ライフサイエンスコーパス: PPD

1 PPD and ManLAM specifically down-regulated CCR2 expressi

2 PPD and relative clinical attachment level (rCAL) improv

3 PPD and the protein cocktails tested induced strong DTH

4 PPD correlated negatively with phenolics and carotenoids

5 PPD is an enzymatically mediated oxidative process with

6 PPD is an inhibitory feedback mechanism that prevents ex

7 PPD is the most common reason for revision with adjustab

8 PPD limits cassava's marketing possibilities in countrie

9 PPD proteins interact with KIX8 and KIX9, which act as a

10 PPD selectively delivered polyIC into PSMA-overexpressin

11 PPD-exposed skin is associated with extensive transcript

12 PPD-modified HSA triggered T-cell responses through a cl

13 PPD-specific immune recovery was lower, whereas levels o

14 PPD-specific isotype/subclass, PPD-specific antibody-dep

15 PPD-specific T cell clones readily trafficked to the air

16 PPD/polyIC invokes antitumor immunity, but unlike many i

17 ter (DP: 430/784, 54.5%; PD: 269/611, 44.0%; PPD: 255/565, 45.1%) than the hospitals of the highest v

18 matitis on day 4 after patch testing with 1% PPD in petrolatum.

19 A total of 70 PPD-specific and 10 PPD-HSA-specific CD4+, CD8+, and CD4+CD8+, Th2-secreting

20 Lymphocytes from 10 PPD-allergic patients, but not tolerant/naive individual

21 meters CAL gain -0.248 mm (-0.618 to 0.122), PPD Reduction -0.397 mm (-0.810 to 0.015), GR Change 0.0

22 A total of 70 PPD-specific and 10 PPD-HSA-specific CD4+, CD8+, and CD4

23 stinguishable from DTH responses driven by a PPD injection.

24 ifty-three out of 72 (73.6%) M2 presenting a PPD >= 4mm at baseline healed at 6 months recall without

25 rence risk of postpartum AD for women with a PPD hospital contact after first birth was 55.4 per 100

26 n the skin of patients with severe ACD after PPD exposure.

27 c target-6, culture filtrate protein-10, and PPD as stimulatory antigens were undertaken, and cytokin

28 gene expression, scopoletin accumulation and PPD symptom development.

29 in biopsies at 8 and 48 h after allergen and PPD challenges, respectively, from 10 allergic rhinitics

30 led human infection model using live BCG and PPD is feasible and safe.

31 levels had no significant impact on CAL and PPD improvements in teriparatide patients at 1 yr, but i

32 ulted in significant improvements in CAL and PPD.

33 +) or perforin(+) Vgamma2Vdelta2 T cells and PPD-specific IFNgamma(+)alphabeta T cells.

34 nal effects on both long-term depression and PPD were eliminated by treatment with an mGluR1-selectiv

35 ET) was also observed during dye-doping, and PPD was detected with a limit of detection (LOD, 3sigma)

36 The proliferative capacity of HIV- and PPD-specific responses increased after 1 year of ART.

37 l corticotropin-releasing hormone (pCRH) and PPD incidence has been hypothesized, but empirical evide

38 ve individuals, were stimulated with PPD and PPD-modified HSA.

39 40 clones were stimulated with both PPD and PPD-modified HSA.

40 Many of the up-regulated and PPD-specific expressed sequence tags were predicted to p

41 cs to generate an extensive cassava root and PPD proteome.

42 ark and BCG-Japan induced more BCG scars and PPD reactions than BCG-Russia.

43 measured showed similar improvement such as PPD reduction, CAL gain, IBD reduction and defect resolu

44 cyanide-induced oxidative stress as well as PPD control strategies involving inhibition of ROS produ

45 stablished a reliable method for image-based PPD symptom quantification and used label-free quantitat

46 Means were adjusted for baseline PPD, education, and cigarette pack-years, and time-depen

47 percentage of sites with gingival bleeding, PPD, CAL, D, M, and F with adjustment for confounders.

48 n total, 40 clones were stimulated with both PPD and PPD-modified HSA.

49 of the murine CES2 homologue, was induced by PPD.

50 II (carcinogenic dye), which was oxidized by PPD doped in P-CNDs.

51 rgets of PPD2, being negatively regulated by PPDs and KIX8/9.

