ライフサイエンスコーパス: ADA

1 ADA coupled to polyethylene glycol or allogeneic hematop

2 ADA development, low TL and need for dose intensificatio

3 ADA enzyme therapy in these mice normalized cochlear ade

4 ADA fasting glucose concentration clinical categories, W

5 ADA positivity and gender were predictors of LOR.

6 ADA-1 expression and enzymatic activity are increased in

7 ADA-deficient patients show specific defects in B-cell d

8 ADA-IFG (4870/11 199 [43.5%), IEC-HbA(1c) (1005 [9.0%]),

9 ADAs arise inconsistently, and it is not clear what fact

10 ADAs may decrease the efficacy of biologic drugs by neut

11 ADAs were detected in 3.8% (95% confidence interval [CI]

12 cells (Hu-NSG mice) and infected with HIV-1(ADA) can recapitulate the salient features of this progr

13 hese data show for the first time that HIV-1(ADA)-infected Hu-NSG mice can recapitulate key left vent

14 nal dynamics and diversity in a cohort of 15 ADA-SCID children treated with gammaretroviral vectors a

15 gender: p < 0.001, OR:7.8 CI 95%: 2.5-24.3, ADA positivity: p = 0.007 OR:3.6 CI 95%: 1.4-9.5).

16 3D-ADA first uses a source domain feature extractor to extr

17 3D-ADA stably improved the cross data source prediction, as

18 ning-based adversarial domain adaptation (3D-ADA) method to timely address the domain shift problem i

19 We tested 3D-ADA on both experimental and realistically simulated sub

20 Furthermore, we demonstrate that 3D-ADA can improve cross data source recovery of novel macr

21 l hernia repair: primary closure 7/109 (6%), ADA 3/30 (10%) and other mesh 2/7 (28%).

22 y VRC01 neutralized the HIV-1 isolates 89.6, ADA, SG3, and SA32 more efficiently than either antibody

23 size all possible 3-mer sequences: AAA, AAD, ADA, DAA, ADD, DAD, DDA, and DDD.

24 ts may develop Abs also called antidrug Abs (ADA), directed against these anti-TNF-alpha Abs after ju

25 acement therapies, can elicit anti-drug Abs (ADA) that may interfere with drug efficacy and impact pa

26 ro studies revealed that the Gcn5-Ada2-Ada3 (ADA) and Esa1-Yng2-Epl1 (Piccolo NuA4) histone acetyltra

27 shown that new anti-TNF agents, adalimumab (ADA) and golimumab, are effective in induction of remiss

28 Compared with patients negative for ADAs, ADA positivity in the radioimmunoassay and drug-tolerant

29 Additionally, ADA enzyme therapy rescued SNHL by restoring nerve fiber

30 reactions proceed via an aryne Diels-Alder (ADA) reaction, followed by a facile aromatization.

31 owed that patients with IL-7 receptor alpha, ADA, and CD3 chain gene mutations can have normal B-cell

32 mpetitive binder (e.g., adamantane ammonium (ADA)) for CB[7], (2) by a dual pH-chemical stimulus invo

33 199 [43.5%), IEC-HbA(1c) (1005 [9.0%]), and ADA-HbA(1c) (2299 [20.5%]) poorly predicted diabetes (3.

34 and metabolism (PCK2, PFKL, IDH2, ACY1, and ADA) are significantly downregulated because of the accu

35 electron microscopy demonstrate that AD and ADA lamellae are made of a double layer of co-oligomers

36 d samples were collected, and adalimumab and ADA concentrations was determined at baseline and at wee

37 Adalimumab and ADA concentrations, clinical response and ADA concentrat

38 Patient PASI and adalimumab and ADA concentrations.

39 ucose concentration clinical categories, and ADA and WHO 2 h glucose concentrations clinical categori

40 structure (AD) or a triad structure (DAD and ADA) in order to understand the correlations between the

41 abling unbiased measurement of both free and ADA-bound drug presents a considerable challenge.

