ライフサイエンスコーパス: presentation

1 (DCs) and promoted DC maturation and antigen presentation.

2 = 0.001) and less likely to have a monofocal presentation.

3 treatment resistance and defects in antigen presentation.

4 at first presentation and in the case of re-presentation.

5 nterocular disparity of the disease stage at presentation.

6 cant gastrointestinal disease were anemic on presentation.

7 e for lung macrophage protrusions in antigen presentation.

8 of infection did not alter antigenic peptide presentation.

9 , potentially indicative of impaired antigen presentation.

10 Presence of pain did not prompt earlier presentation.

11 ction biomarkers were determined at clinical presentation.

12 TEC-infected children without HUS at initial presentation.

13 cess to data and more effective analyses and presentation.

14 SARS-CoV-2 patient peaks just before symptom presentation.

15 studies with microbiome assessment after ASD presentation.

16 ents had bilateral bull's-eye maculopathy at presentation.

17 gth prediction models for endogenous peptide presentation.

18 leukopenia) characterize the most aggressive presentation.

19 little variation in other clusters of caries presentation.

20 d thymidylate synthase, enhanced DLBCL MHC-I presentation.

21 highlight that rtvFTD has a unique clinical presentation.

22 nslation initiation, cell cycle, and antigen presentation.

23 m >200 serum samples collected upon clinical presentation.

24 had distinctive retina-related VF defects at presentation.

25 istries in approximately half of patients on presentation.

26 major histocompatibility complex II (MHC-II) presentation.

27 patients had advanced or terminal disease at presentation.

28 ecialized for delivery of antigens for cross-presentation.

29 onal study with biological samples stored at presentation.

30 howed advanced glaucoma in at least 1 eye at presentation.

31 stly programmed for MHC-I and MHC-II antigen presentation.

32 years of age and showed no ocular issues at presentation.

33 m with lymph node resident DCs through cross-presentation.

34 tic movement disorder with variable clinical presentation.

35 esumably due to increased breadth of peptide presentation.

36 athogenesis and the highly variable clinical presentation.

37 iagnostic evaluations, depending on clinical presentation.

38 4 (67.5%) were found more than 6 weeks after presentation.

39 rial MRI scans over a median of 5 years from presentation.

40 l diagnosis in the case of atypical clinical presentation.

41 n 10%, and 2.5% had corneal complications at presentation.

42 education may promote earlier detection and presentation.

43 Cases with cleared infection had variable presentations.

44 conditions and in those with severe COVID-19 presentations.

45 ted rates (P < .001) for paper and non-paper presentations.

46 to assess demographic variables and clinical presentations.

47 ophrenia including heterogeneity in clinical presentations.

48 s there was considerable overlap in clinical presentations.

49 rd HIV-negative populations who have diverse presentations.

50 in the 2020 cohort showed worse median VA at presentation (1.00 logarithm of the minimum angle of res

51 Invasive pneumonia was the most common presentation (11 424/16 346 [69.9%]) and, overall, 67.0%

52 se with follow-up within 6 months of initial presentation (228 patients, 246 unique encounters) were

53 omen had lower rates of ST-segment elevation presentation (73.0% versus 78.7%), acute noncardiac orga

54 of CME regardless of foveola involvement at presentation (79% vs. 21%; P < 0.001), previous treatmen

55 ae genotype shift and its impact on clinical presentations, additional surveillance programs targetin

56 At the time of presentation after OGI, 64% of eyes showed light percept

57 the 3 PVN disease classes predicted clinical presentation, allograft function, and outcome independen

58 ersons, 7292 were hospitalized directly upon presentation; an additional 882 persons tested positive

59 orrhagic lesions with a more severe clinical presentation and a higher admission rate in intensive ca

60 21 patients had diplopia at presentation and all were improved after surgery.

61 cted, IFN-gamma induced genes involved in Ag presentation and antimicrobial defense.