52 he most common complication of childbearing, PPD has a prevalence of 13%, but there are no widespread

53 e top discriminatory features, with combined PPD IgG titers and Fc domain glycans providing the highe

54 le without interfering with the conventional PPD-based surveillance.

55 Plasma Proteome Database (PPD) was initially described in the year 2005 as a part

56 a/gamma (PAPalpha/gamma)-mediated RNA decay (PPD) pathway and an ARS2-dependent decay pathway.

57 BPN1- and PAPalpha/gamma-mediated RNA decay (PPD) pathway and an ARS2-mediated decay pathway.

58 additional gene candidates to further delay PPD.

59 e peroxidase in storage roots showed delayed PPD and reduced lipid peroxidation as well as decreased

60 Polyphenylene dendrimers (PPDs) represent a unique class of dendrimers based on th

61 We show that this time-dependent PPD evasion by late transcripts requires the host factor

62 Postpartum depression (PPD) affects approximately 10-18% of women in the genera

63 Postpartum depression (PPD) is associated with abnormalities in resting-state f

64 Postpartum depression (PPD) is common and has serious implications for the moth

65 ctively predictive of postpartum depression (PPD) when modeled in antenatal blood.

66 all women experience postpartum depression (PPD), which for many is their first psychiatric disorder

67 a prodromal state for postpartum depression (PPD), with severe PPB strongly associated with an elevat

68 e of GABA undergoes paired-pulse depression (PPD) that recovers in <1 min (single exponential time co

69 s well as increased paired-pulse depression (PPD).

70 Probing pocket depth (PPD) was measured by calibrated examiners.

71 with >= 6 mm residual probing pocket depth (PPD) were included and randomly assigned to one of three

72 missing teeth (M), periodontal pocket depth (PPD), attachment loss (AL), and gingival bleeding in add

73 ary variables included probing pocket depth (PPD), bleeding on probing (BoP), gingival margin level,

74 Probing pocket depth (PPD), clinical attachment level (CAL) and gingival reces

75 l parameters including Probing pocket depth (PPD), Clinical attachment level (CAL) and Horizontal pro

76 Clinical measurements, probing pocket depth (PPD), clinical attachment level (CAL), plaque index (PI)

77 rushes and flossing on probing pocket depth (PPD), plaque indices, and bleeding on probing (BOP) meas

78 bleeding index (GBI), probing pocket depth (PPD), tooth mobility (TM), and alveolar bone height.

79 mm vs. 0.92 mm, p < 0.01) and probing depth (PPD) reduction (0.43 mm vs. 1.83 mm, p < 0.01) than vita

80 post-therapy clinical (probing pocket depth [PPD], clinical attachment level [CAL], gingival recessio

81 months was based upon probing pocket depths (PPD), clinical attachment levels (CAL), and whole-mouth

82 ccumulation for purified protein deritative (PPD)-specific T effector cells producing IFN-gamma durin

83 efore and after purified protein derivative (PPD) and mannosilated lipoarabinomannan (ManLAM) stimula

84 Purified protein derivative (PPD) is a widely used reagent for the diagnosis of Mycob

85 gous T-Regs and purified protein derivative (PPD) preprimed T-Reg-depleted effector cells.

86 G reactions and purified protein derivative (PPD) responses (secondary outcomes).

87 G reactions and Purified Protein Derivative (PPD) responses (secondary outcomes).

88 reby tuberculin purified protein derivative (PPD) was injected into the skin and the local T cell res

89 glutinin (PHA), purified protein derivative (PPD), and T cell epitope peptides derived from merozoite

90 Fab domain, and purified protein derivative (PPD)- and Ag85A-specific IgG from subjects with latent (

91 -incubated with purified protein derivative (PPD)-driven peripheral blood-derived effector cells.

92 atients but not purified protein derivative (PPD)-negative or PPD-positive healthy control subjects,

93 Purified protein derivative (PPD)-specific immune recovery was determined by interfer

94 -4 or -7/8, or purified protein derivative (PPD).

95 cific antigens (purified protein derivative [PPD] and ESAT-6/CFP10), followed by polychromatic flow c

96 evelopment of pigmented purpuric dermatosis (PPD).

97 no postharvest physiological deterioration (PPD) compared to controls and lines with high DMC and st

98 of postharvest physiological deterioration (PPD) in cassava roots.

99 oot postharvest physiological deterioration (PPD) is directly correlated with starch content.