42 od to differentiate between total, free, and ADA-bound drug for recombinant human alpha acid glucosid

43 Female gender and ADA positivity were associated with LOR (female gender:

44 ) was identified as a selective, potent, and ADA-resistant trypanocidal compound that cured T. brucei

45 a relationship between CXCL12 production and ADA development independent of the disease, which is con

46 nd ADA concentrations, clinical response and ADA concentration, and adalimumab concentration and clin

47 ine subunits of the Gcn5-containing SAGA and ADA complexes required for nonhistone protein acetylatio

48 e observation of the revertant of SCIDX1 and ADA deficiency as a kind of natural gene therapy.

49 of STAT3, IL-10, ELL2, XBP1, MYC, TERT, and ADA.

50 An accurate determination of the total and ADA-bound concentrations of the drug gives information o

51 The methods for total and ADA-bound rhGAA allow quantitation of the drug in the ra

52 up to 6 weeks; infliximab-TNF complexes and ADAs were measured by enzyme-linked immunosorbent assay

53 The formation of antidrug antibodies (ADA) can interfere with the accurate quantitation of the

54 unogenicity testing for antidrug antibodies (ADA) faces challenges when high levels of the drug are p

55 with the development of antidrug antibodies (ADAs) against each of the DART molecules.

56 The development of antidrug antibodies (ADAs) is a common cause for the failure of biotherapeuti

57 ncing the occurrence of antidrug antibodies (ADAs) is still limited.

58 he in vivo formation of antidrug antibodies (ADAs), which may reduce the efficacy of the therapy by b

59 ate the development of anti-drug antibodies (ADAs) against protein drugs by immunomodulatory bioconju

60 The formation of anti-drug antibodies (ADAs) may explain part of this variation by reducing the

61 Some patients develop anti-drug antibodies (ADAs), which reduce the efficacy of infliximab, a monocl

62 is the development of anti-drug antibodies (ADAs).

63 eeks, clinically relevant antidrug antibody (ADA) to adalimumab was frequently found.

64 ients were monitored for anti-drug antibody (ADA) development, including inhibitory capacity and chan

65 Anti-drug antibody (ADA) responses are a concern for both drug efficacy and

66 Although anti-drug antibody (ADA) responses restricted mAb delivery, one monkey succe

67 Alternatives to infliximab are ADA and golimumab.

68 nto the lowland Ajkwa River deposition area (ADA) leading to forest inundation and degradation of wat

69 Alternative assays (ADA and IRISA-TB) are significantly more sensitive, with

70 The American Diabetes Association (ADA) annually updates its Standards of Medical Care in D

71 cription: The American Diabetes Association (ADA) annually updates Standards of Medical Care in Diabe

72 cription: The American Diabetes Association (ADA) annually updates the Standards of Medical Care in D

73 IFG based on American Diabetes Association (ADA) criteria (FPG >=5.5 mmol/L [>=100 mg/dL]); IFG base

74 mmol L(-)(1) (American Diabetes Association (ADA) criteria.

75 etes Care, an American Diabetes Association (ADA) journal.

76 The American Diabetes Association (ADA) published the 2016 Standards of Medical Care in Dia

77 The American Diabetes Association (ADA) updates the Standards of Medical Care in Diabetes a

78 award of the American Diabetes Association (ADA).

79 DDK); and the American Diabetes Association (ADA).

80 oncentration (American Diabetes Association [ADA] fasting glucose concentration cutoff 5.6-6.9 mmol/L

81 previously unrecognized association between ADA-SCID and DFSP with unique features, such as multicen

82 In vitro, agents that either block ADA or overexpress adenosine resulted in altered B cell

83 we successfully attenuated priapism in both ADA(-/-) and SCD mice by restoring penile PDE5 gene expr

84 The DPP4 colocalized with membrane-bound ADA on human DCs and enhanced the ability of the latter

85 Lowering adenosine by ADA enzyme therapy or genetic deletion of ADORA2B signif

86 features of all patients with SCID caused by ADA deficiency in a single center were analyzed.

