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1 an early biological marker of the outcome of cerebral malaria.
2 variants may play a role in the pathology of cerebral malaria.
3  promise as potential new drugs for treating cerebral malaria.
4 en for patients with severe liver disease or cerebral malaria.
5 h Plasmodium berghei ANKA, a murine model of cerebral malaria.
6  with potential therapeutic implications for cerebral malaria.
7 uestration in patients with or who died from cerebral malaria.
8 athy, supporting its use in the diagnosis of cerebral malaria.
9  of improving the treatment and prognosis of cerebral malaria.
10 emoglobin was elevated only in patients with cerebral malaria.
11 sculature in retinopathy-positive paediatric cerebral malaria.
12 estations of retinopathy-positive paediatric cerebral malaria.
13 e in Malawian children with uncomplicated or cerebral malaria.
14 ecked and contributes to the pathogenesis of cerebral malaria.
15 nnel AQP4 confers partial protection against cerebral malaria.
16  crucial for the development of experimental cerebral malaria.
17 argets for interventions to treat or prevent cerebral malaria.
18  their contributions to the understanding of cerebral malaria.
19 by P. berghei ANKA, an experimental model of cerebral malaria.
20 e mechanism that could contribute to coma in cerebral malaria.
21 patients diagnosed with severe anemia and/or cerebral malaria.
22 tic, and epidemiological research studies on cerebral malaria.
23  with retinopathy and mortality in pediatric cerebral malaria.
24  receptor were resistant to otherwise lethal cerebral malaria.
25 netic susceptibility to SLE protects against cerebral malaria.
26 eceptor 7 are protected from death caused by cerebral malaria.
27 t of human brain endothelium contributing to cerebral malaria.
28 istics of parasite var genes associated with cerebral malaria.
29  ameliorate adverse neurological outcomes in cerebral malaria.
30 rocyte binding to cerebral blood vessels and cerebral malaria.
31 e without, who were presumed to have died of cerebral malaria.
32 d to kill the parasite is the development of cerebral malaria.
33 utopsy from patients with clinically defined cerebral malaria.
34 ogy of severe malaria-associated anaemia and cerebral malaria.
35  on clinical grounds, from patients dying of cerebral malaria.
36 of the microvasculature in a murine model of cerebral malaria.
37 enotype are at increased risk for developing cerebral malaria.
38 y play an important role in the pathology of cerebral malaria.
39 centrations would be low in individuals with cerebral malaria.
40 , multiple sclerosis, cerebral ischemia, and cerebral malaria.
41 ith severe anaemia being more insidious than cerebral malaria.
42 ed as a neurological sequela in survivors of cerebral malaria.
43 associated with increased risk of developing cerebral malaria.
44 crovasculature is the only one correlated to cerebral malaria.
45 rospective cohorts of Malawian children with cerebral malaria.
46 pathology such as multiple organ failure and cerebral malaria.
47  improved outcomes in a preclinical model of cerebral malaria.
48 be targeted as part of a strategy to prevent cerebral malaria.
49 ue approaches for the effective treatment of cerebral malaria.
50 a T cells and were resistant to experimental cerebral malaria.
51 integrity associated with fatal experimental cerebral malaria.
52  AT2-deficient mice were more susceptible to cerebral malaria.
53 arrier breakdown occurs in three patterns in cerebral malaria.
54 plasma PfHRP-2 concentrations were higher in cerebral malaria (1008 [IQR 342-2572] ng/mL) than in unc
55 e high anti-PS antibodies than children with cerebral malaria (16.4% vs. 7.4%), p = 0.02.
56 inical trials, and even worse in the case of cerebral malaria (18% and 30%, respectively).
57                                In paediatric cerebral malaria a combination of retinal signs correlat
58                    Despite the importance of cerebral malaria, a binding phenotype linked to its symp
59                                              Cerebral malaria, a disorder characterised by coma, para
60                                              Cerebral malaria, a reversible encephalopathy affecting
61 ith Plasmodium falciparum infections develop cerebral malaria, acute respiratory distress, and shock
62 athology of life-threatening malarial coma ("cerebral malaria"), allowing differentiation between 1)
63       132 children with retinopathy-positive cerebral malaria and 264 age-matched, non-comatose contr
64 ed susceptibility of CXCR3-deficient mice to cerebral malaria and also restored brain proinflammatory
65 precursors, which dictated susceptibility to cerebral malaria and conferred protection against recomb
66  Malawi, on pediatric patients who died from cerebral malaria and controls.
67  driven by the competing risks of death from cerebral malaria and death from severe malarial anaemia.