100 id post-harvest physiological deterioration (PPD) of its roots that occurs within 24-72 h of harvest,

101 pid postharvest physiological deterioration (PPD) of the root is a major constraint to commercial cas

102 id post-harvest physiological deterioration (PPD) response that can occur within 24-72 h of harvest.

103 pid postharvest physiological deterioration (PPD) that occurs within 72 h following harvest.

104 rom postharvest physiological deterioration (PPD).

105 Sixteen women developed PPD symptoms.

106 o control (mean percentage point difference [PPD]: DEV vs control, -2.2 [90% CI, -8.0 to 3.49], P = .

107 These responses consistently displayed PPD.

108 rs, SD 16.7; range 26 to 81) and mean distal PPD at baseline of 7 mm was more likely to be associated

109 e cell types in the posterior pars distalis (PPD), and fewer melanotropes in the posterior region of

110 This disynaptic PPD is independent of mGluR-mediated plasticity and depl

111 PAZ/PIWI domain (PPD) proteins carrying small RNAs (sRNAs) function in ge

112 AtTIFY4B has three domains (PPD, TIFY and CCT_2) conserved between homologs from dif

113 Pentyl PABC-Doxaz (PPD) is a Doxaz carbamate prodrug that is hydrolyzed by

114 Pentyl PABC-Doxaz (PPD) is a prodrug of Doxaz that is activated by carboxyl

115 We designed a nonviral vector, PEI-PEG-DUPA (PPD), comprising polyethylenimine-polyethyleneglycol (PE

116 gnificantly higher in the non-atopics during PPD-induced responses (P = 0.003).

117 Degradation of starch granules during PPD was also detected.

118 lvement in the discoloration observed during PPD.

119 owed significant abundance regulation during PPD.

120 in several genotypes of cassava roots during PPD.

121 with Progressive Pseudorheumatoid Dysplasia (PPD).

122 rder progressive pseudorheumatoid dysplasia (PPD).

123 heir expression, KSHV late transcripts evade PPD through the activity of the host factor NRDE2.

124 cumulative numbers of teeth with PPD events (PPD > 3 mm) at each dental examination and the slopes as

125 nerable groups, such as women who experience PPD as a first psychiatric episode.

126 cells by glutamatergic neurons that express PPD, and these are likely to correspond to local neurons

127 Following PPD challenge CD3(+)STAT4(+)cells and CD3(+)T-bet(+)cell

128 ystems were significantly shrunken following PPD/polyIC treatment, in all cases.

129 with 6.2% for DP, 8.3% for PD, and 5.7% for PPD in the 5-year observation period.

130 terase (hiCE) as the agent of activation for PPD.

131 There were 132 cases for PPD requiring surgical intervention before September 201

132 antidepressants and/or hospital contact for PPD within 6 months after childbirth.

133 oximately 100-fold reduction in the IC50 for PPD compared to cells lacking the carboxylesterase.

134 These data reveal a mechanism for PPD in cassava based on cyanide-induced oxidative stress

135 on reprogramming exists in those at risk for PPD.

136 and treatment of pregnant women at risk for PPD.

137 trongly associated with an elevated risk for PPD.

138 control = -2.1 +/- 1.3 mm) and similarly for PPD; the difference between groups was not significant.

139 t subsequently required revision surgery for PPD were assessed and compared with those that did not.

140 e data identify Cys as the single target for PPD-HSA binding, and show that PPD protein adducts are a

141 itive and specific early diagnostic test for PPD symptoms.

142 s non-inferior results in terms of CAL gain, PPD reduction, GR increase and DBL gain in comparison wi

143 , was observed in percentage of both healthy PPDs (pockets < 5 mm) and converted pockets (sites no lo

144 frequent BoP and a higher number of healthy PPDs.

145 rcadian gene expression rhythms and identify PPD as an ELF3 co-ortholog, termed ELF3b Genetic interac

146 Drug-induced PPD is distinct from idiopathic PPD, and it is important to consider isotretinoin as a p

147 In PPD-stimulated peripheral blood mononuclear cells, MPA a

148 Primary study outcomes were changes in PPD, CAL, GR, and bone fill.

149 The delay in PPD in transgenic plants was also observed under field c

150 ter connectivity with the rest of the DMN in PPD (peak voxel: MNI coordinates (2, 58, 32), p = 0.002)

151 Plasma allopregnanolone was higher in PPD (p = 0.03) and positively correlated with intra DMPF

152 cantly enriched the proteomic information in PPD.

