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1 red (2 hydroxyurea, 1 placebo, and none from malaria).
2 cytes perpetuating the cycle responsible for malaria.
3 s been paid to how to measure the absence of malaria.
4 he primary outcome was incidence of clinical malaria.
5 e wedge that balances clinical protection to malaria.
6 vere and uncomplicated Plasmodium falciparum malaria.
7 s to be protective against falciparum severe malaria.
8 and Plasmodium spp., the causative agents of malaria.
9 h phenotypes of numerous diseases, including malaria.
10 s been reported in cases of Plasmodium vivax malaria.
11 jor threat to the control and elimination of malaria.
12 these infections on infant susceptibility to malaria.
13 ative, of whom 365 (33%) tested positive for malaria.
14 commended rescue treatment for uncomplicated malaria.
15 fer the lower susceptibility to P.falciparum malaria.
16 ibitory antibodies through exposure to vivax malaria.
17  appropriate treatment for all children with malaria.
18 s to the development of clinical immunity to malaria.
19 ales that blood feed and thus transmit human malaria.
20 of all fevers) were causally attributable to malaria.
21 y drug available to prevent relapse in vivax malaria.
22 dence for a role of CNV in host responses to malaria.
23 s to limit the spread of multidrug-resistant malaria.
24  Plasmodium species, the causative agents of malaria.
25  patients, 53 (21%) also tested positive for malaria.
26 ssociations between comorbidities and severe malaria.
27 ed in the acute management and prevention of malaria.
28 olor, lactase persistence, and resistance to malaria.
29 lian children with cerebral or uncomplicated malaria.
30 ne (SP) in preventing maternal and placental malaria.
31 ous, most likely by augmenting resistance to malaria.
32 opment of blood stage vaccines against vivax malaria.
33 r rescue treatment for Plasmodium falciparum malaria.
34 ntion target of ongoing efforts to eradicate malaria.
35  and remain the mainstay of therapy to treat malaria.
36 eurological sequela in survivors of cerebral malaria.
37 ntial role in naturally acquired immunity to malaria.
38 ong-lived humoral immunity and resistance to malaria.
39 ), providing further support for the role of malaria.
40 her the use of DSM265 for the prophylaxis of malaria.
41 nferring enhanced protection against febrile malaria.
42 he potential application of this approach to malaria.
43         There was a total of 8,476 confirmed malaria admissions.
44 oing burden of vector-borne diseases such as malaria and dengue.
45 tes to be associated with protection against malaria and further shows IgG3 and GLURP antibodies are
46      Studies were identified by the Maternal Malaria and Malnutrition (M3) initiative using a conveni
47 ty of only 2 cross-sectional measurements of malaria and the limited availability of ultrasound-based
48                                    Together, malaria and the neglected tropical diseases (NTDs) kill
49 on and vitamin A deficiencies, inflammation, malaria, and body mass index) and distal risk factors (e
50  (n = 21) and nonsevere (n = 109) falciparum malaria, and healthy controls (n = 50), we measured para
51 metric measures, micronutrient deficiencies, malaria, and inflammation) and household-level predictor
52 physiological mechanisms underlying knowlesi malaria, and of the age-related increase in risk of seve
53                  As markers of exposure anti-malaria antibody responses can help characterise heterog
54                      Assuming all women with malaria are still parasitaemic at delivery, an estimated
55 on decreases to 12%, assuming all women with malaria are treated during pregnancy.
56 dies suggest that young children (<5 y) with malaria are under-dosed.
57 available in infants and pregnant women with malaria as well as in healthy individuals.
58 od spot samples from patients with suspected malaria at 37 health facilities from 2012 to 2014 in the
59                         The risks of MiP and malaria-attributable low birthweight (mLBW) in unprotect
60 t yet there are no licensed vaccines against malaria based on antigens identified from genomic data.
61 terventions targetting this unique aspect of malaria biology.