87 odified hematopoietic stem/progenitor cells, ADA gene expression, and immune reconstitution.

88 Circulating ADA levels were measured using two assays: a drug-sensit

89 6 mmol/mol]), and 2 h glucose concentration (ADA and WHO 2 h glucose concentration cutoff 7.8-11.0 mm

90 Ten subjects with confirmed ADA-deficient SCID and no available matched sibling or f

91 s, we identify the Gcn5- and Esa1-containing ADA and Piccolo NuA4 complexes as bona fide crotonyltran

92 Samples containing ADAs against V-I-Adnectin and various drug concentration

93 In an effort to control ADA, we focused on identifying regimens of immune tolera

94 The cumulative ADA positivity (>10 ng/mL) and low TL (<5.0 mug/mL) was

95 ives a K(assoc) of 500 M(-1), typical of DAD-ADA dimers.

96 known about the role of adenosine deaminase (ADA) 2 in regulation of immune responses, although recen

97 ve its interaction with adenosine deaminase (ADA) and other extracellular matrix proteins.

98 ay analysis identifying adenosine deaminase (ADA) as a key molecule that delineates a human Tfh helpe

99 nosine, whereas soluble adenosine deaminase (ADA) catabolizes adenosine to inosine.

100 Inherited defects in adenosine deaminase (ADA) cause a subtype of severe combined immunodeficiency

101 Adenosine deaminase (ADA) deficiency causes severe cellular and humoral immun

102 Adenosine deaminase (ADA) deficiency is a rare, autosomal-recessive systemic

103 o genetic evidence that adenosine deaminase (ADA) deficiency leads to excess plasma adenosine and ele

104 Adenosine deaminase (ADA) deficiency results in the accumulation of toxic met

105 eficiency (SCID X1) and adenosine deaminase (ADA) deficiency.

106 epared by entrapment of adenosine deaminase (ADA) into sol-gel derived monolithic silica columns, and

107 Three days later, an adenosine deaminase (ADA) level of 118.1 U/L (normal range, 0.0-11.3 U/L) fro

108 Adenosine deaminase (ADA), IRISA-TB (interferon gamma ultrasensitive rapid im

109 ic models: SCD mice and adenosine deaminase (ADA)-deficient mice.

110 ransplantation (HCT) of adenosine deaminase (ADA)-deficient severe combined immunodeficiency (SCID).

111 Adenosine deaminase (ADA)-severe combined immunodeficiency (SCID) is caused b

112 ve covalent modifier of adenosine deaminase (ADA).

113 etabolic degradation by adenosine deaminase (ADA).

114 tained at low levels by adenosine deaminase (ADA).

115 iency caused by adenosine deaminase defects (ADA-SCID).

116 ibrosis, and adenosine deaminase deficiency (ADA(-/-)).

117 (SCID-X1) and adenine deaminase deficiency (ADA).

118 l benefit for adenosine deaminase-deficient (ADA-deficient) SCID when combined with reduced intensity

119 e plasmon resonance (SPR) assays that detect ADAs against a bispecific Adnectin drug molecule that co

120 e median in serum were more prone to develop ADAs (aHR = 2.329 [1.106-4.90], p = 0.026).

121 Eight patients developed ADA over the 2-year study, with 3 (38%) meeting criteria

122 To model a chronic lung disease, ADA(-/-) mice were used.

123 al reduction of serum proteins to dissociate ADA-drug bindings, followed by tryptic digestion of prot

124 Conditions that lower drug-ADA interaction affinity could also be used to develop d

125 That decrease in the affinity of drug-ADA interaction correlated with an increase of assay dru

126 y, H(MQ(+))H, paired with an electroinactive ADA array, O(NH)O.

