ライフサイエンスコーパス: AMA

1 AMA also fully restored the activity of meropenem agains

2 AMA discharges have risen among individuals with IDU-IE

3 AMA mice (38-41 weeks) at E17.5 had fewer pups, more lat

4 AMA was associated with lower maternal serum PAPP-A and

5 AMA were detectable for the first 4 years after the diag

6 AMAs aggregate among FDRs of PBC probands.

7 AMAs were detected in 28/69 (40.6%) ALF patients with re

8 nts (MA), recombinant apical merozoite Ag 1 (AMA-1), the 42-kDa C-terminal region of merozoite surfac

9 ndidate antigens, apical membrane antigen 1 (AMA-1) and merozoite surface protein 1 (MSP-1).

10 Apical membrane antigen 1 (AMA-1) is a promising vaccine candidate for Plasmodium f

11 ntibodies against apical membrane antigen 1 (AMA-1) of Plasmodium falciparum inhibit merozoite invasi

12 -stage antigen 1, apical-membrane antigen 1 (AMA-1), and merozoite surface proteins (MSP) 1 and 3, in

13 of antibodies to apical membrane antigen 1 (AMA-1), but to none of the other 7 antigens were signifi

14 tigens, including apical membrane antigen 1 (AMA-1), circumsporozoite protein (CSP), erythrocyte bind

15 e protein (TRAP), apical membrane antigen 1 (AMA-1), erythrocyte binding antigen 175 (EBA-175), and m

16 vaccine candidate apical membrane antigen-1 (AMA-1) can inhibit invasion of merozoites into RBC, but

17 1 h in ammonium hydroxide/methylamine (1:1) (AMA) at 80 degrees C).

18 bodies to two P. falciparum antigens (MSP-1, AMA-1).

19 1-AMA fluorescence is enhanced when bound to HSAF.

20 entified a fluorophore, 1-aminoanthracene (1-AMA), that is anesthetic, potentiates GABAergic transmis

21 Furthermore, 1-AMA reversibly immobilizes stage 45-50 Xenopus laevis ta

22 Thus, displacement of 1-AMA from HSAF by other anesthetics attenuates the fluore

23 microM) and fluorescence micrographs show 1-AMA localized to brain and olfactory regions.

24 xperiments in isolated cells indicate that 1-AMA potentiates chloride currents elicited by GABA, simi

25 Thus, 1-AMA provides an unprecedented opportunity for studying g

26 etitive cross-reactivity using sera from 100 AMA-positive and 23 AMA-negative PBC patients and 190 co

27 Moreover, 78 of 80 AMA-positive and 5 of 17 AMA-negative patients with PBC had antibodies against 3

28 data, using sera from 95 AMA-positive and 19 AMA-negative patients with PBC and 76 controls, by testi

29 According to the 2011 AMA-PM, 10,819 physicians were born or trained in 28 SSA

30 175) of its estimated physicians in the 2011 AMA-PM.

31 vity using sera from 100 AMA-positive and 23 AMA-negative PBC patients and 190 controls.

32 Clinical data from 720 of 1,318 AMA-positive patients identified in 1 year were collecte

33 In the healing response study, 35 AMA-BRS and 23 BVS were implanted in 58 coronary arterie

34 tribution of 24 polymorphic sites of the 3D7 AMA-1 vaccine was determined.

35 ty of the IgG3 isotype was found in 52 (52%) AMA-positive PBC patients but in only 1 of the controls

36 Moreover, 78 of 80 AMA-positive and 5 of 17 AMA-negative patients with PBC

37 superior to MTPA and MPA and comparable to 9-AMA.

38 We extended the data, using sera from 95 AMA-positive and 19 AMA-negative patients with PBC and 7

39 Sera from 3 of 95 AMA-positive sera, but none of the controls, reacted wit

40 Although high titers of immunoglobulin (Ig)A AMAs are found in bile, saliva, and urine of patients, a

41 ngal natural product, aspergillomarasmine A (AMA), that is a rapid and potent inhibitor of the NDM-1

42 pithelial cells, and anti-mitochondrial Abs (AMAs).

