ライフサイエンスコーパス: PSM

1 PSM of the PM10 was dominated by gypsum (36%), plagiocla

2 PSM-rich, nanometer-scale domains prefer to partition wi

3 PSMs are required for mobilizing lipoproteins, the TLR2

4 PSMs are small-peptide toxins that have recently been ch

5 PSMs have multiple functions in staphylococcal pathogene

6 PSMs reduced clathrin-mediated endocytosis and inhibited

7 All 14 PSMs passed the u-test with residuals between the gravim

8 etermine a CH(4) response for each of the 14 PSMs where the reproducibility of average measurement ra

9 One of the 14 PSMs, FF4288 at 1836.16 +/- 0.75 nmol mol(-1) (k = 1) am

10 Ultimately 14 of these 36 PSMs define a CH(4) standard suite covering the nominal

11 ber of matched peptide-spectrum-matches (958 PSMs) and identified links (446).

12 airs immune responses, our results support a PSM-dependent mechanism that allows for the development

13 sight into the structural features affecting PSM functions, we analyzed an alanine substitution libra

14 After PSM, patients were matched and included in benign and ma

15 After PSM, the 3-year survival rates and median survival were

16 ity toward secreted PSMs and defense against PSM-mediated bacterial interference.

17 2 is required for protection of mice against PSM-producing S. aureus.

18 Thirty-six CH(4) in dry air PSMs were prepared in 5.9 L high-pressure aluminum cylin

19 unction is responsible for the export of all PSMs, thus representing a single target for complete obs

20 ection was similar to that of the sum of all PSMs.

21 (SEC-1), and phenol-soluble modulin alpha3 (PSM-alpha3).

22 Although PSM cells oscillate autonomously, they coordinate with n

23 ody levels against Hla, Hld, PVL, SEC-1, and PSM-alpha3 may protect against sepsis in patients with i

24 spensable for initiation of PSM assembly and PSM curvature but required for PSM extension.

25 Interactions between cholesterol and PSM have a very particular character: hydrogen bonding b

26 rt to the notions that Agr functionality and PSM production play a major role in defining different f

27 y suggests the coordinated action of Hla and PSMs in host tissue during early pathogenesis, confirmin

28 clock reporter signal increases in anterior PSM cells and that the periodicity of reporter oscillati

29 1, encoding a Notch ligand, in the anterior PSM as a mechanism to specify posterior identity of somi

30 gradual slowing of the clock in the anterior PSM creates peaks of clock expression that are separated

31 ock, but is stably expressed in the anterior PSM during presomite patterning.

32 segmentation clock dynamics in the anterior PSM in developing zebrafish embryos using an in vivo clo

33 periodic expression of PAPC in the anterior PSM triggers rhythmic endocytosis of CDH2, allowing for

34 f the future somite boundary in the anterior PSM.

35 tions stop or are stabilized in the anterior PSM.

36 f DeltaD on the cell surface in the anterior PSM.

37 Second, the more appropriate PSM probability values that are produced by the threshol

38 moting formation of the Ssp2/Smk1 complex at PSMs.

39 IL-18) from keratinocytes and that S. aureus PSMs are necessary and sufficient to stimulate IL-18 rel

40 The amino acid sequences of S. aureus PSMs are well conserved with two exceptions, one of whic

41 The average PSM was 98.1% (95% CI, 97.3% to 98.6%) and increased wit

42 Even more intriguing methods that go beyond PSM are herein termed building block replacement (BBR) w

43 Notably, the course of sepsis caused by PSM-deficient S. aureus is similar in wild-type and TLR2

44 y, we also determined gel phase formation by PSM and DPPC in unsaturated PC mixed bilayers.

45 resence of DNA promotes amyloid formation by PSM peptides.

46 sis, the melting of the gel phases formed by PSM and DPPC in unsaturated PC mixed bilayers (at 45 mol

47 w that production of Hla can be modulated by PSM expression.

48 C, cholesterol is preferentially solvated by PSM.

49 stingly, the induction of tolerogenic DCs by PSMs appeared to be independent of mFPRs, as shown by ex

50 however, the signaling pathways modulated by PSMs remain elusive.

