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1 ei rhodesiense and falcipain-2 of Plasmodium falciparum.
2 irst genome-wide nascent RNA profiling in P. falciparum.
3 activity against liver and blood stages of P falciparum.
4 cking vaccine (TBV) candidate for Plasmodium falciparum.
5 lication throughout schizogony in Plasmodium falciparum.
6 rs of the human malaria parasite, Plasmodium falciparum.
7 difference in the Fulani susceptibility to P.falciparum.
8 ys with proteasomes isolated from Plasmodium falciparum.
9 lled Human Malaria Infection with Plasmodium falciparum.
10  virulent human malaria parasite, Plasmodium falciparum.
11 of malaria in humans is caused by Plasmodium falciparum.
12 he human malaria-causing parasite Plasmodium falciparum.
13 ation, affecting most laboratory lines of P. falciparum.
14 r severe malaria in adults diagnosed with P. falciparum.
15 nt role in asexual development of Plasmodium falciparum.
16 s a potential target for vaccines against P. falciparum.
17  R0 and R2), and AMA1 antigens of Plasmodium falciparum.
18 quito bite: a major challenge for Plasmodium falciparum.
19 nt were Plasmodium vivax (14.3%), Plasmodium falciparum (10.5%) and Plasmodium malariae (3.4%).
20                      Treatment of Plasmodium falciparum 3D7 parasites with peptide corresponding to t
21 s noteworthy growth inhibitors of Plasmodium falciparum (3D7 and W2) in culture.
22 ctron microscopy structure of the Plasmodium falciparum 80S ribosome with the (+)-mefloquine enantiom
23 lts to the species level revealed Plasmodium falciparum (92.0%), Plasmodium ovale (5.6%), and Plasmod
24 active pericentromeric heterochromatin in P. falciparum, a region devoid of the characteristic H3K9me
25 nancy and birth outcomes owing to Plasmodium falciparum accumulation in the placenta.
26           In contrast to canonical actin, P. falciparum actin 1 (PfAct1) does not readily polymerize
27 esent study antibody responses to Plasmodium falciparum AMA-1, MSP-119 and CSP were measured with the
28 ametocyte prevalence decreased 3-fold for P. falciparum and 29% for P. vivax from 2010 to 2014.
29 ecreased 5-fold from 2006 to 2010; 72% of P. falciparum and 87% of P. vivax infections were submicros
30 y against a multidrug resistant strain of P. falciparum and arrest parasites at the ring phase of the
31                            INTERPRETATION: P falciparum and P vivax malaria in pregnancy both increas
32 me motor complex (GAP50, GAPM1-3) of both P. falciparum and P. berghei.
33 tory activity against multiple strains of P. falciparum and P. vivax in vitro, is efficacious against
34  strongly inhibited oocyst development of P. falciparum and Plasmodium berghei expressing PfCelTOS in
35  of five human-infecting species: Plasmodium falciparum and Plasmodium knowlesi.
36 pecies causing malaria in humans, Plasmodium falciparum and Plasmodium vivax, rely on two distinct ho
37              The malaria parasite Plasmodium falciparum and related apicomplexan pathogens contain an
38 hat the unexpected target of actinonin in P. falciparum and Toxoplasma gondii is FtsH1, a homolog of
39 related human parasitic pathogens Plasmodium falciparum and Toxoplasma gondii.
40 ples from Cambodian patients infected with P falciparum and treated with dihydroartemisinin-piperaqui
41 used by the Apicomplexan parasite Plasmodium falciparum, and results in significant global morbidity
42 - and the prevalence of antibodies to two P. falciparum antigens (MSP-1, AMA-1).
43 ning chimeric rodent parasites expressing P. falciparum antigens and a flow cytometric readout of inf
44                   Antibodies specific for P. falciparum antigens were determined in uncomplicated hyp
45 ch may influence the emergence of Plasmodium falciparum artemisinin-resistant phenotypes and genotype
46 re identified: (1) children infected with P. falciparum as detected by rapid diagnostic testing (RDT)
47 ays for a total of six doses) to eliminate P falciparum before the first and last vaccinations.
