ライフサイエンスコーパス: APS

1 APS + ELE may block the up-regulation of alpha-SMA and C

2 APS is a phosphorylated branched mannan that shares a co

3 APS is an autoimmune disease with a confusing name becau

4 APS or ELE treatment alone on LX-2 cells could inhibit c

5 APS patients with atherothrombosis harbor in vivo-activa

6 APS reductase catalyzes the first committed step in bact

7 APS was purified on concanavalin A affinity columns to m

8 APS-IgG and SLE/APS- IgG increased FXa mediated NFkappaB

9 se autoimmune polyglandular syndrome type 1 (APS 1), which manifests in a classic triad of hypoparath

10 Autoimmune polyendocrine syndrome type 1 (APS-1) is caused by mutations of the autoimmune regulato

11 e, autoimmune polyendocrine syndrome type 1 (APS-1), distinguished by multi-organ autoimmunity.

12 re quantified in purified leukocytes from 23 APS and 64 SLE patients, and 56 healthy donors.

13 thrombotic and inflammatory parameters in 43 APS patients was found compared with 38 healthy donors.

14 A sample of 83 APS individuals and 90 healthy controls (HC) were assess

15 ti-FIXa Abs were present in 11 of 38 (28.9%) APS patients.

16 women with a history of recurrent abortion, APS women were at a higher risk than other women of PE,

17 loped for measurement of 5'-adenylylsulfate (APS) reductase (APR), an enzyme of the reductive sulfate

18 ubstrate inhibition by formation of an E.ADP.APS dead end complex.

19 ral data reported for Pseudomonas aeruginosa APS reductase and related enzymes.

20 e resultant MALDI-ISD mass spectra (MS after APS --> MALDI-ISD MS) are almost equivalent to conventio

21 Multiply stage MS after APS addition showed enhanced sensitivity, resolution, an

22 Among APS women, prior fetal loss was a risk factor for fetal

23 Patients diagnosed with an APS by PET or 1-y clinical follow-up showed a significan

24 -imidoadenosine-5'-triphosphate, Mg(2+), and APS provides a view of the Michaelis complex for this en

25 e of Asp(136), which bridges the ATP/ADP and APS/PAPS binding sites, suggest how the ordered nucleoti

26 ts the binding affinities at the ATP/ADP and APS/PAPS sites from those observed in the reduced enzyme

27 has dual specificity for both O-antigen and APS repeating units.

28 lished the linkage of both the O antigen and APS to the lipid A core of O-LPS and A-LPS, respectively

29 outes by having opposing effects on APSK and APS reductase in plants.

30 To investigate the roles of AS and APS, reciprocal exon-exon junctions were interrogated on

31 pregnancy outcomes in mouse models of PE and APS, possibly due to their protective effects on endothe

32 sis, the interplay between APS reductase and APS kinase is important for sulfur partitioning between

33 activation pathway, ATP-sulfurylase (S) and APS-kinase (K), are fused as 'KS' in animals but are fus

34 least in Arabidopsis, the interplay between APS reductase and APS kinase is important for sulfur par

35 In addition, there is overlap between APS and dementia diseases, such as Alzheimer's disease (

36 These compounds, exemplified by APS-2-79, modulate KSR-dependent MAPK signalling by anta

37 Subsequent studies of inhibition by APS and CTIU revealed that both compounds can bind to al

38 increase in K(i) for substrate inhibition by APS compared with the oxidized enzyme.

39 sed effectiveness of substrate inhibition by APS compared with the oxidized form.

40 etely insensitive to substrate inhibition by APS.

41 a(2+) release by FXa that was potentiated by APS-IgG and SLE/APS- IgG compared to healthy control sub

42 o thermal unfolding and the stabilization by APS, PPS-1 behaved like the unstable human PAPSS2 protei

43 HC monocytes was stimulated more strongly by APS IgG from patients with higher-avidity serum AVA.

44 Patients with catastrophic APS also benefit from immunosuppressive therapy and/or p

45 On positively charged APS-treated mica surfaces, amelogenin forms a relatively

46 and reduced penetrance compared to classical APS-1.

47 ine CSF biomarkers was able to differentiate APS from patients with PD and dementia.

48 c analysis of SynAPSK in complex with either APS and a non-hydrolyzable ATP analog or APS and sulfate

49 Recently we showed that the enzyme APS kinase limits the availability of activated sulfate

50 tion of thrombosis in human and experimental APS.