68 ent in CXCR3 were markedly protected against cerebral malaria and had far fewer T cells in the brain
69  citrulline levels in Malawian children with cerebral malaria and in mice infected with Plasmodium be
70 into mechanisms of endothelial activation in cerebral malaria and indicate that the angiopoietin-Tie-
71 ce for pathogenic mechanisms common to human cerebral malaria and neurodegenerative disorders.
72  host-targeted therapeutic possibilities for cerebral malaria and other diseases in which brain endot
73                                Children with cerebral malaria and P. berghei-infected mice demonstrat
74 es the specificity of the diagnosis of fatal cerebral malaria and provides accurate quantitative esti
75  revised to limit inclusion to children with cerebral malaria and retinopathy on the basis of indirec
76  PA predisposes to severe malaria, including cerebral malaria and severe anemia.
77 into the brain and the development of murine cerebral malaria and suggest that the CXCR3 ligands Mig
78 astrointestinal tract, both in patients with cerebral malaria and those with parasitemia in other org
79 te to limited NO production in children with cerebral malaria and to severe disease.
80 riable and World Health Organization-defined cerebral malaria and/or retinopathy as the outcome, was
81  the hospital with severe malaria (excluding cerebral malaria) and 31 age-matched controls.
82             At baseline, 35% had evidence of cerebral malaria, and 17% had severe hepatic impairment.
83  stroke, epilepsy, viral hemorrhagic fevers, cerebral malaria, and acute hemorrhagic leukoencephaliti
84 dent decrease in brain swelling during acute cerebral malaria, and brain volumes did not differ betwe
85 lities in treating hemophilia, inflammation, cerebral malaria, and cancer.
86 owed a reduction of brain AQP4 transcript in cerebral malaria, and immunoblots revealed reduction of
87 evelopment of myocardial infarction, stroke, cerebral malaria, and preeclampsia.
88 icated malaria; the cases (n = 25) developed cerebral malaria, and the controls (n = 125) did not.
89 s have been implicated in the development of cerebral malaria, and the IFN-inducible CXCR3 chemokine
90                     In longitudinal studies, cerebral malaria appeared nearly 1 d earlier in the AQP4
91            In this study, we used a model of cerebral malaria appearing in C57BL/6 WT mice after infe
92 laria syndromes, including severe anemia and cerebral malaria, are associated with high transcript le
93                Of 348 children admitted with cerebral malaria (as defined by the World Health Organiz
94 f potential surrogate markers for paediatric cerebral malaria because, in this condition, the retina
95 malaria, and the proportion of children with cerebral malaria began to change 10 years before hospita
96  and meeting a strict definition of clinical cerebral malaria (Blantyre Coma Score </= 2, Plasmodium
97 se deficiency (G6PDd) was protective against cerebral malaria but increased the risk of severe malari
98 that are beneficial in the immune control of cerebral malaria but that, in the absence of malaria, co
99 in volume was seen in children who died from cerebral malaria but was uncommon in those who did not d
100 sunate remains the mainstay of treatment for cerebral malaria, but it is less effective in later stag
101 t platelets not only have an adverse role in cerebral malaria, but platelets may also be protective i
102 iency are associated with decreasing risk of cerebral malaria, but with increased risk of severe mala
103  after malaria, we created a rodent model of cerebral malaria by infecting C57BL/6 mice with Plasmodi
104 asibility of developing a vaccine preventing cerebral malaria by inhibiting cerebral IE sequestration
105 ction of brain AQP4 protein was confirmed in cerebral malaria by quantitative immunogold EM; however,
106 vels of Ang II may confer protection against cerebral malaria by strengthening the integrity of the e
107 n endothelium of patients who have died from cerebral malaria casts new light on our understanding of
108 ly induced in the brains of mice with murine cerebral malaria caused by Plasmodium berghei ANKA.
109           The most severe form of malaria is cerebral malaria caused by Plasmodium falciparum.
110 emostatic changes as being most prevalent in cerebral malaria caused by Plasmodium falciparum.
111 ere collected from subjects with WHO-defined cerebral malaria (children), all forms of severe malaria
112                                              Cerebral malaria (CM) and severe malarial anemia (SMA) a
113                                              Cerebral malaria (CM) can be classified as retinopathy-p
114                                              Cerebral malaria (CM) from Plasmodium falciparum infecti
115 the role of PGs as immunomodulators of human cerebral malaria (CM) has not been examined, we investig
116 ldren with World Health Organization-defined cerebral malaria (CM) have a nonmalarial cause of death.