51 the modulation of the signaling pathways by PSMs was independent of the known receptor for PSMs, as

52 r perdeuterated or proton-based N-acyl chain PSM and PCer in our (2)H NMR studies has allowed the sep

53 d expression of GATA family members in chick PSM explants blocks induction of hedgehog-dependent gene

54 Cholesterol-PSM hydrogen bonding also locally modifies the hexagonal

55 to effectively generate a model to classify PSMs using decoy hits with increased sensitivity.

56 Comparing PSM with DPPC, we observed that PSM formed a gel phase w

57 parallel the melting of the major component (PSM) except at intermediate (20 and 30 mol %) fractions

58 rking in concert with T-box genes to control PSM formation in zebrafish, although the mechanism is un

59 strongly variable, quorum sensing-controlled PSM expression in biofilm microenvironments, whereas ove

60 how here that, in mice, Msgn1 alone controls PSM differentiation by directly activating the transcrip

61 ing the transcriptional programs that define PSM identity, epithelial-mesenchymal transition, motilit

62 Independent of the cold plasma device, PSM has noticeable advantage of being a flexible platfor

63 We report that directed PSM extension fails in many septin-mutant cells, and, fo

64 in phase transition temperature of equimolar PSM/Cer bilayers was revealed by differential scanning c

65 evels of PSMs were verified against existing PSMs in a balance of air or nitrogen with excellent agre

66 The existing PSMs had been used in a Consultative Committee for Amoun

67 h that on the freestanding membrane parts (f-PSM) under the exact same experimental conditions.

68 ully immobile, whereas those docked to the f-PSM were mobile with a mean diffusion coefficient of 0.4

69 For PSM/chol, L(beta)-L(o) coexistence occurs over the range

70 For PSM/POPC alone, coexistence of L(alpha) and L(beta) phas

71 assembly and PSM curvature but required for PSM extension.

72 h mobility, its validity is questionable for PSMs such as polyurethane foam disks and XAD-resin packe

73 Ms was independent of the known receptor for PSMs, as shown by experiments with DCs lacking the formy

74 Furthermore, PSMs facilitated dissemination from an infected catheter

75 e in a series of structures near the growing PSM, but previous studies noted only mild sporulation de

76 in vitro and in vivo and further implicates PSMs as important contributors to pathogenesis.

77 cells lacking LDs are severely defective in PSM growth and organization and display disrupted spindl

78 tegy is largely used for error estimation in PSM assessment.

79 Based on this finding, both H2O2 in PSM and the anti-cancer capacity of PSM can be significa

80 into the structure-function relationship in PSMs, our study identifies nontoxic PSMalpha3 derivative

81 ion may be satisfied when modeling uptake in PSMs in which chemicals have high mobility, its validity

82 Instead, PSM cells oscillate until they incorporate into somites.

83 Instead, PSMs penetrate the cell membrane most likely by transien

84 ures of mouse embryonic stem (ES) cells into PSM-like cells without the introduction of transgenes or

85 he gel phase, PCer becomes incorporated into PSM:PCer membranes with no evidence of pure solid PCer.

86 is sufficient to predictably switch isolated PSM cells from a quiescent to an oscillatory state in vi

87 We provide evidence that all known PSM classes participate in structuring and detachment pr

88 An S. aureus mutant lacking PSM expression exhibits a transcriptional delay in hla m

89 ration are found for lipid compositions: 25%<PSM<65%, 5%<chol<30-35%, 65%>POPC>10%, and confirmed by

90 athways are required in parallel to maintain PSM progenitor tissue.

91 in triplicate analysis in total 2602 matched PSMs and 1390 linked residue pairs at 5% false discovery

92 We created a propensity score matched (PSM) cohort and a low cardiovascular disease (CVD) risk

93 , 27.1%, and 84.1%, peptide spectra matches (PSMs) produce 17.4% (13.0%), 14.4% (11.5%), and 45.7% (3

94 t generate as many peptide spectrum matches (PSMs) as conventional bottom-up methods; however, UVPDnL

95 The peptide-spectrum matches (PSMs) must also be assessed by computational tools since

96 ies up to 70% more peptide-spectrum matches (PSMs), 40% more peptides, and 20% more proteins at the 0

97 mics, assertion of peptide-spectrum matches (PSMs), generation of consensus spectra and compilation o

98 Propensity score matching (PSM) analysis was used to identify 147 well-balanced pat

99 Moreover, propensity score matching (PSM) was employed in balancing baseline covariates.

100 Propensity score matching (PSM) was utilized.

101 vival models, and propensity score matching (PSM).