62 (ISR) in the United States as well as on its presentation and appropriate treatment strategies.

63 dministered in 21.1% of low-risk episodes at presentation and at 7 days postpresentation, 72.3% of ep

64 as significantly reduced in eyes with RRD at presentation and at the most recent visit compared with

65 is challenging, because of the heterogeneous presentation and both mis- and underdiagnosis are common

66 dendritic cells that are essential for cross-presentation and CD8 T cell-mediated immunity against in

67 is not fully understood, and it may vary by presentation and clinical course.

68 The clinical presentation and course of the disorder have been extens

69 sive NP further strengthened the CTL epitope presentation and CTL responses.

70 In particular, the heterogeneous spectrum of presentation and disease severity in sepsis, as well as

71 actosylated WTA is required for InlB surface presentation and function, cellular invasiveness and pha

72 ptors in live cells, where the native glycan presentation and glycoprotein expression are preserved,

73 rovide important insights into antigen cross-presentation and have implications for development of ap

74 icator tube, and by WGS on isolates at first presentation and in the case of re-presentation.

75 and corrected visual acuity (VA) at initial presentation and last follow-up (up to 1 year) were the

76 the ER-resident MR1 pool and hampers antigen presentation and MAIT cell activation.

77 This study examined clinical presentation and management of a cohort of febrile Kenya

78 bacterium tuberculosis and influence disease presentation and outcome.

79 To examine presentation and outcomes of COVID-19 in patients with E

80 To better understand the contemporary presentation and outcomes of this disease, we analyzed c

81 otype, few co-occurring mutations, high-risk presentation and poor outcomes were specific to multi-hi

82 bial therapy depends on severity of clinical presentation and presence or absence of associated compl

83 integrating peptide features associated with presentation and recognition, we developed a model of tu

84 recurrent tumor cells that dampen DC antigen presentation and recruit innate-like CD8(+) T cells.

85 lcification had the same temporal pattern of presentation and resolution in mdx(betageo) and mdx musc

86 The atypical presentation and severe outcome among IMD-W cases could

87 y the bacterial factors involved in clinical presentation and severity of IMD-W cc11.

88 the impact of HBV/HIV co-infection on age at presentation and survival of HCC.

89 ht upregulation of genes involved in antigen presentation and T cell activation during EAU.

90 DRB expression and subsequently perturbed Ag presentation and T cell activation, higher TLR-mediated

91 that share several similarities in clinical presentation and vascular pathology.

92 ctive cohort study, we describe the clinical presentation and workup of parathyroid carcinoma (PC) an

93 This review summarizes presentations and discussions of some of the key points

94 ism in CDCS patients with different clinical presentations and identify possible brain metabolic phen

95 generate a comprehensive picture of clinical presentations and outcome of patients with Danon disease

96 erential impact of this pandemic on clinical presentations and outcomes in African Americans (AAs) co

97 he working group deliberated on the clinical presentations and used a 3-pronged approach to develop m

98 ates PH through complement, phagocytosis, Ag presentation, and chemokine/cytokine pathways.

99 ny key factors during antigen processing and presentation, and helped to solve several conundrums tha

100 L-10 and IL-6 were significantly elevated at presentation, and IL-6, IL-8 and TNF-alpha levels were h

101 rally engage innate immunity, induce antigen presentation, and mediate CD8 T cell priming against for

102 ociated with protein ubiquitination, antigen presentation, and mitochondrial dysfunction.

103 f their distinct etiologic factors, clinical presentation, and outcomes.

104 en LVEF, New York Heart Association class on presentation, and the end points of mortality and heart

105 After weighing evidence from the review, presentations, and public comments, an independent panel

106 , variation in immune activation and disease presentation are regulated by both host genetic diversit

107 actors influencing cognitive and psychiatric presentations are unknown.