62  Obesity was strongly associated with severe malaria, both independently (aOR, 5.58 [95% CI, 2.03-15.
63 e primary driver of systemic inflammation in malaria, both within the phagolysosome and in the cytoso
64  The radial distribution of Plasmodium vivax malaria burden has evoked enormous concern among the glo
65 to approximately 78% of the reduction in the malaria burden in sub-Saharan Africa since 2000.
66  positively associated with recent fever and malaria but not with other recent illnesses.
67 tment of uncomplicated Plasmodium falciparum malaria, but ACT resistance is spreading across Southeas
68  is not crucial for survival of experimental malaria, but alters its progression in a parasite strain
69 mains the mainstay of treatment for cerebral malaria, but it is less effective in later stages of dis
70 fer protection against Plasmodium falciparum malaria, but the precise nature of the protective effect
71      This variant reduces the risk of severe malaria by 40% and has recently increased in frequency i
72 bola virus was done by real-time PCR and for malaria by a rapid diagnostic test.
73 vectored malaria vaccine in a mouse model of malaria by co-administering it with vaccine adjuvants.
74 blocking vaccines (TBV) which aim to control malaria by inhibiting human-to-mosquito transmission sho
75                              Because EVD and malaria can be difficult to distinguish clinically, and
76  million (95% CrI: 138 million, 230 million) malaria cases and saved 940,049 (95% CrI: 545,228, 1.4 m
77 essarily prevent over-estimation of clinical malaria cases or sub-optimal case management of febrile
78 tion of P. malariae increased (2%-10% of all malaria cases).
79                                           In malaria, CD36 plays several roles, including mediating p
80 ne efficacy and sterile protection following malaria challenge.
81                                     Cerebral malaria (CM) is a severe complication of Plasmodium falc
82 predictor of mortality in pediatric cerebral malaria (CM).
83 ation and, in the longer term, transform the malaria community's ability to eradicate it globally.
84 68.7%, P < .001) for the detection of severe malaria compared to algorithms that incorporate screenin
85 variation in malaria exposure and evaluating malaria control efforts in high endemic area.
86 cally highest in countries where funding for malaria control is also high.
87                                              Malaria control is heavily dependent on chemotherapeutic
88 dual spraying (IRS) is an effective tool for malaria control, its use contributes to high insecticide
89  submicroscopic and represent a challenge to malaria control.
90                           The need to expand malaria diagnosis capabilities alongside policy requirem
91 ets had high sensitivity and specificity for malaria diagnosis, compared to microscopy.
92                       Further correction for malaria does not appear to materially alter regression-a
93          We demonstrate that the common anti-malaria drug chloroquine (CQ) extends the lifespan of ZI
94                                    Few known malaria drug targets are expressed in quiescent parasite
95 ine agents to treat uncomplicated falciparum malaria due to their activity against multidrug resistan
96  correlates with protection against clinical malaria during infancy.
97  is associated with reduced risk of clinical malaria during infancy.
98                                              Malaria during pregnancy constitutes a large health prob
99 d test periods and thus can be utilized in a malaria early warning system.
100 ing with the export element (PEXEL) found in malaria effector proteins from Plasmodium falciparum The
101 ng subregion, which has motivated a regional malaria elimination agenda.
102 esearch and development agenda to accelerate malaria elimination and, in the longer term, transform t
103 ed RDTs, would represent a serious threat to malaria elimination efforts.
104                             A cornerstone of malaria elimination is the effective management of Anoph
105  in natural Anopheles gambiae populations at malaria endemic areas in Kenya, and reducing FBN30 expre
106 nd clinically circulating P. falciparum from malaria endemic areas in Kenya, but not laboratory P. fa
107 HbC) mutations are frequently encountered in malaria-endemic areas of Africa, where they protect chil
108                         Because hospitals in malaria-endemic areas often lack diagnostic facilities t
109 lobulin G (IgG) from individuals residing in malaria-endemic regions in Tanzania, Senegal, and Mali w
110 rtality in the growing population of HEIs in malaria-endemic resource-limited settings.