51 Finally, APS binding more than doubled the half-life for unfoldin

52 AtAPSKDelta96 showed decreased affinity for APS binding, although the N-terminal domain does not dir

53 P site was favored and enhanced affinity for APS in the second site by 50-fold.

54 xin and glutathione as an electron donor for APS reduction.

55 Our results suggest that novel therapies for APS can now be developed targeting these mechanisms.

56 will convert, the appropriate treatment for APS, the ability of treatment to prevent conversion to p

57 We found APS-I-typical autoantibodies and clinical manifestations

58 cal effects of anti-beta2GPI antibodies from APS patients and displaced beta2GPI-bound patient antibo

59 Purified polyclonal IgG derived from APS patients with elevated levels of serum antithrombin

60 e predisposition to phenotypes distinct from APS 1 can be mediated in a dominant-negative fashion by

61 dominant autoimmune phenotype distinct from APS 1.

62 IPD subjects were distinguished from APS with 94% specificity and 96% positive predictive val

63 nfirmed by comparing monocytes isolated from APS patients and HC.

64 were found in monocytes and neutrophils from APS patients.

65 rs could differentiate patients with PD from APS with an area under the curve of 0.95 and subtypes of

66 ta2GP1 autoantibodies affinity-purified from APS patients.

67 Furthermore, APS-2-79 increased the potency of several MEK inhibitors

68 ecimens from individuals suspected of having APS.

69 he autoimmune polyendocrine syndrome type I (APS-I), caused by mutations in the autoimmune regulator

70 We found that, after IgG-APS or 4C5 injections and vascular injury, mean thrombus

71 ular cell adhesion molecule-1 induced by IgG-APS or 4C5 in explanted A2(-/-) aorta was also significa

72 In wild type mice, IgG-APS, E7 and the dimer increased thrombus formation, caro

73 -derived polyclonal aPL IgG preparation (IgG-APS), a murine anti-beta(2)GPI monoclonal antibody (E7)

74 eservation of mitochondria and prevented IgG-APS-induced fission mediated by Drp-1 and Fis-1 proteins

75 patient with antiphospholipid syndrome (IgG-APS), a healthy control subject (IgG-normal human serum)

76 n addition, those effects induced by the IgG-APS, by E7 and by the dimer were inhibited by treatment

77 bound to FIXa and that IgG anti-FIXa Abs in APS patients were significantly higher than those in nor

78 thesis, we searched for IgG anti-FIXa Abs in APS patients.

79 Development of AIH in APS-1 is dependent on specific Aire mutations and geneti

80 To study AIH in APS-1, we generated a murine model of human AIH on a BAL

81 rombosis not only in primary APS but also in APS secondary to lupus.

82 of AnxA5 on PLBs and cultured cells, and in APS patient plasmas.

83 ntigen for clinically relevant antibodies in APS.

84 n and FXa, we hypothesized that some aPLs in APS bind to FIXa and hinder AT inactivation of FIXa.

85 Accelerated atherosclerosis in APS patients was found associated with their inflammator

86 Moreover, naturally occurring changes in APS concentrations may be sensed by changes in the confo

87 and characterize microRNAs linked to CVD in APS and SLE; 2) assess the effects of specific autoantib

88 tes neutrophil activation and fetal death in APS and that statins may be a good treatment for women w

89 be a prototype for an antithrombotic drug in APS.

90 chanisms of thrombosis and pregnancy loss in APS have been proposed.

91 ls of microRNAs in neutrophils were lower in APS and SLE than in healthy donors.

92 nterferes with 2 prothrombotic mechanisms in APS: the binding of beta2GPI to negatively charged cellu

93 s between ToM function and neurocognition in APS subjects were stronger than those in healthy control

94 in AtAPSK is comparable to that observed in APS reductase.

95 In conclusion, the oxidative perturbation in APS patient leukocytes, which is directly related to an

96 Reduction in APS kinase activity led to reduced levels of glucosinola

97 nt system activation play a cardinal role in APS pathogenesis.

98 o the pathogenesis of vascular thrombosis in APS.

99 ge of semiconductors that can be utilized in APS.

100 and finally the decision whether to include APS as a formal psychiatric diagnosis.

101 nd 4 more subjects as level II indeterminate APS.