127 Exogenous ADA-1 enhances less efficient cTfh1 and pro-follicular T

128 AD) has been successfully applied to extract ADA from serum samples prior to conduction of cell-based

129 We demonstrate that the fly ADA complex has histone acetylation activity on histones

130 ncident chronic kidney disease was 0.636 for ADA fasting glucose concentration clinical categories an

131 centration clinical categories and 0.640 for ADA HbA1c clinical categories (difference -0.005, 95% CI

132 The C-statistics were 0.662 for ADA fasting glucose clinical concentration categories an

133 nical concentration categories and 0.672 for ADA HbA1c clinical categories for atherosclerotic cardio

134 r peripheral arterial disease, and 0.683 for ADA fasting glucose concentration clinical categories an

135 centration clinical categories and 0.688 for ADA HbA1c clinical categories for all-cause mortality.

136 osclerotic cardiovascular disease, 0.701 for ADA fasting glucose concentration clinical categories an

137 centration clinical categories and 0.722 for ADA HbA1c clinical categories for peripheral arterial di

138 The strongest selective advantage for ADA-transduced cells occurred at the transition from imm

139 The treatment of choice for ADA-deficient SCID (ADA-SCID) is hematopoietic stem cell

140 l for the first time the outcomes of HCT for ADA-SCID and show that, if patients survive HCT, long-te

141 l therapeutic efficacy from gene therapy for ADA-deficient SCID, with an excellent clinical safety pr

142 e therapeutic benefits with gene therapy for ADA-deficient severe combined immunodeficiency.

143 n Medicines Agency approved gene therapy for ADA-SCID patients without a suitable bone marrow donor.

144 Compared with patients negative for ADAs, ADA positivity in the radioimmunoassay and drug-to

145 In mice, we found ADA formation to increase with dose of infliximab given

146 t/transitional and mature naive B cells from ADA-SCID patients contained more autoreactive and ANA-ex

147 ur method is not prone to interferences from ADA, allowing accurate and precise measurement of the Ig

148 Viscosity of the paste produced from ADA-R-preparation in a wide range of acetylation degrees

149 ntially reduced drug exposure resulting from ADAs formation is associated with impaired clinical resp

150 Strikingly, after HSC-GT, ADA-SCID patients displayed quasi-normal early B cell to

151 concentration cutoff 6.1-6.9 mmol/L), HbA1c (ADA HbA1c cutoff 5.7-6.4% [39-46 mmol/mol] and Internati

152 Hence, ADA plays an essential role in controlling autoreactive

153 educed response to therapy due to ADAs, high ADA-bound concentrations of rhGAA were found, while in t

154 ozygous for the minor allele carrying higher ADA risk (mean: 2,693 pg/ml) than for the other genotype

155 ted with HIV(ADA) or with low numbers of HIV(ADA)-infected leukocytes to limit tissue colonization in

156 mice were either directly infected with HIV(ADA) or with low numbers of HIV(ADA)-infected leukocytes

157 D34+ cells that were modified with the human ADA cDNA (MND-ADA) gamma-retroviral vector after conditi

158 with a retroviral vector encoding the human ADA complementary DNA sequence (GSK2696273) as part of s

159 If ADA is present, dose interval shortening is less useful.

160 -deficient severe combined immunodeficiency (ADA-SCID) patients have been treated with 4 distinct gam

161 deaminase-severe combined immunodeficiency (ADA-SCID), major histocompatibility complex class II def

162 m, causing severe combined immunodeficiency (ADA-SCID), often referred to as the "bubble boy" disease

163 nosine-induced erythrocyte SphK1 activity in ADA-deficient mice.

164 colleagues investigate the B cell defects in ADA-deficient patients.

165 o study alterations in B-cell development in ADA-deficient patients and investigate the ability of ER

166 onary tissue repair, and promote survival in ADA(-/-) mice.

