ライフサイエンスコーパス: PMA

1 PMA also increased internalization and accelerated recep

2 PMA doping over a limited depth of bulk heterojunction p

3 PMA significantly reduced tenting height, tenting area,

4 PMA treatment also caused impairments in insulin-signali

5 PMA, but not DiC8, targeted PKCalpha to detergent-resist

6 PMA- and BzATP-stimulated increases in [Ca2+]i were addi

7 PMA-doped films show increased electrical conductivity a

8 PMA-induced Erk phosphorylation was reduced by ErbB2 inh

9 PMA-induced shedding of Tim-3 was abrogated by deletion

10 PMA-induced shedding was abrogated by an ADAM (A disinte

11 PMA-stimulated ERK activity was also inhibited by 1-buta

12 PMA/Ionomycin treatment of DOCK8-deficient NK cells resc

13 In the presence of rCIL-2, PMA plus ionomycin or Con A stimulated CD4(+)CD25(+) cel

14 Image characteristics at 34 PMA weeks or earlier independently predict TR-ROP.

15 eine treatment or usual care (controls) at a PMA of at least 34 weeks but less than 37 weeks.

16 n electron-rich aldehyde and 5-methoxy-ABAO (PMA), which was observed at pH 4.5, places this reaction

17 tations in both CRE and kappaB fully abolish PMA-activated MIE gene expression.

18 obtained by phorbol 12-myristate 13 acetate (PMA) treatment.

19 lon), while phorbol 12-myristate 13-acetate (PMA) activation of PKCepsilon drives inducible TSPO expr

20 li, such as phorbol-12-myristate-13-acetate (PMA) and androgens, but show differential responses to s

21 D69 in 12-O-tetradecanoylphorbol 13-acetate (PMA) and Ionomycin stimulated Jurkat cells.

22 response to phorbol 12-myristate 13-acetate (PMA) and ionomycin stimulation.

23 reated with phorbol 12-myristate 13-acetate (PMA) and ionomycin, which signal via protein kinase C (P

24 ernatant or phorbol 12-myristate 13-acetate (PMA) from inducing NETosis.

25 e show that phorbol 12-myristate 13-acetate (PMA) immediately activates the expression of HCMV MIE RN

26 bination of phorbol 12-myristate 13-acetate (PMA) plus ionophore A23187 (Io), which induces NFAT acti

27 sponsive to phorbol 12-myristate 13-acetate (PMA) reactivation in the absence of CYLD, indicating tha

28 C activator phorbol 12-myristate 13-acetate (PMA) stimulated apoE secretion, and both PMA-induced and

29 release by phorbol-12-myristate-13-acetate (PMA) stimulation was demonstrated using T-47D human brea

30 tivation by phorbol 12-myristate 13-acetate (PMA) than cells isolated by conventional mucolytic metho

31 ivated with phorbol-12-myristate-13-acetate (PMA) were added back into whole blood, the extent and ra

32 nists (e.g. phorbol 12-myristate 13-acetate (PMA)) indicate that prolonged stimulation leads to PKCal

33 ork we used phorbol 12-myristate 13-acetate (PMA), a well recognized agonist of classical and non-con

34 opoietin or phorbol 12-myristate 13-acetate (PMA), alphaIIbbeta3 became activated as evidenced by bin

35 orbol ester phorbol 12-myristate 13-acetate (PMA), but not by ionomycin.

36 activator, phorbol 12-myristate 13-acetate (PMA), in primary HUVECs was found to require PKCeta- and

37 e (ATP) and phorbol 12-myristate 13-acetate (PMA), results in a cation influx via P2X(4) receptors at

38 peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activity was down regulated and this i

39 1 activator phorbol 12-myristate 13-acetate (PMA), which acts as a DAG mimetic.

40 h H2O2- and phorbol 12-myristate 13-acetate (PMA)-induced decrease in TRPC6 protein expression.