102 fusion (i.e., channeling) of an intermediate APS(2-) between active sites.

103 y methods depend on the use of (35)S-labeled APS or shunt adenosine 5'-monophosphate (AMP) to a coupl

104 e-associated phosphorylated branched mannan (APS) indicated that this locus is also downregulated in

105 (NZW x BXSB)F(1) mice but induces only mild APS and does not induce thrombocytopenia.

106 kyl-terminated porous silicon nanoparticles (APS NPs) have enhanced fluorescence stability and intens

107 with APS and in SLE patients with aPL but no APS (SLE/aPL+) compared to healthy controls, but anti-ac

108 Hematologists-Antiphospholipid Syndrome (NOH-APS) Study Group give us new information about the effec

109 ed to systemic lupus erythematosus (SLE) non APS IgG.

110 evelop late-onset glomerulonephritis but not APS.

111 lications, are urgently needed for obstetric APS and should be evaluated according to the type of pre

112 Advances in the pathogenesis of obstetric APS have occurred, such as the concept of redefining the

113 nocytes treated with thrombotic or obstetric APS IgG, compared with healthy control (HC) IgG.

114 outcomes in women with refractory obstetric APS when taken at the onset of PE or IUGR until the end

115 nti-FIXa Ab occurred in approximately 30% of APS patients and could interfere with AT inactivation of

116 AnxA5 anticoagulant activities of APS patient plasmas were also determined.

117 reased the AnxA5 anticoagulant activities of APS patient plasmas.

118 d to determine the mechanism of anchoring of APS to the surface of P. gingivalis.

119 lfurylase overcomes the energetic barrier of APS synthesis by distorting nucleotide structure and ide

120 d enzyme, consistent with initial binding of APS as inhibitory, and suggests a role for the N-termina

121 an-specific autoantibodies characteristic of APS-I patients, and we assayed 26 thymoma samples for tr

122 ere treated with different concentrations of APS or ELE for 24 or 48 hours.

123 tions: the actual incidence of conversion of APS to full-blown psychosis, the identification of the s

124 nst beta(2)-glycoprotein I as the culprit of APS.

125 emented may yield more accurate diagnoses of APS.

126 Over-expression of APS reductase had no effect on glucosinolate levels but

127 f small molecules as potential inhibitors of APS reductase present in human pathogens, including M. t

128 lopment of potent and specific inhibitors of APS reductase, we have probed the molecular determinants

129 nal features required for the interaction of APS reductase with a ligand and provides a pharmacologic

130 e announced that the planned introduction of APS as a new diagnosis in DSM-5 was cancelled and that A

131 ents with diverse clinical manifestations of APS have differential effects upon phosphorylation of NF

132 e but not all non-criteria manifestations of APS.

133 treatment for non-criteria manifestations of APS.

134 ased neurodegeneration in the mouse model of APS and in the PTB model.

135 ed using a laser-induced thrombosis model of APS in a live mouse and human anti-beta2GP1 autoantibodi

136 A1 reduced thrombus size in a mouse model of APS in the presence of lupus features, suggesting that A

137 L) syndrome (APS) and, in an animal model of APS, with reduction of experimentally induced thrombosis

138 sis, significantly altered in neutrophils of APS and SLE patients, is associated to their atherothrom

139 sis, the wide range of long-term outcomes of APS and finally the decision whether to include APS as a

140 xidative stresses may affect partitioning of APS into the primary and secondary thiol metabolic route

141 Recent insights into the pathogenesis of APS have begun to elucidate pathophysiology and led to t

142 Recent insights into the pathogenesis of APS have unveiled novel areas for treatment intervention

143 nase (APSK) catalyzes the phosphorylation of APS to 3'-phospho-APS (PAPS).

144 ollectively, we demonstrate the potential of APS NPs in sensors for the effective detection of Cu(2+)

145 owed morphological change in the presence of APS or ELE for 24 hours.

146 APR catalyzes the two-electron reduction of APS and forms sulfite and adenosine 5'-monophospahate (A

147 unction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies

148 Recent studies of APS have reflected this uncertainty and debate over its

149 area under the curve of 0.95 and subtypes of APS from one another.

150 itions for Cu(2+), we demonstrate the use of APS NPs in two separate applications - a standard well-b

151 a robust manner to shore up the validity of APS as a diagnostic construct.

