ライフサイエンスコーパス: CNS disease

1 ot result in an invasive phenotype or murine CNS disease.

2 disease during autoimmune and virus-induced CNS disease.

3 ates in the pathogenesis of HIV-1-associated CNS disease.

4 recurrence of viral replication and onset of CNS disease.

5 ndently associated with an increased risk of CNS disease.

6 of CCHF countermeasures, and CCHF-associated CNS disease.

7 or application of therapeutic genes in human CNS disease.

8 sis who underwent CSF analysis, 80 (62%) had CNS disease.

9 inflammatory factors and ROS, culminating in CNS disease.

10 nd injury leads to dysregulated astroglia in CNS disease.

11 e therapeutically targetable in inflammatory CNS disease.

12 individuals who may develop the HIV-induced CNS disease.

13 , or 10 IT treatments, depending on risk for CNS disease.

14 may yield insights into the pathogenesis of CNS disease.

15 S, although it prevented onset of RV-induced CNS disease.

16 lasma virus and monocytes in contributing to CNS disease.

17 inal fluid of humans with chronic infectious CNS disease.

18 te infection outside of the brain in driving CNS disease.

19 also associated with non-lymphocyte-mediated CNS disease.

20 -mediated pathology and reconstitute a fatal CNS disease.

21 bystander CD8+ T cells to the development of CNS disease.

22 p38 may be protective against HIV-associated CNS disease.

23 L36/37 determinant increased both ocular and CNS disease.

24 al, pathogenic role in retroviral-associated CNS disease.

25 ified in protection against MV infection and CNS disease.

26 tial targets for therapeutic intervention in CNS disease.

27 areas of the CNS, only Fr98 induces clinical CNS disease.

28 d potentials were abnormal, indicating early CNS disease.

29 tential for transplantation-based therapy of CNS disease.

30 ovide a therapeutic target for virus-induced CNS disease.

31 -based immunotherapy in this T cell-mediated CNS disease.

32 poorer overall survival among children with CNS disease.

33 ant MOBP inoculated into SJL/J mice produces CNS disease.

34 ting virus in CSF from patients without HCMV CNS disease.

35 anodal sites is a more reliable predictor of CNS disease.

36 e also associated with an increased risk for CNS disease.

37 hat may contribute to white matter injury in CNS disease.

38 e CNS observation, and treatment of emergent CNS disease.

39 rer outcome of patients who had a history of CNS disease.

40 microglia are necessary for the induction of CNS disease.

41 n a proportion of patients with a history of CNS disease.

42 ral LGI1-specific B cells in this autoimmune CNS disease.

43 useful biomarker in the evaluation of fungal CNS disease.

44 e are largely driven by systemic rather than CNS disease.

45 of targeting microglia for the treatment of CNS disease.

46 matter of the brain, causing a rapid, acute CNS disease.

47 icularly when combined with FCM detection of CNS disease.

48 end organ diseases such as HIV-1-associated CNS disease.

49 europrotective interventions in CTL-mediated CNS disease.

50 without >/= 10 RBCs/muL or clinical signs of CNS disease.

51 of CD8(+) T cells in preventing DENV-induced CNS disease.

52 a protective strategy to treat inflammatory CNS disease.

53 processing are considered in the context of CNS disease.

54 lation in reactive astrocytes will alter the CNS disease.

55 n a model of schizophrenia, and degenerative CNS disease.

56 for controlling viral infections that cause CNS disease.

57 ruption of the BBB may contribute to various CNS diseases.

58 e sclerosis as well as other immune-mediated CNS diseases.

59 ion play a central role in a wide variety of CNS diseases.

60 e the cause of neuronal loss in degenerative CNS diseases.

61 antibody-mediated pathology in demyelinating CNS diseases.

62 te CSF production, turnover and clearance in CNS diseases.

63 atory mediators contribute to HIV-associated CNS diseases.

64 emerged as a promising therapy for treating CNS diseases.

65 h sera from patients with other inflammatory CNS diseases.

66 for the development of transplant therapy of CNS diseases.

67 tion of therapeutic antibodies in infectious CNS diseases.

68 rs of mouse models of potential relevance to CNS diseases.

69 on-demand release of therapeutics to prevent CNS diseases.

70 .5 mutant viruses as therapeutic vectors for CNS diseases.

71 ocator protein (TSPO) has been implicated in CNS diseases.

72 herapeutic strategy for ischemic retinal and CNS diseases.

73 and targeted gene delivery for treatment of CNS diseases.

74 iology and potential therapeutic targets for CNS diseases.

75 sport may be protective in neuroinflammatory CNS diseases.