41 le of PK in phorbol 12-myristate 13-acetate (PMA)-induced megakaryocytic differentiation in human leu

42 h basal and phorbol 12-myristate 13-acetate (PMA)-induced MMP13 promoter activity; conversely, Ankrd1

43 h basal and phorbol 12-myristate 13-acetate (PMA)-induced NADPH oxidase activity were increased in Ra

44 itutive and phorbol 12-myristate 13-acetate (PMA)-induced ubiquitination of the receptor at the cell

45 r naive and phorbol 12-myristate 13-acetate (PMA)-stimulated conditions are reliably measured.

46 vated using phorbol-12-myristate-13-acetate (PMA).

47 ith LPS and phorbol 12-myristate 13-acetate (PMA).

48 C isoforms, phorbol 12-myristate 13-acetate (PMA).

49 uced with 4-phorbol 12-myristate 13-acetate (PMA).

50 promoted by phorbol 12-myristate 13-acetate (PMA).

51 oduction of phorbol 12-myristate 13-acetate (PMA)/ionomycin-stimulated human peripheral blood mononuc

52 cell operating on phorbol myristate acetate (PMA) activated THP-1 human monocytic cells.

53 ts of CXCL8 after phorbol myristate acetate (PMA) or cytokine treatment.

54 th the ability of phorbol myristate acetate (PMA) to promote FLNB-mediated cytoplasmic accumulation o

55 fluidic device to phorbol myristate acetate (PMA), a known promoter of oxidative burst, and the produ

56 nregulated during phorbol myristate acetate (PMA)-induced monocyte-to-macrophage differentiation, whi

57 n stimulated with phorbol myristate acetate (PMA).

58 Using phorbol myristate acetate (PMA)/ionomycin and anti-CD3 activation of CD4(+)CD25(-)

59 timulation (phorbol 12-myristate 13-acetate [PMA] plus ionomycin).

60 by phorbol ester (phorbol myristate acetate [PMA]) reduced insulin-induced p-Tyr-IRS2 by 46% +/- 13%

61 nases in response to phorbol myristate acid (PMA), H(2)O(2), UV, and anisomycin stimulation.

62 icacious, we conjugated polymannuronic acid (PMA), containing the blocks of mannuronic acid conserved

63 Poly(mandelic acid) (PMA) is an aryl analogue of poly(lactic acid) (PLA) and

64 yoxometalate solution (phosphomolybdic acid, PMA) in nitromethane.

65 articles grafted with poly(methyl acrylate) (PMA) chains anchored by a maleimide-anthracene cycloaddu

66 l activity was mimicked by the PKC activator PMA, occurred without activation of PKA, and persisted i

67 but was inhibited by the PKC-theta activator PMA, or by CD28 crosslinking, which enhances PKC-theta a

68 In addition, PMA, which activates other transcription factors require

69 he T-cell receptor (TCR) but does not affect PMA-activated interleukin 2 (IL-2) secretion.

70 ent HEK293 cells failed to shed IL-23R after PMA stimulation, demonstrating that ADAM17 but not ADAM1

71 lar domain was not efficiently cleaved after PMA stimulation.

72 mediated increase in IEC wound closure after PMA stimulation was mediated by increased cell spreading

73 und in primary human CD14(+) monocytes after PMA and ionomycin stimulation.

74 60% reduction in superoxide production after PMA stimulation compared with non-CF MDMs.

75 A] = 32.3 weeks) and at term-equivalent age (PMA = 40.2 weeks).

76 of BPD or PH at 36 weeks post-menstrual age (PMA) is unknown.

77 -36 weeks and 37-42 weeks postmenstrual age (PMA).

78 gers starting at 32-weeks postmenstrual age (PMA).

79 without BPD at 36 weeks' postmenstrual age (PMA).