43 t activity (AOA) and antimicrobial activity (AMA) of the samples were determined.

44 more likely to leave against medical advice (AMA) (15.7% vs 1.1%, P<0.001).

45 docarditis (IDU-IE), against medical advice (AMA) discharge is common and linked to adverse outcomes.

46 ently complicated by against medical advice (AMA) discharges.

47 egnancies in women of advanced maternal age (AMA) are susceptible to fetal growth restriction (FGR) a

48 n crater, we determined absolute model ages (AMAs) of 550 million and 720 million years, depending on

49 Although AMA positivity without biochemical cholestasis may indic

50 nfiltrates and biliary cell damage, although AMA levels were not altered.

51 Therefore, although AMAs appear to interact with the biliary cell apotope an

52 Aortic medial amyloid (AMA) is the most common localized human amyloid, occurri

53 f oxidative stress in aortic medial amyloid (AMA) pathogenesis and deposition.

54 n groups and to detect allelic effects of an AMA-1 vaccine in the field.

55 Accuracy Maximization Analysis (AMA) is a recently developed Bayesian ideal observer met

56 ample extracts by advanced mercury analyzer (AMA) and gas chromatography-atomic fluorescence spectrom

57 suppress CpG-mediated B cell activation and AMA production.

58 DrugPoints was not added, and AMA-DE was removed.

59 AFA and AMA growth patterns exhibited sex-specific trends includ

60 l antibodies to preerythrocytic antigens and AMA-1.

61 mouse monoclonal antibody against PDC-E2 and AMA with an immunoglobulin A isotype.

62 We review the ACH, PSH and AMA in relation to levels of APP proteolytic fragments r

63 We cannot fully evaluate the ACH, PSH and AMA in relation to the effects of mutations in APP as th

64 evels of antibodies to CSP, LSA-1, TRAP, and AMA-1 in the oldest age group (>40 years) in the unstabl

65 wed significant differences in MUAC, UAA and AMA (p < 0.001).

66 ut also in proteins of the CDC48/p97/VAT and AMA groups, suggesting a regulatory network of proteasom

67 Mean HKAAs and AMAs as measured by the readers and the algorithm ranged

68 timulating factor-stimulated macrophages and AMAs, produces an intense proinflammatory response.

69 pes, macrophages from patients with PBC, and AMAs.

70 HKAA) and femoral anatomic-mechanical angle (AMA).

71 ructural basis of antigenic escape from anti-AMA-1 exists.

72 es is a common direct mode of action of anti-AMA-1 antibodies, blocking of AMA-1 secondary processing

73 Polyclonal anti-AMA-1 was much more inhibitory than monoclonal antibody

74 g) 3 +/- 1 and antimitochondrial antibodies (AMA), but it remained unknown whether and how AMA enter

75 ice as well as antimitochondrial antibodies (AMA), serum and hepatic levels of proinflammatory cytoki

76 PBC-specific anti-mitochondrial antibodies (AMA) in a 3-year old girl.

77 lobulins, and anti-mitochondrial antibodies (AMA) were assayed at 3 months of age.

78 othesized that antimitochondrial antibodies (AMAs) and development of autoimmune cholangitis would be

79 BC), including antimitochondrial antibodies (AMAs) and extensive portal CD4(+) and CD8(+) lymphocytic

80 Antimitochondrial antibodies (AMAs) directed against the lipoyl domain of the E2 subun

81 high levels of antimitochondrial antibodies (AMAs) in patients with PBC suggest a profound loss ofB c

82 (>or=90%) for antimitochondrial antibodies (AMAs) in serum.