102 ete suite of new primary standard materials (PSMs) of N2O with synthetic air (O2/N2) as the balance g

103 A pressure-sensor matrix (PSM) with full dynamic range can accurately detect and s

104 spheric gas phase to passive sampling media (PSMs) is currently modeled using the two-film approach.

105 mpling rates and the passive sampler medium (PSM)-air partition coefficient (KPSM-A) were calculated

106 om ambient air to a passive sampling medium (PSM).

107 Both the CAP-stimulated medium (PSM) and the CAP-stimulated buffered solution (PSB) are

108 al years, the cold plasma-stimulated medium (PSM) has shown its remarkable anti-cancer capacity in pa

109 direct contacts with the prospore membrane (PSM) that is synthesized de novo during meiosis II to se

110 roducts become encased by prospore membrane (PSMs) and specialized, stress-resistant spore walls.

111 It is localized to prospore membranes (PSMs), the structures that engulf haploid cells during m

112 we employed planar pore-spanning membranes (PSMs) prepared on porous silicon substrates with large p

113 eparated continuous pore-spanning membranes (PSMs).

114 ion in tethered polymer-supported membranes (PSMs), which were obtained by vesicle fusion on a poly(e

115 tically expanded the unsegmented mesenchymal PSM while blocking somitogenesis and notochord different

116 ignals controls whether presomitic mesoderm (PSM) cells will adopt either a chondrogenic or lateral p

117 ate neural and paraxial presomitic mesoderm (PSM) cells, which are the respective progenitors of the

118 llator expressed within presomitic mesoderm (PSM) cells.

119 ed posteriorly from the presomitic mesoderm (PSM) during body formation.

120 mite formation from the presomitic mesoderm (PSM) is controlled by the "segmentation clock," a molecu

121 tes in each cell of the presomitic mesoderm (PSM), but the individual cells drift out of synchrony wh

122 ed somites bud from the presomitic mesoderm (PSM), in a process regulated by a genetic clock called t

123 , which derive from the presomitic mesoderm (PSM).

124 es from the mesenchymal presomitic mesoderm (PSM).

125 ocess from unsegmented, presomitic mesoderm (PSM).

126 thmically produced from presomitic mesoderm (PSM).

127 gnaling pathways in the presomitic mesoderm (PSM).

128 somites form from the pre-somitic mesoderm (PSM) in a periodic manner.

129 FS), prosulfuron (PS), primisulfuron-methyl (PSM) and triflusulfuron-methyl (TSM) in wine samples.

130 for determining particle surface mineralogy (PSM), which is a major control on PM toxicity in the lun

131 ethane (CH(4)) primary standard gas mixture (PSM) suite to support CH(4) measurement needs over a lar

132 trically assigned primary standard mixtures (PSMs) comprising carbon dioxide (CO2), methane (CH4), an

133 xide (CO2) in air primary standard mixtures (PSMs).

134 fication through postsynthetic modification (PSM) and postsynthetic exchange (PSE) processes.

135 Covalent postsynthetic modification (PSM) of metal-organic frameworks (MOFs) has attracted mu

136 can be tuned by postsynthetic modification (PSM) to introduce specific functionalities after their s

137 ccessed through post-synthesis modification (PSM) on the reactive moieties of the linkers and/or node

138 rystal structure of the photosensing module (PSM) from a seed plant Phy in the Pr state using the Phy

139 n is a member of the phenol-soluble modulin (PSM) peptide family.

140 S. aureus depends on phenol-soluble modulin (PSM) peptide toxins, which are known to attract and lyse

141 Phenol-soluble modulin (PSM) peptides are major pathogenicity factors of communi

142 d the staphylococcal phenol-soluble modulin (PSM) peptides as key contributors to these effects, as I

143 -level production of phenol-soluble modulin (PSM) peptides in response to the global virulence activa

144 pathic alpha-helical phenol-soluble modulin (PSM) peptides.

145 ere, we identify the phenol-soluble modulin (PSM) surfactant peptides as key biofilm structuring fact

146 ow production of the phenol-soluble modulin (PSM) surfactant peptides cause agglomerates to grow to e

147 S. aureus-expressed phenol-soluble modulin (PSM)alpha, a group of secreted virulence peptides, is re

148 r-controlled toxins phenol-soluble modulins (PSMs) and alpha-toxin and reduced production of PIA.