117                                              Cerebral malaria (CM) is a deadly complication of Plasmo
118                                              Cerebral malaria (CM) is a leading cause of death in Pla
119                                              Cerebral malaria (CM) is a major cause of death due to P
120                                              Cerebral malaria (CM) is a major cause of mortality in A
121                                              Cerebral malaria (CM) is a major complication of Plasmod
122                                              Cerebral malaria (CM) is a neurological complication of
123                                              Cerebral malaria (CM) is a primary cause of deaths cause
124                                              Cerebral malaria (CM) is a primary cause of malaria-asso
125                                              Cerebral malaria (CM) is a severe clinical complication
126                                              Cerebral malaria (CM) is a severe complication of Plasmo
127                                              Cerebral malaria (CM) is a severe complication of Plasmo
128                                              Cerebral malaria (CM) is associated with long-term neuro
129 The conventional clinical case definition of cerebral malaria (CM) is imprecise but specificity is im
130 Plasmodium falciparum infection, the coma of cerebral malaria (CM) is particularly deadly.
131                        Brain hemodynamics in cerebral malaria (CM) is poorly understood, with apparen
132 ntral to the pathologic progression of human cerebral malaria (CM) is sequestration of Plasmodium fal
133                                              Cerebral malaria (CM) is the deadliest form of severe Pl
134                                              Cerebral malaria (CM) is the most common form of severe
135 ial anemia (SMA) is the most common, whereas cerebral malaria (CM) is the most lethal.
136                                              Cerebral malaria (CM) is the most severe complication of
137                                              Cerebral malaria (CM) is the most severe form of malaria
138                                              Cerebral malaria (CM) is the most severe manifestation o
139 ciation of inflammation and brain edema in a cerebral malaria (CM) mouse model with a combination of
140 capillary brain endothelium is a hallmark of cerebral malaria (CM) pathogenesis.
141 lial activation and dysfunction in pediatric cerebral malaria (CM) pathology.
142 itive impairment persist in more than 20% of cerebral malaria (CM) patients long after successful ant
143 cation of Plasmodium falciparum infection is cerebral malaria (CM) with a case fatality rate of 15-25
144                                              Cerebral malaria (CM), a complication of malaria infecti
145                               Development of cerebral malaria (CM), a severe and fatal form of clinic
146  severe malarial anemia (SMA), children with cerebral malaria (CM), and community children (CC) and 2
147  organ-specific fatal pathologies, including cerebral malaria (CM), driven by a high parasite load, l
148 nd consistent feature in the murine model of cerebral malaria (CM), resulting in significantly increa
149                             In children with cerebral malaria (CM), serum chemokine levels and associ
150 cant mortality and morbidity associated with cerebral malaria (CM), the molecular mechanisms involved
151  neurologic deficits in Kenyan children with cerebral malaria (CM).
152 value in children with Plasmodium falciparum cerebral malaria (CM).
153 died as potential tools for the treatment of cerebral malaria (CM).
154 s, including the most feared and often fatal cerebral malaria (CM).
155 bility for severe malarial anaemia (SMA) and cerebral malaria (CM).
156 ei ANKA is a well-established model of human cerebral malaria (CM).
157  a major predictor of mortality in pediatric cerebral malaria (CM).
158 ven after survival is the salient feature of cerebral malaria (CM).
159 ased risk for Plasmodium falciparum-mediated cerebral malaria (CM).
160 dings have linked brain swelling to death in cerebral malaria (CM).
161 re was significantly higher in patients with cerebral malaria (CM; n = 21) than in patients with non-
162 o-5 y of age with 2 forms of severe malaria: cerebral malaria (CM; n = 79) or severe malarial anemia
163 R [95% CI] >3 to <=4 days versus <=24 hours: cerebral malaria [CM] = 2.42 [1.24-4.72], p = 0.01; resp
164 been associated with coma in severe malaria (cerebral malaria [CM]).
165 g severe malaria, we identified 100 cases of cerebral malaria (coma, seizure, and obtundation), 17 ca
166           Mortality is markedly increased in cerebral malaria combined with acidosis.
167 inal fluid from children with a diagnosis of cerebral malaria, compared with those with a diagnosis o
168 d (fold-decreases, </=4.39) in children with cerebral malaria, compared with those with uncomplicated
169                                              Cerebral malaria complicated by cognitive sequelae is a
170   The events resulting in the development of cerebral malaria complications are multi-factorial, enco
171 ldren with uncomplicated malaria progress to cerebral malaria despite appropriate treatment; identify
172 aran Africa continue to acquire and die from cerebral malaria, despite efforts to control or eliminat
173 um berghei ANKA murine model of experimental cerebral malaria (ECM) and high-density oligonucleotide
174 t C5(-/-) mice are resistant to experimental cerebral malaria (ECM) and suggested that protection was
175  that causes protection against experimental cerebral malaria (ECM) caused by infection with Plasmodi
176 required for the development of experimental cerebral malaria (ECM) during Plasmodium berghei ANKA in
177 Plasmodium berghei ANKA-induced experimental cerebral malaria (ECM) in C57BL/6 mice.
178 that free Heme generated during experimental cerebral malaria (ECM) in mice, is central to the pathog
179 arasitemia in a rodent model of experimental cerebral malaria (ECM) in vivo.