83 Originally, antimitochondrial antibodies (AMAs) were detected by indirect immunofluorescence (IIF)

84 patients with antimitochondrial antibodies (AMAs), but no clinical evidence of primary biliary chola

85 aracterized by antimitochondrial antibodies (AMAs), directed to the E2 component of the pyruvate dehy

86 ow circulating antimitochondrial antibodies (AMAs), liver-infiltrating autoreactive T lymphocytes aga

87 ponse includes antimitochondrial antibodies (AMAs).

88 ic hallmark of antimitochondrial antibodies (AMAs).

89 appearance of antimitochondrial antibodies (AMAs).

90 bunit (PDC-E2) antimitochondrial antibodies (AMAs).

91 Anti-mitochondrial antibodies (AMAs) have long been recognized as a serological hallmar

92 or absence of anti-mitochondrial antibodies (AMAs).

93 positive for anti-mitochondrial antibodies (AMAs).

94 se linked to the antimitochondrial antibody (AMA) diagnostic of the disease, and reduced anaerobic th

95 with PBC and/or antimitochondrial antibody (AMA) positivity with logistic regression.

96 ith PBC and with antimitochondrial antibody (AMA) status and prior orthotopic liver transplantation (

97 ity, gender, and antimitochondrial antibody (AMA) status; 73 of 535 (13.6%) were non-Caucasian (21 we

98 1% (79 of 97) of antimitochondrial antibody (AMA)-positive patients with PBC but not in controls.

99 ce antigen domain of apical membrane antigen AMA-1.

100 erve as ligands for apical membrane antigen (AMA) family surface proteins displayed on the parasite.

101 nd R29, and antibodies to merozoite antigens AMA-1 and MSP2.

102 oid precursor protein (APP) matrix approach (AMA), of which the ACH has held a dominant position for

103 UAC and derived measures of arm muscle area (AMA) and arm fat area (AFA) on the basis of the populati

104 lowed for the derivation of arm muscle area (AMA) and arm fat area (AFA)], breastfeeding, and individ

105 We found this observation intriguing as AMA and indeed an overlap with PBC are virtually absent

106 definable subphenotypes of disease, such as AMA positivity, or definitive measures of disease severi

107 The American Medical Association (AMA) has proposed a system of tax credits for the purcha

108 N = 6542): (1) American Medical Association (AMA) Masterfile nonfederal, office-based physicians per

109 linkage to the American Medical Association (AMA) Masterfile.

110 compared with American Medical Association (AMA) recommended readability parameters (sixth-grade rea

111 h century, the American Medical Association (AMA), specifically its Section on Ophthalmology, played

112 uction of anti-mitochondrial autoantibodies (AMA) that recognize proteins involved in energy metaboli

113 high-titer antimitochondrial autoantibodies (AMAs) and portal cellular infiltrates.

114 oantigens, antimitochondrial autoantibodies (AMAs) are only found in primary biliary cirrhosis (PBC)

115 okines and antimitochondrial autoantibodies (AMAs) closely resembling human primary biliary cirrhosis

116 Antimitochondrial autoantibodies (AMAs), the serological hallmark of primary biliary cirrh

117 s well as anti-mitochondrial autoantibodies (AMAs) IgA and IgM decreased significantly from baseline

118 ts signature antimitochondrial autoantibody (AMA), the homogeneity of clinical characteristics, and t

119 mplications for FDRs of PBC probands because AMA positivity may suggest susceptibility to PBC.

120 irulent clone was less readily controlled by AMA-1-induced immunity than its less virulent progenitor

121 ith purified recombinant Plasmodium chabaudi AMA-1 (PcAMA-1) and/or the 42-kDa C-terminal processing

122 e sequence divergence from all characterized AMA family members.

123 chanism relative to previously characterized AMA-RON2 complexes.

124 igh-impact AER may be useful for classifying AMA-1 strains into inhibition groups and to detect allel

125 interestingly, 20% of the rigorously defined AMA-negative patient group had antibodies to one or more

126 we implement a stochastic gradient descent (AMA-SGD) routine for filter learning.

