ライフサイエンスコーパス: PD

1 PD apparently fuels the inflammation of T2D and associat

2 PD patients with a long disease course have greater hemi

3 PD-1 blockade diminishes exhaustion and improves GVL, wh

4 PD-L1 expression is typically low or absent in SCLC, whi

5 PD-L1 is expressed in tumor cells and its interaction wi

6 PD-L1 positivity appears to be predictive of pembrolizum

7 PD-L1 signaling also induced an anergic T-bet(-)IFN-gamm

8 Likewise, defect morphology (P = 0.02), PD (P = 0.003), and MBL (P = 0.01) were significantly co

9 bitor targeting the programmed cell death 1 (PD-1) axis, has shown promising results for the treatmen

10 immunotherapy with programmed cell death-1 (PD-1) checkpoint blockade.

11 rt by expression of programmed cell death-1 (PD-1) encoded by the Pdcd1 gene.

12 Programmed death ligand 1 (PD-L1) and PD-L2 are ligands for PD-1; the former is ubi

13 subtypes express programmed death-ligand 1 (PD-L1), and natural killer (NK) cells are involved in tr

14 ssion of CD86 and programmed death ligand 1 (PD-L1).

15 d with anti-programmed cell death protein 1 (PD-1) agents (nivolumab or pembrolizumab) was conducted

16 t receptors programmed cell death protein 1 (PD-1) and cytotoxic T lymphocyte-associated protein 4 (C

17 Programmed cell death protein 1 (PD-1) has become one of the most investigated targets fo

18 ve advanced cancer patient treated with PD-1/PD-L1 checkpoint inhibitors.

19 e compound is capable of disrupting the PD-1/PD-L1 complex by antagonizing PD-L1 and, therefore, rest

20 E5 as a mediator of resistance to anti-PD-1/PD-L1 immunotherapy and demonstrates the antitumor activ

21 a novel mechanism of resistance to anti-PD-1/PD-L1 immunotherapy mediated by HPV E5, which can be exp

22 mTOR inhibitors, CTLA-4 inhibitors, or PD-1/PD-L1 inhibitors, etc.

23 The PD-1/PD-L1 interaction was not correlated with clinical PD-L1

24 intervention, we quantitatively imaged PD-1/PD-L1 interactions in tumor samples from patients, emplo

25 Ipilimumab (anti-CTLA-4) or anti-PD-1/PD-L1 monotherapy failed to show a significant benefit.

26 In conclusion, although targeting the PD-1/PD-L1 pathway reinvigorates exhausted CD8(+) T cells, it

27 For every 10 DOT/1000 PD increase in use of third- and fourth-generation cepha

28 miR-127(PD) decreased the viability and motility of TNBC cells,

29 suppressive compared to PD-1 signaling; (2) PD-L1(+) T cells restrained effector T cells via the can

30 even in the absence of endogenous PD-L1; (3) PD-L1(+) T cells engaged PD-1(+) macrophages, inducing a

31 rregulation by the co-receptors BTLA, Tim-3, PD-1, TIGIT, and CD73.

32 ntly higher abundance (43%), richness (32%), PD (25%) and FD (25%) of birds visiting polyculture plot

33 dth of the 95% limit of agreement of +/-11.4 PD.

34 all, 3341 patients were included (2633 (79%) PD and 708 (21%) DP) of whom 60.3% achieved TO; 58.3% fo

35 A PD DBS cohort (N = 37) completed a reward-based Go/No-Go

36 hat NK cells (haNKs) engineered to express a PD-L1 chimeric antigen receptor (CAR) haNKs killed a pan

37 cells at low effector-to-target ratios in a PD-L1-dependent fashion.

38 main-containing protein, is located within a PD risk locus identified by genome-wide association stud

39 one towards the development of an accessible PD screening tool that will passively monitor the subjec

40 t of various neurological disorders like AD, PD, schizophrenia, epilepsy, brain cancer, CNS infection

41 Tinnitus-related risk on developing AD/PD followingly was determined by the Cox regression to i

42 companied with anxiety-like behavior in aged PD-related alpha-syn A53T mice.

