戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1  antigens may also be present on non-group B meningococci.
2 gococci, but not the CPS of serogroup B or C meningococci.
3 o the development of immunity to serogroup B meningococci.
4 ein-labeled ligands to HpuAB on live, intact meningococci.
5 urified PorB inhibited the binding of MBL to meningococci.
6 ine against infections caused by serogroup B meningococci.
7 ent of a mucosal vaccine against serogroup B meningococci.
8 charide vaccines protect against serogroup C meningococci.
9 fter immunization with homologous whole-cell meningococci.
10 f the role of active immune response against meningococci.
11 r cells that had been exposed to heat-killed meningococci.
12 of healthy donors are exposed to heat-killed meningococci.
13 eripheral blood mononuclear cells exposed to meningococci.
14 eripheral blood mononuclear cells exposed to meningococci.
15 rvoirs for all of the exl cassettes found in meningococci.
16 ingioma cell that was not apparent with Cap+ meningococci.
17 osed of polysaccharides from pneumococci and meningococci.
18 confirmed by [3H]-palmitic acid labelling of meningococci.
19 es, we show that these receptors are used by meningococci.
20 ccine antigens may be present on non-group B meningococci.
21 th decline in carriage of disease-associated meningococci.
22  from all 12 macaques enhanced FH binding to meningococci.
23  sepsis and meningitis caused by serogroup B meningococci.
24 confidence interval [CI], 3.2%-3.6%) carried meningococci.
25 d with sepsis and recoverable levels of live Meningococci.
26 on results from reduced carriage of virulent meningococci.
27 required for complement-dependent killing of meningococci.
28 act on immune escape and host persistence of meningococci.
29 ng, we identified five distinct GGI types in meningococci.
30  with overexpressed FHbp elicits SBA against meningococci.
31  their bactericidal activity against group B meningococci.
32 at demonstrated human-specific fH binding to meningococci.
33 ains fH SCR 6, also bound to fHbp-expressing meningococci.
34 majority of disease-associated group B and C meningococci.
35 antly upregulated in blood after exposure to meningococci.
36  four of the five major pathogenic groups of meningococci: A, C, W-135, and Y.
37 e purified human LOS-specific IgG that binds meningococci across LOS glycose-specific serotypes.
38  meningococci that (rate ratio, 0.06); these meningococci also exhibited high rates of capsule expres
39                           We determined that meningococci also release PG fragments during growth, in
40 o explain the preponderance of 3-PEA-bearing meningococci among clinical isolates, because 6-PEA enha
41 permeability-increasing protein, which kills meningococci and binds to and clears bacterial endotoxin
42                               OMVs from both meningococci and commensal neisseriae have shown promise
43  SBA titres most likely reflects exposure to meningococci and consecutive reactive immunity.
44 ents indicated that AutB is not expressed in meningococci and does not cross-react with AutA.
45 -expressing clinical and mucosal isolates of meningococci and gonococci were shown to bind to the CD6
46 g may be an important virulence mechanism of meningococci and other encapsulated bacterial pathogens.
47 oduce vaccines with broad protection against meningococci and pneumococcus, develop an effective vacc
48 surface of wild-type but not Deltamip mutant meningococci and showed bactericidal activity against ho
49  specificity of the bactericidal response to meningococci and the stability of expression of the clas
50 phy enables us to track the dissemination of meningococci and their transmission.