127 Furthermore, 100% of these newly detected AMA-positive patients were anti-nuclear antibody (ANA) p

128 Nearly half of the newly detected AMAs in clinical practice does not lead to a diagnosis o

129 levels of IgG and IgA, but they also develop AMAs with specificity for PDC-E2, which maps to the inne

130 ndred percent of immunized rabbits developed AMA that have each and every characteristic of human AMA

131 Among those who inject drugs, AMA discharges were more common and increases sharper.

132 erican Medical Association Drug Evaluations (AMA-DE), United States Pharmacopoeia Drug Information fo

133 Instead, virulence evolved; AMA-1-selected parasites induced greater anemia in naive

134 e associated with PBC and to a lesser extent AMA status and prior OLT.

135 antibody responses to Plasmodium falciparum AMA-1, MSP-119 and CSP were measured with the aim to des

136 Two hundred and sixty five AMA positive patients without ascites, variceal bleeding

137 For AMA-1, the seroconversion rates (SCRs) ranged from 0.121

138 The overall seroprevalence was 64.0% for AMA-1, 39.5% for MSP-119, and 12.9% for CSP.

139 g the lipoyl loop conformation necessary for AMA recognition.

140 , vaccine adjuvants and delivery systems for AMA-1- and MSP-1-based vaccines can be selected for thei

141 e plotted unadjusted quarter-year trends for AMA discharges and used multivariable logistic regressio

142 mily registry, we prospectively screened for AMAs in the serum of 306 FDRs in 145 pedigrees, 350 PBC

143 Placentas from AMA women exhibited increased syncytial nuclear aggregat

144 a response noise model, and a cost function, AMA returns the filters (i.e. receptive fields) that ext

145 MA), but it remained unknown whether and how AMA enter KCs and why other cell types are not affected

146 have each and every characteristic of human AMAs with reactivity against PDC-E2, E2 subunit of branc

147 he problem of neural systems identification, AMA may be able to overcome a fundamental limitation of

148 fraction, disparities, and timing of IDU-IE AMA discharges are needed.

149 actors and timing is needed to reduce IDU-IE AMA discharges.

150 Furthermore, if AMA development is heritable, this trait will provide a

151 ased serum levels of immunoglobulin A (IgA), AMA and interleukin-17 (IL-17).

152 ce-were monitored for liver immunopathology, AMAs, and intrahepatic cytokine production.

153 0 [19.5-20.5] in BVS versus 4.0 [3.0-4.3] in AMA-BRS).

154 of IDU-IE and 1.9% of non-IDU-IE resulted in AMA discharges.

155 Two previously unreported specificities in AMA-positive sera that recognize free lipoic acid and a

156 investigate the role of oxidative stress in AMA pathogenicity.

157 the manifestations of cholangitis, including AMA production, intrahepatic T-cell infiltrates, and bil

158 he polymerization of such monomers including AMA, VBMA, and DAA.

159 the multilineage immune response, including AMAs, is directed at the E2 component of the 2-oxo-dehyd

160 PBC and possibly plays a role in influencing AMA development as well as progression to OLT among PBC

161 n invasion-inhibitory epitope of P. knowlesi AMA-1 and then fixing the material for ultrastructural a

162 As expected, 90 of 90 previously known AMA-positive patients remained positive with this assay

163 and colon pathological conditions and lacked AMA.

164 y (1.28 [1.20-1.36]; p < 0.001), and leaving AMA (2.32 [1.81-2.98]; p < 0.001).

165 f patients on Medicaid, and rates of leaving AMA among the DU-IE group shows the downstream effects o

166 osition atomic absorption spectrometry (LECO AMA-254) and the rest of the elements by inductively cou

167 The liberated AMA altered mitochondrial membrane potential, respiratio

168 k-specific methods for feature learning like AMA will become increasingly important.

169 Using a unique dataset linking AMA Physician Masterfile data with hospital discharge cl

170 ld improvement was seen, potentially linking AMA with muscle bioenergetics dysfunction; however, this

171 +/- 5.5, respectively; P < 0.001) and lower AMA (40.6 +/- 5.7 compared with 42.9 +/- 6.9 cm(3), resp

172 he patients were slightly younger, had lower AMA titers, and lower sex-ratio imbalance.