76 e neuropathology and central nervous system (CNS) disease.

77 erve as a marker for central nervous system (CNS) disease.

78 olvement, and 9% had central nervous system (CNS) disease.

79 diated demyelinating central nervous system (CNS) disease.

80 use of virus-induced central nervous system (CNS) disease.

81 l deficits following central nervous system (CNS) disease.

82 tent and severity of central nervous system (CNS) disease.

83 and eventually cause central nervous system (CNS) disease.

84 ufficient to mediate central nervous system (CNS) disease.

85 r ADAM8 in modulating TNF-alpha signaling in CNS diseases: a feedback loop integrating TNF-alpha, ADA

86 Central nervous system (CNS) disease (adjusted odds ratio [AOR], 6.23; P = .03)

87 Adult CD-1 mice also develop CNS disease after infection with VEEV and WEEV.

88 l samples from 12 patients with inflammatory CNS disease and 15 patients with other neurological dise

89 mples (79%): 2 of 2 from patients with overt CNS disease and 21 of 27 from patients thought to be CNS

90 order to establish the role of TR3 in acute CNS disease and chronic neurodegeneration, we analysed b

91 r future in vivo studies in animal models of CNS disease and dysfunction.

92 entral TNF-alpha contributes to pathology in CNS disease and injury, and promotes inflammation in the

93 ial to uncover neurobiological insights into CNS disease and lead to the development of therapies.

94 re involved in the molecular pathogenesis of CNS disease and perhaps in ApoE expression in general, a

95 , 16.5-74.5); 2 patients died of progressive CNS disease and small-cell lung cancer, respectively.

96 d to patients with genotypes associated with CNS disease and was reduced following hematopoietic stem

97 between mGlu2/3 inhibition and a variety of CNS diseases and disorders.

98 on the CNS and its potential contribution to CNS diseases and disorders.

99 ibutes to the pathophysiology of a number of CNS diseases and injuries.

100 nt system is activated in a wide spectrum of CNS diseases and is suggested to play a role in degenera

101 criptome data, connects CNS lupus with other CNS diseases and provides an explanation for the neurolo

102 rus (JCV)-associated central nervous system (CNS) disease and has emerged as a major safety concern i

103 ive therapeutics for central nervous system (CNS) diseases and injury.

104 aa 37-60, plays a role in rodent autoimmune CNS disease, and its human MOBP counterpart is associate

105 in better understanding the role of TSPO in CNS disease, and our results implicate TSPO as a potenti

106 chemokine receptor function in inflammatory CNS disease, and support the hypothesis that CCL2 is con

107 neratinib with chemotherapy in patients with CNS disease are ongoing.

108 The microbial determinants involved in CNS disease are poorly characterized.

109 as the potential to fundamentally change how CNS diseases are treated, unlocking potential for combin

110 cing cerebral ischemia, and may apply to non-CNS diseases as well.

111 id (CSF) of rhesus macaques with SIV-induced CNS disease, as we hypothesized that this might provide

112 of antiretroviral therapy on these cells and CNS disease, as well as the need for effective adjunctiv

113 CNS disease associated with the N-terminal portion of th

114 ole in neuropathological changes observed in CNS diseases associated with elevated CNS levels of IL-6

115 ts close relationship with neurofilaments in CNS diseases associated with neurofilament accumulation.

116 Four patients with active CNS disease at BMT and 20 patients with a history of pri

117 By univariate analysis, CNS disease at diagnosis did not significantly impact ev

118 by these studies, the presence of CSF+/Mass CNS disease at diagnosis was associated with a nominally

119 as stage and LDH did; however, children with CNS disease at diagnosis were at 2.0 times greater risk

120 ts on day 7) to induction therapy and lacked CNS disease at diagnosis were randomized to receive syst

121 r detect and treat patients with subclinical CNS disease at diagnosis would be anticipated to result

122 e treatment outcome of children with NHL and CNS disease at diagnosis, suggesting a need for ongoing

123 mated 2% of patients with AML who have overt CNS disease at diagnosis.

124 mes greater risk of death than those without CNS disease at diagnosis.

125 in) appeared to influence outcome except for CNS disease at presentation.

126 Of four patients with active CNS disease at the time of BMT, two had CNS recurrences

127 (ALL) in adults with central nervous system (CNS) disease at diagnosis is unclear.

128 greatest impediment in the treatment of many CNS diseases because it commonly blocks entry of therape

129 a potentially large proportion of treatable CNS disease burden across vast endemic areas and need mo

130 including genes playing a role in Mendelian CNS diseases, but no statistically significant effect wa

131 ich all animals develop AIDS and 90% develop CNS disease by 3 months after inoculation, pigtailed mac

132 The neonatal infection resulted in severe CNS disease by 3-4 weeks after infection.

133 lar role in patients with MS or inflammatory CNS diseases by epitope spreading is unclear.