149 Phenol-soluble modulins (PSMs) are a family of peptides with multiple functions i

150 Phenol-soluble modulins (PSMs) are peptide toxins with multiple key roles in path

151 ith homology to the phenol-soluble modulins (PSMs) from Staphylococcus epidermidis.

152 e role of S. aureus phenol-soluble modulins (PSMs) in proinflammatory cytokine release and inflammati

153 the alpha class of phenol-soluble modulins (PSMs), which were previously implicated as important det

154 ence factors is the phenol-soluble modulins (PSMs).

155 ) phases occurs over the range 50-95.5 mol % PSM.

156 5 mol % PSM with 10 mol % chol, and 60 mol % PSM with 25 mol % chol.

157 ximately by the compositions 40 and 75 mol % PSM with 10 mol % chol, and 60 mol % PSM with 25 mol % c

158 % chol with endpoints at 50 and >/=77 mol % PSM.

159 n identifications resulted in up to 10% more PSMs, 15% more peptides, and 10% more proteins quantifie

160 It identifies more PSMs and peptides than the ion trap-based approach.

161 In this study, novel CA-MRSA PSM derivatives were discovered by the use of microbial

162 CA-MRSA PSMs contribute to skin infection and recruit and lyse n

163 In human neutrophils, PSMs exert their function by binding to the formyl pepti

164 d that the analyzed concentration of the new PSMs was less than the calculated gravimetric concentrat

165 opriate cylinder in which to prepare the new PSMs.

166 ctions of CO2, CH4, and N2O relative to NIST PSMs.

167 ge protein (LEP) complex required for normal PSM and wall biogenesis, and ectopic expression of the L

168 The novel PSM derivatives are compared with their parent full-leng

169 bonding between cholesterol and the amide of PSM rotates the tilt of the amide plane, which primes it

170 on for the future anti-cancer application of PSM.

171 H2O2 in PSM and the anti-cancer capacity of PSM can be significantly stabilized during the storage a

172 e learning curve on a series of 420 cases of PSM on the basis of rates of incomplete cytoreduction an

173 e, into DMEM can mitigate the degradation of PSM at 8 degrees C during 3 days of storage.

174 udy, we first reveal that the degradation of PSM is mainly due to the reaction between the reactive s

175 Currently, the largest disadvantage of PSM is its degradation during the storage over a wide te

176 matically compared the anti-cancer effect of PSM and PSB over pancreatic adenocarcinoma cells and gli

177 ring the CDH2-dependent epithelialization of PSM cells.

178 This work demonstrates the importance of PSM peptides in S. aureus-mediated inflammatory cytokine

179 ciated protein dispensable for initiation of PSM assembly and PSM curvature but required for PSM exte

180 o extremely large sizes owing to the lack of PSM expression under the specific conditions present in

181 a single target for complete obstruction of PSM production.

182 carbon chains in the liquid-ordered phase of PSM mixtures.

183 at oscillations are a collective property of PSM cells that can be actively triggered in vitro by a d

184 hanism leads to the progressive reduction of PSM size.

185 wnstream of Wnt3a as the master regulator of PSM differentiation.

186 s aimed to understand the biological role of PSM recognition by innate host defense.

187 Similar thermal stabilization of PSM-rich domains by the ceramides was observed in POPC b

188 to the nucleus to activate transcription of PSM genes.

189 Specifically, absence of PSMs in isogenic S. aureus psm deletion mutants led to s

190 Moreover, colocalization of PSMs and p38 was observed near the plasma membrane in th

191 nteractions is responsible for the effect of PSMs on biofilm structure.

192 In this study, we analyzed the effects of PSMs on signaling pathway modulation downstream of TLR2.

193 In this study, we analyzed the impact of PSMs on dendritic cells (DCs) playing an essential role

194 The first five levels of PSMs were verified against existing PSMs in a balance of

195 Streptococcus pyogenes, indicating a role of PSMs in the interference of S. aureus strains with the c

196 After the preparation of a new suite of PSMs at ambient level, they were compared to an existing

197 , they were compared to an existing suite of PSMs.

198 for more robust hydrogen bonding with other PSM.

199 ckground with pronounced production of other PSMs.

