ライフサイエンスコーパス: ADA

1 ADA coupled to polyethylene glycol or allogeneic hematop

2 ADA deficiency predisposes to the development of PAP, wh

3 ADA development, low TL and need for dose intensificatio

4 ADA fasting glucose concentration clinical categories, W

5 ADA positivity and gender were predictors of LOR.

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

7 ADAs may decrease the efficacy of biologic drugs by neut

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

9 tulas: 2/109 (2%) primary closure, 1/30 (3%) ADA and 1/7 (14%) synthetic mesh.

10 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).

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

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

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

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

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

16 the formation of alternative donor-acceptor (ADA) stacks.

17 because of the ubiquitous expression of ADA, ADA-deficient patients often present also with nonimmuno

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

19 ough the administration of 1-adamantylamine (ADA), removing CB[7] from the nanoparticle surface, caus

20 tor (BCR) and TLR functions in B cells after ADA inhibition, which may underlie the defects in B cell

21 implantation of acellular dermal allograft (ADA) and 7 (19%) implantation of another mesh.

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

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

24 with ADA-deficient marrow transduced with an ADA-expressing gamma-retroviral vector without precondit

25 e), with gene marking in PBMC of 1%-10%, and ADA enzyme expression in PBMC near or in the normal rang

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

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

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

29 Adalimumab and ADA concentrations, clinical response and ADA concentrat

30 Patient PASI and adalimumab and ADA concentrations.

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

32 are given nonmyeloablative conditioning and ADA enzyme-replacement therapy (ERT) is withheld before

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

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

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

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

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

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

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

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

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

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

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

44 g in the generation of anti-drug antibodies (ADA) with potentially harmful clinical consequences.

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

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

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

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

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

50 n or thymus, of AOD/ADA-resistant B6 and AOD/ADA-susceptible A/J, B6A, and B6-Chr17(A/J) mice.

51 odes (LNs), but not spleen or thymus, of AOD/ADA-resistant B6 and AOD/ADA-susceptible A/J, B6A, and B

52 Alternatives to infliximab are ADA and golimumab.

53 hat the CD8(+)CD28(+) T lymphocytes that are ADA(+) have significantly greater telomerase activity th

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

55 e 2006 and past American Dental Association (ADA) studies on the distribution of dentists provides in

56 The American Diabetes Association (ADA) and American Psychiatric Association (APA) recommen

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

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

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

60 1997 and 2003 American Diabetes Association (ADA) definitions of IFG to predict CVD.

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

62 y 2004 by the American Diabetes Association (ADA).

63 award of the American Diabetes Association (ADA).

64 award of the American Diabetes Association (ADA).

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

66 Because ADA converts adenosine to inosine, cells lacking this en

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

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

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

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

71 lacement therapy (ERT) with pegylated bovine ADA, and autologous haematopoietic stem cell gene therap

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

73 ng is that chronic reduction of adenosine by ADA enzyme therapy successfully attenuated penile fibros

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

75 C, the transgenic cMyBP-C(SAS(t/t)), cMyBP-C(ADA(t/t)), and cMyBP-C(DAD(t/t)) mice showed no increase

76 BP-C(SAS)), Ala-273-Asp-282-Ala-302 (cMyBP-C(ADA)), or Asp-273-Ala-282-Asp-302 (cMyBP-C(DAD)), were g

77 trast, T effector cells are enriched in CD26/ADA but express low levels of CD39 and CD73.

78 sence of CD39 and the low expression of CD26/ADA are responsible for the generation of adenosine, whi

79 y genes comprising Ig molecules, CD83, CD8A, ADA, and CCL8 were the largest subset upregulated, and a

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

81 duced the resistance phenotype in a chimeric ADA envelope containing the C2-V5 region from RU570 pass

82 6 mmol/mol]), and 2 h glucose concentration (ADA and WHO 2 h glucose concentration cutoff 7.8-11.0 mm

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

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

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

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

87 mice were as resistant to D3Tx-AOD and D3Tx-ADA as B6 mice, thereby excluding Foxp3 as a susceptibil

88 so present data mapping QTL controlling D3Tx-ADA to Chr17 (Ada1/H2), Chr1 (Ada2), and Chr3 (Ada3).

89 genesis (AOD) and autoimmune dacryoadenitis (ADA) in A/J and (C57BL/6J x A/J) F(1) hybrids (B6A), but

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

91 rine precursors, making adenosine deaminase (ADA) a key enzyme in the pathway of hypoxanthine formati

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

93 Genetic deficiency of adenosine deaminase (ADA) can cause profound lymphopenia and result in the cl

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

95 ects in the function of adenosine deaminase (ADA) cause severe combined immunodeficiency (SCID) and a

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

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

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

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

100 Adenosine deaminase (ADA) deficiency, a cause of X-linked severe combined imm

101 Adenosine deaminase (ADA) gene defects are among the most common causes of SC

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

103 In the absence of adenosine deaminase (ADA), adenosine and other purine metabolites accumulate,

104 ng from a deficiency in adenosine deaminase (ADA), developed renal dysfunction and fibrosis.

105 ory receptor component, adenosine deaminase (ADA), on the process of replicative senescence.

106 s express low levels of adenosine deaminase (ADA), the enzyme responsible for adenosine breakdown, an

107 mal models of priapism, adenosine deaminase (ADA)-deficient mice and SCD transgenic mice.

108 Adenosine deaminase (ADA)-deficient mice develop progressive airway inflammat

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

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

111 ial in 10 patients with adenosine deaminase (ADA)-deficient severe combined immunodeficiency using 2

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

113 etabolic degradation by adenosine deaminase (ADA).