43 tly enhanced the antitumor activity of alpha-PD-1 and was accompanied by increased tumor infiltration

44 OSAS patients revealed an increased PD-1 and PD-L1 expression in T cells and monocytes, respectively,

45 ll inhibitory checkpoint proteins CTLA-4 and PD(L)1 are efficacious across a broad range of cancers,

46 apomorphine were active in models of AD and PD.

47 Alcohol-exposed mice have reduced Bcl6 and PD-1 expression as well as IL-21 production by T(FH) cel

48 ditions validated the association of CA9 and PD-L1 expression.

49 These data suggest that combined CXCR4 and PD-1 blockade may expand the benefit of chemotherapy in

50 Except for one sample, PD-L1 and PD-1 in all samples were quantifiable using this assay w

51 The PD-1 ligands PD-L1 and PD-L2 are commonly expressed on the surface of cells, wh

52 and preceding studies confirm that PD-L1 and PD-L2 are expressed in a high percentage of OASCs.

53 trinsic mechanisms of constitutive PD-L1 and PD-L2 expression in brain tumors.

54 ng may influence interpretation of PD-L1 and PD-L2 expression in ocular adnexal tumors.

55 The degree of PD-L1 and PD-L2 expression was also associated with the area in mi

56 ssion of the PD-1 pathway ligands, PD-L1 and PD-L2, remain poorly understood.

57 Programmed death ligand 1 (PD-L1) and PD-L2 are ligands for PD-1; the former is ubiquitously e

58 "do not eat me" signal for macrophages) and PD-L1 (a T-cell inactivator) on their surface.

59 ith different combinations of molecules, and PD-1 expression was studied at the mRNA and protein leve

60 ere is increased clinical interest in NK and PD-1 immunotherapy.

61 y)pT and c (y)pN stages, and LI, VI, PN, and PD (poor vs other).

62 Inhibiting VISTA- and PD-L1-signaling relieved immune suppression and reduced

63 ed 2 dietary patterns consistent with WD and PD.

64 pting the PD-1/PD-L1 complex by antagonizing PD-L1 and, therefore, restores activation of T cells sim

65 agent anti-programmed death receptor 1 (anti-PD-1) therapy is modest in patients with metastatic or r

66 of margetuximab plus pembrolizumab (an anti-PD-1 monoclonal antibody) in previously treated patients

67 Conventional treatment with an anti-PD-L1 mAb had no significant antitumor effect, indicatin

68 immunotherapies beyond anti-CTLA-4 and anti-PD(L)1 and discuss how these results are providing new i

69 Combination of ENO1i and anti-PD-L1 Ab or HDAC6i ACY-241 enhances autologous MM-specif

70 he efficacy and safety of atezolizumab (anti-PD-L1) alone and combined with bevacizumab (anti-VEGF) i

71 wn to be an emerging biomarker for both anti-PD-(L)1 treatment and prognosis; however, multiple chall

72 ynergize with immunotherapy, especially anti-PD therapy.

73 edictive blood biomarker for evaluating anti-PD-1 response.

74 ed with the immune checkpoint inhibitor anti-PD-1, strengthening the rationale behind combination the

75 isotype-treated infected control mice, anti-PD-1-treated mice had improved survival, reduced fungal

76 TLA-4), 2542 per 100 000 for nivolumab (anti-PD-1), 2451 per 100 000 for pembrolizumab (anti-PD-1), 5

77 ransplantation (FMT) and reinduction of anti-PD-1 immunotherapy in 10 patients with anti-PD-1-refract

78 In mice, the combination of anti-PD-1 inhibitory and anti-OX40 agonist antibodies reduces

79 ative tumor, the mechanism of action of anti-PD-1 therapy remains undefined.