48 0 pM in a PfPKG kinase assay and inhibits P. falciparum blood stage proliferation in vitro with an EC
49 itical for asexual development of Plasmodium falciparum, but its precise function and substrates rema
50 sinin-resistant and -sensitive strains of P. falciparum by combining liquid chromatography-mass spect
51 t least one P. vivax parasitaemia and 10% P. falciparum, by qPCR, both of which were predominantly su
52 st that the dominant artemisinin-resistant P falciparum C580Y lineage probably arose in western Cambo
53  suggest that protective immunity against P. falciparum can be achieved via multiple mechanisms and h
54 er various environmental perturbations in P. falciparum can yield quantitative insights into fundamen
55  exposure to the malaria parasite Plasmodium falciparum cause an accumulation of specific responses a
56                                   Plasmodium falciparum causes a spectrum of malarial disease from as
57                                   Plasmodium falciparum causes malaria in humans with over 450,000 de
58                                   Plasmodium falciparum causes most life-threatening cases of malaria
59 se promoting factor of the unconventional P. falciparum cell cycle.
60 lysophosphatidylcholine (LysoPC) controls P. falciparum cell fate by repressing parasite sexual diffe
61           Mice immunized with recombinant P. falciparum CelTOS in combination with the glucopyranosyl
62 vel mutation within the gene encoding the P. falciparum chloroquine resistance transporter, PfCRT.
63 didate of malaria is based on the Plasmodium falciparum circumsporozoite protein (CSP), a major surfa
64 reported to be safe and protective against P falciparum controlled human malaria infection in malaria
65 ers of malaria incidence for P. vivax and P. falciparum corresponded to the pre- and first two years
66 xplore antibody binding in the context of P. falciparum CSP, we used negative-stain electron microsco
67  against one of the lead malaria antigens P. falciparum CSP.
68 dazopyridine series targeting the Plasmodium falciparum cyclic GMP-dependent protein kinase (PfPKG).
69                   Among them, the Plasmodium falciparum Cysteine-Rich Protective Antigen (PfCyRPA) is
70                               Immunity to P. falciparum declined prior to 2004, preceding the emergen
71       The human malaria parasite, Plasmodium falciparum, depends on a coordinated regulation of gene
72 2-2.30]; I(2)=26.1%; 34 estimates), as did P falciparum detected in placental samples (OR 1.95 [1.48-
73                       We assessed Plasmodium falciparum drug resistance markers in parasites collecte
74                                   Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) media
75                                           P. falciparum erythrocytic stage growth in vitro is reduced
76 y against asexual blood stages of Plasmodium falciparum, excellent parasite selectivity, and nanomola
77                                           P. falciparum exclusively infects human erythrocytes during
78 This unexpected response of human mDCs to P. falciparum exhibited a transcriptional program distinct
79 fected controls, women with early Plasmodium falciparum exposure had retarded intrauterine growth bet
80 term decline in the prevalence of Plasmodium falciparum from 40% prevalence in the period 1900-1929 t
81 oth P. berghei and clinically circulating P. falciparum from malaria endemic areas in Kenya, but not
82                      We introduce Plasmodium falciparum gametocyte exported protein-5 (PfGEXP5) trans
83     Even submicroscopic levels of Plasmodium falciparum gametocytes can infect mosquitoes and promote
84 ially, also blocks transmission of mature P. falciparum gametocytes to Anopheles stephensi mosquitoes
85      To address this challenge, a Plasmodium falciparum gamma-irradiated long-lived merozoite (LLM) l
86 haracterize the regulatory regions of the P. falciparum gene PF3D7_1234700, encoding a CPW-WPC protei
87                                       The P. falciparum genome encodes 10 aspartic proteases called p
88  reasons that remain unknown, the Plasmodium falciparum genome has an exceptionally high AT content c
89 ingle nucleotide polymorphisms within the P. falciparum genome were identified and only marginal diff
90              Analysis of multiple Plasmodium falciparum genomes showed that ICAM-1-binding PfEMP1s al
91 this article, we demonstrate that Plasmodium falciparum genomic DNA delivered to the cytosol of human
92 Plasmodium gallinaceum (>80%) and Plasmodium falciparum (>40%) models, an activity that was equivalen
93                  Our results suggest that P. falciparum has acquired multiple RIFINs to evade the hos
94 he plasmepsin II/III genes within Plasmodium falciparum has been associated with decreased sensitivit
95  invasion by the malaria parasite Plasmodium falciparum has been possible.
