ライフサイエンスコーパス: CNS disease

1 of targeting microglia for the treatment of CNS disease.

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

3 icularly when combined with FCM detection of CNS disease.

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

5 europrotective interventions in CTL-mediated CNS disease.

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

7 a protective strategy to treat inflammatory CNS disease.

8 processing are considered in the context of CNS disease.

9 lation in reactive astrocytes will alter the CNS disease.

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

11 for controlling viral infections that cause CNS disease.

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

13 disease during autoimmune and virus-induced CNS disease.

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

15 recurrence of viral replication and onset of CNS disease.

16 d parameters were related to the etiology of CNS disease.

17 ndently associated with an increased risk of CNS disease.

18 or application of therapeutic genes in human CNS disease.

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

20 inflammatory factors and ROS, culminating in CNS disease.

21 nd injury leads to dysregulated astroglia in CNS disease.

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

23 /or animal models of NMDAR antibody-mediated CNS disease.

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

25 may yield insights into the pathogenesis of CNS disease.

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

27 lasma virus and monocytes in contributing to CNS disease.

28 inal fluid of humans with chronic infectious CNS disease.

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

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

31 zone (SVZ) contribute to brain repair during CNS disease.

32 -mediated pathology and reconstitute a fatal CNS disease.

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

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

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

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

37 ified in protection against MV infection and CNS disease.

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

39 d potentials were abnormal, indicating early CNS disease.

40 tential for transplantation-based therapy of CNS disease.

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

42 poorer overall survival among children with CNS disease.

43 revention and treatment strategies of EV-D68 CNS disease.

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

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

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

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

48 unopathological processes that cause ongoing CNS disease.

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

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

51 e therapeutically targetable in inflammatory CNS disease.

52 tial targets for therapeutic intervention in CNS disease.

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

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

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

56 useful biomarker in the evaluation of fungal CNS disease.

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

58 powerful therapeutics for neurodegenerative CNS diseases.

59 iology and potential therapeutic targets for CNS diseases.

60 sport may be protective in neuroinflammatory CNS diseases.

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

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

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

64 antibody-mediated pathology in demyelinating CNS diseases.

65 atory mediators contribute to HIV-associated CNS diseases.

66 ated with a wide range of rare but treatable CNS diseases.

67 emerged as a promising therapy for treating CNS diseases.

68 h sera from patients with other inflammatory CNS diseases.

69 for the development of transplant therapy of CNS diseases.

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

71 n, opening a new avenue for the treatment of CNS diseases.

72 R1 signaling pathways in the pathogenesis of CNS diseases.

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

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

75 tion of therapeutic antibodies in infectious CNS diseases.

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

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

78 herapeutic strategy for ischemic retinal and CNS diseases.

79 and targeted gene delivery for treatment of CNS diseases.

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

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

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

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

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

85 diated demyelinating central nervous system (CNS) disease.

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

87 ely to contribute to central nervous system (CNS) disease.

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

89 n cardiovascular and central nervous system (CNS) diseases.

90 functions, and model central nervous system (CNS) diseases.

91 hogenesis of several central nervous system (CNS) diseases.

92 P) type of GBS or in central nervous system (CNS) diseases.

93 trated frequent complications in people with CNS disease; 25 subjects (35.2%) required >1 lumbar punc

94 nya infection was more often associated with CNS disease (26 [47%] of 55 patients with chikungunya in

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

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

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

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

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

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

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

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

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

104 , 16.5-74.5); 2 patients died of progressive CNS disease and small-cell lung cancer, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

118 er astrogliogenesis over neurogenesis during CNS disease are unclear.

119 y expanding and clinically distinct group of CNS diseases are caused by pathogenic autoantibodies tha

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

121 Many central nervous system (CNS) diseases are characterized by deficits in insulin s

122 Central nervous system (CNS) diseases are the leading cause of morbidity and mor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 ost immunity.IMPORTANCE The current trend in CNS disease biology is to attempt to understand the neur

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

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

142 CNS) and analyzing CSF aids the diagnosis of CNS diseases, but our understanding of CSF leukocytes re

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

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

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

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

147 Patients with overt CNS disease (CNS3; >= 5 WBCs/muL with blasts) received H

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

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

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

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

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

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

154 B cells can contribute to CNS disease either through their actions in the peripher

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

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

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

158 estigation of immunotherapy in patients with CNS disease from NSCLC is warranted.

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

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

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

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

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

164 the absence of overt central nervous system (CNS) disease has led to the suggestion that they are vir

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

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

167 For central nervous system (CNS) diseases, however, the efficacy remains limited due

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

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

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

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

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

173 CNS disease in humanized mice was characterized by glios

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

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

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

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

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

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

180 1(G93A) and rotenone models, mimicking these CNS diseases in humans.

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

182 motherapy-induced peripheral neuropathies or CNS diseases in which axonal degeneration is a common fa

183 molecule that may have therapeutic value for CNS diseases in which BDNF signaling is disrupted.SIGNIF

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

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

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

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

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

189 Example of COVID-19 CNS disease include encephalopathy, encephalitis, acute

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

191 CNS disease included meningeal disease or CNS parenchyma

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

193 The etiology of CNS diseases including multiple sclerosis, Parkinson's d

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

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

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

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

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

199 mice, resistance to central nervous system (CNS) disease induced by members of the genus Flavivirus

200 y lead to novel targets for the treatment of CNS diseases involving aberrant complement-mediated syna

201 In CNS diseases involving energy deprivation at times of my

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

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

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

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

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

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

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

209 for the treatment of central nervous system (CNS) diseases is extremely challenging, in large part du

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

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

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

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

214 bnormal MoCA scores (<26) were predictive of CNS disease; low scores (<22) were associated with poor

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

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

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

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

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

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

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

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

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

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

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

226 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

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

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

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

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

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

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

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

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

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

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

237 TB was associated with diffuse CNS disease (P < .05).

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

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

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

241 egions of Env control dramatically different CNS disease patterns.

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

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

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

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

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

247 7 nAChRs) has broad therapeutic potential in CNS diseases related to cognitive dysfunction, including

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

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

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

251 However, the pathogenesis of CNS disease remains unclear.

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

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

254 s in AIDP and those that might be present in CNS diseases should continue.

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

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

257 sease progression in central nervous system (CNS) diseases such as amyotrophic lateral sclerosis (ALS

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

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

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

261 mors (mRECIST) criteria was used to evaluate CNS disease; systemic disease was not required for parti

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

263 , viral protein synthesis recurs, inducing a CNS disease that is distinct from that observed during a

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

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

266 es the therapeutic power of mAbs for various CNS diseases that remain poorly treated.

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

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

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

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

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

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

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

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

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

276 6 of 88), and the mortality in patients with CNS disease was 73.5% (36 of 49).

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

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

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

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

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

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

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

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

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

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

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

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

289 Fragments transferring increased ocular or CNS disease were sequenced.

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

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

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

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

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

295 rapy in patients with multiple sclerosis and CNS diseases with an autoantibody component, such as neu

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

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

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

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

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