167 oncentrations in patient samples may inhibit ADA assays.

168 h 3 (38%) meeting criteria for an inhibitory ADA response.

169 is is reversed by the presence of inhibitory ADA.

170 Conversely, children with inhibitory ADA showed increase in uGAG over time.

171 Intriguingly, ADA-deficient patients have been reported to have bilate

172 This study demonstrated that mice lacking ADA developed COPD manifestations in association with el

173 while in the samples from a patient lacking ADAs, no significant ADA-bound concentrations were found

174 Three patients demonstrated low-level ADA at baseline, though all children tolerated IV-ERT we

175 Using the covalently linked ADA columns, bioactive mixtures identified by IMER were

176 Mechanistically, ADA-1 controls the Tfh program by influencing IL6/IL-2 p

177 AP activity and lower adenosine-metabolizing ADA activity than adult plasma.

178 Hence, we have named it the metazoan 'ADA complex'.

179 t were modified with the human ADA cDNA (MND-ADA) gamma-retroviral vector after conditioning with bus

180 The MND-ADA vector was persistently detected in PBMCs (vector co

181 Untreated murine ADA(-/-) Tregs show alterations in the plasma membrane C

182 hich was enhanced in children with low or no ADA response.

183 Patients with no ADA formation in the first 24 weeks of treatment have li

184 to characterize the neutralizing ability of ADA are vulnerable to interference from endogenous serum

185 olecule attenuates the enzymatic activity of ADA and inhibits proliferation of lymphocytic cells.

186 which is complexed with excessive amounts of ADA and endogenous serum components in the BEAD eluates.

187 t ADA-SCID and 2 healthy newborn carriers of ADA deficiency.

188 Although highly desirable, development of ADA-tolerant bioanalytical methods enabling unbiased mea

189 may be prone to premature discontinuation of ADA due to adverse events.

190 enetic variants that disrupt the function of ADA.

191 ll help, while pharmacological inhibition of ADA-1 activity impedes cTfh2-17/GC-Tfh function and dimi

192 on of post-HCT IV-ERT, but the occurrence of ADA and inhibitory antibodies are a concern and should b

193 The presence of ADA is strongly correlated with adalimumab concentration

194 ersally applicable for the quantification of ADA-bound concentrations of all non-IgG-based biopharmac

195 Drug retention rate of ADA in uveitis at 60 months was 54.28%, with a good safe

196 ence of detectable ustekinumab regardless of ADA status correlated with poor clinical outcome (median

197 otics were associated with decreased risk of ADA development, whereas tobacco smoking and infections

198 assess the long-term efficacy and safety of ADA and golimumab in ulcerative colitis.

199 The use of ADA as a second or further biotherapy could be predictiv

200 natal Fc receptor (FcRn) in the emergence of ADAs in the case of anti-TNF-alpha Abs.

201 licable approach to prevent the formation of ADAs against biologic therapies.

202 pegylated uricase inhibited the formation of ADAs in mice and non-human primates and normalized serum

203 published analyses of the clinical impact of ADAs are incomplete.

204 of 340 patients, we evaluated the impact of ADAs on ustekinumab level and clinical response as asses

205 imumab resulted in the durable inhibition of ADAs, leading to normalized pharmacokinetics of the anti

206 of infliximab produced increasing levels of ADAs.

207 atient-related factors and the occurrence of ADAs.

208 of PEGylation by the proactive prevention of ADAs.

209 onjugate significantly reduced the titers of ADAs compared with a PEGylated protein.

210 =6.1 mmol/L [>=110 mg/dL]); HbA(1c) based on ADA criteria (HbA(1c) >=39 mmol/mol [5.7%]); and HbA(1c)

211 IFG based on ADA criteria has better sensitivity than the others, but

212 birth from all 3 patients with delayed-onset ADA deficiency had normal TREC levels, but TRECs were un

213 birth from the 3 patients with delayed-onset ADA-SCID had adenosine levels of 10, 25, and 19 mumol/L

214 ould identify newborns who had delayed-onset ADA-SCID later in life.