80 at early, self-activating expression of anti-PD-L1-gamma1 can overcome the immunosuppressive environm

81 Ipilimumab (anti-CTLA-4) or anti-PD-1/PD-L1 monotherapy failed to show a significant bene

82 315 patients responded to anti-PD-1 or anti-PD-L1 therapy for immunotherapy-naive disease, and three

83 0 months (2.7-3.9) for the anti-PD-1 or anti-PD-L1-containing groups.

84 In 2014, we administered pembrolizumab (anti-PD-1) for ~9 months to a 57-year-old kidney transplant r

85 1), 2451 per 100 000 for pembrolizumab (anti-PD-1), 5556 per 100 000 for ipilimumab plus nivolumab, a

86 tumor-intrinsic NGFR signature predicts anti-PD-1 therapy resistance, and NGFR(hi) tumor fractions ar

87 combination of IT CMP-001 with systemic anti-PD-1 enhanced antitumor responses in both injected and n

88 roups, and 3.0 months (2.7-3.9) for the anti-PD-1 or anti-PD-L1-containing groups.

89 Responses to anti-PD-1 immunotherapy occur but are infrequent in bladder c

90 ld-type mice and are more responsive to anti-PD-1 immunotherapy.

91 53 (16.8%) of 315 patients responded to anti-PD-1 or anti-PD-L1 therapy for immunotherapy-naive disea

92 T cell infiltration and sensitivity to anti-PD-1.

93 ion sensitizes resistant lung tumors to anti-PD-1.

94 s HPV E5 as a mediator of resistance to anti-PD-1/PD-L1 immunotherapy and demonstrates the antitumor

95 fies a novel mechanism of resistance to anti-PD-1/PD-L1 immunotherapy mediated by HPV E5, which can b

96 demonstrated synergy when combined with anti-PD-1 therapy.

97 -PD-1 immunotherapy in 10 patients with anti-PD-1-refractory metastatic melanoma.

98 and overall survival when combined with anti-PD-1.

99 sponses using checkpoint inhibitors, such as PD-1 or PD-L1 inhibitors.

100 , and 94.3% accuracy of the smartphone-based PD platform for detection of V. cholerae.

101 roglia is central to the association between PD and AD.

102 alse discovery rate <0.05) was found between PD and a positive family history of PD, a positive famil

103 As a result, these bionic PDs offer a signal/noise ratio of ~10(6) , a large bandw

104 n of Abeta in 5xFAD mice was not affected by PD except for a decrease in the dentate gyrus.

105 estrained effector T cells via the canonical PD-L1-PD-1 axis and were sufficient to accelerate tumori

106 therapy (taxane or gemcitabine-carboplatin), PD-L1 expression at baseline (combined positive score [C

107 lso differed by expression patterns of CD95, PD-1, and Tim-3.

108 were identified: one defined by high T-cell PD-1 expression and another by a hyperinflamed profile a

109 ell lines and 4T1 mouse mammary tumor cells, PD-L1 expression was regulated by the nuclear receptor N

110 agents targeting the immunologic checkpoints PD-1 and CTLA-4.

111 interaction was not correlated with clinical PD-L1 expression scores in malignant melanoma.

112 he cell-intrinsic mechanisms of constitutive PD-L1 and PD-L2 expression in brain tumors.

113 dentification of the mechanisms that control PD-1 expression extremely important to increase the resp

114 tinued to drive T cell maturation into CXCR5+PD-1+ T follicular helper cells.

115 infiltrating lymphocytes expressed decreased PD-1 and LAG3, suggesting a less exhausted phenotype.

116 Everolimus treatment also led to decreased PD-1 expression on certain T cell subsets.

117 bstitution that is associated with decreased PD.

118 sel length density (VLD), perfusion density (PD), and foveal avascular zone (FAZ) parameters were mea

119 s 9.56 +/- 1.93 mm with a mean pocket depth (PD) of 8.41 +/- 1.42 mm.