51 ca, was due both to displacement of existing meningococci and to inhibition of new acquisition, and p
52 bster mice were inoculated intranasally with meningococci, and bacteria were recovered from the noses
53  Escherichia coli K1, groups W-135, Y, and C meningococci, and group B Streptococcus capsular polysac
54                                          All meningococci are carried in the nasopharynx, and most ge
55 Serum bactericidal assays (SBAs) for Group B meningococci are considered the methods of choice for th
56                        Individual strains of meningococci are extremely variable and undergo dynamic
57                                              Meningococci are opportunistic pathogens that colonize t
58          Multiple outer-membrane proteins of meningococci are subject to phase-variable switches in e
59 n transglycosylase, elicits protective Ab to meningococci as a result of mimicking an epitope on loop
60                                  Carriage of meningococci, as detected by the combined methods, was 2
61 22%-26%), compared with meningitis caused by meningococci at 9% (95% CI, 8%-10%) or H influenzae at 1
62                              The responsible meningococci belong to a highly virulent and predominant
63                                              Meningococci bind fH via fH binding protein (fHbp), a su
64  acetylated the wild-type CPS of serogroup A meningococci, but not the CPS of serogroup B or C mening
65                We conclude that MBL binds to meningococci by a novel target recognition of two nongly
66 mon resonance and to the mutant expressed on meningococci by flow cytometry.
67 ect individuals can block killing of group B meningococci by human sera that are otherwise bactericid
68  There was no evidence of internalization of meningococci by meningioma cells in vitro, an observatio
69                  Disk diffusion testing with meningococci can be performed in a reproducible manner w
70                     We conclude that group C meningococci can be phagocytosed by neutrophils in the a
71                                              Meningococci can escape being killed by antibodies to LP
72 n analysis of the hemA mutant indicated that meningococci can transport intact porphyrin from heme (H
73 termine the evolutionary relationships among meningococci carrying hmbR, exl2, or exl3, isolates repr
74 d Kingdom in 1999, but the sequence types of meningococci causing disease since that time have not ye
75 c dynamics of C:P1.5.1,10-8:F3-6;ST-11(cc11) meningococci causing outbreaks, as occurred in the Tusca
76                                 In contrast, meningococci contain at least one L-LDH in addition to t
77             Outbreaks due to non-A serogroup meningococci continue to be a significant burden in this
78               However, serogroup C, W, and X meningococci continue to circulate and have been respons
79     The detection of carriage of serogroup B meningococci correlated with an increase in detection of
80 ntains a poly(G) tract, which suggested that meningococci could phase vary each Hb receptor independe
81 by clonal complex ST-11 and ST-8 serogroup C meningococci decreased from 251 of 268 (94%) before, to
82                    Little is known about how meningococci directly influence these receptors.
83 ement-mediated bactericidal activity against meningococci displaying fHbp from any of the 3 different
84                                 On occasion, meningococci disseminate from the nasopharynx to cause i
85                                              Meningococci drive the differentiation of the Men C-spec
86                                 Encapsulated meningococci expressing a Hep2(GlcNAc)-->KDO2-->lipid A
87 y herd protection by reduced colonization of meningococci expressing the MenC capsule.
88 st strains representative of disease-causing meningococci expressing vaccine-heterologous antigens.
89 st strains representative of disease-causing meningococci expressing vaccine-heterologous antigens.
90                              Some strains of meningococci form biofilms, and this process is likely i
91 d multilocus sequence typing to characterize meningococci from patients with invasive disease over a
92 n vitro data suggest that, in these lesions, meningococci gain access from the capillary lumen to the
93 l be safe and effective vaccines for Group B meningococci (GBMs), Escherichia coli K1, and Pasteurell
94                           Disease-associated meningococci (genogroups A, B, C, W, X, Y) were detected
95                  These enzymes are active in meningococci grown in complex media and are not dependen
96                                          For meningococci grown on a complex medium, activity of the
97 , E (3 isolates), and X (2 isolates), and 68 meningococci had the capsule-null intergenic region.
98  MenAfriVac (PsA-TT), disease due to group A meningococci has nearly disappeared.
99                                   Pathogenic meningococci have acquired a 24 kb capsule synthesis isl
100 rane protein (OMP) components of serogroup B meningococci have been shown to be effective in clinical
101                 Thus, App is conserved among meningococci, immunogenic in humans and potentially invo
102    Carriage prevalence of disease-associated meningococci in 2018 was 225/4104 (5.5%).
103 ed carriage prevalence of disease-associated meningococci in 2018-2020 as the proportion of vaccinate
104       Carriage of all strains of serogroup C meningococci in asymptomatic students was low (0.9%), an
105 dy shows high seroprevalence against group A meningococci in Burkina Faso following MenAfriVac introd
106 e disease by serogroup B and non-serogroup B meningococci in children younger than 5 years of age.