152 Recent work on APS has revolved around a series of unresolved questions

153 the AP2 subunits APM-2/mu2, APA-2/alpha, or APS-2/sigma2.

154 her APS and a non-hydrolyzable ATP analog or APS and sulfate revealed the overall structure of the en

155 BD (n = 28; 22/28 with Parkinson disease) or APS (n = 32), in whom dopaminergic responsiveness could

156 nse, either in the pooled group or in LBD or APS subgroups.

157 ical diagnosis of Lewy-body disease (LBD) or APS was made after a mean follow-up of 12 mo.

158 sential autoantigens, as described for other APS-1-related autoimmune diseases.

159 P-APS symptoms peaked 3 days after chemotherapy.

160 Patients with higher P-APS pain scores with the first dose of paclitaxel appear

161 ory of the paclitaxel-acute pain syndrome (P-APS) and paclitaxel's more chronic neuropathy have not b

162 These data support that the P-APS is related to nerve pathology as opposed to being ar

163 d by simple addition of ammonium persulfate (APS) in the matrix solution.

164 zes the phosphorylation of APS to 3'-phospho-APS (PAPS).

165 osine-5'-phospho-sulfate (APS) to 3'-phospho-APS (PAPS).

166 ich synthesizes adenosine 5'-phosphosulfate (APS) from sulfate and ATP.

167 Adenosine-5'-phosphosulfate (APS) kinase (APSK) catalyzes the phosphorylation of APS

168 In plants, adenosine 5'-phosphosulfate (APS) kinase (APSK) is required for reproductive viabilit

169 erculosis (Mtb) adenosine 5'-phosphosulfate (APS) reductase (APR) catalyzes the first committed step

170 um tuberculosis adenosine-5'-phosphosulfate (APS) reductase is an iron-sulfur protein and a validated

171 sphorylation of adenosine 5'-phosphosulfate (APS) to 3'-phosphoadenosine-5'-phosphosulfate (PAPS).

172 the nucleotide adenosine 5'-phosphosulfate (APS), PAPS synthase proteins are stabilized.

173 n of sulfate to adenosine 5'-phosphosulfate (APS).

174 adenylation to adenosine 5'-phosphosulfate (APS).

175 Current artificial photosynthesis (APS) systems are promising for the storage of solar ener

176 ribed a cell surface anionic polysaccharide (APS) in Porphyromonas gingivalis that is required for ce

177 natural products, astragalus polysaccharide (APS) and beta-elemene (ELE) on the activation of human l

178 nterfere with thrombosis not only in primary APS but also in APS secondary to lupus.

179 ontrasting findings were reported in primary APS patients with regard to the increased number of plaq

180 ogate markers for atherosclerosis in primary APS.

181 e in vivo atherosclerotic lesions of primary APS patients with atherothrombosis.

182 esonance spectroscopy of the lectin-purified APS confirmed the previous structure but also revealed a

183 he use of pravastatin in LDA+LMWH-refractory APS in patients at an increased risk of adverse pregnanc

184 and after the decision in May 2012 to remove APS as a new diagnosis in DSM-5, scientific work has pro

185 ing (AS) and alternative promoter selection (APS).

186 e solid-amine sorbent, 3-aminopropyl silane (APS), bound to mesoporous silica (SBA15) using solid-sta

187 n (C(x)F(y)) and poly(aminopropyl siloxane) (APS, a.k.a. siloxane).

188 er (SMPS) and an aerodynamic particle sizer (APS) and revealed four size modes for all measured sampl

189 sizer (SMPS) and aerodynamic particle sizer (APS) were utilized for particle size distributions rangi

190 light scattering aerodynamic particle sizer (APS).

191 ted nanopowders with average particle sizes (APSs) < 20 nm and corresponding specific surface areas o

192 FXa that was potentiated by APS-IgG and SLE/APS- IgG compared to healthy control subjects' IgG, and

193 APS-IgG and SLE/APS- IgG increased FXa mediated NFkappaB signalling and

194 a reactive IgG from patients with APS or SLE/APS- alter these responses.

195 The American Physical Society (APS) published a report, later updated, estimating the c

196 therapeutic approaches that address specific APS disease mechanisms.

197 The anterior physeal step (APS) measured 3.8 mm on the right side.

198 ts required for the ability of the substrate APS to inhibit the reaction at micromolar concentrations

199 from the 3'-hydroxyl group of the substrate APS.