111 stimated 20% of the 1 059 700 stillbirths in malaria-endemic sub-Saharan Africa are attributed to P f
112 inded, placebo-controlled trial conducted in malaria-endemic Uganda, comparing hydroxyurea to placebo
113 tes have had limited efficacy in settings of malaria endemicity.
114 Cs obtained from malaria-naive US donors and malaria-experienced donors from Mali.
115                 Here we report that 5-10% of malaria-exposed individuals, but none of the European bl
116 e further evidence in assessing variation in malaria exposure and evaluating malaria control efforts
117 ted that TMP-SMX prophylaxis during repeated malaria exposures would induce protective long-lived ste
118        We report a case of severe falciparum malaria following nosocomial Plasmodium falciparum trans
119             Research funding data related to malaria for 1997-2013 were sourced from existing dataset
120 ss vaccination program approach to eliminate malaria from geographically defined areas.
121 e both species are common, zoonotic knowlesi malaria has recently become dominant, and cases are reco
122  confer artemisinin resistance in falciparum malaria have multiple independent origins across the Gre
123 lasmodium parasites, the causative agents of malaria, have evolved a unique cell division cycle in th
124 he emergence of other MDR pathogens, such as malaria, HIV, and Gram-negative bacteria.
125  with the use of the national prevalences of malaria, HIV, schistosomiasis, sanitation, and water-qua
126 ositive children are therefore caused by non-malaria illnesses.
127  thought to contribute to the maintenance of malaria immunity.
128                       Mostly, adjustment for malaria in addition to AGP did not significantly change
129 ection-factor approaches, and accounting for malaria in addition to inflammation did not have an adde
130 viously unidentified risk factors for severe malaria in adults diagnosed with P. falciparum.
131 f the age-related increase in risk of severe malaria in general, are poorly understood.
132                 Plasmodium falciparum causes malaria in humans with over 450,000 deaths annually.
133 re we show that the two main species causing malaria in humans, Plasmodium falciparum and Plasmodium
134 iagnostic tests (RDTs) to evaluate suspected malaria in low-endemicity settings has not been well cha
135 species-transcending immunity to blood-stage malaria in mice.
136 creened men (>/=18 years) with uncomplicated malaria in Missira (northeast Mali) and Bamako (capital
137 sk of re-presentation to hospital with vivax malaria in patients prescribed dihydroartemisinin-pipera
138 the treatment of uncomplicated P. falciparum malaria in pediatric patients.
139                      The association between malaria in pregnancy and stillbirth has yet to be compre
140     INTERPRETATION: P falciparum and P vivax malaria in pregnancy both increase stillbirth risk.
141 aharan Africa are attributed to P falciparum malaria in pregnancy; the population attributable fracti
142 a quantification and stage determination for malaria in remote regions.
143 n adults (>/=18 years of age) diagnosed with malaria in Sweden between January 1995 and May 2015.
144     Any IRS protection significantly reduced malaria incidence during pregnancy and placental malaria
145 ions pauci-immune to malaria, risk of severe malaria increases with age.
146 ilable representative household surveys (the Malaria Indicator Surveys, Demographic and Health Survey
147 lecular and cellular processes that modulate malaria-induced innate and adaptive immune responses.
148 aive volunteers infected in controlled human malaria infection (CHMI) clinical trials.
149    We tested the hypothesis that the odds of malaria infection are lower in modern, improved housing
150 tion, acute phase protein concentrations and malaria infection as indices of immune function, and tel
151 ralization of activin activity during murine malaria infection did not affect hepcidin expression, su
152 dies previously indicated that the effect of malaria infection during pregnancy on the risk of low bi
153 l self-reported fevers were accompanied by a malaria infection in 2014, but that only 28.0% of those
154 ta2(+) T cells may play a role in preventing malaria infection in children living in endemic settings
155 between iron deficiency, iron treatment, and malaria infection in endemic areas; the heightened impac
156 ective against P falciparum controlled human malaria infection in malaria-naive individuals.