200 Compared to other PSMs, delta-toxin is usually more strongly expressed but

201 n biofilm microenvironments, whereas overall PSM production remained constant to ascertain biofilm ho

202 holesterol (chol), N-palmitoylsphingomyelin (PSM), and 1-palmitoyl-2-oleoylphosphatidylcholine (POPC)

203 holine (POPC) and/or palmitoylsphingomyelin (PSM), and in more complex bilayers also containing chole

204 Up to at least 50 mol % PCer, PSM and PCer mix ideally in the liquid crystalline phase

205 The PhyB PSM crystallized as a head-to-head dimer with strong str

206 he surrounding, disordered, cholesterol-poor/PSM-rich/DOPC-rich interdomain phase.

207 ately 1.5 times the periodicity in posterior PSM cells.

208 oscillatory Lfng expression in the posterior PSM (Lfng(FCE)) exhibit abnormal anterior development bu

209 levels of oscillatory Lfng in the posterior PSM are sufficient to support relatively normal posterio

210 Lfng oscillates in the posterior PSM as part of the segmentation clock, but is stably exp

211 lock activity is suppressed in the posterior PSM by FGF signaling until it crosses a determination fr

212 clock and wavefront system in the posterior PSM.

213 DeltaD on the cell surface in the posterior PSM; conversely, loss-of-function mutation of DeltaC inc

214 s secreted protease aureolysin in processing PSMs is demonstrated.

215 a3, a strongly cytolytic and proinflammatory PSM of Staphylococcus aureus with a significant contribu

216 of Msgn1 was sufficient to partially rescue PSM differentiation in Wnt3a(-/-) embryos, demonstrating

217 ts demonstrate that vesicles docked to the s-PSM were fully immobile, whereas those docked to the f-P

218 fusion on the supported parts of the PSMs (s-PSMs) with that on the freestanding membrane parts (f-PS

219 s of individual lipid mixing events on the s-PSMs revealed semi-stable post-fusion structures.

220 The same PSM was subsequently sent to the National Oceanic and At

221 A 100 x 100 large-scale PSM gives both electrical and optical signals by itself

222 ributed to producer immunity toward secreted PSMs and defense against PSM-mediated bacterial interfer

223 teins reconstituted in these phase-separated PSMs strictly partitioned into the l(d) phase.

224 phingomyelin (SM; palmitoyl and stearoyl SM (PSM and SSM, respectively)) and phosphatidylcholine (PC;

225 ermal behavior of N-palmitoyl sphingomyelin (PSM) and N-palmitoyl ceramide (PCer) mixtures in excess

226 system composed of palmitoyl sphingomyelin (PSM), cholesterol, and an unsaturated lipid (dioleoylpho

227 ternary mixtures of palmitoyl sphingomyelin (PSM), cholesterol, and either palmitoyl oleoyl phosphati

228 the analogs were able to thermally stabilize PSM, and a chain-length-dependent increase in the main p

229 So far, to stabilize PSM, it must be remained frozen at -80 degrees C.

230 proteasomes by inducing proteasome subunit (PSM) genes [1,2].

231 ves expression of a reporter in the tailbud, PSM and somites during somitogenesis.

232 the possibility that therapeutics targeting PSM production may simultaneously prevent Hla-mediated t

233 However, targeting PSMs for therapeutic intervention is hampered by their m

234 Comparing PSM with DPPC, we observed that PSM formed a gel phase with less order than DPPC at comp

235 Finally, we show that PSM processing occurs in multiple CA-MRSA strains by str

236 mFPR2 as well as its paralog mFPR1 and that PSMs are chemoattractants for DCs at noncytotoxic concen

237 In previous work, we demonstrated that PSMs in combination with TLR2 ligand from S. aureus indu

238 Our results indicate that PSMs function by disrupting interactions of biofilm matr

239 S. aureus wild-type strain, indicating that PSMs inhibit the production of these interleukins.

240 We show that PSMs secreted by S. aureus alter the host cell cycle, re

241 1 (Dll1) ligand vary dynamically across the PSM of both chick and mouse.

242 atiotemporal waves of expression, across the PSM.

243 The sampler housing and the PSM can introduce kinetic resistance to chemical uptake

244 h a stagnant air-side boundary layer and the PSM pores, and the reversible sorption onto the PSM.

245 the same type of PAS using XAD-resin as the PSM.

246 similar to that described previously for the PSM peptide toxins.