80 TI) scans, early in life (postmenstrual age [PMA] = 32.3 weeks) and at term-equivalent age (PMA = 40.

81 (imaged from 30-36 weeks postmenstrual age [PMA]); 78% of term-aged preterm infants (imaged from 37-

82 Circulating platelet-monocyte aggregates (PMAs), p-selectin expression (P-SEL), and integrin alpha

83 However, although PMA potently down-regulated PKCalpha, prolonged activati

84 erellins (GA) in pre-maturity alpha-amylase (PMA) formation in developing wheat grain, two glasshouse

85 ectively activate PKD2, and endothelin-1 and PMA activate both PKD1 and PKD2.

86 actor required for Th17 differentiation, and PMA markedly stimulated the expression of Stat3 in WT bu

87 ies in response to stimulation with fMLF and PMA.

88 Both Ing3A and PMA activated extracellular signal-regulated kinase 1/2

89 Ing3A and PMA both induced acute neutrophilic inflammation on mous

90 Both naive and PMA plus ionomycin-stimulated thymic CD4(+)CD25(+) cells

91 mulated by uridine-5'-triphosphate (UTP) and PMA, agonists inducing LB fusion with the PM, but not ac

92 ayer with perpendicular magnetic anisotropy (PMA).

93 ility and perpendicular magnetic anisotropy (PMA).

94 value of perpendicular magnetic anisotropy (PMA).

95 undersizing restrictive mitral annuloplasty (PMA) associated with complete surgical myocardial revasc

96 permittivity-based phase metering apparatus (PMA).

97 ion HF Monitoring System premarket approval (PMA) application.

98 isk to patients, via the Premarket Approval (PMA) pathway.

99 therapy devices, via the premarket approval (PMA) process, during which manufacturers submit clinical

100 through various kinds of premarket approval (PMA) supplements.

101 rug Administration (FDA) Premarket Approval (PMA).

102 of poly(dimethylsiloxane) micropost arrays (PMAs) with tunable mechanical rigidities.

103 high-profile recalls of devices approved as PMA supplements.

104 canoylphorbol-13-acetate (TPA, also known as PMA).

105 TAT3 knockdown also reduced basal as well as PMA-induced Tspo mRNA levels in NIH-3T3 cells.

106 round the nucleus after stimulation with ATP/PMA was performed.

107 3, not NFATc1, NFATc2, or NFATc4, attenuated PMA/Io-induced REDD1 expression.

108 metformin and AICAR significantly attenuated PMA-induced monocyte-to-macrophage differentiation and p

109 t-mediated uptake requires macrophages to be PMA-primed, untreated cells phagocytose nonopsonized sil

110 lls with the protein kinase C activator beta-PMA and concomitantly decreases PMA-elicited SERT phosph

111 al evidence supporting the interplay between PMAs and CRP in patients with VTE.

112 CD300f also binds PMA/ionomycin-activated splenocytes and Ag-stimulated T

113 te (PMA) stimulated apoE secretion, and both PMA-induced and apoAI-induced apoE secretion were inhibi

114 tobacillus rhamnosus strain GG inhibits both PMA- and Staphylococcus aureus-induced formation of NETs

115 ocks transcriptional activation of SOCS-3 by PMA.

116 induced NF-kappaB, or NF-kappaB activated by PMA or MyD88 overexpression, whereas a mutant protein la

117 PKC activation by PMA promoted surface ErbB2 clearance but without degrada

118 on, and viable cell quantities determined by PMA real-time PCR were approximately 10(4) greater than

119 and this inhibition was further enhanced by PMA and p38 kinase inhibitors reversed this inhibition.

120 Tregs expanded by PMA or in the presence of CN inhibitors maintain Treg ph

121 Downregulation was not induced by PMA-ionomycin, or prevented by PI3K inhibition, implicat

122 in a pattern comparable with that induced by PMA.

123 o cAMP signaling, including ERK induction by PMA, and ERK activation and neuritogenesis induced by NG

124 of dopamine neurons after internalization by PMA, compared with vehicle or amphetamine treatment.