96 Proteases of the malaria parasite Plasmodium falciparum have long been investigated as drug targets.
97 but a higher proportion were positive for P. falciparum histidine rich protein 2 (192/246 [78.0%]) vs
98 t, this sensor was used to detect Plasmodium falciparum histidine-rich protein 2 (PfHRP2), an importa
99   Rapid diagnostic tests based on Plasmodium falciparum histidine-rich protein II (PfHRP-II) and P. f
100 ral flow malaria RDT that targets Plasmodium falciparum histidine-rich protein-II (HRPII) and Plasmod
101         Among potential new biomarkers, a P. falciparum homolog of insulin-degrading enzyme (PfIDEh)
102                  Deletions of the Plasmodium falciparum hrp2 (pfhrp2) gene cause false-negative RDT r
103                  Deletions of the Plasmodium falciparum hrp2 and hrp3 genes can affect the performanc
104 P. vivax in vitro, is efficacious against P. falciparum in in vivo rodent models, produces parasite r
105 nt strains inhibit development of Plasmodium falciparum in mosquitoes.
106 at occur during sporogonic development of P. falciparum in the mosquito host.
107 e findings in the Xenopus model extend to P. falciparum in vivo, our data suggest that PfCRT might pl
108 lassical LPS response, pointing to unique P. falciparum-induced activation pathways that may explain
109              Our results suggest that the P. falciparum- infected human erythrocyte contains numerous
110 immune effector mechanism against Plasmodium falciparum-infected erythrocytes (IE); however, current
111 y cytokine secretion, mDCs incubated with P. falciparum-infected erythrocytes activated antigen-speci
112 tigen expressed on the surface of Plasmodium falciparum-infected erythrocytes.
113                  BRD3914 was evaluated in P. falciparum-infected mice, providing a cure after four or
114                                        In P. falciparum-infected patients, Vgamma9Vdelta2 T cells pre
115 ement and stage determination for Plasmodium falciparum-infected red blood cells (Pf-iRBCs).
116 th a fever within the previous 14 days and P falciparum infection assessed by RDT who received an ACT
117  asymptomatic individuals with or without P. falciparum infection at the end of the 6-month dry seaso
118 oratory efficacy endpoint of time to first P falciparum infection beginning 28 days after the fifth v
119              Pregnancy-associated Plasmodium falciparum infection impacts the health of mothers and n
120 are fast-acting compounds that can cure a P. falciparum infection in a humanized NOD/SCID mouse model
121 rs significant protection against Plasmodium falciparum infection in humans.
122  identified to be associated with Plasmodium falciparum infection in natural Anopheles gambiae popula
123 istent to more susceptible An. gambiae to P. falciparum infection in the field.
124 dren younger than 5 years with a fever and P falciparum infection increased across sub-Saharan Africa
125                      Chronic asymptomatic P. falciparum infection predicted decreased clinical malari
126 dren younger than 5 years with a fever and P falciparum infection received an ACT.
