ライフサイエンスコーパス: toxoplasmosis

1 nd Toxoplasma gondii (the causative agent of toxoplasmosis).

2 s against Pneumocystis carinii pneumonia and toxoplasmosis).

3 were found to be highly susceptible to acute toxoplasmosis.

4 l tool to reduce the incidence of congenital toxoplasmosis.

5 wn whether this finding is relevant in human toxoplasmosis.

6 example concerning the spread and control of toxoplasmosis.

7 ific differences in the clinical spectrum of toxoplasmosis.

8 ing inflammation in many settings, including toxoplasmosis.

9 ites, including those that cause malaria and toxoplasmosis.

10 atent disease during later phases of chronic toxoplasmosis.

11 r for protection against cerebral and ocular toxoplasmosis.

12 designing immunotherapeutics against chronic toxoplasmosis.

13 response of mice to the parasite that causes toxoplasmosis.

14 ight contribute to the development of ocular toxoplasmosis.

15 8 differentiation is impaired during chronic toxoplasmosis.

16 g a more critical role for NAS-TLRs in human toxoplasmosis.

17 ted activity in murine models of malaria and toxoplasmosis.

18 yst stage is the underlying cause of chronic toxoplasmosis.

19 the 3d susceptible phenotype to experimental toxoplasmosis.

20 or events that confer resistance to cerebral toxoplasmosis.

21 s are considered to be at increased risk for toxoplasmosis.

22 ys a central role in the pathology of ocular toxoplasmosis.

23 portant human diseases including malaria and toxoplasmosis.

24 when administered orally to mice with acute toxoplasmosis.

25 p therapies aimed at defending against human toxoplasmosis.

26 control of parasitemia during early-chronic toxoplasmosis.

27 urs in several chronic infections, including toxoplasmosis.

28 ortant human diseases, including malaria and toxoplasmosis.

29 was enhanced during chronic, but not acute, toxoplasmosis.

30 role of this enzyme in the chronic phase of toxoplasmosis.

31 tremely effective against acute experimental toxoplasmosis.

32 racterize subsets of murine DCs during acute toxoplasmosis.

33 ficient mice, which were more susceptible to toxoplasmosis.

34 ch were otherwise highly susceptible to oral toxoplasmosis.

35 rges such as malaria, cryptosporidiosis, and toxoplasmosis.

36 is jirovecii pneumonia and Toxoplasma gondii toxoplasmosis.

37 he initial activation of CD8+ T cells during toxoplasmosis.

38 me as a valid target for the chemotherapy of toxoplasmosis.

39 espread parasites and the causative agent of toxoplasmosis.

40 ss of blood samples for genotyping in ocular toxoplasmosis.

41 on of T. gondii in the chick embryo model of toxoplasmosis.

42 y from blood samples of patients with ocular toxoplasmosis.

43 f new drugs for the treatment of malaria and toxoplasmosis.

44 a promising method for genotypic analysis of toxoplasmosis.

45 a critical protective function during acute toxoplasmosis.

46 unlikely to be efficacious for treatment of toxoplasmosis.

47 pts a reduction in WSX-1 levels during acute toxoplasmosis.

48 ing the contribution of parasite genotype to toxoplasmosis.

49 stem to study CD4(+)-T-cell responses during toxoplasmosis.

50 chemotherapeutic target for the treatment of toxoplasmosis.

51 play a critical role in the pathogenesis of toxoplasmosis.

52 f sera sampling) suggests a cause other than toxoplasmosis.

53 d a novel chicken embryo model of congenital toxoplasmosis.

54 nation and motor impairments associated with toxoplasmosis.

55 tis carinii pneumonia, and Toxoplasma gondii toxoplasmosis.

56 gulation of inflammation during acute ocular toxoplasmosis.

57 IFN-gamma receptor 1 are not susceptible to toxoplasmosis.

58 ice induces long-term protective immunity to toxoplasmosis.

59 diagnosis of Toxoplasma gondii infection and toxoplasmosis.

60 in acute and chronic experimental models of toxoplasmosis.

61 endent pathway of IL-12p40 production during toxoplasmosis.

62 parasite populations from 32 cases of human toxoplasmosis.

63 ion of caspase-8-deficient mice during acute toxoplasmosis.

64 urse and tissue distribution of experimental toxoplasmosis.

