ライフサイエンスコーパス: malarial

1 and the etiology of the coma is entirely non-malarial.

2 st as a tool for screening a library of anti-malarials.

3 e that may lead to development of novel anti-malarials.

4 hly pertinent to the development of new anti-malarials.

5 es, much of our biochemical understanding of malarial actin has instead relied on recombinant protein

6 opyrimidine-based DHODH inhibitors with anti-malarial activity in vivo.

7 of ameobiasis that also displays potent anti-malarial activity.

8 natural products, many of which display anti-malarial activity.

9 Compared to malarial ADA complexes with adenosine or deoxycoformycin

10 sis for MTA and MT-coformycin specificity in malarial ADAs is the subject of speculation.

11 The catalytic site specificity of malarial ADAs permits methylthiocoformycin (MT-coformyci

12 lthioadenosine (MTA) is a substrate for most malarial ADAs, but not for human ADA.

13 metry for 5'-methylthioribosyl groups in the malarial ADAs.

14 Use of partially effective anti-malarial agents for IPTp may exacerbate malaria infectio

15 cient selectivity to allow their use as anti-malarial agents.

16 t could be exploited by next-generation anti-malarial agents.

17 te spatial hospital accessibility for severe malarial anaemia (SMA) and cerebral malaria (CM).

18 a strong predictor of presenting with severe malarial anaemia (SMA) in children, with an OR of 2.79 (

19 Severe malarial anaemia (SMA) is the most common life-threateni

20 The lack of any of these signals ameliorates malarial anaemia during infection in a mouse model.

21 because of a decrease in incidence of severe malarial anaemia since 1997 (4.75 to 0.37 per 1000 child

22 ral malaria but increased the risk of severe malarial anaemia.

23 from cerebral malaria and death from severe malarial anaemia.

24 jor producers of autoantibodies that promote malarial anaemia.

25 l malaria, but with increased risk of severe malarial anaemia.

26 Antibodies to malarial and non-malarial antigens were highly correlate

27 fects) to achieve greater protection against malarial and non-malarial causes of low birthweight.

28 low birthweight (<2,500 g) in women without malarial and reproductive tract infections.

29 curately classified patients into bacterial, malarial, and viral etiologies and misclassified only on

30 Cerebral malaria (CM) and severe malarial anemia (SMA) are the most serious life-threaten

31 animal model of Plasmodium falciparum severe malarial anemia (SMA) has hampered the understanding of

32 c Plasmodium falciparum transmission, severe malarial anemia (SMA) is a leading cause of pediatric mo

33 Among the severe malaria syndromes, severe malarial anemia (SMA) is the most common, whereas cerebr

34 Severe malarial anemia (SMA) remains a major cause of pediatric

35 onditioning the immunopathogenesis of severe malarial anemia (SMA) remains undefined, relationships b

36 Severe malarial anemia (SMA) resulting from Plasmodium falcipar

37 <5 years of age, or in children with severe malarial anemia (SMA), a form of severe malaria estimate

38 inflammatory markers in children with severe malarial anemia (SMA), children with cerebral malaria (C

39 ria: cerebral malaria (CM; n = 79) or severe malarial anemia (SMA; n = 77).

40 Patients with severe malarial anemia alone (hemoglobin level, <5 g/dL) had an

41 d hyperparasitemia are associated with early malarial anemia and pre-existing anemia is the main dete

42 factors, including Hz, contribute to severe malarial anemia by suppressing Epo-induced proliferation

43 A case of malarial anemia emphasizes the complex relationship betw

44 loss of uninfected red blood cells found in malarial anemia from both species.

45 sessed mechanistic and risk factors for post-malarial anemia in Ghanaian and Gabonese children with s

46 (Epo)-induced erythropoiesis are features of malarial anemia in Plasmodium yoelii- and Plasmodium ber

47 The pathophysiology of malarial anemia is multifactorial and incompletely under

48 However, malarial anemia was greatly reduced in primiparous carri

49 T repeats at -794 and increasing severity of malarial anemia was observed.

50 Children with severe malarial anemia were more likely to have high anti-PS an

51 lear implications for the mechanism of human malarial anemia, a severe pathological condition affecti

52 We also found iHPCs during experimental malarial anemia, in which they required endosomal TLR an

53 malaria (cerebral malaria, n = 253 or severe malarial anemia, n = 211) or community children (n = 206

54 To determine whether Hz contributes to malarial anemia, P. yoelii-derived or synthetic Hz was a

55 f this pathway may be exploited for treating malarial anemia.

