ライフサイエンスコーパス: PMA

1 PMA also increased internalization and accelerated recep

2 PMA also induced a 33% decrease in 5-bromo-2'-deoxyuridi

3 PMA and AJH-836 (a DAG-mimetic that preferentially activ

4 PMA doping over a limited depth of bulk heterojunction p

5 PMA significantly reduced tenting height, tenting area,

6 PMA treatment also caused impairments in insulin-signali

7 PMA treatment of human keratinocytes increases the synth

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

9 PMA-doped films show increased electrical conductivity a

10 PMA-induced Erk phosphorylation was reduced by ErbB2 inh

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

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

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

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 nomycin and phorbol 12-myristate 13 acetate (PMA) are used to trigger NETosis.

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

19 ivated with phorbol-12-myristate-13-acetate (PMA) and differentiated into M1 macrophages with IFNgamm

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

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

22 C activator phorbol 12-myristate 13-acetate (PMA) at 10 nM concentration reduced the intensity of alp

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

24 orbol ester phorbol 12-myristate 13-acetate (PMA) mimics CXCL12-mediated desensitization, internaliza

25 induced by phorbol 12-myristate 13-acetate (PMA) more effectively than SOPD-NAC and several control

26 ation using phorbol 12-myristate 13-acetate (PMA) on hERG channels expressed in human embryonic kidne

27 Phorbol 12-myristate 13-acetate (PMA) promotes skin cancer in rodents.

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

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

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

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

32 in vitro by phorbol-12-myristate-13-acetate (PMA) treatment to produce platelet-like-particles (PLPs)

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

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

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

36 atment with phorbol 12-myristate 13-acetate (PMA), ASP translocates to the cytoplasm and is detectabl

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

38 1 activator phorbol 12-myristate 13-acetate (PMA), which acts as a DAG mimetic.

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

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

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

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

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

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

45 pression of phorbol 12-myristate 13-acetate (PMA)/ionomycin-driven activation of a luciferase reporte

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

47 f NF-kappaB2 with phorbol myristate acetate (PMA) upregulated fermentative glycolysis and increased c

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

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

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

51 rbol ester (phorbol 12-myristate 13-acetate, PMA) to induce changes in gene expression in a lung canc

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

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

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

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

56 ated by the protein kinase C (PKC) activator PMA (phorbol 12-myristate 13-acetate) in Xenopus oocytes

57 N terminus (DeltaN 136 hERG) abolished acute PMA (30 nM, 30 minutes)-mediated I(hERG) reduction.

58 centrations in the cerebellum with advancing PMA, which was impaired in infants with brain injury on

59 atio (R -0.5, p value 0.0002) with advancing PMA.

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

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

62 lar domain was not efficiently cleaved after PMA stimulation.

63 larger than untreated control I(hERG) after PMA removal for 4 hours.

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

65 Of 709 eyes treated at or after PMA 36 weeks and 0 days, short-term RD risk did not diff

66 60% reduction in superoxide production after PMA stimulation compared with non-CF MDMs.

67 In addition, we show that after PMA treatment, ASP exits the nucleus and localizes on th

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

69 m infants with advancing post-menstrual age (PMA) and brain injury during ex-utero third trimester pr

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

71 s born less than 30 weeks postmenstrual age (PMA) and participating in the Neonatal Neurobehavior and

72 esults were stratified by postmenstrual age (PMA) at treatment as occurring before versus at or after

73 cal examination at median postmenstrual age (PMA) of 36 weeks (range: 32-43 weeks), 94% to 96% of plu

74 atment was made at a mean postmenstrual age (PMA) of 37w3d (95% CI, +/- 5d; range, 31w1d to 42w1d).

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

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

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

78 sessments beyond 36 weeks postmenstrual age (PMA).

79 ants born before 34 weeks postmenstrual age (PMA).

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

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

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

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

84 uce QEMSCAN Particle Mineralogical Analysis (PMA) to quantify the phase distribution in ash samples c

85 ar to those found in human skin cancers, and PMA promotes proliferation of human skin cells.

86 ies in response to stimulation with fMLF and PMA.

87 increased degranulation response to K562 and PMA/ionomycin but lower capacity to respond to human CMV

88 ture with perpendicular magnetic anisotropy (PMA) and one piezoelectric substrate.