65 mechanisms regulate T cell responses during toxoplasmosis.

66 emiology and efficacious treatment of ocular toxoplasmosis.

67 to be involved in the pathogenesis of ocular toxoplasmosis.

68 tor of humoral and cellular responses during toxoplasmosis.

69 parasites cause diseases such as malaria and toxoplasmosis.

70 ely fifteen million of these have congenital toxoplasmosis.

71 hyzoite life stage, is responsible for acute toxoplasmosis.

72 ule inhibitors of CDPK1 for treatment of CNS toxoplasmosis.

73 ral candidiasis, Pneumocystis pneumonia, and toxoplasmosis.

74 itors for the treatment of acute and chronic toxoplasmosis.

75 e considered critical for control of chronic toxoplasmosis.

76 and 2012, 9260 patients had ICD-9 codes for toxoplasmosis.

77 concerning US incidence and distribution of toxoplasmosis.

78 esis generation about the pathophysiology of toxoplasmosis.

79 s, including causative agents of malaria and toxoplasmosis.

80 ses including malaria, cryptosporidiosis and toxoplasmosis.

81 ence in samples from 12 patients with ocular toxoplasmosis, 1 sample from a patient with congenital t

82 ses, 95% UI 8.29-22.0 million) and foodborne toxoplasmosis (10.3 million cases, 95% UI 7.40-14.9 mill

83 y, and 1.0 per 10 000 infants had congenital toxoplasmosis (13% mean transmission rate).

84 sis, 1 sample from a patient with congenital toxoplasmosis, 22 samples from soldiers operating in the

85 This apicomplexan is the causative agent of toxoplasmosis, a leading cause of central nervous system

86 outcomes of adult patients with disseminated toxoplasmosis admitted to the intensive care unit (ICU)

87 racellular matrix, were resistant to chronic toxoplasmosis after oral infection with T. gondii.

88 famethoxazole (TMP/SMX) in the prevention of toxoplasmosis after orthotopic cardiac transplantation h

89 of certain forms of uveitis (such as ocular toxoplasmosis) after surgery, suggesting that perioperat

90 After a cluster of fatal toxoplasmosis among stem cell transplant recipients at 2

91 n, Clinical Modification codes 130-130.9 for toxoplasmosis and 042-044/795.8/795.71/V08 for HIV infec

92 hat are effective against acute experimental toxoplasmosis and are not toxic in human cell assays, no

93 The subsequent diagnoses were ocular toxoplasmosis and cytomegalovirus retinitis.

94 ht the importance of Flt3L for resistance to toxoplasmosis and demonstrate the existence of Flt3L-ind

95 current prevention strategies of congenital toxoplasmosis and evaluate options to improve protection

96 t the importance of type I IFN in control of toxoplasmosis and illuminate a parasite mechanism to cou

97 46 serum specimens from patients with ocular toxoplasmosis and in 28 serum specimens from patients wi

98 en is associated with severity of congenital toxoplasmosis and indicate that serological testing prov

99 (iMO) are critical for host defense against toxoplasmosis and malaria but their role in leishmaniasi

100 rasites and required for the pathogenesis of toxoplasmosis and malaria.

101 008 and assessed how the risks of congenital toxoplasmosis and of clinical signs at age 3 years vary

102 CD4 T-cell-mediated immune damage in ocular toxoplasmosis and other types of retinal immune response

103 ocumented prenatal exposure to influenza and toxoplasmosis and performance on the Wisconsin Card Sort

104 of more effective compounds for treatment of toxoplasmosis and perhaps related parasitic diseases.

105 g peptide that can confer protection against toxoplasmosis and provide an important tool for the stud

106 recruited Ly6C(high) monocytes upon cerebral toxoplasmosis and reveal the behavior of further differe

107 e recipients are at high risk for developing toxoplasmosis and should be given prophylaxis and receiv

108 ry effector cells in the resistance to acute toxoplasmosis and suggests that the CCR2-dependent recru

109 um includes the causative agents of malaria, toxoplasmosis and theileriosis-diseases with a huge econ

110 e update with emphasis on the new assets for toxoplasmosis and vector research.

111 development of vaccine protocols to control toxoplasmosis and/or neosporosis.