120 bing (BOP), plaque index, and probing depth (PD) were confirmed reliable discriminants between peri-i

121 Probing depth (PD), attachment level, bleeding on probing (BOP), and in

122 Probing depth (PD), CAL, plaque index (PI), and interproximal bone heig

123 e PD-L1-overexpressing platelets (designated PD-L1 platelets) accumulate in the inflamed pancreas and

124 SD), and mean VF sectoral pattern deviation (PD) from SD OCT data.

125 showed a mean value of -2.9 prism diopters (PD) and a half-width of the 95% limit of agreement of +/

126 Parkinson disease (PD) is a devastating, largely nonfamilial, age-related d

127 a pars compacta (SNpc) in Parkinson disease (PD) is not uniform, as dopamine neurons from the ventral

128 lication of the retina in Parkinson disease (PD) pathology and the importance of dopaminergic cells i

129 about the pathogenesis of Parkinson disease (PD) suggests that the brainstem is a convergent area for

130 de association studies of Parkinson disease (PD).

131 anglia of patients with Parkinson's disease (PD) are associated with impaired motor performance.

132 concept of 'idiopathic' Parkinson's disease (PD) as a single entity has been challenged with the iden

133 r increase the risk of, Parkinson's disease (PD) have been identified.

134 Parkinson's disease (PD) is a common neurodegenerative disease with a heterog

135 Parkinson's disease (PD) is a multifactorial malady and the second most commo

136 Parkinson's disease (PD) is a progressive neurodegenerative disorder involvin

137 Parkinson's disease (PD) is characterized by dopaminergic neuronal loss and t

138 rescue motor defects in Parkinson's disease (PD) models, whether and how grafts functionally repair d

139 Parkinson's disease (PD) pathogenesis may involve the epigenetic control of e

140 notype of LRRK2 and GBA Parkinson's disease (PD), and on the prevalence of prodromal features among i

141 to symptom severity in Parkinson's disease (PD), but few studies have characterized beta activity in

142 mptom lateralization in Parkinson's disease (PD), but its molecular determinants are unknown.

143 pA colocalizes with the Parkinson's disease (PD)-associated protein alpha-synuclein in cells and inte

144 Here, we show that the Parkinson's disease (PD)-related kinase LRRK2 is activated in macrophages by

145 somal-dominant familial Parkinson's disease (PD).

146 or cause of early-onset Parkinson's disease (PD).

147 common risk factor for Parkinson's disease (PD).

148 rodegenerative disorder Parkinson's disease (PD); however, it is unclear how mitochondrial impairment

149 emiological studies link Periodontal disease(PD) to age-related macular degeneration (AMD).

150 Dominant PD-associated LRRK2 alleles may suppress EPAC-1 activity

151 ies of inhibitory receptor expression, i.e., PD-1 and coexpression of PD-1 and TIGIT, within the firs

152 rigenesis, even in the absence of endogenous PD-L1; (3) PD-L1(+) T cells engaged PD-1(+) macrophages,

153 dogenous PD-L1; (3) PD-L1(+) T cells engaged PD-1(+) macrophages, inducing an alternative M2-like pro

154 d-type alpha-Syn transgenic mice facilitates PD pathologies and elicits motor disorders associated wi

155 nexpectedly, bacterial diversity (ASV, Faith PD and Shannon) was higher among zoo gorillas than among

156 rodegeneration in both sporadic and familial PD upon parkin loss-of-function remains unknown.

157 1%) DP) of whom 60.3% achieved TO; 58.3% for PD and 67.4% for DP.

158 design are additional causative factors for PD.

159 Glucocorticoids are indispensable for PD-1 induction on human NK cells, in cooperation with a

160 h ligand 1 (PD-L1) and PD-L2 are ligands for PD-1; the former is ubiquitously expressed in inflamed t

161 MVH provide a model for PD outcomes to improve quality and access for patients w

162 nts had baseline tumor biopsies positive for PD-L1 expression (n = 28/40 evaluable), and response rat

163 D-L1 and 16.96-129.89 (amol/mug protein) for PD-1.

164 tions of 27.85-798.43 (amol/mug protein) for PD-L1 and 16.96-129.89 (amol/mug protein) for PD-1.

165 ars to depend on background genetic risk for PD.