215 at birth from 3 patients with delayed-onset ADA-SCID using tandem-MS (PCT EP2010/070517) to evaluate

216 alyzed DBSs from 3 newborns with early-onset ADA-SCID and 2 healthy newborn carriers of ADA deficienc

217 birth can identify newborns with early-onset ADA-SCID and are used in screening programs.

218 ntifies newborns with delayed- or late-onset ADA deficiency.

219 newborns who will have delayed or late-onset ADA-SCID before symptoms appear.

220 Delayed or late-onset ADA-SCID is characterized by insidious progressive immun

221 ET efficiency of a multiplex such as ADAA or ADA can be predicted from that of analogs containing a s

222 e data, in combination with results of other ADA-SCID gene therapy trials, suggest that disease backg

223 Particularly ADA-deficient patients with late-onset forms and after e

224 zed peripheral blood mononuclear cell (PBMC) ADA activity, improved lymphocyte numbers, and normal pr

225 PEG-ADA-treated mice developed multiple autoantibodies and h

226 ms and after enzyme replacement therapy (PEG-ADA) are known to manifest immune dysregulation.

227 We report that Ada(-/-) mice, phenocopying ADA-deficient humans, displayed SNHL.

228 , followed by a gradual maturation of plasma ADA through infancy.

229 servational cohorts reveal a relative plasma ADA deficiency at birth, followed by a gradual maturatio

230 tal degree of esterification of the produced ADA-R-preparation caused an increase in its resistance t

231 g domain of RyR2 (W3587A/L3591D/F3603A, RyR2(ADA)) in mice result in severe cardiac hypertrophy, poor

232 5-day-old wild-type (WT) and homozygous Ryr2(ADA/ADA) mice.

233 tress-induced ventricular arrhythmia in RyR2(ADA/+) mice.

234 The data suggest that RyR2(ADA) mutation produces significant reduction in ICa dens

235 Using RyR2(ADA/+) knock-in mice, in which half of the CaM-RyR2 bind

236 ts a role for VeA and MvlA in modifying SAGA/ADA complex activity.

237 for GcnE (H3K9 acetyltransferase of the SAGA/ADA complex) in ors cluster expression and here we find

238 treatment of choice for ADA-deficient SCID (ADA-SCID) is hematopoietic stem cell transplant from an

239 ge enzyme adenosine deaminase leads to SCID (ADA-SCID).

240 from a patient lacking ADAs, no significant ADA-bound concentrations were found.

241 However, a complex analogous to the small ADA complex in yeast has never been described in metazoa

242 cn5 acetyltransferase) complex and a smaller ADA acetyltransferase complex.

243 ved reduction in alglucosidase alfa-specific ADA.

244 ng acetylated adipate of retrograded starch (ADA-R) with various degrees of substitution with functio

245 Starting ADA in nonbiotherapy-naive patients was a predictor for

246 nes mutated in rare hematological syndromes (ADA, GP6, IL17RA, PRF1 and SEC23B), reported in prior MD

247 ss made in the gene therapy trials targeting ADA-SCID, SCID-X1, CGD and WAS, review the pitfalls, and

248 ood ratio (25.1 versus 6.8 [P = 0.032]) than ADA.

249 a higher specificity and rule-in value than ADA in this high-TB-burden setting where HIV is endemic.