112 malaria, trypanosomiasis, leishmaniasis, and toxoplasmosis) and provides visions into the main issues

113 eba), Toxoplasma gondii (the agent for human toxoplasmosis), and other protists, Skp1 is regulated by

114 tunistic infections and no signs of cerebral toxoplasmosis, and 18 immunocompetent patients with neur

115 high impact human diseases such as malaria, toxoplasmosis, and cryptosporidiosis.

116 important human diseases including malaria, toxoplasmosis, and cryptosporidiosis.

117 hat include the causative agents of malaria, toxoplasmosis, and cryptosporidiosis.

118 ntation anti- serology, development of acute toxoplasmosis, and the occurrence of other infections.

119 been described in diseases such as malaria, toxoplasmosis, and trypanosomiasis.

120 at mediate protective immunity during murine toxoplasmosis, and yet their effector development remain

121 59 cases of POT and 4 cases of active ocular toxoplasmosis (AOT).

122 hat regulate IL-12 production during chronic toxoplasmosis are incompletely defined.

123 mining the pathogenesis and course of ocular toxoplasmosis are poorly understood.

124 Recurrence rates of ocular toxoplasmosis are probably not higher during pregnancy,

125 The drugs currently available to treat toxoplasmosis are unable to clear the cyst form of the p

126 ristics of disease due to Toxoplasma gondii (toxoplasmosis) are dependent on the infecting strain, we

127 eutic implications in combating recrudescent toxoplasmosis as well other chronic infections.

128 etic cells and can cause cerebral and ocular toxoplasmosis, as a result of either congenital or postn

129 In CNS toxoplasmosis, astrocytes are critical to controlling pa

130 or Toxoplasma gondii, responsible for human toxoplasmosis, Babesia belongs to the Apicomplexa family

131 equences from Colombian patients with ocular toxoplasmosis belonged to the group of mouse-virulent st

132 iosis was lower than those due to congenital toxoplasmosis but accords with those due to echinococcos

133 CD4 not only become exhausted during chronic toxoplasmosis but this dysfunction is more pronounced th

134 L-23, plays a dominant role in resistance to toxoplasmosis but, in the absence of IL-12, IL-23 can pr

135 1, HLA-A*02:01, and HLA-B*07:02 mice against toxoplasmosis by (i) this novel chimeric polypeptide, co

136 Toxoplasmosis can be due to congenital infection or acqu

137 Diagnosis of toxoplasmosis can be established by direct detection of

138 Usually asymptomatic, toxoplasmosis can be severe and even fatal to many hosts

139 rth America (NA) and Europe, the majority of toxoplasmosis cases are benign and generally asymptomati

140 cerebrospinal fluid samples from congenital toxoplasmosis cases in Poland.

141 Toxoplasmosis causes morbidity and mortality in the Unit

142 Toxoplasmosis causes significant morbidity and mortality

143 We reported earlier that during chronic toxoplasmosis CD8(+) T cells become functionally exhaust

144 sequences (83.3%) from patients with ocular toxoplasmosis clustered with those of mouse-virulent str

145 of 51 serum cytokines from acute and chronic toxoplasmosis cohorts of pregnant women from the United

146 Nevertheless, prevention of toxoplasmosis commonly targets mainly pregnant women.

147 12/15-LOX-deficient mice died during chronic toxoplasmosis, compared to no deaths in wild-type contro

148 can expedite the development of novel human toxoplasmosis control strategies.

149 uman and animal diseases, including malaria, toxoplasmosis, cryptosporidiosis, coccidiosis and babesi

150 Congenital toxoplasmosis (CT) and cytomegalovirus infection (cCMV)

151 ly identification of infants with congenital toxoplasmosis (CT).

152 -Schiff staining for fungi, PCR analysis for toxoplasmosis, cytomegalovirus, Epstein-Barr virus (EBV)

153 In this cohort, acute toxoplasmosis developed after transplantation in one cas

154 emonstrated that screening and treatment for toxoplasmosis during gestation result in a decrease of v

155 a serologic panel for the diagnosis of acute toxoplasmosis during pregnancy.

156 There were 128 episodes of ocular toxoplasmosis during the study period (6 during pregnanc

157 in patients without classic presentation of toxoplasmosis encephalitis.

158 aradigm-shifting vaccine approach to prevent toxoplasmosis, extendable to other diseases.