166 Kv1.3 as a potential therapeutic target for PD.

167 vide a key for developing new treatments for PD.

168 t information about the likelihood of future PD not captured by classical HRV metrics.

169 n to the periodontal parameters of VPI, GBI, PD, CAL, or BOP 2 years after completion of the periodon

170 In the high PD-L1 population, median overall survival was 14.4 month

171 Programmed death-1 homolog (PD-1H), a CD28/B7 family molecule, coinhibits T cell act

172 elanoma protein B (GPNMB) signaling in human PD SN.

173 1.9- angstrom crystal structure of the human PD-1H extracellular domain.

174 point intervention, we quantitatively imaged PD-1/PD-L1 interactions in tumor samples from patients,

175 optic material to have a lower I/R improved PD symptoms in the large majority of patients.

176 To address the role of NK cells in PD pathogenesis, NK cell function was investigated in a

177 ibited significant expression differences in PD associated with all four mycobacteria.

178 for alleviating L-DOPA-induced dyskinesia in PD patients.

179 se in cytosine modifications at enhancers in PD neurons, which is partly explained by elevated hydrox

180 re gait and balance, and to prevent falls in PD.SIGNIFICANCE STATEMENT In persons with Parkinson's di

181 microbiome approximated clinical findings in PD patients, characterized by increased abundance of Ver

182 and SMARCB1 mutations were more frequent in PD.

183 valuable), and response rates were higher in PD-L1-positive (8/28; 29%) versus PD-L1-negative (0/12;

184 mplant health and disease, while increase in PD (PD > 4 mm) and suppuration were good discriminants a

185 sease and was highest in GO, intermediate in PD, and lowest in R patients (P = 0.017).

186 neurodegeneration and is highly involved in PD pathology.

187 nd vesicular transport genes are observed in PD with and without dementia and Lewy body dementia, but

188 he hallmark pathological amyloid observed in PD, is also elevated in melanoma, where its expression i

189 reaffirmed the importance of this process in PD aetiology.

190 Remarkably, Netrin1 is reduced in PD patient brains, associated with MST1 activation and U

191 rs, yet oHSV infection led to a reduction in PD-1+ CD8+ T cells in injected GBMs and an increase in I

192 Both groups showed significant reductions in PD, GI, and CAL gain overtime.

193 centuating the neuroinflammatory response in PD and identify Kv1.3 as a potential therapeutic target

194 d variation may not have a prominent role in PD etiology, but some related drug targets could influen

195 A key therapeutic target in PD is alpha-synuclein (alphaS), which is both geneticall

196 NA translation and resulting in an increased PD-1 amount in NK cells.

197 OSAS patients revealed an increased PD-1 and PD-L1 expression in T cells and monocytes, resp

198 In vitro IFNgamma treatment increased PD-L1 expression in the tumor cell lines and caused up t

199 ut some related drug targets could influence PD via alternate pathways.

200 r understanding how GBA1 mutations influence PD pathogenesis and provides a platform for testing nove

201 ned effector T cells via the canonical PD-L1-PD-1 axis and were sufficient to accelerate tumorigenesi

202 The PD-1 ligands PD-L1 and PD-L2 are commonly expressed on the surface of

203 late expression of the PD-1 pathway ligands, PD-L1 and PD-L2, remain poorly understood.

204 MS does not seem to influence GBA and LRRK2-PD phenotype.

205 bacterium utilizes an effector to manipulate PD-mediated host intercellular communication for maximiz

206 ses were observed regardless of tumor MCPyV, PD-L1, or TMB status.

207 iatal axonal dysfunction in mild to moderate PD.

208 s loss, whereas 26 (29%) had relatively more PD loss.

209 Moreover, PD-L1 deficiency leads to compromised expression of mult

210 n a preformed fibril alpha-syn-induced mouse PD model.

211 erior colliculus visual responses in de novo PD patients are present early in the course of the disea

212 tigated whether miRNAs have potential as NTM-PD biomarkers.

