen 85B [Ag85B]) (rLm30) as heterologous booster vaccines in animals primed with BCG.

288 Booster vaccines made in chloroplasts prevent global inf

289 rLmI/h30 vaccines were generally more potent booster vaccines than r30 with an adjuvant and a recombi

290 major adverse events were allowed to receive booster vaccines.

291 A fifth and final booster was administered 6 months after the fourth immun

292 After 7.5 years, a vaccine booster was administered.

293 uld have lost protective antibodies before a booster was proposed.

294 , delivered as a three-dose series without a booster, was introduced into the childhood vaccination p

295 in elevated and do not increase with vaccine boosters, whereas in whole-cell vaccine-primed children,

296 1 year later, after a booster with an inactivated H5N1 vaccine (part 2), 39 (9

297 ys 42 and 225; cynomolgus monkeys received a booster with either PA or licensed anthrax vaccine (BioT

298 A parenteral booster with purified PA83 plus alum was given to rhesus

299 (eg, replacing decennial tetanus-diphtheria booster with tetanus, diphtheria, and acellular pertussi

300 ources, and an attempted 10-minute telephone booster within 2 weeks (n = 435) or enhanced care as usu