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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

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