107 ereas endotoxin was at least as effective as meningococci in inducing ICAM-1 and VCAM-1.
108                  We compared the carriage of meningococci in isolates we obtained from 14,064 student
109 asis for LOS sialylation in AP regulation on meningococci in more than one animal species.
110                                   Killing of meningococci in reactions containing bactericidal mAbs a
111 ide (LOS) are bactericidal for L3,7 and L2,4 meningococci in the presence of human complement.
112 duction of oropharyngeal carriage of group A meningococci in vaccinated and unvaccinated individuals,
113 rnatants of inflammatory cells stimulated by meningococci in vitro abolished the negative inotropic a
114 le effect on the carriage of disease-causing meningococci, including group B.
115                                              Meningococci incubated with human serum bound MBL as det
116 ty and morbidity associated with serogroup B meningococci infections, but uncertainty remains about t
117  situation with gonococci, the mtr system in meningococci is not subject to the MtrR or MtrA regulato
118    We conclude that the mtr efflux system in meningococci is subject to transcriptional regulation by
119               Six clusters contained carried meningococci isolated during 1997-2001, suggesting tempo
120 tial iron scavenging capacity amongst Y:cc23 meningococci isolated from older compared to younger pat
121  repertoires in 190 asymptomatically carried meningococci isolated in the United Kingdom from a conte
122    Opa repertoires in 227 disease-associated meningococci, isolated in the United Kingdom over a peri
123                                  The lack of meningococci killing by blood containing eculizumab resu
124   Over the past 50 years one such lineage of meningococci, known as serogroup A, clonal complex 5 (A:
125                               The ability of meningococci lacking expression of fHbp and NspA to caus
126 is aggregated and recruited to intracellular meningococci (MC).
127        An equivalent vaccine against group B meningococci (menB) has remained elusive due to the poor
128                     Following challenge with meningococci, meningioma cells secreted specifically the
129                                       As for meningococci, mutation of the gonococcal lldA reduced L-
130                The transcriptome of adherent meningococci obtained after 4 h of coculture was markedl
131                                              Meningococci obtained from cerebrospinal fluid or oropha
132                Understanding why carriers of meningococci occasionally develop invasive disease is a
133 enicity and cross-reactivity of AutA amongst meningococci of different serogroups and strains represe
134 us-mediated adhesion to host cells by either meningococci or gonococci triggers the rapid, localized
135 rmine whether carried and disease-associated meningococci possess different Opa repertoires and wheth
136                                              Meningococci possessing a capsule null locus (cnl) typic
137            At both surveys, nongenogroupable meningococci predominated, followed by genogroups Y, B,
138 ely formed amide linkages, whereas C4B bound meningococci preferentially via ester linkages.
139 protein-based vaccines targeting serogroup B meningococci protect against invasive disease but impact
140  meningitidis and N. gonorrhoeae showed that meningococci release less of the proinflammatory PG mono
141                No studies have determined if meningococci release PG or activate Nod1 during infectio
142 ngitis and septicaemia caused by serogroup B meningococci remain uncontrolled.
143 t, efficient stimulation of RANTES by intact meningococci required pilus-mediated adherence, which se
144         To ascertain the mechanisms by which meningococci resist PxB, mutants that displayed increase
145 ns and mortality of IMD-W with IMD caused by meningococci serogroup B, Y, or C, adjusting for age, ge
146        Purified CPSs bound to unencapsulated meningococci, simulated findings with naturally encapsul
147 might induce against the diverse serogroup B meningococci strains that cause disease.