159 Twenty patients (17%) with ocular toxoplasmosis had a localized RNFL defect associated wit

160 Eleven of the 12 patients with confirmed toxoplasmosis had positive PCR results in either blood o

161 ctive therapeutics for cryptosporidiosis and toxoplasmosis has led to the discovery of novel inhibito

162 Toxoplasmosis has no cure but it can be controlled by th

163 The rate of HIV-associated toxoplasmosis hospitalizations among all HIV-related hos

164 HIV-associated toxoplasmosis hospitalizations dropped markedly after 19

165 Non-HIV-associated toxoplasmosis hospitalizations have been more stable.

166 Estimated HIV-associated toxoplasmosis hospitalizations increased from 9395 in 19

167 he rates of both HIV- and non-HIV-associated toxoplasmosis hospitalizations were higher in Hispanic p

168 Estimated non-HIV-associated toxoplasmosis hospitalizations were less variable from 1

169 CD-9) codes, including treatment specific to toxoplasmosis, identified patients with this disease.

170 e of IL-2 in the expansion of T cells during toxoplasmosis, IL-2(-/-) mice were infected with T. gond

171 er analysis of host-pathogen interactions in toxoplasmosis in a secondary host.

172 ctions with Toxoplasma gondii and congenital toxoplasmosis in Austria, a country with a nationwide pr

173 Toxoplasma gondii is the causative agent of toxoplasmosis in human and animals.

174 tinochoroiditis in the setting of congenital toxoplasmosis in human infants.

175 that causes the severe opportunistic disease toxoplasmosis in humans.

176 ed with genes that confer resistance against toxoplasmosis in humans.

177 In addition, toxoplasmosis in immune-compromised individuals usually

178 A major challenge in treating toxoplasmosis in immunocompromised patients is lack of t

179 tion in risk of clinical signs of congenital toxoplasmosis in infected children born from mothers dia

180 h dexamethasone, we detected reactivation of toxoplasmosis in mice infected with S23-luc7 and S22-luc

181 ro and is effective against acute and latent toxoplasmosis in mice.

182 mining susceptibility to experimental ocular toxoplasmosis in murine models.

183 Type II and NE-II parasites cause congenital toxoplasmosis in North America.

184 Family clusters and epidemics of toxoplasmosis in North, Central, and South America led u

185 entified susceptibility genes for congenital toxoplasmosis in our cohort of infected humans and found

186 nel of tests done for the diagnosis of acute toxoplasmosis in pregnant women in a reference laborator

187 Although uncommon, toxoplasmosis in SOT patients causes substantial morbidi

188 factors, clinical features, and outcomes of toxoplasmosis in SOT recipients.

189 e clear with the first reports of congenital toxoplasmosis in the 1940s.

190 s plays an important role in pathogenesis of toxoplasmosis in the mouse model.

191 trophils are important for controlling acute toxoplasmosis in the mouse model.

192 ecific inhibitor of ABA synthesis to prevent toxoplasmosis in the mouse model.

193 ound 24 was also effective at treating acute toxoplasmosis in the mouse, reducing dissemination to th

194 howed a significant delay in producing acute toxoplasmosis in vivo.

195 or sulfonamide use, particularly in cases of toxoplasmosis in which the initial response to drug trea

196 N-gamma), a cytokine known to control latent toxoplasmosis, in chronically infected prerecrudescent m

197 te Toxoplasma gondii, the causative agent of toxoplasmosis, includes both CBS and CGL enzymes.

198 T-regulatory cells is an important factor in toxoplasmosis-induced retinal damage.

199 te Toxoplasma gondii, the causative agent of toxoplasmosis, induces a protective CD8 T-cell response

200 he implementation of universal screening for toxoplasmosis infection during gestation.