125 Stimulation with CD3/CD28, PMA/ionomycin, or latency reversing agents prostratin an

126 TE had a significant increase in circulating PMAs and CRP post-operatively, compared to those without

127 study to identify that increased circulating PMAs and CRP levels are early markers associated with po

128 uantifying the anthracene-containing cleaved PMA polymers, which are generated via retro-[4 + 2] cycl

129 Subjecting the corresponding PMA (>30 kDa) chains to ultrasound at 0 degrees C result

130 secondary motor cortex: the premotor cortex (PMA) and the accessory motor area (SMA).

131 cal IDR-1002 treatment successfully dampened PMA-induced ear edema, proinflammatory cytokine producti

132 d1 overexpression in control cells decreased PMA-induced MMP13 promoter activity.

133 tivator beta-PMA and concomitantly decreases PMA-elicited SERT phosphorylation.

134 nding sites were required for ERK-dependent, PMA-stimulated SOCS-3 gene activation.

135 play bryostatin-like behavior, WN-1 displays PMA-like behavior in U937 cell attachment and proliferat

136 racene/phorbol 12-myristate 13-acetate (DMBA/PMA) treatment developed in sites of preexisting hyperem

137 guided PK-dependent metabolic changes during PMA induction, which are important in megakaryocytic dif

138 In addition to metabolic effects, PMA treatment also translocated PKM2, but not PKR, into

139 C-theta, or WT PKC-theta activated by either PMA or TCR cross-linking, stimulated expression of a luc

140 protein kinase C (PKC) by the phorbol ester PMA has been shown to down-regulate cell surface DAT.

141 tor region is inducible by the phorbol ester PMA, a potent activator of the protein kinase C (PKC) pa

142 n contrast, the PKC-activating phorbol ester PMA, often used as a strong inducer of ADAM17, causes no

143 ivation of gene expression by phorbol ester (PMA).

144 Activating PKC with the phorbol ester, PMA, enhanced Ca(2+) entry, and potentiated stimulus-evo

145 f the Nox4 TM and Nox2 DH domains, exhibited PMA-dependent activation that required coexpression of r

146 y at 5 years, but freedom from MACCE favored PMA in the last year of follow-up.

147 isk therapeutic devices approved via the FDA PMA pathway, total product life cycle evidence generatio

148 TRPM5 was required for PMA and ATP-induced secretion of MUC5AC from the post-Go

149 n with self-MHC class II is not required for PMA-induced Treg proliferation.

150 lement, is both necessary and sufficient for PMA-induced transactivator activity in PAI-2-expressing

151 Further, PMA-induced ATP production reduced greatly upon PK silen

152 BV-transformed B cell lines (resting and 6 h PMA stimulated) and purified CD4(+) and CD8(+) T cells.

153 ed under controlled conditions in the highly PMA-susceptible genotype Rialto.

154 In PMA/alphaCD3-activated Jurkat T cells, MPTP opening and

155 iated by the reduction of ADAM17 activity in PMA stimulated cells although the expression ADAM17 is n

156 ession of TIMP-1 and gelatinases activity in PMA stimulated cells.

157 Changes in PMA and CRP in VTE patients were significantly correlate

158 ariety of HIV-1 stimulating agents including PMA and TSA.

159 D1 mRNA and protein expression and increased PMA/Io-mediated REDD1 promoter activity.

160 and progressively decreases with increasing PMA.

161 n rate determined by the culture-independent PMA-qPCR method (1.5-log removal at 664 mg.min/L) was lo

162 ion in response to oxidative stress inducers PMA or soluble cigarette smoke extract.

163 cule C-reactive protein (CRP), which induces PMA formation in vitro, along with plasma d-dimer and fi

164 extracts and rACP were also able to inhibit PMA-induced formation of NADPH oxidase complex on PMN me

165 f c-Jun N-terminal kinase activity inhibited PMA-induced inflammation but not differentiation, sugges

166 ore expressed by Escherichia coli, inhibited PMA-induced generation of reactive oxygen species (ROS)

167 ly, silencing of PK (PKM2 and PKR) inhibited PMA-induced megakaryocytic differentiation, as revealed

168 al-I, and found that this strongly inhibited PMA-induced apoptosis.