200 rs N4-(6-aminopyrimidin-4-yl)-sulfanilamide (APS) and 1-(5-cyclobutyl-thiazol-2-yl)-3-isoquinolin-5-y

201 phorylation of adenosine-5'-phospho-sulfate (APS) to 3'-phospho-APS (PAPS).

202 rvival in patients with clinically suspected APS.

203 Seventy-eight patients with suspected APS at study inclusion underwent a follow-up of up to 5.

204 del of obstetrics antiphospholipid syndrome (APS) and a mouse model of preterm birth (PTB).

205 F(1) mice develop antiphospholipid syndrome (APS) and proliferative glomerulonephritis that is marked

206 egnant women with antiphospholipid syndrome (APS) are at a high risk of obstetrical complications.

207 patients with the antiphospholipid syndrome (APS) bind to the homologous enzymatic domains of thrombi

208 rom patients with antiphospholipid syndrome (APS) display higher avidity binding to FXa with greater

209 H]) for obstetric antiphospholipid syndrome (APS) does not prevent life-threatening placenta insuffic

210 and treatment of antiphospholipid syndrome (APS) from current literature.

211 The antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by

212 Antiphospholipid syndrome (APS) is an autoimmune disease characterized by venous th

213 Antiphospholipid syndrome (APS) is an autoimmune disorder with increased risk for t

214 gulability in the antiphospholipid syndrome (APS) is antiphospholipid Ab-mediated upregulation of tis

215 Antiphospholipid syndrome (APS) is characterized by recurrent arterial/venous throm

216 The antiphospholipid syndrome (APS) is defined by the persistent presence of antiphosph

217 Antiphospholipid syndrome (APS) is defined by thrombosis, fetal loss, and the prese

218 purely obstetric antiphospholipid syndrome (APS) or inherited thrombophilia.

219 mmatory status of antiphospholipid syndrome (APS) remain unknown.

220 ome patients with antiphospholipid syndrome (APS) that are negative for other isotypes.

221 obstetric form of antiphospholipid syndrome (APS) treated with prophylactic low-molecular-weight hepa

222 patients with the antiphospholipid syndrome (APS) upon monocyte activation have not been fully charac

223 Women with antiphospholipid syndrome (APS), a condition characterized by the presence of antip

224 In antiphospholipid syndrome (APS), antiphospholipid antibodies (aPL) binding to beta2

225 ding catastrophic antiphospholipid syndrome (APS), atypical presentations of thrombotic thrombocytope

226 ers, particularly antiphospholipid syndrome (APS), in which autoantibodies to phospholipid/protein co

227 manifestations of antiphospholipid syndrome (APS).

228 scarriages in the antiphospholipid syndrome (APS).

229 ing patients with antiphospholipid syndrome (APS).

230 rom patients with antiphospholipid syndrome (APS).

231 osis in the antiphospholipid (aPL) syndrome (APS) and, in an animal model of APS, with reduction of e

232 ly suspected atypical parkinsonian syndrome (APS) were prospectively recruited for imaging.

233 known as Autoimmune Polyglandular Syndrome (APS) Type I, which classically manifests as a triad of a

234 ual status of attenuated psychosis syndrome (APS) as a psychiatric disorder.

235 is as well as attenuated psychosis syndrome (APS).

236 atypical parkinsonian look-alike syndromes (APS), can be clinically challenging.

237 the symptoms of antiphospholipid syndromes (APS), including thrombosis and repeated pregnancy loss.

238 RD), the autoimmune polyglandular syndromes (APS), the association of IgG4 with APS, and possible pat

239 h suspected atypical parkinsonian syndromes (APSs) for optimal treatment and counseling.

240 mportant as atypical parkinsonian syndromes (APSs) such as progressive supranuclear palsy (PSP), mult

241 Based on hybrid array pattern synthesis (APS) and particle swarm optimization (PSO) algorithm, th

242 ew diagnosis in DSM-5 was cancelled and that APS was being moved to 'Section III' of the manual as a

243 er of the major researchers have argued that APS does not yet enjoy a degree of validity that warrant

244 e results contrast with reported claims that APS and CTIU are competitive inhibitors of the binding o

245 We tested the hypothesis that APS increases dependence on neurocognition during the in

246 ATP-sulfurylase domain and the latter by the APS-kinase domain.

247 In the APS group, ToM was associated with an apparent increase

248 synthetase influences these elements in the APS kinase domain, we propose that this could be a commu

249 tion of C3 deposition in the placenta in the APS model was associated with placental insufficiency ch

250 In the APS model, foetuses that showed increased C3 in their br

251 lectrostatics plays an essential role in the APS(2-) channeling.