89 Perpendicular magnetic anisotropy (PMA) ferromagnetic CoFeB with dual MgO interfaces is an

90 ility and perpendicular magnetic anisotropy (PMA).

91 value of perpendicular magnetic anisotropy (PMA).

92 ayer with perpendicular magnetic anisotropy (PMA).

93 of a weak perpendicular magnetic anisotropy, PMA.

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

95 permittivity-based phase metering apparatus (PMA).

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

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

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

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

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

101 ons between plants, microbes and arthropods (PMA).

102 ns between Plants, Microbes, and Arthropods (PMA): Impacts, Mechanisms, and Prospects for Sustainable

103 ns between plants, microbes, and arthropods (PMA): Impacts, mechanisms, and prospects for sustainable

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

105 However, the difficulty in attaining PMA in ultrathin CoFeB layers has imposed the use of thi

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

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

108 Among 458 eyes treated before PMA 36 weeks and 0 days, the short-term RD rate was high

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

110 ivation and transcriptional networks between PMA and DAG-lactones.

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

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

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

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

115 n, using FRET to detect robust activation by PMA that was absent during whole-cell patch clamp.

116 he possibility that induction of APOBEC3A by PMA causes genomic accumulation of uracils that may lead

117 Thermal hyperalgesia induced by PMA or burn injury in KI was identical to WT.

118 among the genes most prominently induced by PMA, an effect impaired by RNAi silencing of PKCalpha, b

119 in a pattern comparable with that induced by PMA.

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

121 hERG channels, chronic activation of PKC by PMA (30 nM, 16 hours) increased both Delta2-354 hERG and

122 ERG)) and I(Kr) Chronic activation of PKC by PMA (30 nM, 16 hours) increased I(Kr) in cardiomyocytes

123 Acute activation of PKC by PMA (30 nM, 30 minutes) reduced both hERG current (I(hER

124 tracellular reactive oxygen species (ROS) by PMA-stimulated HL-60D, whereas PgPE-untreated PDLSCs sup

125 With stimulation by PMA/ionomycin, TNF-alpha, or H(2)O(2), PBMCs from ulcera

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

127 Phenylmethylammonium lead chloride (PMA(2) PbCl(4) ) crystals are grown that exhibit a nonce

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

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

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

131 multiple examples of simple and more complex PMA interactions.

132 In contrast, PMA-evoked nocifensive responses and sensitization of ca

133 Similar to CXCL12, PMA promotes PKC-dependent phosphorylation of serine res

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

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

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

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

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

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

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

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

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

143 ction of differentiation with phorbol ester (PMA) and transduction with the full-length cDNA of GLS2.

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

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

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

147 ced expression of Gal-9 on T cells following PMA stimulation via protein kinase C suggests persistent

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

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

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

151 proteins; however, chronic (30 nM, 16 hours) PMA treatment decreased I(hERG), which became larger tha

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

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

154 cking of the non-growing B. bacteriovorus in PMA-differentiated U937 cells.

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

156 the crystal surface, the linear EO effect in PMA(2) PbCl(4) is reported and its EO coefficient is det

157 Overexpression of FENDRR in PMA-activated THP-1 cells increased the IFNgamma-induced

158 IFNgamma-induced phosphorylation of STAT1 in PMA-activated THP-1 cells.

159 re was little increase in genomic uracils in PMA-treated wild-type or uracil repair-defective cells.

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

161 RA- and SLE-IgG both increased PMA-induced beta(1) integrin-mediated adhesion to fibron

162 and progressively decreases with increasing PMA.

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

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

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

169 stability owing to the enhanced interfacial PMA that arises from the two CoFeB-MgO interfaces.

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

171 action of NETs released by freshly isolated, PMA-stimulated primary human neutrophils with primary hu

172 n gestational age (GA) of 25 weeks, and mean PMA of 33 weeks at first examination met study criteria.

173 ease developed in 10% of infants at a median PMA of 37 weeks, with the majority being bilateral and m

174 During September and October 2016, model PMA (mPMA) were produced from seawater by bursting bubbl

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

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

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

178 (v-dPCR) protocol using propidium monoazide (PMA) was developed, allowing for the first time the sele

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

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

181 rodevelopmental outcomes at 18 to 24 months' PMA.

182 rodevelopmental outcomes at 18 to 24 months' PMA.

183 Moreover, PMA downregulated the expression of collagen-encoding ge

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

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

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

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

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

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

190 macrophage differentiation in the absence of PMA.

