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1 ed as a neurological sequela in survivors of cerebral malaria.
2 of improving the treatment and prognosis of cerebral malaria.
3 emoglobin was elevated only in patients with cerebral malaria.
4 sculature in retinopathy-positive paediatric cerebral malaria.
5 estations of retinopathy-positive paediatric cerebral malaria.
6 e in Malawian children with uncomplicated or cerebral malaria.
7 ecked and contributes to the pathogenesis of cerebral malaria.
8 nnel AQP4 confers partial protection against cerebral malaria.
9 crucial for the development of experimental cerebral malaria.
10 argets for interventions to treat or prevent cerebral malaria.
11 their contributions to the understanding of cerebral malaria.
12 by P. berghei ANKA, an experimental model of cerebral malaria.
13 e mechanism that could contribute to coma in cerebral malaria.
14 patients diagnosed with severe anemia and/or cerebral malaria.
15 tic, and epidemiological research studies on cerebral malaria.
16 with retinopathy and mortality in pediatric cerebral malaria.
17 pathology such as multiple organ failure and cerebral malaria.
18 receptor were resistant to otherwise lethal cerebral malaria.
19 netic susceptibility to SLE protects against cerebral malaria.
20 eceptor 7 are protected from death caused by cerebral malaria.
21 t of human brain endothelium contributing to cerebral malaria.
22 improved outcomes in a preclinical model of cerebral malaria.
23 istics of parasite var genes associated with cerebral malaria.
24 ameliorate adverse neurological outcomes in cerebral malaria.
25 rocyte binding to cerebral blood vessels and cerebral malaria.
26 e without, who were presumed to have died of cerebral malaria.
27 d to kill the parasite is the development of cerebral malaria.
28 utopsy from patients with clinically defined cerebral malaria.
29 ogy of severe malaria-associated anaemia and cerebral malaria.
30 on clinical grounds, from patients dying of cerebral malaria.
31 enotype are at increased risk for developing cerebral malaria.
32 y play an important role in the pathology of cerebral malaria.
33 be targeted as part of a strategy to prevent cerebral malaria.
34 centrations would be low in individuals with cerebral malaria.
35 thy Tanzanian children but low in those with cerebral malaria.
36 ovide new opportunities for the treatment of cerebral malaria.
37 the role of blood-brain barrier breakdown in cerebral malaria.
38 predispositions to severe malarial anemia or cerebral malaria.
39 thway leading to neurological dysfunction in cerebral malaria.
40 e model is a well-recognized model for human cerebral malaria.
41 infection, a well-recognized model for human cerebral malaria.
42 of exchange transfusion for the treatment of cerebral malaria.
43 in the lethal malaria disease complication, cerebral malaria.
44 can populations, which increased the risk of cerebral malaria.
45 barbital in preventing seizures in childhood cerebral malaria.
46 o main causes of death are severe anemia and cerebral malaria.
47 ue approaches for the effective treatment of cerebral malaria.
48 a T cells and were resistant to experimental cerebral malaria.
49 associated with increased risk of developing cerebral malaria.
50 integrity associated with fatal experimental cerebral malaria.
51 AT2-deficient mice were more susceptible to cerebral malaria.
52 crovasculature is the only one correlated to cerebral malaria.
53 an early biological marker of the outcome of cerebral malaria.
54 variants may play a role in the pathology of cerebral malaria.
55 promise as potential new drugs for treating cerebral malaria.
56 en for patients with severe liver disease or cerebral malaria.
57 h Plasmodium berghei ANKA, a murine model of cerebral malaria.
58 with potential therapeutic implications for cerebral malaria.
59 uestration in patients with or who died from cerebral malaria.
60 athy, supporting its use in the diagnosis of cerebral malaria.
61 plasma PfHRP-2 concentrations were higher in cerebral malaria (1008 [IQR 342-2572] ng/mL) than in unc
67 ith Plasmodium falciparum infections develop cerebral malaria, acute respiratory distress, and shock
69 athology of life-threatening malarial coma ("cerebral malaria"), allowing differentiation between 1)
71 ed susceptibility of CXCR3-deficient mice to cerebral malaria and also restored brain proinflammatory
74 precursors, which dictated susceptibility to cerebral malaria and conferred protection against recomb
76 ent in CXCR3 were markedly protected against cerebral malaria and had far fewer T cells in the brain
78 citrulline levels in Malawian children with cerebral malaria and in mice infected with Plasmodium be
79 into mechanisms of endothelial activation in cerebral malaria and indicate that the angiopoietin-Tie-
80 chanisms responsible for the pathogenesis of cerebral malaria and lead to interventions or vaccines t
82 host-targeted therapeutic possibilities for cerebral malaria and other diseases in which brain endot
84 es the specificity of the diagnosis of fatal cerebral malaria and provides accurate quantitative esti
85 revised to limit inclusion to children with cerebral malaria and retinopathy on the basis of indirec
88 into the brain and the development of murine cerebral malaria and suggest that the CXCR3 ligands Mig
89 astrointestinal tract, both in patients with cerebral malaria and those with parasitemia in other org
91 riable and World Health Organization-defined cerebral malaria and/or retinopathy as the outcome, was
94 stroke, epilepsy, viral hemorrhagic fevers, cerebral malaria, and acute hemorrhagic leukoencephaliti
96 owed a reduction of brain AQP4 transcript in cerebral malaria, and immunoblots revealed reduction of
98 icated malaria; the cases (n = 25) developed cerebral malaria, and the controls (n = 125) did not.