213 pported the discriminative potential for NTM-PD and their combination provided an improved diagnostic

214 rovided an improved diagnostic value for NTM-PD.

215 this period, SF recovered ~76% of TD, 84% of PD and 96% of FD found within PFs.

216 tumors correlated with long-term benefit of PD-1 blockade therapy.

217 r expression, i.e., PD-1 and coexpression of PD-1 and TIGIT, within the first year of infection.

218 The degree of PD-L1 and PD-L2 expression was also associated with the

219 Enrichment of PD-1(+)CD4(+) T cells only within a granulocyte CN posit

220 While the expression of PD-1 on NK cells has been controversial, with papers pub

221 lips et al. explore the distinct features of PD-L2 and identify a specific evolutionary event linked

222 between PD and a positive family history of PD, a positive family history of dementia, non-smoking,

223 r, these results highlight the importance of PD-1 agonistic treatment in allergic asthma and undersco

224 implicated in the unresolved inflammation of PD, regardless of host metabolic health.

225 mprehensive assessment of the inheritance of PD in the common bean (Phaseolus vulgaris), a major dome

226 mor sampling may influence interpretation of PD-L1 and PD-L2 expression in ocular adnexal tumors.

227 s with high levels of OX40 and low levels of PD-1 were associated with longer survival times of patie

228 ownregulated cellular and membrane levels of PD-L1 in tumor cells by 50% as measured by Western blott

229 erformed for real-time in vivo monitoring of PD-L1 positive tumor cells and CTLs with cellular resolu

230 was developed to map the epitope/paratope of PD-1/nivolumab.

231 ay have an impact on the prognostic power of PD-L1.

232 was associated with a 17% decreased rate of PD (rate ratio = 0.83, 95% confidence interval: 0.75, 0.

233 However, the regulation of PD-L1 expression on tumor cells is still poorly understo

234 receptor CD44 as a key positive regulator of PD-L1 expression in these cancers.

235 r main postsynaptic neurons in the retina of PD.

236 subject-smartphone interaction for signs of PD and which could be used to reduce the critical gap be

237 lpha-synuclein across reflects all stages of PD model progression.

238 The clinical study of PD-L1 CAR haNKs is warranted.

239 teraction, whereby the effect of diabetes on PD risk appears to depend on background genetic risk for

240 using checkpoint inhibitors, such as PD-1 or PD-L1 inhibitors.

241 tors, mTOR inhibitors, CTLA-4 inhibitors, or PD-1/PD-L1 inhibitors, etc.

242 illance; this can be overcome using PD-L1 or PD-1 immunotherapy antibodies.

243 injection with the oncolytic virus overcomes PD-L1-mediated immunosuppression during both the priming

244 ls are genetically engineered to overexpress PD-L1 to produce immunosuppressive platelets.

245 cts the outcomes of pancreaticoduodenectomy (PD).

246 nt health and disease, while increase in PD (PD > 4 mm) and suppuration were good discriminants among

247 lity, pharmacokinetic (PK), pharmacodynamic (PD) and behavioral effects of a novel ghrelin receptor i

248 pharmacokinetics (PK), and pharmacodynamics (PD) of the human anti-C5 monoclonal antibody tesidolumab

249 PK/PD/behavioral findings support continued research of PF-

250 ly interacts with and destabilizes the plant PD-located protein PDLP7 and possibly PDLP5.

251 oprene (PI), the two most common polydienes (PD), are involved in a large number of materials and use

252 is an option in select cases of low positive PD-L1.

253 responses in patients with HR-NB with prior PD.

254 NMC with probability rates for prodromal PD above 50% had higher frequencies of hypertriglyceride

255 expression of the immunosuppressive protein PD-L1 in tumors.

256 s express the inhibitory checkpoint receptor PD-1.

257 We also observed that LXA4 treatment reduces PD-L1 expression and that PD-L1 expression is an importa

258 and down-regulation of checkpoint regulator PD-L1 on the cancer cells.

259 Except for one sample, PD-L1 and PD-1 in all samples were quantifiable using th

260 d clinical progression before imaging showed PD, and one participant was lost to follow-up.