56 C) output, is an important feature of severe malarial anemia.

57 l of hyperparasitemia and protection against malarial anemia.

58 altose as an adjunctive treatment for severe malarial anemia.

59 y be a host protective effect against severe malarial anemia.

60 a rural hospital with various severities of malarial anemia.

61 ic disease, myelodysplasia, thalassemia, and malarial anemia.

62 that expose PS and have been linked to late malarial anemia.

63 B-cells and anti-PS autoantibodies in human malarial anemia.

64 erythrocytes is an important contributor to malarial anemia; however, the mechanisms underlying this

65 as a cause of erythropoietic suppression in malarial anemia; however, the role of iron in malaria re

66 Our findings demonstrate that human anti-malarial antibodies have evolved to function by fixing c

67 e have demonstrated that acquired human anti-malarial antibodies promote complement deposition on the

68 methodology was developed for the sensing of malarial antibodies.

69 her SM in pregnancy is associated with lower malarial antibody responses and higher cytokine response

70 m in urine for clinical analysis, and (iv) a malarial antigen (Plasmodium falciparum histidine-rich p

71 Injecting SpyCatcher-VLPs decorated with a malarial antigen efficiently induced antibody responses

72 on in a TNF-alpha-dependent manner following malarial antigen processing by monocytes/macrophages.

73 luorescent beads covalently-coupled with the malarial antigen VAR2CSA.

74 We have cloned a malarial antigen-containing fusion protein, MBP-pfMSP1(1

75 Humoral responses to the malarial antigens circumsporozoite protein, liver-stage

76 Antibodies to malarial and non-malarial antigens were highly correlated between materna

77 e antibody responses to TT, but not those to malarial antigens, in infants.

78 a marker for the extent of fetal exposure to malarial antigens.

79 ittle effect on the antibody response to the malarial antigens.

80 Therefore, inhibition of malarial arginase may serve as a possible candidate for

81 tion of two polypeptide insertions unique to malarial arginase: a 74-residue low-complexity region co

82 in is a potent peptidyl inhibitor of various malarial aspartic proteases, and also has parasiticidal

83 For this study we focus on the anti-malarial, atovaquone.

84 sulfadoxine-pyrimethamine shows greater non-malarial benefits for birth outcomes than does dihydroar

85 ique model for studying conserved aspects of malarial biology as well as species-specific features of

86 l label free spectrophotometric detection of malarial biomarker HRP-II following an indicator displac

87 and then was applied to the detection of the malarial biomarker Plasmodium falciparum histidine-rich

88 ine-containing branched peptide mimic of the malarial biomarker Plasmodium falciparum histidine-rich

89 n lack diagnostic facilities to identify non-malarial causes of coma, it has not been possible to eva

90 greater protection against malarial and non-malarial causes of low birthweight.

91 The current model is that PKG, a malarial cGMP-dependent protein kinase, triggers egress,

92 the 3-day atovaquone/proguanil schedule for malarial chemoprophylaxis.

93 exploit PfDHODH for the development of anti-malarial chemotherapy.

94 d by combining it with the FDA-approved anti-malarial, chloroquine, a known lysosomotropic compound,

95 the underlying pathology of life-threatening malarial coma ("cerebral malaria"), allowing differentia

96 tly required for use in next generation anti-malarial combinations.

97 immunomodulatory effects of Hz, its role in malarial complications, and its potential effects after

98 esponse may contribute to the development of malarial complications.

99 ceuticals such as azidothymidine (AZT), anti-malarial compounds and novel vaccines saving millions of

100 Several heme-binding anti-malarial compounds, such as chloroquine, efficiently inh

101 One of the challenges faced in malarial control is the acquisition of insecticide resis

102 t could discriminate bacterial from viral or malarial diagnoses.