169 s which modifications occurred after initial PMA) and median number of supplements approved per devic

170 We find that interfacial PMA in the three-layer structures comes from both the Mg

171 developed and applied a propidium monoazide (PMA) real-time PCR assay to quantify viable (with PMA) a

172 technique combined with propidium monoazide (PMA) to simultaneously detect viable Legionella pneumoph

173 live cells was based on propidium monoazide (PMA) treatment to selectively remove DNA from membrane-c

174 at the combination of a propidium monoazide (PMA) treatment with haRPA, the so-called viability haRPA

175 lled organisms, we used propidium monoazide (PMA), a DNA-binding dye that penetrates damaged bacteria

176 home, at 1 year, and at age 18 to 24 months' PMA and neurodevelopmental assessments at 18 to 24 month

177 evelopmental assessments at 18 to 24 months' PMA did not differ between groups.

178 rodevelopmental outcomes at 18 to 24 months' PMA.

179 rodevelopmental outcomes at 18 to 24 months' PMA.

180 Moreover, PMA treatment increased the association of p65 with hist

181 d sensitivity, this newly invented multiplex PMA-qPCR assay took a much shorter time than did convent

182 The sensitivity of the multiplex PMA-qPCR assay achieved two colony-forming units (CFU) p

183 The viable multiplex PMA-qPCR assay was further successfully applied to patho

184 onstitutive endocytosis in dopamine neurons, PMA induces ubiquitination of DAT and leads to accumulat

185 FcepsilonRI-mediated degranulation, but not PMA/ionomycin-induced degranulation, as shown by beta-he

186 macrophage differentiation in the absence of PMA.

187 Conjugation of PMA to FLA appears to be a promising path for developing

188 n (representing chromatin decondensation) of PMA-treated serpinb1-deficient neutrophils compared with

189 rentiated into macrophages after 24 hours of PMA induction.

190 FAT-mediated T-cell activation in a model of PMA-elicited peritonitis, whereas topical application of

191 o enhance the dead bacterial permeability of PMA.

192 mulated CD4+ T cells and immune responses of PMA/ionomycin stimulated CD4+ T cells by FACS analysis p

193 ession or its inactivation on the surface of PMA-treated monocytes reduced the extent and rate of clo

194 The trend of PMA variation with different capping materials agrees we

195 proval of panel-track supplements (a type of PMA supplement pathway that is used for significant chan

196 The variation of PMA with different capping materials is attributed to th

197 y either method, at mid-grain development on PMA in mature grains.

198 unts to alter grain metabolism and impact on PMA.

199 s and these cells expressed CXCL8 protein on PMA stimulation.

200 Compared with RA only, PMA exerted a long-term beneficial effect on left ventri

201 ulated with IFNgamma, TNFalpha, alphaFas, or PMA/alphaCD3, in the presence or absence of CsA.

202 tes of internalized DAT after amphetamine or PMA treatment.

203 using the calcium ionophore ionomycin and/or PMA on Jurkat T cells, we show that the gene expression

204 Upon exposure to bacteria or PMA, protein kinase C activity in Slamf8(-/-) MPhis is i

205 with a median of 50 supplements per original PMA (interquartile range [IQR], 23-87).

206 ears (IQR, 8-20), and 79% of the 77 original PMAs approved during our study period were the subject o

207 the PMA supplement process, not as original PMAs.

208 lated the number of supplements approved per PMA and analyzed trends relating to different supplement

209 und a mean (SD) of 2.6 (0.9) supplements per PMA per year.

210 matched against 10 patients with persistent (PMA) microalbuminuria.

211 thway, we treated MKs with polymethacrylate (PMA), which markedly increased MARCKS phosphorylation wh

212 Moreover, bryostatin 1 prevented PMA-induced PKCdelta peripheral translocation.

213 ven at high concentrations, and it prevented PMA-induced apoptosis in these cells.

214 ells to serum, lipids, or the tumor promoter PMA suppressed formation of these complexes.