134 ese results demonstrate that the severity of CNS disease can be reduced through the use of a neutrali

135 us, TGF-beta1 may exert a protective role in CNS diseases characterized by microglial cell activation

136 s (BDV) results in a central nervous system (CNS) disease characterized by behavioral abnormalities.

137 ant to both the onset and the progression of CNS disease compared with wild-type (WT) littermates.

138 rus (HIV)-associated central nervous system (CNS) disease, consistent with previously reported dopami

139 h high likelihood of central nervous system (CNS) disease could be identified in whom CSF analysis mu

140 en of the eight (88%) patients with sinus or CNS disease demonstrated stabilization of the IFI.

141 Many central nervous system (CNS) diseases display sexual dimorphism.

142 nificant potential as therapeutic targets in CNS disease due to HIV.

143 To study the prevalence of CNS disease due to VZV, cerebrospinal fluid (CSF) specim

144 esentations consistent with ocular and other CNS disease due to VZV; 4 were without zoster on present

145 tection from initial systemic and subsequent CNS disease following DENV infection and demonstrate the

146 in the periphery and favor susceptibility to CNS disease following peripheral routes of infection.

147 ncer Agency data set showed similar rates of CNS disease for low-risk (0.8%; CI, 0.0% to 1.6%), inter

148 hanistically diverse central nervous system (CNS) diseases from autoimmune diseases such as multiple

149 for degenerative, developmental, or acquired CNS diseases, functional integration may depend critical

150 ive gliosis are prominent in virtually every CNS disease, glia are largely viewed as passive responde

151 The presence of CNS disease had 88% specificity and a 92% positive predi

152 ce of HIV-associated central nervous system (CNS) disease has increased despite suppression of plasma

153 ct on VZV-associated central nervous system (CNS) disease has not been assessed.

154 lapse (such as T-cell immunophenotype, overt CNS disease, high-risk cytogenetic features, or poor res

155 ived imaging agents for routine diagnosis of CNS diseases (i.e., Parkinson's disease) in which change

156 ection from the consequences of inflammatory CNS disease in an experimental allergic uveitis model.

157 une responses to and therapeutic options for CNS disease in an immunologically defined, genetically m

158 in CSF, for more accurate identification of CNS disease in DLBCL and BL patients.

159 e burden of these pathogens in patients with CNS disease in endemic countries.

160 Both viruses are associated with CNS disease in horses, humans, and mouse infection model

161 CNS disease in humanized mice was characterized by glios

162 patients also express RAC2 and give rise to CNS disease in mice.

163 offer new insights into the pathogenesis of CNS disease in MPS patients, and support the use of sper

164 rituximab eliminates the increased risk for CNS disease in patients with ECFI.

165 rocesses are involved in the pathogenesis of CNS disease in pre-B-cell ALL, support a model in which

166 he treated group versus 4 of 20 animals with CNS disease in the control group; P = 0.036).

167 ation with increased viral load and onset of CNS disease in vivo, suggests that SOCS3 may allow HIV-1

168 exert beneficial effects for immune-mediated CNS diseases in vivo.

169 S) RNA virus, causes central nervous system (CNS) disease in a broad range of vertebrate species, inc

170 were associated with central nervous system (CNS) disease in addition to endocarditis, UTI, and sepsi

171 ses ocular and other central nervous system (CNS) disease in human immunodeficiency virus (HIV)-infec

172 ne pathogens causing central nervous system (CNS) disease in humans and equids.

173 ae is known to cause central nervous system (CNS) disease in humans, and neurological signs have been

174 CSF) and active HCMV central nervous system (CNS) disease in patients with human immunodeficiency vir

175 ed in the CSF of 26 (76%) of 34 infants with CNS disease, in 13 (93%) of 14 infants with disseminated

176 Other important mechanisms to control CNS disease include targeting pathways downstream of ALK

177 CNS disease included meningeal disease or CNS parenchyma

178 Complications in CNS disease included raised intracranial pressure (42%),

179 ation of function in central nervous system (CNS) diseases including stroke and ischemic retinopathie

180 edge about the isolated role of microglia in CNS diseases, including degenerative conditions of the r

181 ctor of outcome in a number of diverse human CNS diseases, including head and spinal cord trauma, met

182 mediate white matter injury in a variety of CNS diseases, including multiple sclerosis (MS).