153 reviously identified as dominant proteins in PPD were tested for the capacity to induce delayed-type

154 more effective in gain in CAL, reduction in PPD and achieving greater bone fill as compared with tre

155 howed that the observed greater reduction in PPD and BOP in persons using interdental brushing than i

156 nths, statistically significant reduction in PPD in Group 1 and Group 2 was evident.

157 The mean reduction in PPD, CAL and HPD was 1.85 +/- 0.59 mm, 1.9 +/- 0.64 mm a

158 en starch/dry matter content and its role in PPD and canopy architecture traits in cassava.

159 accharides and may play an important role in PPD delay.

160 to cortical GABA concentrations and RSFC in PPD as compared to healthy comparison women (HCW).

161 Incident PPD occurred in 5.1% and 1.3% of women and men, respecti

162 Drug-induced PPD is distinct from idiopathic PPD, and it is important

163 t with other described cases of drug-induced PPD.

164 first reported case of isotretinoin-induced PPD.

165 in pull-down assays to identify interacting PPD products.

166 Six-month M2 PPD improved at disto-vestibular (T0-5.2/T1-3.0 mm) and

167 Since many PPD-expressing dorsal horn neurons respond to noxious st

168 entage of sites with gingival bleeding, mean PPD, AL, F, and either gastritis, the presence of oral o

169 ndation did not achieve noninferiority (mean PPD: DEV vs control, 0.9 [90% CI, -4.9 to 6.7], P = .23

170 rmal weight) were associated with worse mean PPD (p < .005), percentage of PPD > 4 mm (p = .01), but

171 e, we demonstrate that in two murine models, PPD was effective at slowing tumor growth and demonstrat

172 mporal expression of its genes by modulating PPD activity.

173 > 0.14-0.39 or > 0.39 cm/yr experienced more PPD events than men in the lowest tertile (</= 0.14 cm/y

174 lb during follow-up) had significantly more PPD events than men in the lowest tertile of weight gain

175 uberculosis purified protein derivative (Mtb PPD) in UK adolescents, but not in Malawian adolescents.

176 We hypothesized that Mtb PPD-induced IFN-gamma after BCG vaccination would be sim

177 UK infants had an IFN-gamma response to Mtb PPD, compared to 41 (53%) of 78 of Malawian infants, in

178 were recognized by T-cells from in-vitro Mtb-PPD and ESAT6/CFP10-positive donors by proliferation and

179 ate Tetrahymena thermophila encodes numerous PPD proteins exclusively of the Piwi clade.

180 of 106 Da, corresponding to the addition of PPD and not to the secondary products of self conjugatio

181 Recently, the molecular composition of PPD was defined, with hundreds of mycobacterial protein

182 torage and were correlated with the delay of PPD.

183 major functional role in the development of PPD symptoms, rather than merely paralleling symptom dev

184 posure to PPD is frequent, but the effect of PPD exposure in nonallergic occupationally exposed subje

185 We sought to investigate the effects of PPD exposure on the skin of occupationally exposed subje

186 an epidermis was used to test the effects of PPD in vitro.

187 The potent antitumor effects of PPD/polyIC should spur its development for clinical use.

188 The frequency of PPD-specific interferon gamma (IFNgamma) secreting cells

189 However, the molecular identity of PPD has so far remained elusive.

190 In contrast, inactivation of PPD has more widespread effects, including premature acc

191 biochemical events during the initiation of PPD is a rapid burst of reactive oxygen species (ROS) ac

192 s to define the nature of the interaction of PPD with the protein and the antigenic determinant that

193 grouped samples according to their levels of PPD and chemical compositions.

194 between pea ELF3 genes suggest that loss of PPD function does not affect flowering time in the prese

195 ation was associated with a delayed onset of PPD by 14 to 21 d after harvest of greenhouse-grown plan

196 ith worse mean PPD (p < .005), percentage of PPD > 4 mm (p = .01), but not with FMBS (p > .05) or CAL

197 these specific products drive the potency of PPD remains in question.

198 resulted in a cross-sectional prediction of PPD status with an AUC of 0.81 (95% CI: 0.68-0.93, p=0.0

199 is sensitivity enable accurate prediction of PPD.