201 Toxoplasmosis is a disease of prominent health concern t

202 in bacterial or fungal endophthalmitis, and toxoplasmosis is a major cause of ocular morbidity and p

203 Toxoplasmosis is a neglected disease that affects millio

204 NCMD, and in this single family, congenital toxoplasmosis is a phenocopy of grade 3 NCMD.

205 Ocular toxoplasmosis is a prominent and severe condition of hig

206 Congenital toxoplasmosis is a serious condition but little is known

207 Congenital toxoplasmosis is a severe, life-altering disease in the

208 Because congenital toxoplasmosis is almost solely the result of maternal in

209 Toxoplasmosis is an infection caused by the protozoan pa

210 asymptomatic, whereas in South America (SA) toxoplasmosis is associated with much more severe sympto

211 The diagnosis of ocular toxoplasmosis is based most often on the presence of cha

212 Although congenital toxoplasmosis is generally considered to contribute most

213 Protection from toxoplasmosis is mediated by CD8(+) T cells, but the T.

214 Toxoplasmosis is the clinical and pathological consequen

215 Toxoplasmosis is the most common cause of posterior uvei

216 Toxoplasma gondii, the causative agent of toxoplasmosis, is an intracellular parasite that demonst

217 Toxoplasma gondii, the causative agent of toxoplasmosis, is an obligate intracellular protozoan pa

218 Severe disseminated toxoplasmosis leading to ICU admission has a poor progno

219 IDO inhibition during murine toxoplasmosis led to 100% mortality, with increased para

220 The initially active toxoplasmosis lesions were successfully treated in all c

221 that are effective against acute and latent toxoplasmosis, likely acting as inhibitors of the Q(i) s

222 eserine presents interesting anti-parasitic (toxoplasmosis, malaria) potential.

223 table for the diseases they cause, including toxoplasmosis, malaria, and cryptosporidiosis.

224 impact on improving outcomes for those with toxoplasmosis, malaria, and ~2 billion persons chronical

225 th both typical and atypical forms of ocular toxoplasmosis may be good.

226 Congenital macular lesions attributed to toxoplasmosis may limit potential visual acuity.

227 A murine toxoplasmosis model has been developed that results in c

228 tients with Behcet uveitis (n = 259), ocular toxoplasmosis (n = 120), and multiple sclerosis (MS)-ass

229 r brain biopsy were diagnosis unlikely to be toxoplasmosis (n=8, 42.1%), focal brain lesion (n=5, 26.

230 First episodes of ocular toxoplasmosis occurred between ages 9.6 and 38.5 years.

231 ion was the only independent risk factor for toxoplasmosis (odds ratio, 15.12 [95% confidence interva

232 Professor Silvia Moreno studies toxoplasmosis, one of the most common parasitic infectio

233 h primarily within the context of congenital toxoplasmosis or postnatally acquired disease in immunoc

234 Worldwide, ocular toxoplasmosis (OT) is the principal cause of posterior u

235 d to refer to congenital infections, such as toxoplasmosis, other infections (such as syphillis, vari

236 mester maternal infection, chorioamnionitis, toxoplasmosis, other infections, rubella, cytomegaloviru

237 e neurological and muscular pathologies that toxoplasmosis patients present with.

238 and 89 parent/case trios of presumed ocular toxoplasmosis (POT) to evaluate associations with polymo

239 In a mouse model of toxoplasmosis, pyrazolopyrimidine inhibitors of Toxoplas

240 The Austrian Toxoplasmosis Register included 2147 pregnant women with

241 nalyzed retrospective data from the Austrian Toxoplasmosis Register of pregnant women with Toxoplasma

242 Results from the Austrian Toxoplasmosis Register show the efficiency of the prenat

243 d Utilization Project, we examined trends in toxoplasmosis-related hospitalizations by HIV infection

244 Toxoplasmosis-related hospitalizations often occur in pe

245 The rates of toxoplasmosis-related hospitalizations varied markedly a

246 gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for consid

247 iological agents of severe human malaria and toxoplasmosis, respectively.

248 anifestations include punctate outer retinal toxoplasmosis, retinal vasculitis, retinal vascular occl

249 The primary outcome was recurrent toxoplasmosis retinochoroiditis within 1 year, and the s

250 The incidence of recurrent toxoplasmosis retinochoroiditis within 12 months was 0 o

251 susceptibility alleles for human congenital toxoplasmosis (rs6502997 [P, <0.000309], rs312462 [P, <0

252 The differential diagnosis included toxoplasmosis, rubella, cytomegalovirus, herpes simplex

253 Serologic testing ruled out toxoplasmosis, rubella, cytomegalovirus, syphilis, and h

254 Toxoplasmosis, rubella, cytomegalovirus, syphilis, and h

255 Children with presumed foveal toxoplasmosis scars who underwent amblyopia treatment.

256 of amblyopia therapy in children with foveal toxoplasmosis scars.