183 therapeutic goal in the treatment of certain CNS diseases, including multiple sclerosis, amyotrophic

184 omy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the in

185 HIV-1 associated central nervous system (CNS) disease involves neuronal damage and prominent reac

186 In CNS diseases involving energy deprivation at times of my

187 lomyelitis, multiple sclerosis, and/or other CNS diseases involving myelomonocytic lineage cells.

188 ituation in which the extent of inflammatory CNS disease is determined by the balance between antivir

189 ials, but the effectiveness of crizotinib in CNS disease is limited by poor blood-brain barrier penet

190 therapy for their brain metastases and whose CNS disease is radiographically stable at study entry; t

191 However, its role in HIV-1 CNS disease is unknown.

192 Central nervous system (CNS) disease is a frequent complication of human immunod

193 Central nervous system (CNS) disease is the most common extrarespiratory complic

194 e only available and effective treatment for CNS disease, is associated in up to 10% of cases with a

195 o-orbital-cerebral zygomycosis, particularly CNS disease, is associated with substantial mortality ra

196 usses the issues of diagnosis and staging of CNS disease, its neuropathogenesis, and the possibility

197 e chronic pain is considered by some to be a CNS disease, little is understood about underlying neuro

198 , it is not understood why in HIV-associated CNS disease, macrophages and microglia are biased toward

199 used in this study, curcumin aggravates some CNS disease manifestations in experimental lupus brain.

200 The incidence of CNS disease manifestations in humans depends on the infe

201 Indeed, B. hermsii infection did not induce CNS disease manifestations in T cell-deficient mice (TCR

202 Moreover, chronic inflammatory CNS disease may induce autoantibodies by virtue of epito

203 CNS disease may result owing to the sensitivity of the C

204 Similarities to the pathogenesis of common CNS diseases mean that common neuroprotective strategies

205 s as targets for therapeutic intervention in CNS disease might now have to be considered in the conte

206 CNS disease occurred in 57% (51 of 90).

207 Parenchymal and leptomeningeal CNS disease occurred in four and three patients, respect

208 PCR-positive CNS disease occurred in patients ranging in age from 13

209 in pre-B-cell ALL, support a model in which CNS disease occurs as a result of external invasion, and

210 high-risk group (12%) showed 2-year rates of CNS disease of 0.6% (CI, 0% to 1.2%), 3.4% (CI, 2.2% to

211 ief contributor to this phenomenon; however, CNS diseases of childhood and the elderly also demonstra

212 s of humans with infectious and inflammatory CNS diseases of unknown etiology such as multiple sclero

213 s of humans with infectious and inflammatory CNS diseases of unknown etiology such as multiple sclero

214 Whether it is associated with CNS disease or a marker of inflammation requires further

215 roles of specific T cells in causing lethal CNS disease or curing pervasive and life-long CNS infect

216 ive and either amphotericin-B for those with CNS disease or fluconazole for those without.

217 be neuroprotective in other animal models of CNS disease or injury known to be responsive to unmodifi

218 years, had normal organ function, and had no CNS disease or serious infections, including human immun

219 ith HCMV CNS disease, other non-HCMV-related CNS diseases, or no CNS disease were tested for the pres

220 HIV-1-positive patients diagnosed with HCMV CNS disease, other non-HCMV-related CNS diseases, or no

221 y-eight out of 625 patients (4.5%) developed CNS disease over time.

222 mutation was associated with (18)F-FDG-avid CNS disease (P = 0.0357), higher SUVmax (P = 0.0044), an

223 he evaluation of mechanisms and treatment of CNS disease, particularly those where glutathione may pl

224 tribution of PilA in central nervous system (CNS) disease pathogenesis are unknown.

225 egions of Env control dramatically different CNS disease patterns.

226 Those with CNS disease, pleural effusion, circulating lymphoma cell

227 proteins are profoundly upregulated in many CNS diseases prior to signs of neuron loss, suggesting a

228 a support the hypothesis that in HIV-induced CNS disease products of activated macrophages and astroc

229 weeks, defined by an absence of CNS or extra-CNS disease progression, no tumour-related worsening of

230 it was a combination of systemic and distant CNS disease progression.

231 7 nAChRs) has broad therapeutic potential in CNS diseases related to cognitive dysfunction, including

232 uelae, although the cellular contributors to CNS disease remain poorly defined.

233 al cells-during multiple sclerosis and other CNS diseases remain controversial.

234 icial or detrimental contributions of ASC to CNS diseases remain to be defined, virus-specific ASC ar

235 However, the pathogenesis of CNS disease remains unclear.

236 ent of these chronic central nervous system (CNS) diseases, remains a critical unsolved issue.