127 icant protection in African adults against P falciparum infection throughout an entire malaria season
128       Anti-FBG serum also reduced >81% of P. falciparum infection to A. gambiae Finally, we showed th
129                                   Plasmodium falciparum infection was assessed by blood smear microsc
130  during the early immune response against P. falciparum infection, we investigated whether they could
131 red with women with no detected antenatal P. falciparum infection, women with positive RDT findings d
132  27 (66%) from the vaccine group developed P falciparum infection.
133 vaccinees who were protected from Plasmodium falciparum infection.
134 HCM) is a serious complication of Plasmodium falciparum infection.
135 ets the pre-erythrocytic stage of Plasmodium falciparum infection.
136 ignificantly differentially expressed upon P.falciparum infection.
137 eneous effects on the clinical outcome of P. falciparum infection.
138  (CM) is a severe complication of Plasmodium falciparum infection.
139 gens are widely deployed for detection of P. falciparum infection; however, these tests often miss ca
140 s that support liver stage human malaria (P. falciparum) infection in vitro, and also after implantat
141 vo IC50 64 nM), and murine P. berghei and P. falciparum infections (day 4 ED90 0.34 and 0.57 mg kg(-1
142              Chronic asymptomatic Plasmodium falciparum infections are common in endemic areas and ar
143 e studied spatial distribution of Plasmodium falciparum infections to compare simulated effects of th
144 (2) RDT-negative children whose untreated P. falciparum infections were detected retrospectively by P
145                       Subpatent antenatal P. falciparum infections were not associated with adverse d
146 e the first line of treatment for Plasmodium falciparum infections worldwide, but artemisinin resista
147 anism proposed for maintenance of chronic P. falciparum infections(7-9).
148                            During Plasmodium falciparum infections, erythrocyte-stage parasites inhib
149 en who did or did not harbor asymptomatic P. falciparum infections.
150  low-dose primaquine (PQ) reduces Plasmodium falciparum infectivity before it impacts gametocyte dens
151 he most virulent form of malaria, Plasmodium falciparum, invade erythrocytes.
152          For the malaria parasite Plasmodium falciparum, invasion of host red blood cells (RBCs) is e
153 d with the human malaria parasite Plasmodium falciparum (iRBCs) adhere to the vascular endothelium th
154                            Pfhrp2-deleted P. falciparum is a common cause of RDT-/PCR+ malaria among
155         In conclusion, high AT content in P. falciparum is driven by a systematic mutational bias and
156 ity of pepstatin against cultured Plasmodium falciparum is highly variable depending on the commercia
157                Gene expression in Plasmodium falciparum is tightly regulated to ensure successful pro
158 ever, the human malaria parasite, Plasmodium falciparum, is incapable of pyrimidine salvage for mRNA
159 ssociated with drug resistance in Plasmodium falciparum isolated from subjects receiving DP or SP.
160 did a genome-wide association study of 297 P falciparum isolates from Cambodia to investigate the rel
161 rospectively sequenced the genomes of 194 P. falciparum isolates from five sites in Northwest Thailan
162 is observational study, we tested Plasmodium falciparum isolates from Myanmar, northeastern Thailand,
163 re performed by sequential cloning of six P. falciparum isolates growing in human erythrocytes in vit
164 on in malaria parasites, clinical Plasmodium falciparum isolates were sampled from patients and cultu
165  the benzoxaborole AN3661 against Plasmodium falciparum laboratory-adapted strains (mean IC50 32 nM),
166                                Reports of P. falciparum lacking this protein are increasing, creating
167  histidine-rich protein II (PfHRP-II) and P. falciparum lactate dehydrogenase (PfLDH) antigens are wi
168 icans to fatal pathogens, such as Plasmodium falciparum, Lassa Virus and Trypanosoma brucei rhodesien
169 generation of transgenic DiCre-expressing P. falciparum lines in any genetic background.
170                                  Multiple P. falciparum lines selected in vitro for resistance to AN3
171  individuals or from in vitro cultures of P. falciparum, making them prone to high variation.
