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 hly pertinent to the development of new anti-malarials.

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

4 e that may lead to development of novel 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 natural products, many of which display anti-malarial activity.

8 of ameobiasis that also displays potent 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 cy can lead to the transplacental passage of malarial Ags that are capable of inducing acquired immun

18 ned IgM to MA but 78% had IgG to one or more malarial Ags, with 53% having IgG to AMA-1, 38% to MSP-1

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

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

21 jor producers of autoantibodies that promote malarial anaemia.

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

23 Malarial and HIV infections may hinder efforts to elimin

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

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

26 -PGE2/TNF-alpha, compared with children with malarial anemia (P<.01), with systemic bicyclo-PGE2 and

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

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

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

30 Severe malarial anemia (SMA) is a primary cause of morbidity an

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

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

33 Severe malarial anemia (SMA) resulting from Plasmodium falcipar

34 <5 years of age, or in children with severe malarial anemia (SMA), a form of severe malaria estimate

35 Severe malarial anemia (SMA), caused by Plasmodium falciparum i

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

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

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

39 A case of malarial anemia emphasizes the complex relationship betw

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

41 The pathogenesis of malarial anemia is multifactorial, and the mechanisms re

42 However, malarial anemia was greatly reduced in primiparous carri

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

44 k of severe malaria phenotypes (particularly malarial anemia) in comparison with the frameshift delet

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

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

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

48 l of hyperparasitemia and protection against malarial anemia.

49 altose as an adjunctive treatment for severe malarial anemia.

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

51 a rural hospital with various severities of malarial anemia.

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

53 TNF-alpha, which is associated with enhanced malarial anemia.

54 hich correlated with an enhanced severity of malarial anemia.

55 (aged <3 years, n = 357) with P. falciparum malarial anemia.

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

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

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

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

60 methodology was developed for the sensing of malarial antibodies.

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

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

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

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

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

66 Now, the availability of well characterized malarial antigens allows us to test whether serological

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

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

69 o TT were reduced, but levels of antibody to malarial antigens were not.

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

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

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

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

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

75 pepsin, human pepsin (h. pepsin) and several malarial aspartic proteases, the plasmepsins.

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

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

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

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

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

81 A number of malarial blood-stage candidate vaccines are currently be

82 demonstrated that natural HZ is coated with malarial but not human DNA.

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

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

85 In contrast to the outcome in malarial challenge, death of alphaD-/- animals was accel

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

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

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

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

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

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

92 t could discriminate bacterial from viral or malarial diagnoses.

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

94 Malarial dihydrofolate reductase (DHFR) is the target of

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

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

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

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

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

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

101 To estimate the burden of malarial disease, and evaluate the likely effects of con

102 stages of the parasite life cycle that cause malarial disease.

103 e to protect African children against severe malarial disease.

104 etic mechanisms of protection against severe malarial disease.

105 Purified malarial DNA activated TLR9 but only when DNA was target

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

107 responses was even greater than transfecting malarial DNA.

108 uantities of natural HZ contain <1 microg of malarial DNA; its potency in activating immune responses

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

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

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

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

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

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

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

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

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

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

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

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

121 Artemisinin derivatives are effective anti-malarial drugs.

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

123 Artemisinins are the cornerstone of anti-malarial drugs.

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

125 iscovered several compounds that inhibit the malarial enzyme in the sub- to low-nanomolar range and t

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

127 le in the design of potent inhibitors of the malarial enzyme Plasmodium falciparum enoyl acyl carrier

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

129 p to 136-fold selectivity), that inhibit the malarial enzyme with IC50 values down to 1 nM, and that

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

131 ther with a homology structural model of the malarial enzyme.

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

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

134 The implications are that malarial erythrocyte remodeling events occur at a signif

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

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

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

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

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

140 Thus, although the malarial genome is extremely AT-rich, its DNA is highly

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

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

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

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

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

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

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

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

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

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

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

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

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

154 Malarial infection in nonimmune pregnant women is a majo

155 Malarial infection in nonimmune women is a risk factor f

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

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

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

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

160 latent hypnozoites acquired from a previous malarial infection.

161 the virulence of intraerythrocytic stages of malarial infection.

162 ment in the triggering of the lytic cycle of malarial infection.