237 inversely correlated with the development of CNS disease; RON was maintained in animals that did not

238 le cell neuronopathy (GCN), a JCV-associated CNS disease, so far unreported amongst patients treated

239 ns and neurologic disability in inflammatory CNS diseases such as multiple sclerosis (MS) result from

240 ing therapeutics for central nervous system (CNS) diseases such as Parkinson's disease, we have been

241 ring plasticity paradigms or after models of CNS disease, such as stroke, where the weighting within

242 ages and activated microglial cells in human CNS diseases, suggesting that CCR8 may be a feasible tar

243 al indication of CMV central nervous system (CNS) disease, suggesting that the development of gancicl

244 uch as CD14(-/-) mice, exhibited more severe CNS disease than Wt mice.

245 be considered when selecting therapy for CMV CNS disease that develops in patients receiving treatmen

246 we found high incidence of distinct signs of CNS disease that ranged from a flaccid tail to complete

247 The classifier that differentiates MS from CNS diseases that mimic MS clinically, pathophysiologica

248 ting photoreceptor apoptosis in RD and other CNS diseases that share a common etiology.

249 e virus (BDV) causes central nervous system (CNS) disease that is frequently manifested by behavioral

250 tics, cardiovascular risks, lupus nephritis, CNS disease, the antiphospholipid syndrome, assessment o

251 Among patients with CNS disease, those with neuroimaging abnormalities (P =

252 We developed a murine model of CNS disease to obtain a better understanding of the path

253 This relationship may extend to other CNS diseases typified with an inflammatory component.

254 trated well in several preclinical models of CNS diseases, validating TrkB as a promising drug target

255 atients with CNS cryptococcosis; the risk of CNS disease was 14% if none, 39% if one, and 94% if two

256 ylaxis with methotrexate, the 2-year rate of CNS disease was 4.2% compared with 2.3% in 191 patients

257 6 of 88), and the mortality in patients with CNS disease was 73.5% (36 of 49).

258 Morbidity and mortality of the acute viral CNS disease was augmented by the presence of the autoant

259 Induction of CNS disease was dependent on the B. hermsii strain as we

260 Thirty-eight patients were enrolled; CNS disease was detected at presentation in 16 patients.

261 logic symptoms; the diagnosis of VZV-related CNS disease was facilitated by this assay; improvement i

262 In a multivariate analysis, CNS disease was not significantly associated with either

263 Among cases of SNCC NHL/B-ALL, CNS disease was significantly associated with event-free

264 LPs and amphotericin therapy for those with CNS disease was small and additional costs were large (U

265 r cumulative rate of central nervous system (CNS) disease was increased in 205 ECFI patients compared

266 t-free survival +/- SE for all patients with CNS+ disease was 45% +/- 7%.

267 d functional factors involved in HIV-induced CNS disease, we analyzed the viral loads and T cell infi

268 ls greater than 500 IU/L after adjusting for CNS disease were 1.4 (95% CI, 0.96 to 2.0; P =.029) and

269 serum cryptococcal antigen (CRAG) titers in CNS disease were 563.9 (vs 149.3 in isolated lung infect

270 The outcomes of those with a history of CNS disease were compared with those of a matched contro

271 NPV, respectively) for the diagnosis of HCMV CNS disease were determined.

272 BMT and 20 patients with a history of prior CNS disease were identified.

273 nally, multiple hallmarks of immune-mediated CNS disease were observed including upregulation of MHC

274 Fragments transferring increased ocular or CNS disease were sequenced.

275 , other non-HCMV-related CNS diseases, or no CNS disease were tested for the presence of HCMV pp67 mR

276 oms resembling viral central nervous system (CNS) disease were examined for the presence of herpes si

277 in CSF has good correlation with active HCMV CNS disease, whereas CSF culture is insensitive and qual

278 CNS-HL at diagnosis, 2 of whom had isolated CNS disease, while 8 patients developed CNS-HL at relaps

279 delivery to the brain in relevant models of CNS diseases, while in few cases proof of concept had be

280 l to improve efficacy of treatments for many CNS diseases, while reducing systemic side effects by pr

281 alpha7 nAChRs, with therapeutic potential in CNS diseases with cognitive dysfunction.

282 VZV continues to be associated with CNS disease, with meningitis being the most frequent cli

283 gray matter has been identified in multiple CNS diseases, yet the deleterious consequences, if any,

284 ecimens collected from patients without HCMV CNS disease yielded the following results: pp67 assay ne

285 specimens collected from patients with HCMV CNS disease yielded the following results: pp67 assay po