252 s scientists in scientific networks like the APS, where the commonly used number of citations can be

253 was confirmed by fatty acid analysis of the APS and matrix-assisted laser desorption ionization-time

254 Here, we report the structure of the APS-kinase domain of PAPSS isoform 1 (PAPSS1) representi

255 atients with different manifestations of the APS.

256 This work builds on the APS report to investigate the effect of modifications to

257 t effects on the overall price, reducing the APS estimate from $610 to $309/tCO2 avoided.

258 ransfer of electrons from glutathione to the APS reduction site on the amino-terminal domain.

259 sizes from 0.6 to 2.5 mum, measured with the APS, were similar for all samples.

260 00 particles/cm(3) for measurements with the APS.

261 e monitored for potentially life-threatening APS-I manifestations such as AI and hypoparathyroidism.

262 vel therapeutic interventions for thrombotic APS.

263 ins the mainstay of treatment for thrombotic APS.

264 her characterized the proteome of thrombotic APS IgG-treated monocytes using a label-free proteomics

265 ore, the clinical and serologic parallels to APS-I in patients with thymomas are not explained purely

266 r involvement in atherothrombosis related to APS and SLE patients.

267 sduction functions which are all relevant to APS and may therefore provide potential new therapeutic

268 ovative approach potentially useful to treat APS patients refractory to standard therapy.

269 en with prior fetal loss, LMWH + LDA-treated APS women had lower pregnancy loss rates but higher PE r

270 oagulant therapeutic strategies for treating APS.

271 ively charged 3-aminopropyl triethoxysilane (APS) silanized mica.

272 model has been developed for M. tuberculosis APS reductase that is in accord with the results present

273 -SMA and CD44 expressions was inhibited upon APS + ELE treatment through TGF-beta pathway in LX-2 cel

274 ants in which activities of enzymes that use APS as a substrate were increased or reduced.

275 The combinational treatment using APS + ELE significantly increased the killing efficiency

276 ssible binding models (i.e. ATP first versus APS first) differs and implies that active site structur

277 dependently predicted diagnosis of PD versus APS.

278 fects of aPL antibodies in vivo and in vitro APS.

279 flow of sulfur to primary assimilation when APS kinase activity was reduced.

280 increased in 11 of 27 patients (40.7%) with APS.

281 habited the cell proliferation compared with APS or ELE treatment alone on LX-2 cells.

282 for reproductive viability and competes with APS reductase to partition sulfate between the primary a

283 Glycine max ATP sulfurylase) in complex with APS was determined.

284 Consistent with APS, AR patients exhibited a 30% reduction in platelet c

285 yndromes (APS), the association of IgG4 with APS, and possible pathobiology.

286 asaccharide repeating units) and A-LPS (with APS repeating units).

287 were significantly elevated in patients with APS and in SLE patients with aPL but no APS (SLE/aPL+) c

288 in the risk stratification of patients with APS and provide new molecular therapeutic targets.

289 UVEC and FXa reactive IgG from patients with APS and/or SLE potentiate this effect.

290 Patients with APS are at increased risk for accelerated atherosclerosi

291 Moreover, IgG purified from patients with APS displayed higher avidity for thrombin and significan

292 ation of thrombin, distinguish patients with APS from SLE/aPL+ patients, and thus may contribute to t

293 whether FXa reactive IgG from patients with APS or SLE/APS- alter these responses.

294 protein C were compared in 32 patients with APS, 29 patients with systemic lupus erythematosus (SLE)

295 In 38 patients with APS-I, by contrast, we observed neither autoantibodies a

296 Treatment with APS + ELE for 24 or 48 hours significantly inhabited the

297 g new pregnancies between treated women with APS (n = 513; LMWH + LDA) and women negative for antipho

298 al and fetal/neonatal outcomes in women with APS given pravastatin after the onset of preeclampsia an

299 We studied 21 pregnant women with APS who developed PE and/or IUGR during treatment with L

300 ti-phospholipid Ab-positive patients without APS, or healthy controls.