173 an Medical Association Physician Masterfile (AMA-PM) on physicians trained or born in SSA countries w

174 ics: 78% female; median age 58 years; median AMA titer 1:160; extrahepatic autoimmune disorders 46%;

175 acid-based BRS (APTITUDE, Amaranth Medical [AMA]) to Absorb (bioresorbable vascular scaffold [BVS])

176 inyl methacrylate (VMA), allyl methacrylate (AMA), 4-vinylbenzyl methacrylate (VBMA), and N,N-diallyl

177 inyl methacrylate (VMA), allyl methacrylate (AMA), and N,N-diallyl acrylamide (DAA) by Cs-ligated zir

178 e (M) domain, while maintaining a monolithic AMA fold of the bifunctional enzyme.

179 The murine AMAs also inhibit PDC-E2 activity.

180 ly, we showed that T. gondii harbors a novel AMA designated as TgAMA4 that shows extreme sequence div

181 More than 30% of AMA discharges for both groups occurred before hospital

182 To address the 5% of AMA-negative patients with PBC, we have generated and va

183 teins studied herein and also the ability of AMA-negative sera to react with HiBEC apotopes.

184 ls had reduced levels of B cells, absence of AMA, and increased levels in sera of tumor necrosis fact

185 entry, trafficking, and pathogenic action of AMA in PV.

186 action of anti-AMA-1 antibodies, blocking of AMA-1 secondary processing and redistribution are additi

187 ctivity, demonstrating that a combination of AMA and a carbapenem antibiotic has therapeutic potentia

188 The main protein component of AMA, medin, readily assembles into amyloid-like fibrils

189 We show that medin, the main constituent of AMA, can induce an environment rich in oxidative species

190 validated a bead assay for the detection of AMA.

191 that although the pathobiological effects of AMA on KCs are reversible, they become irreversible, lea

192 alous processing to a 52-kDa soluble form of AMA-1).

193 d secondary processing of the 66-kDa form of AMA-1, only polyclonal IgG caused its anomalous processi

194 tribution, and cross-linked soluble forms of AMA-1 on merozoites.

195 the mechanisms leading to the generation of AMA are enigmatic, we have postulated that xenobiotic-in

196 Then, we examine the geometry of AMA's unique combination of properties that distinguish

197 mmon acceptor protein for internalization of AMA and, perhaps, for PV autoantibodies to other intrace

198 , and KCa3.1 concurrent with measurements of AMA and responses to a control antigen, tetanus toxoid,

199 The mortality of AMA-positive patients without PBC is increased irrespect

200 Over nearly 6-years, odds of AMA discharge increased 12% per year for IDU-IE [AOR 1.1

201 2 (95% CI: 1.03-1.69)] had increased odds of AMA discharge, which differed from non-IDU-IE.

202 4.48)] was associated with increased odds of AMA discharge.

203 The prevalence of AMA in FDRs and controls was 13.1% and 1%, respectively.

204 Greater prevalence of AMA was found in female FDRs of PBC probands [sisters (2

205 Despite the prevalence of AMA, little is known about the self-assembly mechanism o

206 Prevalence of AMA-positive patients without evidence of PBC was 16.1 p

207 zing therapeutics targeting a broad range of AMA-RON2 pairs and apicomplexan invasive stages.

208 tic processing and surface redistribution of AMA-1 on merozoites.

209 y, K+ channel blockers suppress secretion of AMA without a reduction of CpG-B-enhanced IgM production

210 male-to-female ratio, and seroprevalence of AMA positivity were similar between the 2 groups.

211 A prospective study of AMA incidence was conducted through a nation-wide networ

212 Women of AMA (>/=35 years) and young controls (20-30 years) with

213 ed for B cell development, the appearance of AMAs, liver pathology, and cytokine production.

