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1 and P. falciparum, and the liver stage of P. yoelii.
2 n was only critical in protection against P. yoelii.
3 I) of the rodent malaria parasite Plasmodium yoelii.
4 parum, and its rodent-infectious relative, P.yoelii.
5 in vivo using the rodent parasite Plasmodium yoelii.
6 ALB/c mice were solidly protected against P. yoelii.
7 ic characterization of PanK1 and PanK2 in P. yoelii.
8 mily exist in the rodent parasite Plasmodium yoelii.
9 ed in the murine malaria parasite Plasmodium yoelii.
10 )) of the murine malaria parasite Plasmodium yoelii.
11 and subsequent resistance to infection by P. yoelii.
12 ABA diets do not die from lethal doses of P. yoelii.
13 on from challenge with a lethal strain of P. yoelii.
14 s and the rodent malaria parasite Plasmodium yoelii.
15 andidiasis or initial hepatic invasion by P. yoelii.
16 alaria parasites, Plasmodium chabaudi and P. yoelii.
17 plexans Plasmodium falciparum and Plasmodium yoelii.
18 ll up-regulated 24 h after infection with P. yoelii.
19 r numbers in response to coinfection with P. yoelii.
20 artemisinin in the rodent malaria Plasmodium yoelii.
21 eting techniques to delete PAT in Plasmodium yoelii.
22 3) in the rodent malaria parasite Plasmodium yoelii.
23 modium liver stages in vivo using Plasmodium yoelii.
24 y spleen macrophages and DCs from Plasmodium yoelii 17NXL-infected and P. berghei ANKA-infected mice.
25 re, we test chemically attenuated Plasmodium yoelii 17X and demonstrate significant protection follow
26 PyMIF were generated, one in a nonlethal P. yoelii 17X background [Py17X-MIF(+)] and the other in a
29 d do not suppress the growth of nonlethal P. yoelii 17X, a parasite that primarily replicates in reti
32 tible than C57BL/6 mice to infection with P. yoelii 17XL and were not protected against lethal malari
35 ecific antibodies preferentially suppress P. yoelii 17XL growth in mature erythrocytes compared to gr
36 with M. tuberculosis CDC1551 and Plasmodium yoelii 17XL had a lower peak parasitemia and increased s
39 ene expression in reticulocyte-restricted P. yoelii 17XL parasites that escaped neutralization by PyM
43 ow that co-infection of mice with Plasmodium yoelii 17XNL (Py17XNL) and Salmonella enterica serovar T
46 nous, Plasmodium berghei ANKA- or Plasmodium yoelii 17XNL-parasitized red blood cells (pRBCs) after t
47 6 background were challenged with Plasmodium yoelii (17XNL strain) sporozoites, and then liver parasi
48 and amino acid homology with the Plasmodium yoelii 235-kDa rhoptry protein family, which is also rel
50 tic machinery to synthesize PABA, Plasmodium yoelii, a rodent malaria species, requires exogenous die
52 circumsporozoite (CS) protein of Plasmodium yoelii (AdPyCS), followed by a booster with an attenuate
53 al pathogens Candida albicans and Plasmodium yoelii, an accepted experimental malaria model in mouse.
54 tage by using the rodent malaria parasite P. yoelii, an important model for malaria vaccine developme
55 f a linear peptide construct specific for P. yoelii and compared the responses of antigen-presenting
56 structure of the TRAP A-domain of Plasmodium yoelii and located regions surrounding the MIDAS (metal
59 cells (RBC) of all ages (RBC generalist); P. yoelii and P. vivax preferentially infect young RBCs (RB
60 g TMP-SMX effects on the rodent parasites P. yoelii and Plasmodium berghei and on the human malaria p
62 es of the rodent malaria parasite Plasmodium yoelii and studied the early events in the development o
63 nt extracts and Hz from P. falciparum and P. yoelii and synthetic Hz suppressed Epo-induced prolifera
64 kDa family of rhoptry proteins in Plasmodium yoelii and the two reticulocyte binding proteins of P. v
68 re features of malarial anemia in Plasmodium yoelii- and Plasmodium berghei ANKA-infected mice, simil
70 odent models of malaria, commonly Plasmodium yoelii, are frequently used for studies of malaria patho
71 nnotated genes will facilitate the use of P. yoelii as a model system for studying human malaria.
72 redicted interactions is observed against P. yoelii, because of missing ortholog partners in pairs of
73 circumsporozoite protein (CS) of Plasmodium yoelii between 17D nonstructural proteins NS2B and NS3.