108 We highlight phenotypic presentation as a reflection of pathogenesis and outline

109 re reviewed and data on age at detection and presentation as well as other clinical information was c

110 MOGAD patients differ in the clinical presentation at onset, showing an age-related shift in t

111 lationship between pathological and clinical presentation at single symptom level, including neuropsy

112 We searched for presentation biomarkers to identify such patients.

113 portion of patients who were not cultured at presentation but later required culturing decreased (13.

114 ompatible with lymph node homing and antigen presentation, but unexpectedly express both BDCA-2 and C

115 , W-TBP, is used to facilitate tumor antigen presentation by enabling immunogenic photodynamic therap

116 chanisms of evasion include impaired antigen presentation caused by mutations or loss of heterozygosi

117 pression signature of antigen processing and presentation, cell-cycle arrest, and execution phase of

118 stercoralis co-infection influenced clinical presentation, cerebrospinal fluid (CSF) inflammation, an

119 EVALI typically have a nonspecific clinical presentation characterized by a combination of respirato

120 the gene mutations leads to similar clinical presentations, characterized by increased susceptibility

121 We retrospectively reviewed clinical presentation, chemotherapy regimens, hematologic respons

122 on in a prospective manner to report patient presentation, clinical course, treatment, and outcomes i

123 d to understand the infection rate, clinical presentation, clinical outcomes, and transmission dynami

124 020 were reviewed for demographics, clinical presentation, comorbidities, and surgeries performed.

125 ctions including antibody secretion, antigen presentation, cytokine production, and generation of imm

126 We aimed to investigate whether neurological presentations differed according to the infecting arbovi

127 Case presentations drawn from actual clinical scenarios were

128 lity is caused by both the dominant clinical presentation, e.g. paralysis or tremor and additional sy

129 (BCVA), intraocular pressure (IOP), clinical presentation, eye culture results, and treatments perfor

130 bition of two negative regulators of antigen presentation, EZH2 and thymidylate synthase, enhanced DL

131 three major criteria: a compatible clinical presentation, finding nonnecrotizing granulomatous infla

132 body posture emerged shortly after stimulus presentation, followed by OMA selectivity.

133 ce in the likelihood of emergency department presentation for chest pain or hospital admission for AM

134 The median age at presentation for congenital cataracts that were noticed

135 Obstructive jaundice is an uncommon presentation for patients with HCC.

136 dence included longer duration of uveitis at presentation (for 2 to 5 years vs. less than 6 months: a

137 The presentation form of eating disorders might vary for men

138 neuron mechanisms for processing of stimulus presentation frequency in PPC.

139 however, these diseases have unique clinical presentations, genetics, and available therapies.

140 delines based on histopathology and clinical presentation, genomic classification enables earlier tre

141 At presentation he was febrile at 40.1 degrees C but hemody

142 ity pneumonitis (HP) is hampered by variable presentation, heterogeneous or undetected causal antigen

143 ity, and acceptability.Results: The clinical presentation, histopathology, and exclusion of alternati

144 ve response through (i) manipulating antigen presentation, (ii) repressing T cell-activating costimul

145 On presentation, IL-10 was elevated in mortality (P = .008)

146 n and exocytosis in beta cells to uptake and presentation in islets and peripheral sites.

147 ial for SteD to suppress both mMHCII antigen presentation in mouse dendritic cells and MHCII-dependen

148 itionally ablating MHC class I-restricted Ag presentation in targeted APC subpopulations.

149 int expression, as well as increased antigen presentation in tumor cells.

150 int expression, as well as increased antigen presentation in tumor cells.

151 ead, whereas tumor antigen transfer into and presentation in tumor-draining lymph nodes induce activa

152 rent disaccharidases with general GI symptom presentations in a large cohort of pediatric patients.