172                                            P falciparum malaria detected and treated during pregnancy
173                                   Plasmodium falciparum malaria detected at delivery in peripheral sa
174  as first-line agents to treat uncomplicated falciparum malaria due to their activity against multidr
175                   We report a case of severe falciparum malaria following nosocomial Plasmodium falci
176                               Elimination of falciparum malaria from this region should be accelerate
177 ations that confer artemisinin resistance in falciparum malaria have multiple independent origins acr
178 arative analysis of treatment regimen for P. falciparum malaria in adults in Stockholm during 2000-20
179 laria test (UMT) for diagnosis of Plasmodium falciparum malaria in febrile patients.
180 reasing, creating a problem for diagnosis of falciparum malaria in locations without quality-assured
181  to AL for the treatment of uncomplicated P. falciparum malaria in pediatric patients.
182                    The association between P falciparum malaria in pregnancy and stillbirth was two t
183 demic sub-Saharan Africa are attributed to P falciparum malaria in pregnancy; the population attribut
184            Although the burden of Plasmodium falciparum malaria is gradually declining in many parts
185 administration for elimination of Plasmodium falciparum malaria is recommended by WHO in some setting
186 5a and 5c showed activity against Plasmodium falciparum malaria parasites (IC50 approximately 1 muM).
187 a-regression analysis of cure rates from all falciparum malaria treatment trials (n = 40) with monoth
188                       Adults with Plasmodium falciparum malaria were randomized to receive 1 of 3 art
189  pre-erythrocytic) prophylaxis of Plasmodium falciparum malaria with prolonged activity would substan
190 ended treatment for uncomplicated Plasmodium falciparum malaria worldwide.
191 ria, severe (n = 21) and nonsevere (n = 109) falciparum malaria, and healthy controls (n = 50), we me
192                                           In falciparum malaria, angiopoietin-2 increased with age, i
193 relatively better protection from Plasmodium falciparum malaria, as reflected by fewer symptomatic ca
194 urrent treatment of uncomplicated Plasmodium falciparum malaria, but ACT resistance is spreading acro
195 eved to confer protection against Plasmodium falciparum malaria, but the precise nature of the protec
196 ia correlates with the development of severe falciparum malaria, suggesting that platelets either con
197 acious treatment of uncomplicated Plasmodium falciparum malaria.
198 fectively treating drug-resistant Plasmodium falciparum malaria.
199 ts aged 6 months to 12 years with Plasmodium falciparum malaria.
200 besity, is associated with severe Plasmodium falciparum malaria.
201 nsidered for rescue treatment for Plasmodium falciparum malaria.
202 sults of PCR for the detection of Plasmodium falciparum malaria.
203 opoietin-2, and microvascular dysfunction in falciparum malaria.
204 oscopy or rapid test confirmed uncomplicated falciparum malaria.
205 ren from severe and uncomplicated Plasmodium falciparum malaria.
206 ms that confer the lower susceptibility to P.falciparum malaria.
207 n on maintenance of antibodies to Plasmodium falciparum merozoite antigens and infected erythrocytes
208       Invasion of erythrocytes by Plasmodium falciparum merozoites is necessary for malaria pathogene
209                                           P. falciparum merozoites that lack PfMSP3.1 showed a marked
210     In this article, we show that Plasmodium falciparum merozoites, the invasive form of blood stage
211  have slowed the development of a Plasmodium falciparum multiantigen vaccine.
212                  Spread of pfhrp2-deleted P. falciparum mutants, resistant to detection by HRP2-based
213 cking robust adaptive immunity to Plasmodium falciparum Nevertheless, the host may partly control blo
214 he mitochondria of Plasmodium falciparum (P. falciparum) NF54-attB blood-stage parasites and evaluate
215  a deadly outcome of infection by Plasmodium falciparum, occurring when parasite-infected erythrocyte
216 e cytosol and the mitochondria of Plasmodium falciparum (P. falciparum) NF54-attB blood-stage parasit
217 ce and spread of fit artemisinin-resistant P falciparum parasite lineages, which then acquire partner
218 approach to detect hotspots using Plasmodium falciparum parasite prevalence and serological evidence
219 cations of human infection by the Plasmodium falciparum parasite.