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

164 Malarial infections are often genetically diverse, leadi

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

166 After continuous exposure to malarial infections in regions of Africa where malaria i

167 We studied malarial infections to understand the contribution of PD

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

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

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

171 The domain adopts a fold similar to malarial invasion proteins, with extensive loop insertio

172 blishment of memory CD8+ T cell responses to malarial liver stages.

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

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

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

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

177 olizing P450s in natural populations of this malarial mosquito.

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

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

180 resistance protein homologues found in this malarial parasite (PfMDR1) may further modify or tailor

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

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

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

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

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

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

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

188 ecognition and killing of ookinetes from the malarial parasite Plasmodium berghei, a model for the hu

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

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

191 Our in vitro investigations with the human malarial parasite Plasmodium falciparum document a remar

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

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

194 In the malarial parasite Plasmodium falciparum, a multifunction

195 he prokaryote Vibrio harveyi, the eukaryotic malarial parasite Plasmodium falciparum, the parasitic A

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

197 te Plasmodium berghei, a model for the human malarial parasite Plasmodium falciparum.

198 The malarial parasite Plasmodium must complete a complex lif

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

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

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

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

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

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

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

206 n of pathogens such as Plasmodium falciparum malarial parasite.

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

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

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

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

211 DH) is a key enzyme for energy generation of malarial parasites and is a potential antimalarial chemo

212 D DIC transmittance "z stack" images of live malarial parasites and use those to quantify hemozoin (H

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

214 d2) (CQR via transfection with mutant pfcrt) malarial parasites as they develop within the human red

215 The malarial parasites assemble flagella exclusively during

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

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

218 t cell-mediated immunity against blood-stage malarial parasites during chronic malaria (i) requires t

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

220 Malarial parasites have evolved resistance to all previo

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

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

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

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

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

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

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

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

229 Its mode of action against malarial parasites, however, has remained undefined.

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

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

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

233 for lipid biosynthesis of intraerythrocytic malarial parasites.

234 s in humans and purine auxotrophs, including malarial parasites.

235 as HIV/SIV, Mycobacterium tuberculosis, and malarial parasites.

236 quine sensitive (CQS) versus resistant (CQR) malarial parasites.

237 versus time data for live, intraerythrocytic malarial parasites.

238 zed, intraerythrocytic Plasmodium falciparum malarial parasites.

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

240 stant to the growth of Plasmodium falciparum malarial parasites.

241 Our findings reveal the presence in the malarial parasitophorous vacuole of a regulated, PfSUB1-

242 onse to challenge with Plasmodium berghei, a malarial pathogen that models systemic infection and inf

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

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

245 Since deposition of malarial pigment (hemozoin [Hz]) contributes to suppress

246 Ingestion of naturally acquired malarial pigment (hemozoin [PfHz]) by monocytes promoted

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

248 ion of Plasmodium falciparum hemozoin (pfHz; malarial pigment) by peripheral blood mononuclear cells

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

250 s produced more MIF when stimulated with the malarial product hemozoin compared with cells carrying l

251 Intermittent malarial prophylaxis and insecticide-treated bednets sho

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

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

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

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

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 ascribe the novel catalytic activity of the malarial PTPS to a Cys to Glu change at its active site

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

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

261 However, the malarial PVM lacks PIP(2), although another raft lipid,

262 valent to calculating the human component of malarial R0 .

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

264 Malarial retinopathy (MR) has diagnostic and prognostic

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

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

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

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

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

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

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

272 sistance for screening and quantification of malarial retinopathy.

273 etecting retinal hemorrhages associated with malarial retinopathy.

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

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

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

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

278 e assessed by ELISA for Abs to an extract of malarial schizonts (MA), recombinant apical merozoite Ag

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

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

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

282 inhibitors block the proteolytic activity of malarial SPP (mSPP).

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

284 clinically approved drugs as potential anti-malarial therapies.

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

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

287 4.93 (95% CI, 3.79-6.42), those with severe malarial thrombocytopenia alone had an adjusted OR of 2.

288 ody responses to recombinant Pfs25H, a human malarial transmission-blocking protein vaccine candidate

289 This is the first report that a malarial vaccine candidate induced different specificiti

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

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

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

293 A1) is one of the most promising blood-stage malarial vaccine candidates.

294 Synthetic antimalarial drugs and malarial vaccines are currently being developed, but the

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

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

297 Recently, TEP1 from the malarial vector Anopheles gambiae was shown to mediate r

298 genetic structure of four populations of the malarial vector Anopheles scanloni in Thailand was studi

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