153 tion in humans, with a heterogenous clinical presentation including medical, behavioural and psychiat

154 We report new disease presentations, including atypical patterns of dystonia e

155 ving IABP on demographics, clinical history, presentation, infarct location, coronary anatomy, and cl

156 Clinical presentation, initial management decisions, and subseque

157 rials and Methods The demographics, clinical presentation, injuries, and radiologic findings of patie

158 on through the IL18-IL18RAP axis and antigen presentation involving HLA-DRB1, which might help to ide

159 th tumor antigen material for processing and presentation is a common strategy for stimulating antige

160 sents a diagnostic challenge as the clinical presentation is often blurred by concomitant autonomic a

161 Although the predominant clinical presentation is with respiratory disease, neurological m

162 Clinical presentation, laboratory values, immunosuppression, and

163 ents exhibited specific characteristics (ACS presentation, low use of invasive procedures, coronary a

164 c HLA class I (HLA-I) antigen processing and presentation machinery (APM) in therapy resistance.

165 ssociated with downregulation of the antigen-presentation machinery.

166 nd its wide spectrum of nonspecific clinical presentations makes dietary FB perforation extremely dif

167 This severe presentation may result from the virus using a virus rec

168 l acuity was better in the subsequent eye at presentation (mean, 20/62 vs. 20/149; P < 0.001) and pos

169 5.1%; P = .005) and had less severe clinical presentations (median Pitt score, 0 [interquartile range

170 increased markers of antigen processing and presentation; more lymphocytes and associated cytokines;

171 entially facilitates MHC class II-restricted presentation, negative selection, and increased Treg cel

172 D8(+) T cell clones as biosensors of antigen presentation, neither HDACi-treated CD4(+) T cell condit

173 The median age at presentation of 35 children was 26 days (interquartile r

174 with a mean (standard deviation [SD]) age at presentation of 35.2 (14.2) years, and mean refractive e

175 D3 and anti-CD28 antibodies) and the surface presentation of a cytokine (IL-2) on ICEp were shown to

176 After the presentation of a visual stimulus, neural processing cas

177 osomal frameshifting, and the generation and presentation of aberrant trans-frame peptides at the cel

178 d access to lymph nodes, optimal packing and presentation of antigens, and induction of a persistent

179 Because the most common presentation of BIA-ALCL is swelling of the breast with

180 years (range, 1-22 years), and median age at presentation of Coats-like exudative vitreoretinopathy w

181 mutation in NFKB1 leads to a severe clinical presentation of combined immunodeficiency.

182 The presentation of cysticercosis is very heterogeneous both

183 GILT facilitated MHC class II-restricted presentation of endogenous TRP1 by pooled thymic APCs.

184 Given the presentation of fevers, rashes, and mucosal symptoms obs

185 ling of the cell surface, increasing surface presentation of HLA proteins known to inhibit the activa

186 1/1947(H1N1) IAV significantly increased the presentation of HLA-B, -C, and -E on lung epithelial cel

187 Without Rab39a, MHC-I presentation of intraphagosomal peptides is inhibited, i

188 We describe a case of an adolescent presentation of Kawasaki Disease presenting with a predo

189 This case highlights a unique presentation of late stage appendiceal MAA.

190 Clinical presentation of LCV is variable and frequently mistaken

191 rans-Golgi network (TGN), is involved in the presentation of ligands from Mycobacterium tuberculosis

192 gnizing a breadth of important pathogens via presentation of microbial riboflavin metabolite Ags by M

193 onsistently lower for binaural than monaural presentation of modulated tones.

194 y should be strongly considered whenever the presentation of orbital myositis is not typical or when

195 nally derived exosomes predates the clinical presentation of Parkinson's disease (PD), offering a mea

196 Use of 18F-FDG-PET/CT at the initial presentation of patients with suspected PVE increases th

197 ion (PFDR = 0.02) and antigen processing and presentation of peptide antigen via MHC class I (PFDR =

198 This case report presents a rare presentation of PG with bilateral dense pigment deposits

199 ortantly, simultaneous delivery and activity presentation of protein antigen and nucleic acid ligands

200 r, and pharmacologic assays characterize the presentation of renal disease and enable useful pharmaco

201 a desire for clarity and objectivity in the presentation of results and are a prerequisite for the s

202 d physical structure of O-Ag are key for the presentation of specific epitopes within proteinaceous s

203 ia demonstrate considerable variation in the presentation of symptoms.