191 etail as well as the evolutionary aspects of PMA interactions.

192 m-negative bacteria to improve the effect of PMA.

193 SK, S264A, and S264E prevented the effect of PMA.

194 rentiated into macrophages after 24 hours of PMA induction.

195 plication forks may explain the inability of PMA-induced APOBEC3A/APOBEC3B to increase genomic uracil

196 o enhance the dead bacterial permeability of PMA.

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

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

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

200 Finally, the use of PMA interactions for crop protection in sustainable plan

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

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

203 of human neutrophils and only mild effect on PMA-activated CL.

204 unts to alter grain metabolism and impact on PMA.

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

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

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

208 ber and the use of sodium dodecyl sulfate or PMA enhancer for Gram-negative bacteria to improve the e

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

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

211 the PMA supplement process, not as original PMAs.

212 duction of primary marine aerosol particles (PMA) at the sea surface via modulation of bubble surface

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

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

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

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

217 ese results suggest that the proinflammatory PMA is unlikely to promote extensive APOBEC3A/APOBEC3B-m

218 This study presents QEMSCAN PMA as a new resource to identify generation mechanisms

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

220 pectively, compared with coverslips or rigid PMAs.

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

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

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

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

225 e adjusted for recruitment site, infant sex, PMA, and tissue heterogeneity.

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

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

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

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

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

231 CoFeB layer is essential to obtain a strong PMA.

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

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

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

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

236 ofiling analysis using RNA-Seq revealed that PMA caused major changes in gene expression, whereas AJH

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

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

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

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

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

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

243 channel (PQAAAS-AQAP) did not influence the PMA-induced increase of potassium current.

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

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

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

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

248 received initial marketing approval via the PMA pathway.

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

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

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

252 The organism groups that contribute to PMA interactions are presented as well as types of inter

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

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

255 luciferase activity by DNAJB3 in response to PMA and TNF-alpha that was consistent with a decrease in

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

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

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

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

260 Unexpectedly, PMA treatment, but not APOBEC3A plasmid transfection, ca

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

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

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

264 1)H-MRS at median 33.0 (IQR 31.6-35.2) weeks PMA from a voxel placed in the cerebellum of 53 prematur

265 inal cohort of premature infants (<=32 weeks PMA, n = 188; Washington D.C).

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

267 Adding BPD status at 36 weeks PMA to the model did not change the accuracy (area under

268 equiring O2 (without restricting at 36 weeks PMA) improved the prediction of respiratory outcomes acc

269 inal cohort of premature infants (<=36 weeks PMA, n = 130; Bogota).

270 ograms were performed at 7 days and 36 weeks PMA.

271 hocardiogram and BPD assessments at 36 weeks PMA.

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

273 untreated eyes of infants at 36 +/- 1 weeks' PMA were compared with demographic data and clinical ROP

274 PS at a single time point of 36 +/- 1 weeks' PMA.

275 e of prior ROP treatment) at 36 +/- 1 weeks' PMA.

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

277 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

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

279 when type 1 ROP is treated before 36 weeks' PMA.

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

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

282 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

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

284 r recordings were obtained through 40 weeks' PMA.

285 increased by treatment of SH-SY5Y cells with PMA and it correlated with cell cycle arrest at G2/M, up

286 is particularly important for children with PMA between 36 and 38 weeks, which is considered to be t

287 1 monocyte cell line by differentiation with PMA and vitamin D3, respectively.

288 cells, when induced for differentiation with PMA, supported an enhanced viral replication.

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

290 5 years, mean LVEDD was 56.5 +/- 5.7 mm with PMA versus 60.6 +/- 4.6 mm with RA (mean change from bas

291 f chronically infected cells stimulated with PMA, and upon viral budding, ASP becomes a structural pr

292 nd to or protect neutrophils stimulated with PMA.

293 ulating CD8 + PD-1 + T cells stimulated with PMA/ionomycin as well as with HLA-A*24:02 CMV peptide wa

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

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

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

297 Following ex vivo stimulation with PMA/Ionomycin, PSC patients showed significantly increas

298 uman keratinocyte cell line was treated with PMA, both APOBEC3A and APOBEC3B gene expression increase

299 Treatment with PMA and ionomycin significantly prevented the decrease i

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

301 Of the 221 subjects (median, 27 wk PMA; interquartile range, 25-28 and 920 g; interquartile