ライフサイエンスコーパス: PID

1 PID binding rate was also sensitive to H4B and Arg site

2 PID bound to iNOS heme to generate an irreversible PID-i

3 PID could also interact with nascent iNOS monomers in iN

4 PID has been observed to undergo transient internalizati

5 PID skin displayed increased ecological permissiveness w

6 PID, but not D6PK, can also induce PIN1 polarity shifts,

7 PIDs are hugely beneficial in promoting our knowledge of

8 a comprehensive gene panel incorporating 162 PID genes.

9 A total of 162 PID genes were screened in 261 patients by using the Ion

10 ed bacterial and fungal skin microbiomes (41 PID, 13 AD, 49 healthy controls) at four clinically rele

11 A PID control loop automatically stabilizes the stage agai

12 ns were abnormal in 26 children (16%), and a PID was identified in 17 patients (10%), including 1 cas

13 ribe activated PI3K-delta syndrome (APDS), a PID associated with a dominant gain-of-function mutation

14 y when cytopenia is the initial symptom of a PID, the order and depth of diagnostic steps have to be

15 Information about PIDs is often widely scattered throughout the clinical a

16 hods for gene editing might allow additional PIDs to be treated by gene therapy because they will all

17 3 was sufficient for binding to Shc, CH1 and PID domains of Shc were responsible for binding to Jak3.

18 The differential effects of D6PK and PID on PIN1 polarity had so far been attributed to their

19 explain the differential effects of D6PK and PID on PIN1 polarity, and suggest that a more complex mo

20 At the same time, we reveal that D6PKs and PID have differential phosphosite preferences.

21 ate an association between M. genitalium and PID, and limited data suggest associations with infertil

22 Our data suggest that IID and PID ripple-like oscillations (150-250Hz) in human epilep

23 rocal regulation of gravitropism by RCN1 and PID.

24 We observed that the apparent PID affinity for the monomer was 11 times higher than th

25 ations, particularly those aged >2 years, as PIDs may be discovered in up to 26% of cases.

26 Several studies assessed PID diagnosis after untreated chlamydial infection, but

27 We investigated the association between PID and the risk of epithelial ovarian cancer according

28 No association was observed between PID and ovarian cancer risk overall (pOR = 0.99, 95% CI:

29 tify and functionally annodate lipid-binding PIDs on a genomic scale, we performed experimental and c

30 hypothesis that phosphorylation mediated by PID kinase and dephosphorylation regulated by the ROOTS

31 is, and endemic mycoses can all be caused by PIDs.

32 ons in more than 170 different genes causing PIDs have been described.

33 the greatest risk was associated with T-cell PIDs and common variable immunodeficiency.

34 PIDO characterizes PIDs in terms of the phenotypes commonly observed by cli

35 bility that a CT episode will cause clinical PID was 0.16 (95% credible interval (CrI): 0.06, 0.25),

36 i-infectious prophylaxis for the most common PIDs.

37 In conclusion, PID was associated with an increased risk of borderline

38 In contrast, PID ripples were associated with depolarizing synaptic i

39 a much larger impact and reduces cumulative PID incidence in women due to M. genitalium by 31.1% (95

40 o a running wheel (RW) from post-injury-day (PID) 14 to 20.

41 At postinoculation day (PID) 28, pigs either were euthanized or were challenged

42 irus shedding began at postinoculation days (PID) 1 to 3 and continued up to PID 16 (1 x 10(5) to 2 x

43 literature on PML in primary immune defects (PIDs).

44 ld of genetics, primary immune deficiencies (PIDs) can be diagnosed and treated earlier to provide be

45 n patients with primary immune deficiencies (PIDs) have led to important breakthroughs in our underst

46 ances in treating primary immune deficiency (PID) disorders by stem cell transplantation (SCT); we ha

47 Peri-infarct depolarizations (PIDs) are seemingly spontaneous spreading depression-lik

48 s, detrimental peri-infarct depolarizations (PIDs) contribute to secondary infarct growth and negativ

49 xing and a proportional-integral-derivative (PID) temperature controller minimised temperature based

50 glycemia), proportional-integral-derivative (PID), model predictive control (MPC) and fuzzy logic bas

51 imidazole core compound and its derivative (PID), having low cellular toxicity and high affinity for

52 typical presentation of previously described PIDs.

53 settings, 2%-5% of untreated women developed PID within the approximately 2-week period between testi

54 ype-phenotype correlations for the different PID disorders.

55 all the clinical trials targeting different PIDs has been extremely encouraging but not without cave

56 armacologically induced preictal discharges (PIDs) preceding ictal-like events.

57 ciation between pelvic inflammatory disease (PID) and ovarian cancer risk are few and inconsistent.