157                      Exposure to blood-stage malaria infection is often persistent, leading to genera
158 he 2La inversion are associated with natural malaria infection levels in wild-captured vectors from W
159                                   Preventing malaria infection through vaccination requires preventin
160 een possible to evaluate the contribution of malaria infection to retinopathy-negative CM.
161 l children surveyed, 139,318 were tested for malaria infection using microscopy (n = 131,652) or RDT
162                  During the liver stage of a malaria infection, Plasmodium parasites are targeted by
163  and were protected against controlled human malaria infection.
164  the human skin odour profile is affected by malaria infection.
165 mediated pathology during potentially lethal malaria infections.
166 Andrew Lover and colleagues discuss regional malaria initiatives, the strengths and challenges.
167 spatial analysis on available data to target malaria interventions in areas where hotspot boundaries
168                                      Because malaria is a host immune response-driven disease, one ap
169                                              Malaria is a mosquito-borne disease affecting millions o
170                                              Malaria is a reportable disease in Israel.
171                                              Malaria is a worldwide health problem that affects two-t
172                                              Malaria is caused by mosquito-borne Plasmodium spp. para
173                                              Malaria is caused by parasites of the genus Plasmodium.
174 e find that a nearby association with severe malaria is explained by a complex structural rearrangeme
175 , sustain elimination, and free the world of malaria is greater than ever.
176 onses and development of severe pathology of malaria is largely unknown.
177  the subsequent risk of clinical episodes of malaria is unclear.
178                 Here, using a mouse cerebral malaria model and small-molecule inhibitors, we demonstr
179                         Using a unique mouse malaria model, here we investigated the mechanisms of sp
180 t sporozoite challenge in a stringent rodent malaria model.
181                                 Using rodent malaria models, we previously showed that TMP-SMX, at pr
182                            However, mosquito-malaria molecular interactions in nature are not clear.
183 sequently enrolled 229 cases with P knowlesi malaria mono-infection and 91 cases with other Plasmodiu
184 imethamine in vulnerable populations reduces malaria morbidity in Africa, but resistance mutations in
185 r aim in this study was to assess changes in malaria morbidity in an area of Uganda with historically
186 (Brazzaville) and Guinea had reasonably high malaria mortality, yet Congo (Brazzaville) ranked 38th a
187 iparum controlled human malaria infection in malaria-naive individuals.
188 results were obtained with DCs obtained from malaria-naive US donors and malaria-experienced donors f
189 ased in parallel with hepcidin in serum from malaria-naive volunteers infected in controlled human ma
190 d not significantly protect against clinical malaria (odds ratio [OR]=0.95, 95% CI 0.68-1.32, p=0.745
191                   A longitudinal analysis of malaria parasite genomes has revealed new markers that c
192  constitute a major change in our concept of malaria parasite invasion, suggesting it is, in fact, a
193                Sexual differentiation of the malaria parasite is a pre-requisite for transmission fro
194 tage infections of two strains of the rodent malaria parasite Plasmodium chabaudi that differ in viru
195 een, red blood cells infected with the human malaria parasite Plasmodium falciparum (iRBCs) adhere to
196                                          The malaria parasite Plasmodium falciparum and related apico
197 lular resolution of red cell invasion by the malaria parasite Plasmodium falciparum has been possible
198 e emergence of artemisinin resistance in the malaria parasite Plasmodium falciparum poses a major thr
199                     The hepatic stage of the malaria parasite Plasmodium is accompanied by an autopha
200           These data strongly imply that the malaria parasite primes the erythrocyte surface through
201  strategies to impact liver infection by the malaria parasite through the modulation of Arg uptake an
202                                    The human malaria parasite, Plasmodium falciparum, depends on a co
203 es are key effectors of calcium signaling in malaria parasite.