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

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

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

117 deficient severe combined immune deficiency (ADA-SCID) can provide significant long-term benefit when

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

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

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

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

124 rase activity than those that do not express ADA and that ADA is progressively lost as cultures progr

125 ene therapy with a retrovirus that expresses ADA resulted in the apparent correction of these defects

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

127 /109 (2%) for primary closure, 0/30 (0%) for ADA and 1/7 (14%) for other mesh.

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

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

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

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

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

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

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

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

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

137 CID forms, 2 other options are available for ADA-SCID: enzyme replacement therapy (ERT) with pegylate

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

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

140 tle data are available on outcome of HCT for ADA-SCID in particular.

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 l transplantation is the major treatment for ADA-SCID, although survival following different donor so

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

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

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

148 was that genetic removal of the A(2B)R from ADA-deficient mice would lead to diminished pulmonary in

149 Plasmodium gallinaceum ADA does not use MTA as a substrate, is not inhibited by

150 A(2B)R signaling in this model by generating ADA/A(2B)R double-knockout mice.

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

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

153 Hence, ADA plays an essential role in controlling autoreactive

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

155 te for most malarial ADAs, but not for human ADA.

156 n state analogue with low affinity for human ADA.

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) and set out to evaluate the association of the

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

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

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

164 leading to severe combined immunodeficiency (ADA-SCID).

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

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

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

168 nosinergic machinery and loss of function in ADA-deficient Tregs provide new insights into a predispo

169 contributing to autoimmune manifestations in ADA deficiency.

170 clear antibodies (ANAs), frequently occur in ADA-SCID patients after treatment.

171 Furthermore, pharmacological studies in ADA-deficient mice demonstrate that A(2B)R antagonism ca

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

173 ms causing defective peripheral tolerance in ADA-SCID.

174 immunodeficiency with recurrent infections (ADA-SCID).

175 oncentrations in patient samples may inhibit ADA assays.

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

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

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

179 Compared to malarial ADA complexes with adenosine or deoxycoformycin, 5'-meth

180 TA and MT-coformycin specificity in malarial ADAs is the subject of speculation.

181 osine (MTA) is a substrate for most malarial ADAs, but not for human ADA.

182 The catalytic site specificity of malarial ADAs permits methylthiocoformycin (MT-coformycin) to act

183 5'-methylthioribosyl groups in the malarial ADAs.

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

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

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

187 ministration of polyethylene glycol-modified ADA to reduce adenosine levels and the inhibition of the

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

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

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

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

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

193 t antibodies isolated from single B cells of ADA-SCID patients before and after HSC-GT.

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

195 ver, because of the ubiquitous expression of ADA, ADA-deficient patients often present also with noni

196 enetic variants that disrupt the function of ADA.

197 The inhibition of ADA activity on effector T cells enhanced Treg-mediated

198 The presence of ADA is strongly correlated with adalimumab concentration

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

200 ngs provide the first evidence for a role of ADA in modulating the process of replicative senescence

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

202 the natural course of DFSP in the setting of ADA-SCID is unknown, this observation should prompt regu

203 Here, the crystal structure of ADA from Plasmodium vivax (PvADA) in a complex with MT-c

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

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

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

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

208 ransplantation cytoreduction and remained on ADA enzyme-replacement therapy (ERT) throughout the proc

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

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

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

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

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

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

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

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

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

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

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

220 n B cell tolerance in the setting of partial ADA deficiency that is corrected by gene therapy.

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

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

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

224 Tregs isolated from PEG-ADA-treated mice lacked suppressive activity, suggesting

225 Tregs isolated from PEG-ADA-treated patients are reduced in number and show decr

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

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

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

229 nd kinetic analysis of five other Plasmodium ADAs establish the unique structural basis for its speci

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 ved reduction in alglucosidase alfa-specific ADA.

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

243 icles displaying CCR5-tropic clade B (strain ADA) or clade C (IN98012) Envs.

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

245 than those that do not express ADA and that ADA is progressively lost as cultures progress to senesc

246 They demonstrate that ADA patients receiving enzyme replacement therapy had B

247 studies to investigate the possibility that ADA deficiency is associated with a stem cell defect.

248 The ADA Professional Practice Committee performed a systemat

249 The ADA stacks can be expediently obtained in high yield as

250 istically significant improvements after the ADA guidelines were issued, monitoring for plasma lipids

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

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

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

254 , suggestions are offered for efforts by the ADA and/or the American Academy of Periodontology to dra

255 The high-avidity Ab elicited by the ADA Env had excellent breadth for the Envs of incident c

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

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

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

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

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

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

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

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

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

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

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

269 trypanotoxicity while gaining resistance to ADA-mediated metabolism.

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

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

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

273 Unexpectedly, ADA/A(2B)R double-knockout mice exhibited enhanced pulmo

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

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

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

277 To assess whether ADA deficiency affects the establishment of B cell toler

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

279 a surface-bound glycoprotein associated with ADA.

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

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

282 inflammation in obesity by interacting with ADA.

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

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

285 We have diagnosed PAP among patients with ADA deficiency more commonly in the last 10 years than p

286 absolute neutrophil counts of patients with ADA deficiency vary inversely with the accumulation of d

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

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

289 alveolar proteinosis (PAP) in patients with ADA deficiency.

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

291 d investigational therapies to patients with ADA-SCID and support further studies to investigate the

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

293 Twelve patients with ADA-SCID were evaluated with a complete dermatologic exa

294 analyzed outcome of HCT in 106 patients with ADA-SCID who received a total of 119 transplants.

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

296 regular screening for DFSP in patients with ADA-SCID.

297 cellularity are often found in patients with ADA-SCID.

298 Abdominal wall reconstruction with ADA biologic mesh provides an expeditious means of perfo

299 Mice were transplanted with ADA-deficient marrow transduced with an ADA-expressing g

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