58 ode of clinical pelvic inflammatory disease (PID) and the reduction in such episodes among women with

59 a infection and pelvic inflammatory disease (PID) is a key parameter for models evaluating the impact

60 Pelvic inflammatory disease (PID) is a leading cause of both tubal factor infertility

61 Pelvic inflammatory disease (PID) is an important cause of infertility and ectopic pr

62 is, cervicitis, pelvic inflammatory disease (PID), and tubal factor infertility.

63 dometritis, and pelvic inflammatory disease (PID), including an association with risk for human immun

64 is, cervicitis, pelvic inflammatory disease (PID), infertility and ectopic pregnancy.

65 es, can lead to pelvic inflammatory disease (PID), infertility, ectopic pregnancy, and chronic pelvic

66 cally suspected pelvic inflammatory disease (PID).

67 mong women with pelvic inflammatory disease (PID).

68 t severe primary immune deficiency diseases (PIDs) have been successfully treated with allogeneic hem

69 for rare primary immune deficiency diseases (PIDs), including severe combined immune deficiency (SCID

70 Primary immunodeficiency diseases (PIDs) are Mendelian conditions of high phenotypic comple

71 utated in primary immunodeficiency diseases (PIDs) where reversions have been described also revealed

72 ecognized primary immunodeficiency diseases (PIDs), including their clinical, genetic and laboratory-

73 any human primary immunodeficiency diseases (PIDs).

74 tool for primary immunodeficiency diseases (PIDs).

75 Primary immunodeficiency disorders (PIDs) represent a range of genetically determined diseas

76 nts with primary immunodeficiency disorders (PIDs) than in the general population.

77 several primary immunodeficiency disorders (PIDs) with gene therapy.

78 nts with primary immunodeficiency disorders (PIDs), but there are no large studies looking at long-te

79 The use of laboratory testing to distinguish PIDs from HIV infection was clarified.

80 so known as principal immunodominant domain (PID) because of its high immunogenicity, and it is essen

81 retrovirus expressing Pak inhibitory domain (PID), a well-characterized inhibitor of Pak activation.

82 e newly identified PALB2-interacting domain (PID) in RNF168 and the WD40 domain in PALB2, and drives

83 n we have termed the PSF-interacting domain (PID).

84 efined C-terminal P-TEFb-interacting domain (PID).

85 main and phosphotyrosine interaction domain (PID) of Shc.

86 nteracting with protein-interaction domains (PIDs).

87 nd that astroglial calcium elevations during PIDs are mediated by inositol triphosphate receptor type

88 tracellular accumulation of glutamate during PIDs is strongly curtailed in Ip3r2-deficient mice, resu

89 advocacy efforts of established and emerging PID networks promote excellence in clinical recognition

90 Thus, our study establishes PID as a versatile iNOS inhibitor and therefore a potent

91 were sacrificed immediately after exercise (PID 21).

92 trachomatis is an important risk factor for PID, but the proportion of PID cases caused by C. tracho

93 Analyses of the outcomes of SCT for PID by specific molecular defect have clarified which co

94 years since the last major review of SCT for PID.

95 antation with RIC by using Flu/Melph and for PIDs by using bone marrow (n = 93) or peripheral blood s

96 rs, the French National Reference Center for PIDs aimed at elaborating recommendations for anti-infec

97 m morbidity, the French Reference Center for PIDs initiated a prospective multicenter cohort: the Fre

98 nel and its utility as a diagnostic tool for PIDs.

99 l in children undergoing transplantation for PIDs using RIC with fludarabine and melphalan (Flu/Melph

100 hematopoietic stem cell transplantation for PIDs was reviewed, with recommendations to give priority

101 c regimens associated with the most frequent PIDs.

102 s endowed with a 1,2-diketone functionality (PIDs) as efficient intermediates to easily access peryle

103 situ FTIR spectroscopy, HPLC-UV/FID, and GC-PID and quantified in a yield of (24 +/- 5) %.

104 RPOSE OF REVIEW: Primary immunodeficiencies (PIDs) are an often-devastating class of genetic disorder

105 Primary immunodeficiencies (PIDs) are inherited diseases associated with a considera

106 Some primary immunodeficiencies (PIDs) are known to confer predisposition to IPD.

107 racterization of primary immunodeficiencies (PIDs) in human subjects is crucial for a better understa

108 understanding of primary immunodeficiencies (PIDs) in pathogenesis, diagnosis, and treatment were pub

109 st children with primary immunodeficiencies (PIDs) now reach adulthood.

110 Primary immunodeficiencies (PIDs) represent exquisite models for studying mechanisms

111 Primary immunodeficiencies (PIDs) that predispose to EBV-associated malignancies hav

112 mutations cause primary immunodeficiencies (PIDs) that predispose to infections.