103 selective, simple, portable, and inexpensive malarial diagnostic device for point-of-care and low res

104 Malarial dihydrofolate reductase (DHFR) is the target of

105 We estimated antimalarial (indirect) and non-malarial (direct) effects of IPTp on birth outcomes usin

106 tive resistance to both infection and severe malarial disease (SM).

107 se that any parasite can cause uncomplicated malarial disease and that these diverse parasite reperto

108 Plasmodium falciparum causes a spectrum of malarial disease from asymptomatic to uncomplicated thro

109 sk and support the hypothesis that pediatric malarial disease has fetal origins.

110 ogen in other parts of the world, may expand malarial disease in Africa.

111 rotropic P. berghei NK65 (PbN) causes severe malarial disease in C57BL/6 mice but does not cause ECM.

112 ed with UM, but its level and role in severe malarial disease remains to be investigated.

113 etic mechanisms of protection against severe malarial disease.

114 prompted us to examine the possibility that malarial DNA triggered TLR9-independent pathways.

115 Artesunate is a clinically effective anti-malarial drug and has recently been shown to attenuate a

116 demonstrate that PDI-Trans is a viable anti-malarial drug and vaccine target blocking malarial trans

117 odium species that are resistant to the anti-malarial drug atovaquone.

118 For over a half-century the anti-malarial drug chloroquine (CQ) has been used as a therap

119 cation with, for example, the weak-base anti-malarial drug chloroquine prevents exogenous Tat degrada

120 zoites attenuated by radiation or under anti-malarial drug coverage.

121 romising source of suitable targets for anti-malarial drug development.

122 ntext of both anti-bacterial as well as anti-malarial drug discovery.

123 sphorylation, but also define potential anti-malarial drug targets within the parasite kinome.

124 hway inhibitors and chloroquine (CQ)-an anti-malarial drug used as a cancer therapy adjuvant in over

125 Atovaquone is an anti-malarial drug used in combination with proguanil (e.g. M

126 ns that contain important antigenic and anti-malarial drug-resistance genes.

127 men need access to information on which anti-malarial drugs are safe to use at different stages of pr

128 amined in vitro susceptibility to seven anti-malarial drugs for 40 fresh P. falciparum field isolates

129 emerging resistance of the parasite to anti-malarial drugs such as chloroquine, demonstrates an urge

130 uently a target for many of the current anti-malarial drugs.

131 Artemisinins are the cornerstone of anti-malarial drugs.

132 Artemisinin derivatives are effective anti-malarial drugs.

133 doxine-pyrimethamine conferred a greater non-malarial effect than did dihydroartemisinin-piperaquine

134 ine-pyrimethamine appears to have potent non-malarial effects on birthweight.

135 -pyrimethamine (or another compound with non-malarial effects) to achieve greater protection against

136 ely 400 million G6PD deficient people across malarial endemic regions of the world.

137 olunteers and Tanzanians from an area of low malarial endemicity, who were subjected to the identical

138 ted 15-, 57-, and 3-fold selectivity for the malarial enzyme over human TopoII.

139 s allowed species-specific inhibitors of the malarial enzyme to be identified.

140 mammalian PFT and the homology model of the malarial enzyme.

141 ial parasites are critical for prevention of malarial epidemic, especially in developing and tropical

142 tiple episodes were common, with 551 and 618 malarial episodes in the RTS,S/AS01E and control groups,

143 itivity and specificity for determination of malarial etiology among febrile persons.

144 Bayesian latent class modeling to attribute malarial etiology to the fevers and to estimate the sens

145 2 cohorts with different levels of previous malarial exposure.

146 wo cohorts with different levels of previous malarial exposure.

147 potential of anti-PDI agents to act as anti-malarials, facilitating the future development of novel

148 nown due to potential coinfection with a non-malarial febrile illness.

149 st be rationally managed for malaria and non-malarial febrile illnesses (NMFI).