78 g a B cell epitope derived from a Plasmodium yoelii circumsporozoite (CS) protein (referred to as the
79 g vaccine constructs based on the Plasmodium yoelii circumsporozoite protein (CSP) and P. yoelii mero
80 naked DNA plasmid expressing the Plasmodium yoelii circumsporozoite protein (pPyCSP) protects mice a
81 evious studies indicated that the Plasmodium yoelii circumsporozoite protein (PyCSP) 57-70 region eli
82 DNA vaccine plasmids encoding the Plasmodium yoelii circumsporozoite protein (PyCSP) and murine granu
83 nized as neonates (7 days) with a Plasmodium yoelii circumsporozoite protein (PyCSP) DNA vaccine mixe
86 ected with a non-lethal strain of Plasmodium yoelii Compared with Cd36(-/-) mice, WT mice had lower p
98 ation of mice with yeast-secreted Plasmodium yoelii-derived 19-kilodalton merozoite surface protein 1
99 hether Hz contributes to malarial anemia, P. yoelii-derived or synthetic Hz was administered to naive
100 r the circumsporozoite protein of Plasmodium yoelii develop a severely impaired memory response after
103 important for liver-stage development of P. yoelii, during which it is likely to play an intrinsic r
105 n agreement with the presence of genes in P. yoelii encoding for proteins with homology to NADH-Q oxi
106 d that during the acute phases of Plasmodium yoelii erythrocyte stage infection, APC upregulate the e
107 dentification method approach used 192 P. y. yoelii exons from genes expressed during the sporozoite
108 imental immunization of mice with Plasmodium yoelii fabb/f(-) (Pyfabb/f(-)), a genetically attenuated
114 P1 in the rodent malaria parasite Plasmodium yoelii generated mutant parasites that traverse and inva
116 tified and manually curated a further 510 P. yoelii genes which have clear orthologs in the P. falcip
117 sterile protection conferred by a Plasmodium yoelii genetically attenuated parasite (PyGAP) vaccine w
118 suggests that improvements of the current P. yoelii genome annotation should focus on genes expressed
119 ry and matching the cDNA sequences to the P. yoelii genome yielded 25 redundantly tagged genes includ
121 ch shows that apicoplast-targeted Plasmodium yoelii glycerol 3-phosphate dehydrogenase and glycerol 3
123 n the murine malaria model system Plasmodium yoelii has been cumbersome and requires terminal procedu
124 rozoites of Plasmodium berghei or Plasmodium yoelii has been used extensively to evaluate liver-stage
126 rial activity against multidrug-resistant P. yoelii in mice in the dose range of 5-100 mg/kg x 4 days
130 rray analysis of CD4(+) T cells following P. yoelii-induced exhaustion shows upregulation of effector
131 ction and are therefore more resistant to P. yoelii-induced exhaustion than their wild-type counterpa
132 us protein 14K (A27) to the CS of Plasmodium yoelii, induces strong effector memory CD8(+) T cell res
133 -specific memory CD8 T cell protection in P. yoelii-infected BALB/c or P. berghei-infected B10.D2 mic
134 fic ablation of Foxp3(+) Tregs in Plasmodium yoelii-infected DEREG-BALB/c mice leads to an increase i
136 in vivo and cleared malaria from Plasmodium yoelii-infected mice, resulting in 100% mice survival ra
139 n of effector cytokines following Plasmodium yoelii infection and are therefore more resistant to P.
140 e changes suggest the immune responses to P. yoelii infection are both parasite and organ specific.