204     Secondary outcomes included incidence of malaria, parasite prevalence, and adverse birth outcomes
205 lly inherited traits, and find evidence that malaria parasitemia does contribute to the pathogenesis
206                          Having asymptomatic malaria parasitemia was associated with a 40% increase i
207 doses, can arrest liver stage development of malaria parasites and speculated that TMP-SMX prophylaxi
208                                              Malaria parasites are thought to influence mosquito attr
209 ontinue (the STOP-CTX arm) were examined for malaria parasites by quantitative reverse transcription
210 e now demonstrate that repeated exposures to malaria parasites during TMP-SMX administration induces
211                                              Malaria parasites modify their human host cell, the matu
212 merozoites, the invasive form of blood stage malaria parasites, actively recruit C1-INH to their surf
213 ifestyle of intracellular pathogens, such as malaria parasites, is intimately connected to that of th
214 -binding domains (ApiAP2s) was identified in malaria parasites.
215                                           In malaria pathophysiology, divergent hypotheses on the inh
216 rum proteome alterations in non-severe vivax malaria patients before and during patient recuperation
217 compare the serum proteome profiles of vivax malaria patients with low (LPVM) and moderately-high (MP
218 essed the efficacy and safety of re-treating malaria patients with uncomplicated failures with the sa
219 te responsible for the most virulent form of malaria, Plasmodium falciparum, invade erythrocytes.
220  consistent predictors of severe anemia were malaria, poor sanitation, and underweight.
221                            Most fevers among malaria-positive children are therefore caused by non-ma
222 ulness in hot and low-income countries where malaria prevails.
223                                              Malaria prevalence decreased in only 1 of 3 study villag
224                   Within individual surveys, malaria prevalence measured by microscopy ranged from 0.
225 urkina Faso 2010) in traditional houses, and malaria prevalence measured by RDT ranged from 0.3% (Sen
226  to derive 2 alternative measures of overall malaria propensity of a location across different time s
227 sought cellular immunity-based correlates of malaria protection and risk associated with RTS,S/AS01E
228 duced immunity and identifying correlates of malaria protection, which could, for instance, inform th
229 participants and compare the prevalence of 3 malaria-protective red blood cell polymorphisms in BWF c
230  2012, to Feb 27, 2014, who were tested with malaria rapid diagnostic tests (RDTs), and administered
231 nes can affect the performance of HRP2-based malaria rapid diagnostic tests (RDTs).
232  enhance a popular dual-antigen lateral flow malaria RDT that targets Plasmodium falciparum histidine
233 cycles, the signature and exclusive cause of malaria-related morbidity and mortality.
234     We describe the trends of investments in malaria-related research in sub-Saharan Africa and compa
235          Hemoglobin AC, which reduces severe malaria risk, reduced IE binding to the receptors CD36 a
236 ria incidence during pregnancy and placental malaria risk.
237               In populations pauci-immune to malaria, risk of severe malaria increases with age.
238   Through amplicon deep-sequencing placental malaria samples from women in Malawi and Benin, we asses
239 e vaccine to children in the months prior to malaria season could maximize impact of the vaccine.
240  P falciparum infection throughout an entire malaria season.
241 ere (n = 47) and nonsevere (n = 99) knowlesi malaria, severe (n = 21) and nonsevere (n = 109) falcipa
242 , FCGR2C, and FCGR3 genes is associated with malaria severity, and our results provide evidence for a
243  and adjustment of sTfR for inflammation and malaria should be considered.
244 iptomics profiling of virulent and avirulent malaria shows the validity of this approach to inform se
245 romotes increased transplacental transfer of malaria-specific antibodies and a prolonged IgG3 half-li
246 the transplacental transfer and half-life of malaria-specific IgG3 in young infants and is associated
247 metabolically active, non-replicating, whole malaria sporozoite vaccine that has been reported to be
248           IPTp-SP appears to protect against malaria, STIs/RTIs, and other unspecified causes of adve
249 n a pooled analysis of surveys that measured malaria, stunting was associated with elevated AGP but n
250                 The spatial heterogeneity of malaria suggests that interventions may be targeted for
251                                              Malaria surveillance data provide opportunity to develop
252                             Individual-level malaria surveillance data were collected from 1 outpatie
253  biological characteristic of macular CNP in malaria that had previously only been described subjecti
254 n quantifying the international movements of malaria to improve our understanding of these phenomena
255 on this foundation, the goal is now to drive malaria towards elimination.