214 llected for up to 7 years after detection of AMAs.

215 The rapid disappearance of AMAs in these patients provides further support for the

216 The strikingly high frequency of AMAs in ALF supports the thesis that oxidative stress-in

217 nflammatory cytokines, but similar levels of AMAs compared with dnTGFbetaRII controls.

218 with BEC apoptotic bodies in the presence of AMAs markedly increase tumor necrosis factor-related apo

219 Indeed, the presence of AMAs represents the most highly directed and specific au

220 We investigated the prevalence of AMAs in first-degree relatives (FDRs) of PBC probands to

221 man PBC, including spontaneous production of AMAs directed to the same mitochondrial autoantigens, na

222 patients with PBC, CpG induces secretion of AMAs in PBMCs andalso up-regulates B cell expression of

223 increased the sensitivity and specificity of AMAs, and they are now considered positive in approximat

224 correlation of disease severity and titer of AMAs.

225 s but were not prescribed any antibiotics on AMA discharge, and (3) received a partial course of IV a

226 tics and were prescribed oral antibiotics on AMA discharge.

227 A review of published reports on AMA positivity in paediatric age shows that the antibody

228 o did not receive oral antibiotic therapy on AMA discharge (adjusted hazard ratio [aHR], 2.32; 95% co

229 g PWID prescribed oral antibiotic therapy on AMA discharge (aHR, .99; 95% CI, .62-1.62).

230 o did not receive oral antibiotic therapy on AMA discharge (n = 46, 68.7%), compared with inpatient I

231 re then serially passaged through control or AMA-1 vaccinated mice and evaluated after 10 and 21 roun

232 ern RON2 ligand binding selectivity in other AMAs.

233 with NDM-1-expressing Klebsiella pneumoniae, AMA efficiently restored meropenem activity, demonstrati

234 loride-co-2-hydroxyethyl methacrylate) (poly(AMA-co-HEMA)) was first grafted from initiator-coated go

235 Invasion-inhibitory polyclonal AMA-1 antibodies inhibit secondary proteolytic processin

236 biliary cirrhosis (PBC) and that a positive AMA is virtually pathognomonic of either PBC or future d

237 g a non-random group of 30 rigorously proven AMA-negative patients, 50 healthy subjects, and 74 contr

238 technical advances that significantly reduce AMA's compute time: we derive gradients of cost function

239 ents at (5)Ile, (12)Ile, and (15)Glu reduced AMA reactivity even further.

240 , (12)Ile, and (15)Glu significantly reduced AMA recognition.

241 ge, 100% of animals exhibit high-titer serum AMA of all isotypes.

242 f AIH type 2 with an unexpected PBC-specific AMA positivity in a young child.

243 f AIH-2-specific anti-LKM-1 and PBC-specific AMA was confirmed by indirect immunofluorescence (IIF),

244 -purpose atomic absorption spectrophotometer AMA 254.

245 sets BRalibase II and BRalibase 2.1, Stemloc-AMA has comparable sensitivity to and better specificity

246 his leads to a new software program, Stemloc-AMA, that is both accurate and specific in the alignment

247 gnments of non-homologous sequences, Stemloc-AMA aligns only sequences with detectable homology and l

248 Histopathology revealed lower area stenosis (AMA-BRS, 21.0+/-6.1% versus BVS 31.0+/-4.5%; P=0.002) in

249 sing inhibition assay that uses a C-terminal AMA-1-specific MAb, 28G2dc1, to detect merozoite-bound r

250 ergetic abnormality related to AMA, and that AMA reduction with B-cell depletion therapy will improve

251 Thus, it appears that AMA enter a keratinocyte in a complex with FcRn, become

252 We conclude that AMA-1 may be directly responsible for reorientation or t

253 autoepitope of PDC-E2 and demonstrated that AMA in PBC reacted against several organic modified mimo

254 The fact that AMA-containing sera reacted with PDC-E2 on apoptotic BEC

255 idative stress, raising the possibility that AMA may be found in patients with keratin mutations that

256 These data suggest that AMA-1 and MSP-119 sero-epidemiological analysis may prov

257 The recent demonstration that AMAs recognize xenobiotic modified PDC-E2 with higher ti

258 ial aggregation of PBC, we hypothesized that AMAs also aggregate among relatives of PBC probands.