215 WC1 cytoplasmic domain significantly reduced PMA-induced endocytosis in both cell types and enhanced

216 pectively, compared with coverslips or rigid PMAs.

217 We used the FDA's PMA Database to identify and characterize initial approv

218 mic devices initially approved via the FDA's PMA pathway between January 1, 1979 and December 31, 201

219 st ophthalmic devices approved via the FDA's PMA pathway have undergone extensive revisions, includin

220 Poly(methyl acrylate)s (PMAs) of varying molecular weights were grown from a [4+

221 es accounted for birth gestational age, sex, PMA, dose of analgesics/sedatives (fentanyl, morphine, m

222 m hPSCs within 23 days of culture using soft PMAs were improved more than fourfold and tenfold, respe

223 The preparation of stereoregular PMA was realized using a pyridine/mandelic acid adduct (

224 CH 23390, but the infusion of PKC stimulator PMA does not.

225 stimulator Sp-cAMP or of the PKC stimulator PMA.

226 he NETosis pathways induced by five stimuli; PMA, the calcium ionophore A23187, nigericin, Candida al

227 CoFeB layer is essential to obtain a strong PMA.

228 FDA approved 77 original and 5829 supplement PMA applications for CIEDs, with a median of 50 suppleme

229 oes not rely on its relocalisation, but that PMA-induced PKC activity drastically dysregulates the lo

230 It is found that PMA treatment not only elevates the average protease act

231 We found that PMA treatment of wounded IEC monolayers resulted in 5.8+

232 Given that PMA-mediated apoptosis is thought to result from up-regu

233 We observed that PMA treatment decreased cancer-type anabolic metabolism

234 Further mechanistic analysis revealed that PMA fails to promote phosphorylation of Bad in Ser(112)

235 ophoretic mobility shift assay revealed that PMA stimulated DNA binding activity of NF-kappaB.

236 We show that PMA, C. albicans and GBS use a related pathway for NET i

237 ite-specific mutational analysis showed that PMA increased serine phosphorylation at three sites on I

238 matin immunoprecipitation assays showed that PMA treatment induced p65 binding to the TRPC6 promoter.

239 Further experiments showed that PMA, but not its inactive analog 4alpha-phorbol 12, 13-d

240 The PMA effect was specifically mediated by PKCbetaII, as it

241 The PMA response is also partially attenuated by the RNAi-me

242 The PMA-dependent IkappaBalpha phosphorylation was significa

243 The PMA-FLA conjugate was highly immunogenic in mice and rab

244 its inhibition significantly diminished the PMA-induced increase in wound closure.

245 Importantly, the PMA-FLA conjugate vaccine did not elicit antibodies that

246 Ejection fraction was 44.1 +/- 6% in the PMA group versus 39.9 +/- 3.9% in the RA group (mean cha

247 ion of the underlayer via suppression of the PMA by a critical ion-irradiation step.

248 this paper, we investigate the origin of the PMA in MgO/CoFe/metallic capping layer structures by usi

249 tive AMPKalpha2 mutant (S491A) prevented the PMA-induced reduction in AMPK activity.

250 oved 168 original ophthalmic devices via the PMA pathway and 2813 subsequent modifications.

251 received initial marketing approval via the PMA pathway.

252 tly used by clinicians were approved via the PMA supplement process, not as original PMAs.

253 ammatory mechanisms of IDR-1002 in vivo, the PMA-induced mouse ear inflammation model was used.

254 Furthermore, the PMAs in the CoFe/capping layer interfaces are analyzed t

255 This PMA-qPCR assay is useful as a rapid 3-day first- and sec

256 ruginosa, but nonetheless rabbit antibody to PMA-FLA showed evidence of protective efficacy against b

257 coli or Staphylococcus aureus, as well as to PMA.

258 nors with inhibitors of molecules crucial to PMA-induced NETs including protein kinase C, calcium, re

259 4-3-3-binding site S312, whereas exposure to PMA led to phosphorylation of PDE3A2 at an alternative 1

260 t not unmodified PKCdelta, was refractory to PMA-stimulated T(505) phosphorylation, similar to PKCdel

261 pression, and calcium release in response to PMA and CF pathogens.