180                                 Experimental cerebral malaria (ECM) is a gamma interferon (IFN-gamma)
181             The pathogenesis of experimental cerebral malaria (ECM) is an immunologic process, mediat
182 a through the use of the murine experimental cerebral malaria (ECM) model.
183 brain, directly contributing to experimental cerebral malaria (ECM) mortality.
184 bA) model in which mice develop experimental cerebral malaria (ECM) to study the roles of IRGM1 and I
185 g pathway in the development of experimental cerebral malaria (ECM) using the murine Plasmodium bergh
186  the protein cargo of MP during experimental cerebral malaria (ECM) with the overarching hypothesis t
187 ty hypothesis in the setting of experimental cerebral malaria (ECM), but find instead that low NO bio
188 riptomic analysis in a model of experimental cerebral malaria (ECM), in which C57BL/6 mice are infect
189  an established murine model of experimental cerebral malaria (ECM), in which wild-type (WT) C57BL/6J
190 um berghei ANKA murine model of experimental cerebral malaria (ECM), we have identified over 300 puta
191 mice and the P. berghei-induced experimental cerebral malaria (ECM).
192  DR) prevents neuropathology in experimental cerebral malaria (ECM).
193 lethal neuroinflammation during experimental cerebral malaria (ECM).
194 ficantly to the pathogenesis of experimental cerebral malaria (ECM).
195 dium berghei ANKA (PbA)-induced experimental cerebral malaria (ECM).
196 o limits disease progression in experimental cerebral malaria (ECM).
197  role for this T cell subset in experimental cerebral malaria (ECM).
198 Plasmodium berghei ANKA-induced experimental cerebral malaria (ECM).
199 neuroinflammatory responses, in experimental cerebral malaria (ECM).
200  mice is a widely used model of experimental cerebral malaria (ECM).
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
203                                Patients with cerebral malaria have significantly reduced levels of se
204                                        Human cerebral malaria (HCM) is a serious complication of Plas
205 smodium falciparum infection can cause human cerebral malaria (HCM) with high mortality rates.
206                                        Human cerebral malaria (HCM), a severe encephalopathy associat
207  brain swelling in the pathogenesis of fatal cerebral malaria in African children.
208 ence of differentially expressed proteins in cerebral malaria in both plasma and cerebrospinal fluid
209               Clinical signs and symptoms of cerebral malaria in children are nonspecific and are see
210                    The clinical diagnosis of cerebral malaria in Plasmodium falciparum-endemic region
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
214                       The immune response in cerebral malaria involves elevation of circulating level
215                          The pathogenesis of cerebral malaria involves parasitized red blood cell (RB
216                                              Cerebral malaria is a common presentation of severe Plas
217                                              Cerebral malaria is a dangerous complication of Plasmodi
218                                              Cerebral malaria is a deadly outcome of infection by Pla
219                                              Cerebral malaria is a pathology involving inflammation i
220 ed to establish whether retinopathy-positive cerebral malaria is a risk factor for epilepsy or other
221                                              Cerebral malaria is a severe and often fatal complicatio
222                                              Cerebral malaria is a severe form of the disease that ma
223                                              Cerebral malaria is a severe multifactorial condition as
224                                              Cerebral malaria is a significant cause of global mortal
225                                              Cerebral malaria is associated with decreased production
226                                              Cerebral malaria is characterized by cytoadhesion of Pla
227 common among children in sub-Saharan Africa, cerebral malaria is characterized by rapid progression t
228                             The pathology of cerebral malaria is characterized by the accumulation of
229  role of nitric oxide (NO) in the genesis of cerebral malaria is controversial.