200 25 weeks' GA, pCRH was a strong predictor of PPD symptoms (R(2) = 0.21; beta = 0.46 [P < .001]), an e

201 Presentation of PPD to several clones was dependent on protein complex f

202 Younger women are at higher risk of PPD after LAGB surgery than men and women older than 50

203 Main Outcome Measure Symptoms of PPD were assessed at a mean (SD) of 8.7 (2.94) weeks aft

204 trategies that allow for the modification of PPDs at the core, scaffold, and surface to introduce num

205 w is aimed to demonstrate the versatility of PPDs through their site-specific chemical functionalizat

206 nd the effects of changing hormone levels on PPD biomarker loci.

207 The optimal PPD and BCG dose was 0.5 TU and 10(4) cfu, respectively,

208 vitro stimulation with either Antigen-mix or PPD jhonin, than PBMC from MAP316F vaccinated animals.

209 urified protein derivative (PPD)-negative or PPD-positive healthy control subjects, demonstrating its

210 pylorus-preserving pancreatoduodenectomies (PPD) performed between 2011 and 2015.

211 e axons was counted in paraphenylenediamine (PPD)-stained sections and compared between EphB mutants

212 f rodents stained with paraphenylenediamine (PPD).

213 Here, we characterized PEAPOD (PPD) proteins, the only transcriptional regulators known

214 of the regioisomeric pairs MME/MEM, PPE/PEP, PPD/PDP, EEP/EPE and DDP/DPD (M=14:0, P=16:0, E=20:5, D=

215 nting with moderate to severe periodontitis (PPD = 5 to 8 mm) in at least 2 pockets per contralateral

216 In contrast, IFN- gamma responses to PHA, PPD, and Plasmodium falciparum MSP-1 peptides did not si

217 Accordingly, kix8 kix9 mutants phenocopied PPD loss-of-function producing larger leaves resulting f

218 an electrodeposited poly-m-phenylenediamine (PPD) layer and an R. gracilis D-amino acid oxidase (RgDA

219 A polymer, poly-o-phenylenediamine (PPD) layer was electropolymerized onto a 50 um Pt wire t

220 was to determine whether p-phenylenediamine (PPD) and/or Bandrowski's base (BB) stimulate T cells fro

221 p-Phenylenediamine (PPD) is a strong contact allergen used in hair dye that

222 Exposure to p-phenylenediamine (PPD) is associated with the development of T-cell-mediat

223 ocytes after exposure to p-phenylenediamine (PPD).

224 A fourth pea locus, PHOTOPERIOD (PPD), also contributes to the photoperiod response in a

225 Preaxial polydactyly (PPD) is a common limb-associated birth defect characteri

226 nterior limb bud and a preaxial polydactyly (PPD) skeletal phenotype.

227 echanism that leads to preaxial polydactyly (PPD).

228 utine practice, all 875 adults with positive PPD skin test results at pre-employment examinations per

229 or TB screening of individuals with positive PPD skin test results.

230 a from purified protein derivative-positive (PPD+) healthy subjects confirms its expression only duri

231 high-risk women, we prospectively predicted PPD status in an independent N=51 women using first trim

232 at the HP1BP3 and TTC9B genes that predicted PPD with an area under the receiver operator characteris

233 ugh the dynorphin precursor preprodynorphin (PPD) was only present in 4-7% of VGLUT2 boutons in lamin

234 atients were 41 times more likely to present PPD >= 4 mm after healing (OR = 41.4; 95% CI = 10.9 to 1

235 inotecan, a clinical CES2-activated prodrug, PPD produced no visible gastrointestinal damage.

236 en synthetic achievements that have produced PPDs with a range of polarities that break the hydrophob

237 eveloped via introduction of protoporphyrin (PPD, a photosensitizer) which has great doping affinity

238 , CRY2, ELF4, GHD7, VGT1, HY1/SE5, TOC1/PRR7/PPD-1, PIF3, ZCN8, and ZCN19.

239 release with NMDA receptors, did not reduce PPD.

240 hione peroxidase as a candidate for reducing PPD.

241 Pocket Probing Depth reduction (PPD), Clinical Attachment Level (CAL) gain and radiograp

242 Remarkably, PPD inactivation has no effect on late transcripts at th

243 atients with mild and 5 patients with severe PPD-related ACD and 7 hairdressers without contact derma

244 In addition both loci showed PPD-specific trajectories with age, possibly mediated by

245 roups demonstrated statistically significant PPD reduction, CAL gain and radiographic bone gain.

