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 consists of the sum of total P present in the produc

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 versus controls analyses revealed 11 CSF markers wit

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

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

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

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

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

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

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

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

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

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

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

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

19 -reactive CD4(+) memory T cell clones and an APS-derived, pathogenic monoclonal antibody cross-reacte

20 biopsy specimen of a femoral artery from an APS patient.

21 Here, we present an APS CMOS-probe technology for Simultaneous Neural record

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

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

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

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

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

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

28 ngest effect size in APS versus controls and APS versus PD analyses.

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

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

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

32 f biomarker concentrations were made between APS (n=114), PD (n=37) and control (n=34) groups using l

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

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

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

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

37 etely insensitive to substrate inhibition by APS.

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

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

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

41 ition) were present in 85.7% of catastrophic APS (CAPS), 35.6% of APS (and 68.5% of samples collected

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

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

44 and reduced penetrance compared to classical APS-1.

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

46 significant PEA biomarkers in distinguishing APS, PD and controls.

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

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

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

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

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

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

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

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

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

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

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

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

59 were found in monocytes and neutrophils from APS patients.

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

61 ta2GP1 autoantibodies affinity-purified from APS patients.

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

63 ecimens from individuals suspected of having APS.

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

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

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

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

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

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

70 arkers also reached significance (p<0.05) in APS versus PD analyses.

71 similar activities of anti-beta2-GPI Abs in APS and possibly act independently of Abs, raising the i

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

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

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

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

76 ntigen for clinically relevant antibodies in APS.

77 vides a strategy to block pathogenic aPLs in APS.

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

79 velopment and persistence of autoimmunity in APS, which may apply more broadly to human autoimmune di

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

81 imal studies showing a role of complement in APS-related clinical events, we used the modified Ham (m

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

83 be a prototype for an antithrombotic drug in APS.

84 pe IgG titers were significantly elevated in APS patients and correlated with anti-beta(2)GPI IgG aut

85 tion is associated with thrombotic events in APS.

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

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

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

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

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

91 an anti-inflammatory therapeutic paradigm in APS, which may extend to thrombotic disease in the gener

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

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

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

95 ptor (DNER) had the strongest effect size in APS versus controls and APS versus PD analyses.

96 e complement and contribute to thrombosis in APS, whereas patients with CAPS have underlying mutation

97 o the pathogenesis of vascular thrombosis in APS.

98 ge of semiconductors that can be utilized in APS.

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

100 nd 4 more subjects as level II indeterminate APS.

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

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

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

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

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

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

107 evelop late-onset glomerulonephritis but not APS.

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

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

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

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

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

113 n 85.7% of catastrophic APS (CAPS), 35.6% of APS (and 68.5% of samples collected within 1 year of thr

114 reased the AnxA5 anticoagulant activities of APS patient plasmas.

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

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

117 ntify novel diagnostic protein biomarkers of APS using multiplex proximity extension assay (PEA) test

118 ied potential novel diagnostic biomarkers of APS.

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

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

121 two independent cohorts, each consisting of APS and PD cases, and controls, were analysed for neurof

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

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

124 emented may yield more accurate diagnoses of APS.

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

126 A new form of APS based on IgA anti-beta-2-glycoprotein-I (B2GPI) anti

127 There are 3 forms of APS, primary (the most common form), associated to other

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

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

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

131 treatment for non-criteria manifestations of APS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 ke organic matter production depends only on APS if the latter falls below the threshold of 0.54 g P

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

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

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

153 a coli (E. coli) were not affected by CTL or APS diets.

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

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

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

157 ous arterial thrombosis, livedo racemosa, or APS-related cardiac valvular disease.

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), plays a significant role in controlling sulfur met

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

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

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

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

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

179 ogate markers for atherosclerosis in primary APS.

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

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

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

183 d to other systemic autoimmune diseases (SAD-APS), and catastrophic.

184 Nevertheless, patients with SAD-APS and renal failure only represent 2% to 5% in hemodia

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

186 the use of the modular Active Pixel Sensor (APS) concept, in which a small front-end circuit is loca

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

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

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

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

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

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

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

197 O(2) m(-2) d(-1)) as long as areal P supply (APS) exceeded 0.54 +/- 0.06 g P m(-2) during the product

198 rvival in patients with clinically suspected APS.

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

200 lants in antiphospholipid antibody syndrome (APS) remains uncertain.

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

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

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

204 Using antiphospholipid syndrome (APS) as a model, we demonstrate cross-reactivity between

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

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

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

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

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

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

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

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

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

214 The antiphospholipid syndrome (APS) is characterized by thrombosis and/or pregnancy mor

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

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

217 Antiphospholipid syndrome (APS) is well recognized as an important cause of kidney

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 ibodies (aPLs) in antiphospholipid syndrome (APS), a life-threatening autoimmune thrombotic disease.

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 percoagulation of antiphospholipid syndrome (APS), our approach focused on antiphospholipid antibodie

228 rom patients with antiphospholipid syndrome (APS).

229 in patients with antiphospholipid syndrome (APS).

230 manifestations of antiphospholipid syndrome (APS).

231 in patients with antiphospholipid syndrome (APS).

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

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

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

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

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

237 lap between atypical parkinsonian syndromes (APS) and Parkinson's disease (PD) makes diagnosis challe

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 nd 2.03 x 10(4) m(-2) s(-1) for UV-APS and T-APS oxidative treatment systems, respectively.

243 nd thermally activated persulfate (UV-APS, T-APS) batch systems, and the loss of rhodamine B (RhB) se

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

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

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

247 . int), and T and B cell autoepitopes in the APS autoantigen beta(2)-glycoprotein I (beta(2)GPI).

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

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

252 atients with different manifestations of the APS.

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

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

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

256 00 particles/cm(3) for measurements with the APS.

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

258 riority to dose-adjusted VKAs for thrombotic APS and, in fact, showed a non-statistically significant

259 ins the mainstay of treatment for thrombotic APS.

260 vel therapeutic interventions for thrombotic APS.

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

262 ti-beta2GPI), that are considered central to APS pathogenesis.

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

264 zation rate (AHM) decreased in proportion to APS.

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

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

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

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

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

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

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

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

273 x 10(4) and 2.03 x 10(4) m(-2) s(-1) for UV-APS and T-APS oxidative treatment systems, respectively.

274 in UV and thermally activated persulfate (UV-APS, T-APS) batch systems, and the loss of rhodamine B (

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

276 dependently predicted diagnosis of PD versus APS.

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

278 ) ratios in settling particulate matter when APS declined.

279 Only when APS sank below this threshold, the areal hypolimnetic mi

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 ory genes (60%), compared with patients with APS (21.8%) or SLE (28.6%) or normal controls (23.3%), a

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.