261 Patients with early-stage PD (duration <3 years) who were not taking dopaminergic

262 ith DSR (4.5+/-0.4 g) compared with standard PD solution (1.0+/-0.3 g; P<0.0001).

263 blockade was remarkably more effective than PD-1 blockade alone in enhancing T cell cycling and diff

264 treatment reduces PD-L1 expression and that PD-L1 expression is an important immune evasion strategy

265 e current and preceding studies confirm that PD-L1 and PD-L2 are expressed in a high percentage of OA

266 The data demonstrated that PD increases neuroinflammation in WT mice and disrupts t

267 y, functional in vitro studies revealed that PD-1 expression on NK cells is associated with diminishe

268 The PD-1 ligands PD-L1 and PD-L2 are commonly expressed on t

269 The PD-1/PD-L1 interaction was not correlated with clinical

270 The PD-L1-overexpressing platelets (designated PD-L1 platele

271 The compound is capable of disrupting the PD-1/PD-L1 complex by antagonizing PD-L1 and, therefore,

272 The discovery of the role of the PD familial genes PTEN-induced putative kinase 1 (PINK1)

273 r mechanisms that regulate expression of the PD-1 pathway ligands, PD-L1 and PD-L2, remain poorly und

274 imal germinal center (GC)-rich region of the PD-L1 gene promoter.

275 nts (100%) received prior ICIs targeting the PD-1 pathway.

276 In conclusion, although targeting the PD-1/PD-L1 pathway reinvigorates exhausted CD8(+) T cell

277 tion at the SNCA locus in RBD as compared to PD, with an opposite direction of effect at the 3' of SN

278 ells and was equally suppressive compared to PD-1 signaling; (2) PD-L1(+) T cells restrained effector

279 nges in spontaneous SPN discharge related to PD and Dystonia are likely amplified by basal ganglia do

280 ns associated with response or resistance to PD-1 blockade.

281 atic murine TNBC models poorly responsive to PD-1 blockade.

282 RE1-silencing transcription factor (REST) to PD and also Alzheimer's disease.

283 ed the sensitivity of HR(+) 59-2-HI tumor to PD-L1 blockade, suggesting that antiprogestins may impro

284 well-recognised non-motor feature of treated PD, much remains unknown about the influence of risk fac

285 All 280 patients who underwent PD at our institution from January 2008 to December 2018

286 and newborn Tregs exhibiting a more uniform PD-1(+)CD39(+) phenotype.

287 NK cells of malaria-naive adults upregulated PD-1 following P. falciparum stimulation in vitro Additi

288 rtoire of sebocytes, notably by upregulating PD-L1 and IL10.

289 une surveillance; this can be overcome using PD-L1 or PD-1 immunotherapy antibodies.

290 higher in PD-L1-positive (8/28; 29%) versus PD-L1-negative (0/12; 0%) patients.

291 pecific strategies used were associated with PD sex and the presence of under-represented minority tr

292 epigenome-wide significant associations with PD, including cg06690548 on chromosome 4.

293 produce several well-known associations with PD, to demonstrate the validity of a PRS and to demonstr

294 ased vaccine, NEO-PV-01, in combination with PD-1 blockade in patients with advanced melanoma, non-sm

295 The degree of insomnia correlates with PD severity and it responds to treatments that decrease

296 ssed in tumor cells and its interaction with PD-1 plays an important role in evading immune surveilla

297 activity in brain metastases from NSCLC with PD-L1 expression at least 1% and is safe in selected pat

298 hanges of the basal ganglia in patients with PD who underwent staged STN DBS.

299 y overall survival analysis in patients with PD-L1 immune cell-positive tumours, median overall survi

300 ance over 1, 2, and 4 years in patients with PD.

301 ut higher scores compared with patients with PD.

302 i during rest and movement in 37 people with PD undergoing DBS.

303 ecutive advanced cancer patient treated with PD-1/PD-L1 checkpoint inhibitors.