148                However, different strains of meningococci, such as those within the electrophoretic t
149 thelial cells were invaded by Opa-expressing meningococci, suggesting that epithelial cell invasion m
150 any years in other, unrelated, hyperinvasive meningococci, suggesting that the epidemic clones emerge
151 of sequence type (ST)-11 complex serogroup C meningococci that (rate ratio, 0.06); these meningococci
152                          The presence of cnl meningococci that can escape serum killing and cause inv
153 expression did not alter factor H binding to meningococci that express gonococcal Por.
154 hat MCC vaccines protect against carriage of meningococci that express serogroup C polysaccharide cap
155 pa protein increased the association of Cap+ meningococci that expressed low-adhesive pili, but did n
156 re found to be constitutively transcribed in meningococci, the biosynthesis operon about fourfold hig
157 growing evidence for RNA-based regulation in meningococci, their transcriptome structure and output o
158                                           In meningococci, three different TPS systems exist, and of
159  proteins mediated by phase variation enable meningococci to escape killing in vitro by bactericidal
160 c mutant strains of groups A, B, C, W, and Y meningococci to express similar amounts of the same fact
161 ein that is required for optimal adhesion of meningococci to human cells.
162  in an increased resistance of gonococci and meningococci to the same compounds, as well as to norflo
163             Factor H binding to unsialylated meningococci transfected with gonococcal Por1B was simil
164 y altered in a TonB- mutant and in wild-type meningococci treated with the protonophore carbonylcyani
165    Taken together, these data indicated that meningococci utilize multiple mechanisms including the a
166 he IS1106 element downstream of porA in some meningococci was absent in the gonococcus.
167 ine on the prevalence of carriage of group C meningococci was consistent with herd immunity.
168                                  Immunity to meningococci was determined in infected and uninfected s
169  was restored when binding of blocking Ab to meningococci was inhibited using either synthetic peptid
170 his intervention on asymptomatic carriage of meningococci was investigated to establish whether serog
171                      Carriage of serogroup C meningococci was reduced by 66% (p=0.004).
172 e molecules in AP regulation in encapsulated meningococci was studied using isogenic mutants.
173 acid, the capsular polysaccharide of Group B meningococci, we have investigated its solution dynamics
174                                              Meningococci were added to anticoagulated blood from 12
175 viduals colonized long term with serogroup B meningococci were also upregulated during prolonged cocu
176                                              Meningococci were detected by culture and polymerase cha
177                           Once internalized, meningococci were effectively killed, although more rapi
178 immediately cultured on selective media, and meningococci were identified and serologically character
179 n a total of 48,309 samples, from which 8599 meningococci were isolated and characterized by genotypi
180                                              Meningococci were isolated from oropharyngeal swabs coll
181                                              Meningococci were more potent stimuli of CD62E expressio
182                                              Meningococci were recovered from the animals by nasophar
183 of 25 other genetically diverse nongroupable meningococci were studied in detail.
184 dal and opsonophagocytic for P1.7-expressing meningococci, whereas human MAb SS269 (IgG3) and murine
185 the interactions of piliated and nonpiliated meningococci, whereas lipopolysaccharide (LPS) had a min
186  Opc did not influence the adherence of Cap+ meningococci, whereas loss of capsule was associated wit
187 sis factor-alpha by monocytes in response to meningococci, whereas lower concentrations enhanced the
188 n about classical pathway (CP) inhibition by meningococci, which forms the basis of this study.
189 ms, including encapsulated serogroup B and C meningococci, which leads to increased bacterial killing
190 However, meningococcal lipid A, expressed by meningococci with defects in 3-deoxy-D-manno-octulosonic
191 lic acid capsule modifies the interaction of meningococci with human macrophages at multiple steps, i
192      MBL increased the association of killed meningococci with neutrophils, monocytes, and macrophage
193                               Interaction of meningococci with nonhuman complement is relevant for an

 
Page Top