99 s have been implicated in the development of cerebral malaria, and the IFN-inducible CXCR3 chemokine
102 laria syndromes, including severe anemia and cerebral malaria, are associated with high transcript le
104 f potential surrogate markers for paediatric cerebral malaria because, in this condition, the retina
105 malaria, and the proportion of children with cerebral malaria began to change 10 years before hospita
106 and meeting a strict definition of clinical cerebral malaria (Blantyre Coma Score </= 2, Plasmodium
107 that are beneficial in the immune control of cerebral malaria but that, in the absence of malaria, co
108 in volume was seen in children who died from cerebral malaria but was uncommon in those who did not d
109 sunate remains the mainstay of treatment for cerebral malaria, but it is less effective in later stag
110 t platelets not only have an adverse role in cerebral malaria, but platelets may also be protective i
111 iency are associated with decreasing risk of cerebral malaria, but with increased risk of severe mala
112 after malaria, we created a rodent model of cerebral malaria by infecting C57BL/6 mice with Plasmodi
113 asibility of developing a vaccine preventing cerebral malaria by inhibiting cerebral IE sequestration
114 ction of brain AQP4 protein was confirmed in cerebral malaria by quantitative immunogold EM; however,
115 vels of Ang II may confer protection against cerebral malaria by strengthening the integrity of the e
117 n endothelium of patients who have died from cerebral malaria casts new light on our understanding of
118 ly induced in the brains of mice with murine cerebral malaria caused by Plasmodium berghei ANKA.
121 ading causes of death in African children is cerebral malaria caused by the parasitic protozoan Plasm
122 ere collected from subjects with WHO-defined cerebral malaria (children), all forms of severe malaria
126 the role of PGs as immunomodulators of human cerebral malaria (CM) has not been examined, we investig
127 ldren with World Health Organization-defined cerebral malaria (CM) have a nonmalarial cause of death.
139 The conventional clinical case definition of cerebral malaria (CM) is imprecise but specificity is im
142 ntral to the pathologic progression of human cerebral malaria (CM) is sequestration of Plasmodium fal
147 itive impairment persist in more than 20% of cerebral malaria (CM) patients long after successful ant
148 cation of Plasmodium falciparum infection is cerebral malaria (CM) with a case fatality rate of 15-25
151 severe malarial anemia (SMA), children with cerebral malaria (CM), and community children (CC) and 2
152 nd consistent feature in the murine model of cerebral malaria (CM), resulting in significantly increa
154 cant mortality and morbidity associated with cerebral malaria (CM), the molecular mechanisms involved
165 re was significantly higher in patients with cerebral malaria (CM; n = 21) than in patients with non-
166 g severe malaria, we identified 100 cases of cerebral malaria (coma, seizure, and obtundation), 17 ca
168 inal fluid from children with a diagnosis of cerebral malaria, compared with those with a diagnosis o
169 d (fold-decreases, </=4.39) in children with cerebral malaria, compared with those with uncomplicated
171 The events resulting in the development of cerebral malaria complications are multi-factorial, enco
172 ldren with uncomplicated malaria progress to cerebral malaria despite appropriate treatment; identify
173 aran Africa continue to acquire and die from cerebral malaria, despite efforts to control or eliminat
174 modium falciparum and its rapid clearance of cerebral malaria, development of clinically useful semis
175 um berghei ANKA murine model of experimental cerebral malaria (ECM) and high-density oligonucleotide
176 t C5(-/-) mice are resistant to experimental cerebral malaria (ECM) and suggested that protection was
177 that causes protection against experimental cerebral malaria (ECM) caused by infection with Plasmodi
178 required for the development of experimental cerebral malaria (ECM) during Plasmodium berghei ANKA in
180 that free Heme generated during experimental cerebral malaria (ECM) in mice, is central to the pathog
185 bA) model in which mice develop experimental cerebral malaria (ECM) to study the roles of IRGM1 and I
186 g pathway in the development of experimental cerebral malaria (ECM) using the murine Plasmodium bergh
187 the protein cargo of MP during experimental cerebral malaria (ECM) with the overarching hypothesis t
188 ty hypothesis in the setting of experimental cerebral malaria (ECM), but find instead that low NO bio
189 ice, a well-recognized model of experimental cerebral malaria (ECM), exhibit many of the hallmarks of
190 riptomic analysis in a model of experimental cerebral malaria (ECM), in which C57BL/6 mice are infect
191 an established murine model of experimental cerebral malaria (ECM), in which wild-type (WT) C57BL/6J
192 um berghei ANKA murine model of experimental cerebral malaria (ECM), we have identified over 300 puta
201 ain unknown and no adjunctive therapy during cerebral malaria has been shown to reduce the rate of su