220                                   Plasmodium falciparum parasitemia was less frequent than in non-BWF
221  gametocytes and asynchronous blood-stage P. falciparum parasites by microarray technology.
222 sess potent antimalarial activity against P. falciparum parasites comparable to the known antimalaria
223 hallenged with double chimeric P. berghei-P. falciparum parasites expressing both PfUIS3 and PfTRAP,
224 e recalled in human volunteers exposed to P. falciparum parasites in a controlled human malaria infec
225  PfHRP2-only RDTs is sufficient to select P. falciparum parasites lacking this protein, thus posing a
226  of Mali) for eligibility (>/=2000 asexual P falciparum parasites per muL of blood).
227 g whether successful sporogony of Plasmodium falciparum parasites through to human-infectious transmi
228                     Therefore, binding of P. falciparum parasites to the erythrocyte directly activat
229 usly enriches pLDH and HRPII from Plasmodium falciparum parasitized blood samples.
230 ne knockouts were not viable in the human P. falciparum pathogen, we used conditional knockdowns to d
231  observational cohort study, we evaluated P. falciparum pathogenesis in vitro in RBCs from pregnant w
232        The best ligands inhibited Plasmodium falciparum (Pf) and Arabidopsis thaliana (At) SHMT in ta
233 s, children acquired equal numbers of new P. falciparum (Pf) and Pv blood-stage infections/year (Pf-m
234 phoribosyltransferase (HGPRT) and Plasmodium falciparum (Pf) hypoxanthine-guanine-xanthine phosphorib
235 man malaria infection (CHMI) with Plasmodium falciparum (Pf) parasites homologous to the vaccine stra
236 ization with radiation-attenuated Plasmodium falciparum (Pf) sporozoites (PfSPZ) inoculated by mosqui
237 SP), the major surface antigen of Plasmodium falciparum (Pf) sporozoites, can protect from malaria in
238 ter of the human malaria parasite Plasmodium falciparum, PfCRT, is an important determinant of resist
239                               The Plasmodium falciparum Pfs25 protein (Pfs25) is a leading malaria tr
240                                           P. falciparum phenotypic plasticity is linked to the varian
241     Bicyclic azetidines targeting Plasmodium falciparum phenylalanyl-tRNA synthetase comprise one pro
242 pyridine that selectively targets Plasmodium falciparum PKG, inhibits blood stage parasite growth in
243                                           P. falciparum population genetic approaches offer promising
244 esistance in the malaria parasite Plasmodium falciparum poses a major threat to the control and elimi
245                              A total 1392 P. falciparum positive samples collected from eight endemic
246  to serve a different function in Plasmodium falciparum, protecting ookinetes from the mosquito immun
247     Placental accumulation is mediated by P. falciparum protein VAR2CSA, a leading PAM-specific vacci
248 eened proteomic data for highly expressed P. falciparum proteins and compared their features to those
249 asmodium yoelii orthologs of four Plasmodium falciparum proteins identified by an antibody-based geno
250                                              falciparum proteins prepared using the wheat germ cell-f
251  have almost entirely focussed on Plasmodium falciparum, providing a highly informative means to inve
252 th the homologous Brd PfGCN5 from Plasmodium falciparum rationalizes the high selectivity for PCAF an
253 ibrate close to the level seen across the P. falciparum reference genome (80.6% AT).
254                  The emergence of Plasmodium falciparum resistant to frontline therapeutics has promp
255 he Erythrocyte binding antigen family and P. falciparum reticulocyte binding-like families.
256                     For instance, Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5
257                                   Plasmodium falciparum reticulocyte-binding protein homologue 2b (Pf
258 parasitaemia undetectable in vivo using a P. falciparum SCID mouse model.