144 ple and noninvasive method for monitoring P. yoelii infection in the liver provides an efficient syst
145 ysis of cytokine production revealed that P. yoelii infection induced two distinct peaks of IFN-gamma
146 om uninfected mosquitoes prior to Plasmodium yoelii infection influences the local and systemic immun
147 initiation of a PABA-deficient diet after P. yoelii infection is established leads to the clearance o
150 phenotypic changes in DCs during Plasmodium yoelii infection represent a mechanism of controlling ho
152 /6 mice show comparable susceptibility to P. yoelii infection with sporozoites and that bioluminescen
160 or T cells as the main mechanism, because P. yoelii infections did not suppress the recruitment or pr
162 ure erythrocytes) had negligible levels of P yoelii invasion compared with wild-type normocytes, demo
165 rotein PY01515 (PDB ID 2aqw) from Plasmodium yoelii, it is shown that the putative annotation, Orotid
167 chimeric multistage recombinant protein (P. yoelii linear peptide chimera/recombinant modular chimer
168 sites allows for quantitative analysis of P. yoelii liver stage burden and parasite development, whic
170 a showed NNRTI treatment modestly reduced P. yoelii liver stage parasite burden and minimally extende
172 e protection against normocyte-associated P. yoelii malaria parasites is mediated by antibodies that
173 e immunized and protected against Plasmodium yoelii malaria, we identified a novel blood-stage antige
176 r the C-terminal 19-kDa region of Plasmodium yoelii merozoite surface protein 1 (MSP119), a major tar
178 yoelii circumsporozoite protein (CSP) and P. yoelii merozoite surface protein-1 (MSP-1) showed encour
181 ised against purified, non-epitope-tagged P. yoelii MIF (PyMIF) were used to localize expression in t
184 smodium yoelii sequence-related molecules P. yoelii MSP-7 (merozoite surface protein 7) and P. yoelii
186 the rodent system demonstrated that both P. yoelii MSP-7 and P. yoelii MSRP-2 could be isolated from
187 Immunofluorescence studies colocalized P. yoelii MSP-7 and P. yoelii MSRP-2 with the amino-termina
188 mmunization with P. yoelii MSRP-2 but not P. yoelii MSP-7 protected mice against a lethal infection w
189 del, we tested the ability of recombinant P. yoelii MSP-8 (rPyMSP-8) to complement rPyMSP-1-based vac
190 Plasmodium yoelii murine model, we fused P. yoelii MSP1(1)(9) (PyMSP1(1)(9)) with full-length P. yoe
191 i MSP-7 (merozoite surface protein 7) and P. yoelii MSRP-2 (MSP-7-related protein 2) by their ability
192 s establish that both P. yoelii MSP-7 and P. yoelii MSRP-2 are expressed on the surface of merozoites
194 emonstrated that both P. yoelii MSP-7 and P. yoelii MSRP-2 could be isolated from parasite lysates an
195 s and released from the parasite and that P. yoelii MSRP-2 may be the target of a protective immune r
196 e studies colocalized P. yoelii MSP-7 and P. yoelii MSRP-2 with the amino-terminal portion of MSP-1 a
199 n proof-of-concept studies in the Plasmodium yoelii murine model, we produced a chimeric vaccine anti
200 to infections with two strains of Plasmodium yoelii (N67 and N67C) and discovered differences in inna
202 l showed that 5 days after coinoculation, P. yoelii nigeriensis infection increased the recovery of S
205 se data suggested that both hemolysis and P. yoelii nigeriensis-specific factors contributed to the i
208 activity of 1.6 and 3.7 mg/kg against the P. yoelii NS strain compared to 7.9 and 7.4 mg/kg for amodi
213 0 P. falciparum genes, more than 3,300 P. y. yoelii orthologues of predominantly metabolic function w
214 19% (Plasmodium berghei) and 26% (Plasmodium yoelii) overall identity to the different Plasmodium AMA
215 es infecting rodents, monkeys and humans (P. yoelii, P. berghei, P. chabaudi, P. knowlesi and P. viva
216 tion and characterization of a transgenic P. yoelii parasite expressing the reporter protein lucifera
217 e, we generated p52/p36-deficient Plasmodium yoelii parasites by the simultaneous deletion of both ge
218 Infection of mice with strains of Plasmodium yoelii parasites can result in different pathology, but
219 form are highly effective against Plasmodium yoelii parasites in mice and against Plasmodium falcipar
222 ice born of mothers previously exposed to P. yoelii parasites or immunized with the vaccine were prot
224 ion of the E1alpha or E3 subunit genes of P. yoelii PDH caused no defect in blood stage development,
225 e E1 alpha or E3 subunit genes of Plasmodium yoelii PDH caused no defect in blood stage development,
229 Consequently the cellular integrity of P. yoelii plasmei2(-) liver stages became increasingly comp
231 d late in development and the majority of P. yoelii plasmei2(-) underwent cell death by the time wild
232 cByJ mice are more susceptible to Plasmodium yoelii preerythrocytic infection than BALB/cJ mice.
233 d approach of developing chimeric Plasmodium yoelii proteins to enhance protective efficacy, we desig
234 Green fluorescent protein-tagged Plasmodium yoelii (PyGFP) was used to efficiently isolate LS-infect
235 the 60-kDa heat shock protein of Plasmodium yoelii (PyHsp60) was cloned into the VR1012 and VR1020 m
236 Plasmodium falciparum (PfMIF) and Plasmodium yoelii (PyMIF)) non-competitively in a reversible fashio
238 nt CD4(+) T cells into mice infected with P. yoelii results in increased production of antibodies to
239 omes of Plasmodium falciparum and Plasmodium yoelii revealed a conserved core of 4500 Plasmodium gene
240 ce infected with malaria-inducing Plasmodium yoelii revealed that chloroquine treatment could lead to
241 of the UIS3 and UIS4 loci in the Plasmodium yoelii rodent malaria model (Pyuis3[-] and Pyuis4[-]).