202 other diseases in causing severe anaemia and cerebral malaria has increased substantially, and at the
206 ence of differentially expressed proteins in cerebral malaria in both plasma and cerebrospinal fluid
209 ed with fourfold increased susceptibility to cerebral malaria in large case-control studies of West A
211 gile can induce clinical symptoms, including cerebral malaria in rhesus macaques, that resemble those
212 CENT FINDINGS: Prospective data suggest that cerebral malaria-induced brain injury may explain the hi
213 r 18 years of surveillance, the incidence of cerebral malaria initially increased; however, malaria m
220 ed to establish whether retinopathy-positive cerebral malaria is a risk factor for epilepsy or other
227 common among children in sub-Saharan Africa, cerebral malaria is characterized by rapid progression t
236 smodium falciparum, the parasite that causes cerebral malaria, is reported in complex with the boroni
237 of inhibition exhibited by domains from two cerebral malaria isolates was sufficient to interfere wi
238 ovide novel insight into the pathogenesis of cerebral malaria, linking loss of the endothelial protei
239 bodies from young African children suffering cerebral malaria (Mann-Whitney test, P = 0.029) but not
240 The understanding of the pathogenesis of cerebral malaria may aid in the development of better th
241 concentrations were low in individuals with cerebral malaria (mean 46 micromol/L, SD 14), intermedia
242 ) and was markedly elevated in children with cerebral malaria (median [95% confidence interval], 163
246 contradictory roles for platelets extend to cerebral malaria models and are dependent on the timing
248 ral malaria, partially restored experimental cerebral malaria mortality and symptoms in CD40-KO recip
250 or Mig were both partially protected against cerebral malaria mortality when infected with P. berghei
254 st that sequestration in patients with fatal cerebral malaria occurs in multiple organs and does not
256 FNGR1-56 polymorphism were protected against cerebral malaria (odds ratio, 0.54; P=.016) and against
257 seful for study of the pathogenesis of fatal cerebral malaria, of which one feature is densely packed
258 d children who met a stringent definition of cerebral malaria (one that included the presence of reti
259 at admission was positively associated with cerebral malaria (P = .011) and with malaria-related mor
260 KO mice, which are resistant to experimental cerebral malaria, partially restored experimental cerebr
261 ause they may represent a process central to cerebral malaria pathogenesis: neurovascular sequestrati
262 topsy studies have improved understanding of cerebral malaria pathology in fatal cases, information a
265 A unifying hypothesis for the genesis of cerebral malaria proposes that parasite antigens (releas
266 milar effects, leading to protection against cerebral malaria, reduced cerebral hemorrhages, and incr
269 es across most organs in patients with fatal cerebral malaria, supporting the hypothesis that the dis
270 rosclerosis, sepsis, multiple sclerosis, and cerebral malaria, supporting their role as effectors and
274 was 1:1 but, in 2006, enrolment criteria for cerebral malaria survivors were revised to limit inclusi
275 hich was recently found to be a biomarker of cerebral malaria susceptibility in the murine model, and
277 te load was higher in patients with presumed cerebral malaria than in parasitemic patients with assum
278 P staining were more severe in patients with cerebral malaria than in those with no clinical cerebral
279 s to be discovered about the pathogenesis of cerebral malaria, The American Journal of Pathology has
280 ere malarial anemia is much more common than cerebral malaria, the distributions of tumor necrosis fa
281 xchanger 1 protein gene) and protection from cerebral malaria, this mutation was observed in only 1 o
284 ies on the nitric oxide-related pathology of cerebral malaria, we show that the antioxidative enzyme
285 e risk factors for epilepsy in children with cerebral malaria were a higher maximum temperature (39.4
290 The most devastating form of the disease is cerebral malaria, which occurs most frequently in young
291 Tie-2 levels are increased in children with cerebral malaria who had retinopathy compared with those
292 Tie-2 levels were elevated in children with cerebral malaria who subsequently died and angiopoetin-2
293 asites from children with clinically defined cerebral malaria, who either had or did not have accompa
294 ia than in parasitemic patients with assumed cerebral malaria with a nonmalaria cause of death identi
295 QP4-null mice exhibited more severe signs of cerebral malaria with greater brain edema, although disr
296 d a prospective cohort study of survivors of cerebral malaria with malaria retinopathy in Blantyre, M
297 mia (hemoglobin, <5 g/dl), 18 cases combined cerebral malaria with severe anemia, and 92 cases with h
298 n HRP2 level of >0 U/mL had a MAF of 93% for cerebral malaria, with a MAF of 97% observed for HRP2 le
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