150 Improving the quality of management of non-malarial febrile illnesses should be a priority in the e

151 nd p53 activation associated with control of malarial fever and coordinated with Pf-specific immunogl

152 dium falciparum malaria-attributable and non-malarial fever in sub-Saharan African children from 2006

153 (3)P under thermal conditions recapitulating malarial fever.

154 mutagenesis of essential asexual blood-stage malarial genes is available, hindering their functional

155 d for large-scale functional analysis of the malarial genome.

156 assay to assess the neutralizing capacity of malarial GPI-specific IgG.

157 ance to the cytotoxic effects of heme during malarial hemolysis but might impair resistance to NTS by

158 and after a malaria infection, but in mice, malarial hemolysis impairs resistance to nontyphoid Salm

159 ies to term despite high parasite burden and malarial hemozoin accumulation in the placenta at midges

160 chemical sandwich ELISA for the detection of malarial histidine-rich protein from Plasmodium falcipar

161 Maternal-foetal transfer of anti-malarial IgG to Plasmodium spp. antigens occurs in low t

162 een G6PD deficiency and both malaria and non-malarial illnesses among children in Kenya.

163 ty to directly or indirectly coordinate anti-malarial immune responses in the offspring.

164 endemic regions, and the passive transfer of malarial immunity confers protection.

165 Finally, we discuss evidence that anti-malarial immunity develops in parallel with advancing NK

166 long-lived pre-erythrocytic protective anti-malarial immunity, mediated primarily by CD8(+) T-cells.

167 nated skin confers immune protection against malarial infection almost as effectively as IV immunizat

168 o also met criteria for bacterial, viral, or malarial infection based on clinical, radiographic, and

169 sk of histopathologically detected placental malarial infection between the daily TMP-SMX plus DP arm

170 me was detection of active or past placental malarial infection by histopathologic analysis.

171 Malarial infection in nonimmune pregnant women is a majo

172 In the asexual blood stages of malarial infection, merozoites invade erythrocytes and r

173 and provided nearly full protection against malarial infection, whereas ID immunization alone was in

174 es of icterus such as sickle cell disease or malarial infection.

175 latent hypnozoites acquired from a previous malarial infection.

176 ntal angiogenesis, in women with and without malarial infection.

177 nse is crucial in determining the outcome of malarial infection.

178 rstanding of the composition of multi-clonal malarial infections and the epidemiological factors whic

179 Malarial infections are often genetically diverse, leadi

180 We compared prevalence of malarial infections in forest birds that were sampled at

181 We studied malarial infections to understand the contribution of PD

182 ure on genes that improve survival in severe malarial infections.

183 es correlates with protection against severe malarial infections; however, understanding the relation

184 m to screen and evaluate the effects of anti-malarial interventions in vivo and in real-time.

185 o survival benefit among HEU children in non-malarial, low-breastfeeding areas with a low risk of mot

186 posed but uninfected (HEU) children in a non-malarial, low-breastfeeding setting with a low risk of m

187 Some of the biochemical properties of malarial mitochondria also appear to be unconventional.

188 stigate the impact of nematode infections on malarial morbidity and antimalarial immunity.

189 olizing P450s in natural populations of this malarial mosquito.

190 ummarize recent studies that reveal that the malarial motif may function differently than previously

191 a member of a family of anti-tumor and anti-malarial natural products.

192 tion of FCGR3B CNV with vasculitis, nor with malarial or bacterial infection.

193 -Saharan Africa, targeting susceptible HIV+, malarial, or malnourished individuals.

194 reciate the complex relationship between the malarial parasite and the human immune system.

195 This probe localizes to the malarial parasite digestive vacuole (DV) during initial

196 s has been heme biomineralization within the malarial parasite digestive vacuole.

197 Data on confirmed malarial parasite infections from health facilities in i

198 Women with >/=2 malarial parasite infections tended to have lower z scor

199 he mosquito resists infection with the human malarial parasite P. falciparum by engaging the NF-kappa

200 ations and resistance to CQ in the important malarial parasite P. vivax.

201 e Gulu case, ebolavirus antigen localized to malarial parasite pigment-laden macrophages.

202 wild-type pfcrt allele into the rodent model malarial parasite Plasmodium berghei.