242 ty and efficacy studies using the Plasmodium yoelii rodent model, we tested the ability of recombinan
243 ubtractive hybridization (SSH) of Plasmodium yoelii salivary gland sporozoites versus merozoites to i
244 we described the isolation of the Plasmodium yoelii sequence-related molecules P. yoelii MSP-7 (meroz
245 ciparum, P. gallinaceum, P. knowlesi, and P. yoelii species representing human, avian, simian, and ro
246 w that dendritic cells presenting Plasmodium yoelii sporozoite antigens are able to activate specific
247 cells are required for protection against P. yoelii sporozoite challenge than for protection against
248 erum with a luciferase-expressing Plasmodium yoelii sporozoite challenge to assess Ab-mediated inhibi
249 om naive mice that had survived wild-type P. yoelii sporozoite infection targeted mainly sporozoite-t
250 n the BALB/c mouse model of P. berghei or P. yoelii sporozoite infection to examine the role of immun
251 of human Plasmodium falciparum and rodent P. yoelii sporozoite infectivity, CD81 may also play a vita
252 nst the 100-kDa protein inhibited Plasmodium yoelii sporozoite invasion of salivary glands >/=75%.
253 using mice singly immunized with Plasmodium yoelii sporozoites and high-throughput screening, we ide
254 assays reveal that Plasmodium berghei and P. yoelii sporozoites attach to and enter Kupffer cells, bu
255 to 2 days prior to challenge with Plasmodium yoelii sporozoites conferred sterile protection against
258 duce sterile protection from challenge by P. yoelii sporozoites in the absence of T cells in 50% of m
259 ministered with either irradiated Plasmodium yoelii sporozoites or a recombinant adenovirus expressin
260 by immunization with radiation-attenuated P. yoelii sporozoites or with plasmid DNA encoding preeryth
261 In BALB/c mice, repeated small doses of P. yoelii sporozoites progressively expand the population o
262 n against the experimental challenge with P. yoelii sporozoites than passive immunization with purifi
263 d 2 weeks later with 2 x 10(3) irradiated P. yoelii sporozoites, and were challenged several weeks la
264 not from vector control groups recognized P. yoelii sporozoites, liver stages, and infected erythrocy
265 ia in immunized mice challenged with live P. yoelii sporozoites, revealing an adjuvant activity for D
274 me rodent malaria parasites, like Plasmodium yoelii strain 17XNL (Py17XNL), induce a transient (self-
276 propose an alternative mechanism whereby P. yoelii suppresses Listeria-specific T cell responses.
277 f mice with Plasmodium berghei or Plasmodium yoelii synthetic linear peptide chimeras (LPCs) based on
278 haracterized the MIF homologue of Plasmodium yoelii throughout the life cycle, with emphasis on preer
279 of three apicomplexan pathogens--Plasmodium yoelii, Toxoplasma gondii, and Cryptosporidium parvum--d
280 d for both Plasmodium berghei and Plasmodium yoelii, two different rodent malaria parasites, suggesti
282 rcumsporozoite protein (PyCSP) of Plasmodium yoelii was engineered into a T. gondii temperature-sensi
283 nt malaria models (Plasmodium berghei and P. yoelii), we were unable to show that saliva had any dete
284 of mice were similarly protected against P. yoelii, we could not correlate vaccine-induced responses
285 el mimicking natural infection by Plasmodium yoelii, we delineated early events governing the develop
286 and MyD88(-/-) mice infected with Plasmodium yoelii, we show that TLR9 and MyD88 regulate pro/anti-in
287 rs from Plasmodium falciparum and Plasmodium yoelii, which likely diverged >or=100 million years ago
289 virulence loci using the offspring from a P. yoelii YM and N67 genetic cross, and identify a putative
290 sequent challenge to a lethal inoculum of P. yoelii YM and to challenge from P. yoelii 17XNL, another
296 ly in the rodent malaria parasite Plasmodium yoelii yoelii code for 235-kilodalton proteins (Py235) t
298 hosphorylation of mitochondria of Plasmodium yoelii yoelii trophozoites were assayed in situ after pe
299 shotgun sequence of one species, Plasmodium yoelii yoelii, and comparative studies with the genome o
300 amilies in both P. falciparum and Plasmodium yoelii yoelii, where no orthologs were predicted uniquel
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