259 The AMA mouse model complements the human studies, demonstra

260 The AMA supports the development of new health insurance mar

261 The AMA's plan would empower individuals to choose their hea

262 ns, two out of three CDC48 proteins, and the AMA protein, function as proteasomal gatekeepers.

263 Collectively, the AMA binding studies and EPR analysis demonstrate the nec

264 At 14 days, the AMA-BRS demonstrated a higher percentage of embedded str

265 quiring surgery was 11.7, which exceeded the AMA parameters.

266 stereospecificity is slightly lower for the AMA polymerization but still leading to highly isotactic

267 6.1% versus BVS 31.0+/-4.5%; P=0.002) in the AMA-BRS at 28 days.

268 echanical testing showed no fractures in the AMA-BRS when overexpanded 1.3 mm above nominal dilatatio

269 e demonstrated living characteristics of the AMA polymerization by 1.

270 emy of Ophthalmology and Otolaryngology, the AMA's contributions to the formation of the American Boa

271 We apply this concept to the AMA-1 protein of the malaria parasite Plasmodium falcipa

272 did not lead to a significant change on the AMAs of the juices.

273 The Abs to AMA-1 and MSP-1(42) were predominantly IgG1 and IgG3.

274 (P < .0001), and lower levels of antibody to AMA-1 (P = .01) and MSP2 (P < .0001).

275 of HiBEC apotope reactivity was confined to AMA-positive sera.

276 ues within the lipoyl domain are critical to AMA recognition by maintaining conformational integrity.

277 dies to FCR3 (P = .04), and levels of IgG to AMA-1 (P </= .03) and MSP2-3D7 (P = .05).

278 or more malarial Ags, with 53% having IgG to AMA-1, 38% to MSP-1(42), 3% to RESA, and 0% to CSP.

279 tive stress-induced liver damage may lead to AMA induction.

280 a severe liver oxidant injury would lead to AMA production.

281 Measurement of antibody levels to AMA-1 at the time of malaria may offer a quantitative bi

282 y muscle bioenergetic abnormality related to AMA, and that AMA reduction with B-cell depletion therap

283 We also review the literature in relation to AMA positivity in paediatric age and adolescence.

284 aria once parasitemic, stronger responses to AMA-1, MSP-1, and MSP-3 were associated with protection

285 266-280) LACDE antibodies were restricted to AMA-positive patients (54 of 95, 57%) and belonged to im

286 er highlights the diminished number of truly AMA-negative PBC patients.

287 ay to incorporate inhibitory epitopes of two AMA-1 strains into a single protein.

288 The antigen we used, AMA-1, is a component of several candidate malaria vacci

289 tile of primary care physician measure using AMA Masterfile counts, beneficiaries in the highest quin

290 Interestingly the mother was AMA positive without other features of PBC.

291 to epidermal blistering (acantholysis), when AMA synergize with anti-Dsg antibodies.

292 es (FDRs) of PBC probands to examine whether AMAs aggregate in such pedigrees.

293 gression to identify factors associated with AMA discharge among IE hospitalizations, comparing IDU-I

294 CTLA4 49AG was significantly associated with AMA positivity among the PBC patients.

295 ficiency and altered placental function with AMA in women, with evidence of placental adaptations in

296 ) and CD8(+) T cell biliary infiltrates with AMA.

297 occurrence of PBC could imply screening with AMA of FDR with at least another autoimmune disease.

298 id residues of PDC-E2 lipoyl beta-sheet with AMA specificity is lacking.

299 or susceptibility to FGR and stillbirth with AMA.

300 Only 1 in 6 patients with AMAs and normal ALP will develop PBC after 5 years.