203 he structurally similar SSB protein from the malarial parasite Plasmodium falciparum (Pf-SSB) also bi

204 For instance, the malarial parasite Plasmodium falciparum and the Lyme dis

205 aerythrocytic development cycle of the human malarial parasite Plasmodium falciparum is subject to ti

206 ent inhibitors of the APN homologue from the malarial parasite Plasmodium falciparum M1 aminopeptidas

207 Resistance of the human malarial parasite Plasmodium falciparum to the antimalar

208 In the malarial parasite Plasmodium falciparum, a multifunction

209 complexity regions (LCRs) in proteins of the malarial parasite Plasmodium falciparum.

210 The malarial parasite Plasmodium must complete a complex lif

211 urface that is the known entry point for the malarial parasite Plasmodium vivax.

212 Despite increasing prevalence of malarial parasite resistance to sulfadoxine-pyrimethamin

213 3 plays a critical role in the regulation of malarial parasite RNA splicing and is essential for the

214 ediates signal transduction processes in the malarial parasite that regulate host erythrocyte invasio

215 OH-inducible expression of the P. falciparum malarial parasite transporter PfCRT in P. pastoris yeast

216 enetically encoding this sensor in the human malarial parasite, Plasmodium falciparum, we have quanti

217 charomyces cerevisae and the non-model human malarial parasite, Plasmodium falciparum.

218 unctional analysis of essential genes in the malarial parasite, Plasmodium, is hindered by lack of ef

219 ms are a result of selective pressure by the malarial parasite.

220 n of pathogens such as Plasmodium falciparum malarial parasite.

221 Dietary supplementation of malarial-parasite-infected mice with L-arginine or L-cit

222 Our findings reveal that malarial-parasite-infected mice, like humans, develop L-

223 A subset of HEIs (n = 471) were tested for malarial parasitemia using dried blood spots from 12, 24

224 gnostic/triaging kits for early detection of malarial parasites are critical for prevention of malari

225 The malarial parasites assemble flagella exclusively during

226 hypothesized that the killing of liver-stage malarial parasites by IFN-gamma involves autophagy induc

227 host red blood cell hemoglobin is toxic, so malarial parasites crystallize heme to nontoxic hemozoin

228 Tryptophan-rich antigens of malarial parasites have been proposed to be the potentia

229 Malarial parasites have evolved resistance to all previo

230 with this device: 1) BSDF-based detection of Malarial parasites inside unstained human erythrocytes;

231 Human infection by malarial parasites of the genus Plasmodium begins with t

232 se (HG(X)PRT) is crucial for the survival of malarial parasites Plasmodium falciparum (Pf) and Plasmo

233 iosensor shows the lowest detection limit of malarial parasites reported in the literature spanning d

234 for addressing the problem of resistance in malarial parasites that are solidly based in evolutionar

235 It is likely that hypnozoites of relapsing malarial parasites will prove to be directly sporozoite-

236 ines (TBV), which prevent the development of malarial parasites within their mosquito vector, thereby

237 f activities against human tumor cell lines, malarial parasites, and bacterial pathogens including lo

238 n is highly effective against drug-resistant malarial parasites, which affects nearly half of the glo

239 ely on the detection of antigens specific to malarial parasites.

240 stant to the growth of Plasmodium falciparum malarial parasites.

241 tein synthesis in Gram-positive bacteria and malarial parasites.

242 isi and wallikeri are perceived as relapsing malarial parasites.

243 ned model for altered CQ accumulation in CQR malarial parasites.

244 suggesting that MIF plays a complex role in malarial pathogenesis.

245 ng cytokinesis, intracellular development of malarial pathogens, and replication of a wide range of R

246 g target with similar utility as that of the malarial PfFNT.

247 n of novel genes dysregulated in response to malarial pigment (hemozoin [PfHz]) revealed that stem ce

248 Malarial pigment, or hemozoin (Hz), is an undegradable c

249 rganisms investigated in this study; (ii) no malarial PP clustered with the tyrosine-specific subfami

250 Intermittent malarial prophylaxis and insecticide-treated bednets sho

251 protein kinase, triggers egress, activating malarial proteases and other effectors.