246 Live BCG, sterile PPD, and saline were bronchoscopically instilled into se

247 PPD-specific isotype/subclass, PPD-specific antibody-dependent phagocytosis, cellular c

248 in, PINK1, and DJ-1 formed a complex (termed PPD complex) to promote ubiquitination and degradation o

249 based primarily on the tuberculin skin test (PPD).

250 llen allergen) and a cutaneous model of Th1 (PPD) responses in man.

251 We believe that PPD will facilitate both clinical and basic research by

252 These results provide initial evidence that PPD is associated with altered DMN connectivity; cortica

253 Overall, our studies indicate that PPD is selectively hydrolyzed to the active metabolite b

254 ithout cyanide complementation, we show that PPD is cyanide dependent, presumably resulting from a cy

255 In contrast, here we show that PPD is required to dampen the expression of viral late t

256 Mass spectrometry was employed to show that PPD oxidation products bind irreversibly to cysteine (Cy

257 le target for PPD-HSA binding, and show that PPD protein adducts are antigenic determinants in patien

258 the growing body of evidence suggesting that PPD is mediated by differential gene expression and epig

259 significant change in expression during the PPD response we have used cDNA microarray technology to

260 Here, we show that the PPD locus also has a role in maintenance of diurnal and

261 We found that the PPD phenotype observed in Etv mutants is suppressed by a

262 ults demonstrate for the first time that the PPD response can be mimicked at the molecular level with

263 efficacy and because it interferes with the PPD test.

264 eration of skin-derived responder T cells to PPD challenge.

265 gic amacrine cells is a major contributor to PPD.

266 de of delayed-type hypersensitivity (DTH) to PPD in the skin.

267 Both private and occupational exposure to PPD is frequent, but the effect of PPD exposure in nonal

268 h respond poorly and express little hiCE, to PPD together with hiCE resulted in a dramatic decrease i

269 asticity may be of etiological importance to PPD.

270 We hypothesized that predisposition to PPD risk is due to an altered sensitivity to estrogen-me

271 showed upregulation of FLG-1 in response to PPD but downregulation of FLG-2.

272 ly, we demonstrate that cellular response to PPD may be predicted with good accuracy using CES2 expre

273 Responses to PPD were significantly higher in IRIS patients compared

274 amming events in the hippocampus and risk to PPD using a cross-species translational design.

275 roduces the transcripts that then succumb to PPD.

276 ental (ORI) cultivar was more susceptible to PPD.

277 rkers for sensitivity of a specific tumor to PPD treatment.

278 e onset of the oxidative burst that triggers PPD.

279 in derivative of Mycobacterium tuberculosis (PPD), as expected.

280 obacterial protein representatives making up PPD.

281 om these studies, we conclude that KSHV uses PPD to fine-tune the temporal expression of its genes by

282 me in the presence of functional HR, whereas PPD can compensate only partially for the lack of HR The

283 We found that while PPD-specific CD4(+) and CD8(+) T effector clones employe

284 hocytes from allergic individuals alone with PPD represents an important discrimination between aller

285 f 7 mm was more likely to be associated with PPD >= 4 mm 6 months postextraction (P < 0.05).

286 DNA methylation associated with PPD risk correlated significantly with E2-induced DNA me

287 up to 50%, when T-Regs were cocultured with PPD-primed CD4(+) effector T cells.

288 total protein amounts to be correlated with PPD.

289 in Mtb-infected macrophages co-cultured with PPD-driven effector cells at physiologically relevant co

290 tributes to cartilage failure in humans with PPD.

291 no acid substitutions found in patients with PPD had reduced activity in these assays.

292 tes from allergic patients proliferated with PPD and BB (n=8).

293 rant/naive individuals, were stimulated with PPD and PPD-modified HSA.

294 ed the mean cumulative numbers of teeth with PPD events (PPD > 3 mm) at each dental examination and t

295 The mean age of those with PPD was 39.9 +/- 9.25 compared with 43.9 +/- 11.0 for th

296 rgic patients proliferated when treated with PPD and Bandrowski's base (BB) and secreted IL-1alpha, -

297 ; however, 12% of clones were triggered with PPD directly.

298 rtum AD was markedly higher among women with PPD hospital contact after first birth compared to women

299 r year of birth and mother's age, women with PPD hospital contact after first birth had a 46.4 times

300 that the trajectories of pCRH in women with PPD symptoms are significantly accelerated from 23 to 26