247 atic, and no displacement of sterol from the PSM environment was observed with 12:1- and 14:1-PCer.

248 nesis can be recapitulated in vitro from the PSM-like cells, providing an efficient, serum-free proto

249 r reduction of Lfng expression levels in the PSM does not increase disruption of anterior development

250 d chains via its smooth face, whereas in the PSM mixtures, cholesterol interacts preferentially with

251 e is one of the most common reactions in the PSM of MOFs.

252 863 HCV-positive and HCV-negative men in the PSM population.

253 that progressively lowers Lfng levels in the PSM.

254 olling supply and movement of cells into the PSM during gastrulation and tailbud outgrowth.

255 be the wavefront signal, which maintains the PSM in an undifferentiated state.

256 er area of the PSM but not the amount of the PSM because chemicals mainly accumulated in the outer la

257 onal to the interfacial transfer area of the PSM but not the amount of the PSM because chemicals main

258 mainly accumulated in the outer layer of the PSM during the deployment time of the PAS.

259 further evidence of the stabilization of the PSM gel state by PCer.

260 s mechanisms, but more potent members of the PSM peptide family may overshadow that impact in vivo.

261 In contrast, tethering of the PSM with oleic acid interfered with the phase separation

262 mobility to the geometric confinement of the PSM, because the drag force is increased substantially d

263 pores, and the reversible sorption onto the PSM.

264 ed by changes in R caused by positioning the PSM at different distances from the opening of the sampl

265 Using spray drying, we show the PSM of two MOFs, the amine-terminated UiO-66-NH2 and the

266 ed by the air boundary layer surrounding the PSM because that layer was deemed to be the main factor

267 y pattern of gene expression that sweeps the PSM in a caudal-rostral direction.

268 g wave of cyclic gene expression through the PSM that has a periodicity equal to that of somite forma

269 ave slows as it moves anteriorly through the PSM, although the dynamics of clock slowing have not bee

270 ssive waves of Notch activity throughout the PSM.

271 The kinetics of chemical sorption to the PSM from the gas phase in the macro-pores is a knowledge

272 uctural and functional similarities with the PSM family of toxins.

273 on that engages multiple features within the PSM to stabilize the Pr and Pfr end states after rotatio

274 to those mass transfer processes within the PSM.

275 The PSMs harbor the t-SNARE DeltaN49-complex to investigate

276 e that chemicals distribute uniformly in the PSMs.

277 We observe that N-AgrD, like the PSMs, is found in the amyloid fibrils of S. aureus biofi

278 ing and fusion on the supported parts of the PSMs (s-PSMs) with that on the freestanding membrane par

279 d-shaped lo domains within the center of the PSMs.

280 lo) domains in the freestanding parts of the PSMs: (i) immobile domains that were attached to the por

281 ed to be used to gravimetrically prepare the PSMs, adjusting the calculated mole fraction for the los

282 Mass transfer of chemicals through the PSMs may be subject to a large resistance because of the

283 coherent probability values assigned to the PSMs.

284 Thus, PSMs from highly virulent pathogens affect DC functions,

285 Thus, PSMs from S. aureus directly modulate the signaling path

286 Conversely, administration of BMP signals to PSM or forced expression of GATA family members in chick

287 ht result in the specific vulnerabilities to PSM and PSB.

288 astoma cells were specifically vulnerable to PSM and PSB, respectively.

289 CA-MRSA virulence determinants (alpha-toxin, PSM alpha, Agr) in that isolate for in-vitro and in-vivo

290 CRS and HIPEC to treat PSM has a steep learning curve requiring 140 procedures

291 CRS and HIPEC to treat PSM is a complex procedure with a significant morbidity.

292 Typically, PSM is carried out on pendant functional groups or throu

293 Using PSM development as a guide, we establish conditions for

294 Using PSM, adults aged 50-64 years (but not other age groups)

295 opening of the sampler housing and by using PSM of different diameters.

296 chol mixtures, nor for ternary mixtures with PSM content <24 mol %.

297 PCer formed sterol-excluding gel phases with PSM, reducing the overall bilayer affinity of sterol.

298 s, cholesterol interacts preferentially with PSM via its rough face.

299 As a consequence, treatment with PSMs impaired the capacity of DCs to induce activation a

300 ture for the assembly of l(o) domains within PSMs into defined structures by binary micropatterning o