259  humans and appears to be protective against falciparum severe malaria.
260 any genes of the malaria parasite Plasmodium falciparum show clonally variant expression regulated at
261                                   Plasmodium falciparum-specific antibody kinetics during the dry sea
262                The performance of Plasmodium falciparum-specific histidine-rich protein 2-based rapid
263                                   Plasmodium falciparum sporozite (PfSPZ) Vaccine is a metabolically
264 nsgenic P. berghei parasites that express P. falciparum sporozoite antigens, we have been able to use
265 t the prevalence and intensity of Plasmodium falciparum sporozoite infection is significantly lower i
266  live-attenuated malaria vaccine, Plasmodium falciparum sporozoite vaccine (PfSPZ Vaccine), confers s
267 ) of 3200 aseptic, purified, cryopreserved P falciparum sporozoites (PfSPZ Challenge; Sanaria Inc, Ro
268 t CHMI with a low or high dose of Plasmodium falciparum sporozoites.
269 ndemic areas in Kenya, but not laboratory P. falciparum strain NF54.
270 ests can give false-negative results when P. falciparum strains do not express this antigen.
271                               Alarmingly, P. falciparum strains have acquired resistance to ART acros
272 itive (NF54) and -resistant (Dd2 and 7G8) P. falciparum strains with 5/6 having IC50 < 100 nM against
273 d stages of drug-sensitive and -resistant P. falciparum strains, inhibits development of P. berghei i
274   The earliest transcriptomics studies in P. falciparum suggested a cascade of transcriptional activi
275  genome-wide association study of ex vivo P. falciparum susceptibility to piperaquine.
276 ent or replication of blood-stage Plasmodium falciparum The percentage of Plasmodium-infected (iRBCs)
277 und that the activation of DCs by Plasmodium falciparum, the main causative agent of human malaria, i
278                               For Plasmodium falciparum, the most widespread and virulent malaria par
279                               For Plasmodium falciparum, the species responsible for the most severe
280 tro activity against different strains of P. falciparum, the toxicity, and the metabolic stability is
281 in malaria effector proteins from Plasmodium falciparum These findings imply a role for the RxLR moti
282 coadministered with the vaccine candidate P. falciparum thrombospondin-related adhesion protein (PfTR
283 ave characterised replication dynamics in P. falciparum throughout schizogony, using DNA fibre labell
284         In this study, we report that the P. falciparum translation enhancing factor (PTEF) relieves
285 established mathematical model of Plasmodium falciparum transmission dynamics with epidemiological, i
286 thogen recognition molecule in inhibiting P. falciparum transmission in malaria endemic areas.
287 arum malaria following nosocomial Plasmodium falciparum transmission in nonendemic Germany.
288 efforts to model the changing patterns of P. falciparum transmission intensity in Africa have been li
289 gent-based stochastic simulation model of P. falciparum transmission was used to investigate the sele
290 ested at each antenatal visit for Plasmodium falciparum, using an RDT and polymerase chain reaction a
291 enotypes and Abs specific for the Plasmodium falciparum vaccine candidate apical membrane Ag-1 (AMA1)
292                                           P. falciparum virulence is related to adhesion and sequestr
293 ted mice and the 48-hour in vitro cycle of P falciparum was <10%.
294                      Antibody response to P. falciparum was determined in 4,112 individuals by ELISA
295 malaria treatment until resistant Plasmodium falciparum was identified.
296 r in the human malarial parasite, Plasmodium falciparum, we have quantified cytosolic labile heme lev
297 tage-specific molecular methods to detect P. falciparum, we show that gametocytes-and not their nonin
298 The study suggests that early exposure to P. falciparum, which is not targeted for prevention by curr
299 ction with the protozoan parasite Plasmodium falciparum, which requires immediate treatment.
300  (PA) is critical for survival of Plasmodium falciparum within human erythrocytes.

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