230                                              Cerebral malaria is more lethal in children than adults.
231                                              Cerebral malaria is one of the most severe complications
232                                              Cerebral malaria is one of the most severe complications
233                             The diagnosis of cerebral malaria is problematic in malaria-endemic areas
234 attenuated and the incidence of experimental cerebral malaria is significantly decreased in Pbyop1Del
235                                              Cerebral malaria is the most deadly manifestation of inf
236                                              Cerebral malaria is the most severe complication of Plas
237 smodium falciparum, the parasite that causes cerebral malaria, is reported in complex with the boroni
238  of inhibition exhibited by domains from two cerebral malaria isolates was sufficient to interfere wi
239 ovide novel insight into the pathogenesis of cerebral malaria, linking loss of the endothelial protei
240 bodies from young African children suffering cerebral malaria (Mann-Whitney test, P = 0.029) but not
241 se findings suggest that the mouse model for cerebral malaria may accurately reflect human disease pa
242     The understanding of the pathogenesis of cerebral malaria may aid in the development of better th
243 ) and was markedly elevated in children with cerebral malaria (median [95% confidence interval], 163
244 eficits are also present in our experimental cerebral malaria model (ECM).
245                          Here, using a mouse cerebral malaria model and small-molecule inhibitors, we
246 ibitor prolonged survival in an experimental cerebral malaria model.
247  contradictory roles for platelets extend to cerebral malaria models and are dependent on the timing
248                          In a mouse model of cerebral malaria, modulation of angiotensin II receptors
249 ral malaria, partially restored experimental cerebral malaria mortality and symptoms in CD40-KO recip
250 o be the only serum biomarker that predicted cerebral malaria mortality in Ghanaian children.
251 or Mig were both partially protected against cerebral malaria mortality when infected with P. berghei
252                        Using an experimental cerebral malaria mouse model, we also demonstrate that p
253 ian children with uncomplicated (n = 61) and cerebral malaria (n = 45; 7 deaths).
254  months to 12 years old with severe malaria (cerebral malaria, n = 253 or severe malarial anemia, n =
255                                           In cerebral malaria, natural log plasma PfHRP-2 was associa
256 st that sequestration in patients with fatal cerebral malaria occurs in multiple organs and does not
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
263  that shows no upregulation in the brains of cerebral malaria patients.
264     A unifying hypothesis for the genesis of cerebral malaria proposes that parasite antigens (releas
265 milar effects, leading to protection against cerebral malaria, reduced cerebral hemorrhages, and incr
266 e fatality rates among African children with cerebral malaria remain in the range of 15 to 25%.
267                 Despite decades of research, cerebral malaria remains one of the most serious complic
268 es across most organs in patients with fatal cerebral malaria, supporting the hypothesis that the dis
269 rosclerosis, sepsis, multiple sclerosis, and cerebral malaria, supporting their role as effectors and
270       Almost a third of retinopathy-positive cerebral malaria survivors developed epilepsy or other n
271                                    12 of 132 cerebral malaria survivors developed epilepsy versus non
272                                    28 of 121 cerebral malaria survivors developed new neurodisabiliti
273 was 1:1 but, in 2006, enrolment criteria for cerebral malaria survivors were revised to limit inclusi
274 hich was recently found to be a biomarker of cerebral malaria susceptibility in the murine model, and
275                                         When cerebral malaria symptoms were manifest, genes involved
276                 Three parasitic infections - cerebral malaria, Taenia solium cysticercosis and onchoc
277 te load was higher in patients with presumed cerebral malaria than in parasitemic patients with assum
278 s to be discovered about the pathogenesis of cerebral malaria, The American Journal of Pathology has
279                                           In cerebral malaria, the retina can be used to understand d
280 ormed for the first time in 65 patients with cerebral malaria to compare disease signatures between c
281                                              Cerebral malaria was associated with significantly eleva
282           To study the pathogenesis of fatal cerebral malaria, we conducted autopsies in 31 children
283 e risk factors for epilepsy in children with cerebral malaria were a higher maximum temperature (39.4
284                                Children with cerebral malaria were identified at the time of their in
285                        IE from patients with cerebral malaria were more likely to bind EPCR and ICAM-
286       Within cases of histologically defined cerebral malaria, which includes phenotypes termed "sequ
287  The most devastating form of the disease is cerebral malaria, which occurs most frequently in young
288 ddress, of which 272 (5%) were classified as cerebral malaria while 1001 (10%) were severe malaria an
289                             In children with cerebral malaria who had a lumbar puncture performed, an
290  Tie-2 levels are increased in children with cerebral malaria who had retinopathy compared with those
291  Tie-2 levels were elevated in children with cerebral malaria who subsequently died and angiopoetin-2
292 asites from children with clinically defined cerebral malaria, who either had or did not have accompa
293 ia than in parasitemic patients with assumed cerebral malaria with a nonmalaria cause of death identi
294 t pathogenic patterns in pediatric and adult cerebral malaria with a stronger cytotoxic component in
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
299                          Upon development of cerebral malaria, WT and AQP4-null mice exhibited simila
300       To further examine the role of AQP4 in cerebral malaria, WT mice and littermates genetically de

 
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