204 eptor loss were consistent with the clinical presentation of the affected siblings.

205 nfluenza was neither linked to a more severe presentation of the disease nor to a worse outcome.

206 Presentation of the familiar context, both in the absenc

207 Here, we investigate the role in antigen presentation of the ribosome-associated quality control

208 ound evidence that there are errors with the presentation of the standard deviations and statistical

209 Presentation of these HLA-abacavir-peptide complexes to

210 The autosomal dominant presentation of trichilemmal cysts is one of the most co

211 ivates GPR81 in dendritic cells and prevents presentation of tumor-specific antigens to other immune

212 d saccade trajectory curvature following the presentation of visual, auditory, and audiovisual distra

213 Different CMR presentations of ARVC are associated with different prog

214 that generalizable patterns exist in diverse presentations of critical illness.

215 single symptom-based subtype rather than all presentations of FND.

216 With the presentations of new concepts, this review opens for new

217 resent a full spectrum of individual patient presentations of pancreatic fistula risk, and to define

218 trongest early predictors (within 5 years of presentation) of secondary progressive MS at 30 years we

219 STEC-infected children, 41 (4.4%) had HUS at presentation; of the remaining 886, 126 (14.2%) develope

220 This is the first presentation on 8,395 low-risk patients treated in 2019.

221 antigens previously shown to be TAAs, their presentation on major histocompatibility complex classes

222 th MacTel 2, four years prior to the current presentation on the basis of an OCT demonstrating bilate

223 define the inhibition in LANA expression and presentation on the cell surface through MHC class I.

224 in cardiac troponin at the time of clinical presentation or during the hospitalization.

225 comorbidities such as classically syndromic presentation or immune deficiency are often present, in

226 have Foster stage 3 conjunctival scarring on presentation or worsening of scarring during follow-up,

227 was independently associated with fovea-off presentation (OR, 1.47, 95% CI, 1.24-1.74, P < 0.001) an

228 dvances in our understanding of its clinical presentation, pathomechanism and role of various tick sp

229 This suggests that the MHC-II antigen presentation pathway is required for PIV-mediated protec

230 es is the most selective step in the antigen presentation pathway.

231 lex class II (MHCII) antigen-processing and -presentation pathway.

232 e three bottleneck issues in the CTL epitope presentation pathway: vaccine uptake, phagolysosomal esc

233 tion of infected cells by disrupting antigen presentation pathways.

234 gradation enzymes, and disruption of antigen presentation pathways.

235 The mean time of presentation post injury was 33.85 +/- 27.5 and 40.6 +/-

236 ific conferences by uploading all conference presentations, posters, and abstracts to highly traffick

237 Striatal dopamine synthesis capacity at presentation predicts the subsequent worsening of sub-cl

238 on, considerable variation exists in disease presentation, progression and response to therapy, highl

239 illions of patients worldwide, with clinical presentation ranging from isolated thrombosis to acute r

240 Given the rapid presentation rate and absence of explicit instruction to

241 antibodies, suggesting a predominant antigen presentation role.

242 Eight weeks before this presentation, she had been traveling in Italy and had be

243 Four weeks before this presentation, she had presented to an emergency departme

244 ging was not available at the time of recent presentation, so comparison was made with gadolinium-enh

245 methods study evaluated how the content and presentation style of new information influences decisio

246 results, both for all CIDP and typical CIDP presentations, support a twofold increased relative risk

247 ney transplant recipients with COVID-19 have presentations that are similar to that of the general po

248 complex disease with heterogeneous clinical presentations that can affect virtually any organ.