252 a model system of a sandwich immunoassay for malarial protein detection.

253 factor 2 (FGF2) and its receptor FGFR1, the malarial protein VAR2CSA, and tumor necrosis factor-alph

254 ngineer infected erythrocytes to present the malarial protein, VAR2CSA, which binds a distinct type c

255 g was efficiently coupled to two blood-stage malarial proteins (from PfEMP1 or CyRPA), with SnoopTagJ

256 d drug targets and 15 novel binders among 61 malarial proteins.

257 insect fossils in which trypanosomes and the malarial protozoan Plasmodium have been found.

258 ty of bioinformatics tools, we identified 27 malarial putative PP sequences within the four major est

259 reveal a proteolytic activation step in the malarial PV that may be required for release of the para

260 valent to calculating the human component of malarial R0 .

261 oline (8-AQ) antimalarial drugs approved for malarial radical cure - the elimination of liver stage h

262 evidence of selection near genes involved in malarial resistance and increased multiple sclerosis ris

263 mechanisms for host immune evasion and anti-malarial resistance has enabled the Plasmodium falciparu

264 on, for example, mdr1 duplications with anti-malarial resistance, no large-scale, genome-wide study o

265 Malarial retinopathy (MR) has diagnostic and prognostic

266 r CM misclassifies 25% of patients, but when malarial retinopathy (MR) is added to the clinical case

267 ofiles to develop machine-learning models of malarial retinopathy and brain swelling.

268 to determine the extent to which paediatric malarial retinopathy reflects cerebrovascular damage by

269 mages per patient) previously diagnosed with malarial retinopathy was examined.

270 proach to a set of images from patients with malarial retinopathy, and found it compares favourably w

271 l to become a powerful new tool for studying malarial retinopathy, and other conditions involving ret

272 a high attributable fraction for features of malarial retinopathy, supporting its use in the diagnosi

273 nd validated it on images from patients with malarial retinopathy.

274 sel segments in images from 10 patients with malarial retinopathy.

275 hod will be a powerful new tool for studying malarial retinopathy.

276 sistance for screening and quantification of malarial retinopathy.

277 etecting retinal hemorrhages associated with malarial retinopathy.

278 vels, are strong indicators of CM cases with malarial retinopathy.

279 Malarial rhythmic fevers are the consequence of the sync

280 antibodies remains to be proven, given that malarial schizonts contain other proinflammatory moietie

281 to cells stimulated with either bacterial or malarial soluble products.

282 Neither of these important malarial species can be cultured in human cells in vitro

283 de a blueprint for the design of future anti-malarials targeting both the glideosome motor and its re

284 be considered during the development of anti-malarial therapeutics.

285 clinically approved drugs as potential anti-malarial therapies.

286 P. falciparum provides a focus for new anti-malarial therapies.

287 smodium PGP may hold promise for use in anti-malarial therapies.

288 y and represents a potential target for anti-malarial therapy.

289 4.93 (95% CI, 3.79-6.42), those with severe malarial thrombocytopenia alone had an adjusted OR of 2.

290 cterial infections but is protective against malarial toxin hemozoin.

291 a protein disulphide isomerase essential for malarial transmission (PDI-Trans/PBANKA_0820300) to the

292 ti-malarial drug and vaccine target blocking malarial transmission with the use of PDI inhibitor baci

293 evidence that PDI function is essential for malarial transmission, and emphasize the potential of an

294 pical membrane antigen 1 (AMA1) is a leading malarial vaccine candidate; however, its polymorphic nat

295 mportant targets for the development of anti-malarial vaccine candidates and chemoprophylaxis approac

296 gical activity of Abs induced by blood stage malarial vaccine candidates, we explored this discrepanc

297 t be important for the future design of anti-malarial vaccines based on PfEMP1 antigens.

298 sist in the design and development of future malarial vaccines.

299 re Anopheles gambiae mosquitoes, the primary malarial vectors in sub-Saharan Africa, were fed with ei

300 d with resistance of artemisinin family anti-malarials, we observe growth inhibition synergism with l