257 including amebiasis, malaria, leishmaniasis, toxoplasmosis, schistosomiasis, and paracoccidioidomycos

258 tested all samples from patients with ocular toxoplasmosis sent to the Palo Alto Medical Foundation T

259 ional Collaborative Chicago-Based Congenital Toxoplasmosis Study (NCCCTS) have a high incidence of To

260 ional Collaborative Chicago-based Congenital Toxoplasmosis Study (NCCCTS), 1981-2009.

261 ional Collaborative Chicago-based Congenital Toxoplasmosis Study.

262 igh the recognised overt morbidity caused by toxoplasmosis, substantially raising the public health i

263 n disease burden of 10 helminth diseases and toxoplasmosis that may be attributed to contaminated foo

264 lesion formation in infants with congenital toxoplasmosis that may be relevant in the establishment

265 Together these studies suggest that during toxoplasmosis the major role of STAT1 is not in the deve

266 I interferon-gamma (IFN-gamma) in control of toxoplasmosis, the role of type I IFN is less clear.

267 lines and represent promising candidates as toxoplasmosis therapeutics.

268 , including the causative agents of malaria, toxoplasmosis, trypanosomiasis, and leishmaniasis, conta

269 patients presented with reactivated chronic toxoplasmosis, underscoring the importance of an intact

270 velopment of an effective, safe, and durable toxoplasmosis vaccine.

271 the lesions in patients with presumed foveal toxoplasmosis, visual potential may be better than expec

272 one episode of rejection, the risk of acute toxoplasmosis was 5% (1 of 22 patients).

273 Susceptibility to toxoplasmosis was associated with an inability to up-reg

274 ility of 12/15-LOX-deficient mice to chronic toxoplasmosis was associated with reduced production of

275 Disseminated toxoplasmosis was defined as microbiological or histolog

276 CD4(+) T cells in the pathogenesis of ocular toxoplasmosis was investigated in murine models utilizin

277 Toxoplasmosis was statistically associated with substant

278 A murine model of toxoplasmosis was thus used to examine the importance of

279 a prospective clinical study of acute ocular toxoplasmosis, we assessed the cytokine pattern in aqueo

280 the role of interleukin-10 (IL-10) in ocular toxoplasmosis, we compared C57BL/6 (B6) and BALB/c backg

281 o understand the basis of acute virulence in toxoplasmosis, we compared low and high doses of the RH

282 f strains of T. gondii associated with human toxoplasmosis, we have developed a set of four highly se

283 In an experimental model of toxoplasmosis, we have identified the presence of a nonl

284 tionality during the later phases of chronic toxoplasmosis, we next examined if adoptive transfer of

285 Nineteen confirmed congenital cases of toxoplasmosis were analyzed, including both severe and a

286 Although in the past most cases of ocular toxoplasmosis were considered to result from reactivatio

287 Isolated cases of cerebral toxoplasmosis were excluded.

288 Twenty-two cases (0.14%) of toxoplasmosis were identified among 15 800 SOTs performe

289 susceptibility alleles for human congenital toxoplasmosis were identified in the NALP1 gene.

290 c role for IL-22 was, however, identified in toxoplasmosis when infections were established by the na

291 rding all pregnancies and episodes of ocular toxoplasmosis, whether or not episodes were observed at

292 ew therapies are needed for the treatment of toxoplasmosis, which is a disease caused by the protozoa

293 Toxoplasmosis, while often an asymptomatic parasitic dis

294 aled that p40(-/-) mice rapidly succumbed to toxoplasmosis, while p35(-/-) mice displayed enhanced re

295 us-infected patients with suspected cerebral toxoplasmosis who had neither CDC diagnostic criteria no

296 consecutive adult patients with disseminated toxoplasmosis who were admitted from January 2002 throug

297 and the contribution of P2X7 during cerebral toxoplasmosis, wild-type and P2rx7 knockout mice were in

298 LYs (95% UI 1.65-2.48 million) and foodborne toxoplasmosis with 825,000 DALYs (95% UI 561,000-1.26 mi

299 type I, suggesting an association of ocular toxoplasmosis with this type.

300 n and livestock diseases such as malaria and toxoplasmosis, yet most of their genes remain uncharacte