249 1) subpopulation important for antigen cross-presentation, that CD40L-overexpressing CAR T cells elic

250 Consistent with late presentations, the mortality rate was high, whereas freq

251 e different types of epilepsy, the different presentations, the signs, the radiologic approach to man

252 Despite leading to similar clinical presentations, the underlying cardiac disease and precip

253 ation of its promoters and by inhibiting its presentation through interaction with the proteins of cl

254 icroglobulin (beta2M) and affects class I Ag presentation through sequestration of beta2M inside endo

255 the mother increases the likelihood of early presentation; thus, focused maternal education may promo

256 ptic shock with multiple organ failure up on presentation to emergency room.

257 -78) days, (P=0.017)], whereas the time from presentation to first intervention was significantly sho

258 ns that include antibody production, antigen presentation to T cells, costimulation, and the producti

259 a dominant pathway to load resident DCs for presentation to T cells.

260 by ligands with varying valency and mode of presentation to the B-cell receptor (BCR).

261 rly LUS findings (acquired within 24hours of presentation to the ED) between patient groups based on

262 onelderly) patients with COVID-19 at initial presentation to the emergency department (ED); outcomes

263 d, died, or discharged within 24 hours after presentation to the emergency department (study baseline

264 patients were treated within 24 hours after presentation to the emergency department, and 85.9% with

265 Hayes Agnew, and the presentation to the University of Thomas Eakins' remarka

266 ic acid architectures for multivalent ligand presentation to unravel the mechanisms of multivalency-e

267 This article will use 3 case presentations to discuss some of the new treatment chall

268 ould be tailored to the severity of clinical presentation, to comorbidities, and to the potential to

269 mong 10 SOT patients, including the clinical presentation, treatment modalities, and outcomes of 7 re

270 an analysis of the temporal trends, clinical presentation, treatment strategies, and in-hospital outc

271 olumes of symptomatic patients delayed their presentation until after lockdown.

272 The clinical presentation varies between adults and children based on

273 et of immunoevasins known to disrupt antigen presentation via MHC class I.

274 Ag presentation via the nonclassical MHC class Ib molecule

275 were measured from emergency department (ED) presentation vs discharge.

276 The median age of presentation was 10 months.

277 Mean time from surgery to presentation was 51 days (range, 4-137 days).

278 The median age at initial presentation was 72.5 years, and 33.3% were men.

279 Presence of TTV at presentation was associated with a higher rate of second

280 Older age at presentation was associated with higher incidence of rem

281 Presentation was commonly clinical or biochemical jaundi

282 Appendectomy within 16 hours of presentation was considered early, whereas those between

283 The primary reason for presentation was defective vision (55.2%) followed by ro

284 , the time from onset of symptom to clinical presentation was significantly longer [31(1-105) days vs

285 Breech presentation was the strongest determinant for PCS as we

286 ed sustained activation following visual cue presentation, was correlated with monkeys' behavior and

287 nts referred for ophthalmic care after an ED presentation were LTFU.

288 Eyes with delayed presentation were more likely to have conjunctival injec

289 ent appendectomy within 24 hours of hospital presentation were obtained from the American College of

290 Symptoms at presentation were similar between the two groups, althou

291 Etiologies and clinical presentations were similar between men living with and w

292 and absolute neutrophil count <5 x 109/L at presentation, which had a negative predictive value (NPV

293 ndicate that aberrant IAV RNAs stimulate HLA presentation, which may aid viral evasion of innate immu

294 inhibits its translation to control antigen presentation, which was supported by treatment of cells

295 nterpretation, and the different patterns of presentation, which will help orient the diagnosis.

296 patient characteristics mentioned above and presentation with advanced glaucoma.

297 active versus inactive lever, and pairing CS presentation with BLA-ChR2 photo-stimulation intensified

298 Detailed assessment at the point of presentation with CIS provides fewer clues to calculate

299 echocardiographic GLS by speckle tracking at presentation with ICI myocarditis (cases, n = 101) to th

300 ve lever or an active lever that produced CS presentation, without water delivery.