262 his cytokine from LNCaP cells in response to PMA.

263 eptor CD4, WC1 is endocytosed in response to PMA.

264 H547A displays a differential sensitivity to PMA- or BIM-induced activation or inhibition of DAT func

265 rked reactivation of HIV latency, similar to PMA stimulation.

266 erformed on samples that were not subject to PMA treatment.

267 Pepsilon) in MCF-7 cells and MDA-MB-231 upon PMA, FGF, and serum stimulation, which depended on EGFR

268 of CD63 and CD203c in mononuclear cells upon PMA stimulation, suggesting a role in sensitization to a

269 ted during monochloramine disinfection using PMA-pyrosequencing, while the community structure appear

270 ity on the U937 cells to confirm that it was PMA-like for growth and attachment, as predicted by the

271 ations at 7 days of age (early) and 36 weeks PMA (late).

272 hocardiogram and BPD assessments at 36 weeks PMA.

273 ged preterm infants (imaged from 37-42 weeks PMA); 49% of term infants; and 39% of adult subjects.

274 At 37-42 weeks PMA, preterm infants had larger vCD and vCDR than term i

275 ot improve survival without BPD at 36 weeks' PMA or respiratory and neurodevelopmental outcomes at 18

276 me at less than 90% Sao2 at 35 and 36 weeks' PMA was 106.3 (89.0) and 100.1 (114.6) s/h, respectively

277 Survival without BPD at 36 weeks' PMA was similar between the placebo and inhaled nitric o

278 ginally below their peak values at 37 weeks' PMA (AOR, 1.8; 95% CI, 1.3-2.6; AUC, 0.743).

279 decreased significantly from 35 to 39 weeks' PMA (P = .01).

280 ory impairment, the AOR and AUC at 40 weeks' PMA (AOR, 1.5, 95% CI, 1.0-2.1; AUC, 0.740) were only ma

281 In particular, oxygen/RS at 40 weeks' PMA was identified as the best predictor for serious res

282 r recordings were obtained through 40 weeks' PMA.

283 covalently linked to a high molecular weight PMA.

284 (n) < 20 kDa, (ii) for high molecular weight PMAs (M(n) > 60 kDa) featuring terminal cycloaddition ad

285 phages, we treated U937 monocytic cells with PMA, which stimulates both macrophage differentiation an

286 1 monocyte cell line by differentiation with PMA and vitamin D3, respectively.

287 in culture medium, whereas incubations with PMA, TNF-alpha, IL-13, or IL-4 enhanced levels of C3 1.7

288 Stimulation of Raw 264.7 macrophages with PMA augmented the amount of mu1A associated with anti-L-

289 5 years, mean LVEDD was 56.5 +/- 5.7 mm with PMA versus 60.6 +/- 4.6 mm with RA (mean change from bas

290 uman polymorphonuclear cells stimulated with PMA did not bind to zymosan or E. coli, but when incubat

291 ected to in vitro mitogenic stimulation with PMA and ionomycin.

292 expressed on NK cells, and stimulation with PMA or N-ethyl-maleimide resulted in the shedding of Fcg

293 HIV mRNA and protein after stimulation with PMA/ionomycin and latency-reversing agents (LRAs).

294 Activation of PKC-theta with PMA promoted Th17 differentiation in wild type (WT) but

295 Treatment with PMA and ionomycin significantly prevented the decrease i

296 In contrast, treatment with PMA or ionomycin alone induces chromatin remodeling at f

297 Treatment with PMA/Io increased expression of the goblet cell different

298 Treatment with PMA/Io increased REDD1 promoter activity and increased N

299 real-time PCR assay to quantify viable (with PMA) and total (without PMA) E. coli O157:H7 cells on gr

300 uantify viable (with PMA) and total (without PMA) E. coli O157:H7 cells on growth chamber and field-g