250 Mass spectrometry analysis revealed that ADA and Piccolo NuA4 crotonylate lysines in the N-termin

251 " However, they also serve as a warning that ADAs may be a problem for practical application of this

252 The ADA Professional Practice Committee comprises physicians

253 The ADA Professional Practice Committee performed a systemat

254 e expansion and levee construction along the ADA in the mid-1990s, we recorded significantly (p < 0.0

255 eads was used to determine the total and the ADA-bound fractions of rhGAA in samples from Pompe patie

256 anada, received the prestigious award at the ADA's 74th Scientific Sessions, 13-17 June 2014, in San

257 For the 2017 Standards of Care, the ADA Professional Practice Committee did MEDLINE searches

258 tion of other biotherapeutic proteins in the ADA-positive clinical matrices.

259 n and did not increase drug tolerance of the ADA assay.

260 d approved by the Executive Committee of the ADA Board of Directors, which includes health care profe

261 d approved by the Executive Committee of the ADA Board of Directors, which includes health care profe

262 HIV infected-individual fail to regulate the ADA pathway.

263 For the 2017 Standards, the ADA Professional Practice Committee updated previous MED

264 To develop the 2020 Standards, the ADA Professional Practice Committee, comprising physicia

265 do not overlap with Spt3 suggesting that the ADA complex binds chromosomal sites independent of the l

266 This demonstrates that the ADA-bound rhGAA fraction can be accurately and precisely

267 tion of chrysenes (and tetraphene) using the ADA approach.

268 Prediabetes defined using the ADA fasting glucose concentration cutoff (prevalence 411

269 The definition of prediabetes using the ADA fasting glucose concentration cutoff was more sensit

270 r major clinical outcomes, whereas using the ADA HbA1c cutoff (2027 [19%] of 10 884 people; 18.0-19.4

271 Prediabetes defined using the ADA HbA1c cutoff showed a significant overall improvemen

272 At least 85% of the ADAs were neutralizing.

273 These ADAs can lead to a decrease in biologic concentration, w

274 Thus, ADA-1 regulates human Tfh and represents a potential tar

275 ts complex with TNF that might contribute to ADA generation.

276 trypanotoxicity while gaining resistance to ADA-mediated metabolism.

277 pendently negatively associated with time to ADA development, whereas infections during the study (aH

278 g the first 12 months of therapy for time to ADA development.

279 nt with a reduced response to therapy due to ADAs, high ADA-bound concentrations of rhGAA were found,

280 (i.e., DA and AD) and a fluorescent triplex (ADA).

281 wing that two of the apparent hits were true ADA inhibitors and demonstrating the ability of this met

282 thus a new column format was developed using ADA that was covalently immobilized to monolithic silica

283 Moreover, using ADA enzyme therapy to reduce adenosine or a specific ant

284 ise, the "adaptive combination of P-values" (ADA) method removes variants with larger P-values.

285 HO criteria and 20.2% (95%CI 17.5-22.9) with ADA criteria.

286 nd biochemical complications associated with ADA deficiency.

287 lexes; complex formation was associated with ADA formation with an area under the curve of 0.944 (95%

288 s due to formation of protein complexes with ADA or nonspecific binding with the beads.

289 one person with AGR was two US dollars with ADA and three point seven dollars with WHO cut-offs.

290 inflammation in obesity by interacting with ADA.

291 The DPP4 interaction with ADA in human DC/macrophages was competitively inhibited

292 tributed to the death of only 1 patient with ADA deficiency.

293 ologic characteristics between patients with ADA deficiency with or without PAP.

294 Among 16 consecutive patients with ADA deficiency, 7 had BAL fluid containing periodic acid

295 peripheral B-cell lymphopenia, patients with ADA-deficient severe combined immunodeficiency showed a

296 ome of gene therapy (GT) in 18 patients with ADA-SCID for whom an HLA-identical family donor was not

297 cacy observed in more than 100 patients with ADA-SCID who received gammaretrovirus- or lentivirus-med

298 the immune deficiency seen in patients with ADA-SCID, patients should be followed for specific nonin

299 the known DNA repair defect in patients with ADA-SCID.

300 fficacy in 15 patients, 7 with and 8 without ADA; improvement in responder status occurred in 1 of 7