256 lFOB) is a quantitative surrogate metric for malaria transmission at population level and for exposur
257                       Over a period in which malaria transmission declined markedly, AMA1 and MSP2 an
258 he vaccine according to seasonal patterns of malaria transmission in regions of Africa.
259 ame regardless of the geographic distance or malaria transmission intensity.
260                                              Malaria transmission is influenced by climate, land use
261                                              Malaria transmission is known to be strongly impacted by
262                                      Using a malaria transmission model we demonstrate that in such r
263 multi-regional assessment of population-wide malaria transmission potential based on 1209 mosquito fe
264    Sustained control has resulted in reduced malaria transmission potential, but an increasing propor
265 le may form reservoirs of persistent outdoor malaria transmission requiring novel measures for survei
266 ish antibody titers that persist for several malaria transmission seasons.
267 dium berghei has served as a model for human malaria transmission studies and played a pivotal role i
268 onses can help characterise heterogeneity in malaria transmission.
269 ing humans, reproducing, and contributing to malaria transmission.
270 act of the mosquito immune response on human malaria transmission.
271 eleterious effect on sporozoites and reduces malaria transmission.
272                                     Changing malaria treatment practices have been accompanied by pro
273 n analysis of cure rates from all falciparum malaria treatment trials (n = 40) with monotherapy arms
274                     Chloroquine was used for malaria treatment until resistant Plasmodium falciparum
275 its (ETUs), guidelines recommended empirical malaria treatment.
276 es for new and underused vaccines, HIV/AIDS, malaria, tuberculosis, and maternal and child health.
277                     Microscopic diagnosis of malaria using Giemsa-stained blood smears is the standar
278                         RTS,S is an advanced malaria vaccine candidate and confers significant protec
279  production and suboptimal immunogenicity of malaria vaccine candidates have slowed the development o
280 e to express three different AMA1-DiCo-based malaria vaccine candidates to develop a vaccine cocktail
281                To identify novel blood-stage malaria vaccine candidates, we constructed a library of
282             As our search for an efficacious malaria vaccine continues, the development of a whole-or
283                                              Malaria vaccine development has been dominated by the su
284 fficacy of a single dose adenovirus-vectored malaria vaccine in a mouse model of malaria by co-admini
285 , which could contribute to a cost-effective malaria vaccine.
286 iving further impetus for the development of malaria vaccines targeting GLURP.
287 under way to improve the efficacy of subunit malaria vaccines through assessments of new adjuvants, v
288 find in a high transmission region in India, malaria vector populations show a high propensity to fee
289 o improve the surveillance and monitoring of malaria vector populations under control.
290 dance of total Anopheles species and primary malaria vectors and the EIR (P<.001).
291 ed stimuli could be used to attract and kill malaria vectors more successfully than individual stimul
292                We also estimated exposure to malaria vectors through genetic matching of blood from 1
293  meets key requirements of the Medicines for Malaria Venture drug candidate profiles.
294 use Of Hydroxyurea in an African Region with Malaria) was a randomized, double-blinded, placebo-contr
295 omics of var genes in cases of uncomplicated malaria, we set out to determine if there was any eviden
296 d bednets (ITNs) are effective in preventing malaria where vectors primarily bite indoors and late at
297 ent sporozoite challenge in rodent models to malaria, where IgG2a antibodies were associated with pro
298 ases with microscopy-positive, PCR-confirmed malaria who presented to two primary referral hospitals
299       The risk of re-presentation with vivax malaria within 1 year was 33.8% (95% confidence Interval
300 s infected with 6 spores unable to transmit malaria within 5 days post-infection, surpassing the Wor

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