113 We review the primary immunodeficiencies (PIDs) underlying an increasing variety of superficial an

114 s (21%) of human primary immunodeficiencies (PIDs) were initially reported in single patients.

115 or patients with primary immunodeficiencies (PIDs) who require hematopoietic stem cell transplantatio

116 wide spectrum of primary immunodeficiencies (PIDs), but outcome is heavily dependent on the availabil

117 The primary immunodeficiencies (PIDs), rare inherited diseases characterized by severe d

118 of patients with primary immunodeficiencies (PIDs), the application of a prophylactic regimen is ofte

119 features of many primary immunodeficiencies (PIDs).

120 in actin-related primary immunodeficiencies (PIDs).

121 xpanding area of primary immunodeficiencies (PIDs).

122 tic approach for primary immunodeficiencies (PIDs).

123 own to cause the primary immunodeficiencies (PIDs).

124 being Mendelian primary immunodeficiencies (PIDs).

125 Primary immunodeficiency (PID) disorders are a heterogeneous group of inherited di

126 Primary immunodeficiency (PID) patients suffer recurrent microbial infections, pro

127 Autoimmunity in PID raises a conundrum: How can an immune system fail to

128 ances in treatment options for cytopenias in PID is provided to facilitate multidisciplinary manageme

129 ons that may reconstitute genetic defects in PID is related to an increased propensity of those genes

130 me of increased ecological permissiveness in PID skin was counterbalanced by the maintenance of a phy

131 to uncertainty in the absolute reduction in PID and sequelae.

132 bial colonization and community stability in PID skin and informs our understanding of host-microbiom

133 tion than that observed for genes mutated in PIDs where revertants have not been identified or contro

134 echanisms underlying disease pathogenesis in PIDs, and developments in immune cell-mediated therapy t

135 i (Candida, Aspergillus) supported increased PID skin permissiveness, suggesting that skin may serve

136 und to iNOS heme to generate an irreversible PID-iNOS monomer complex that could not be converted to

137 og of the Arabidopsis PINOID protein kinase (PID), and tested for trait associations with bif2 in bot

138 tate a genetic diagnosis in any of 170 known PID-related genes by using next-generation sequencing (N

139 s detection of mutations in 161 of 170 known PID-related genes.

140 patients with atypical presentation of known PID genes.

141 ted atypical clinical presentations of known PIDs.

142 th malignancies and on malignancies in large PID cohorts, we conclude that a large part of tumor pred

143 This has been driven by linking PID-specific genetic defects to the associated unique ab

144 achomatis infection; better tools to measure PID and tubal damage; and studies on the natural history

145 microbiomes in patients with rare monogenic PIDs: hyper-IgE (STAT3-deficient), Wiskott-Aldrich, and

146 r discharge photoionization detector (muHDBD-PID) on chip with dimensions of only approximately 15 mm

147 Furthermore, the muHDBD-PID can be driven with a miniaturized ( approximately 5

148 The muHDBD-PID developed here can have a broad range of application

149 The dependence of the muHDBD-PID performance on bias voltage, auxiliary helium flow r

150 Finally, the muHDBD-PID was employed to detect permanent gases and a sublist

151 aires registry (CEREDIH; the French national PID registry) for the occurrence of autoimmunity and inf

152 lk to signaling pathways in the KEGG and NCI-PID databases.

153 the literature (81% for KEGG and 78% for NCI-PID).

154 a set of more than 7000 pathway pairs in NCI-PID.

155 However, new PIDs are being discovered at an ever-increasing rate.

156 The targeted NGS PID gene panel is a sensitive and cost-effective diagnos

157 Nine PID-related genes proved not eligible for evaluation by

158 We have recently characterized a novel PID now named "X-linked immunodeficiency with magnesium

159 ndependent groups have begun to define novel PIDs caused by defects in the caspase recruitment domain

160 and PITT, have been prepared from the novel PIDs.

161 fic association with PID, the association of PID with ovarian cancer risk is still somewhat uncertain

162 pectively screened 2183 consecutive cases of PID in the Centre de Reference Deficits Immunitaires Her

163 Thirty-six patients with 12 classes of PID diagnoses received 37 VST products before or after H

164 infected women to measure the development of PID.

165 among many women who receive a diagnosis of PID, the incidence and timing of PID and long-term seque

166 ex model is needed to explain the effects of PID.

167 Women with at least 2 episodes of PID had a 2-fold increased risk of borderline tumors (pO

168 among women who had had multiple episodes of PID.

169 Further studies of the etiology of PID in different age groups are required.

170 were associated with engraftment failure of PID-LSK.

171 The field of PID continues to expand and advancements have been made

172 early diagnosis of the most severe forms of PID before the onset of symptoms.

173 rials have been conducted for other forms of PID including chronic granulomatous disease and Wiskott-

174 Novel forms of PID were identified by using whole-exome sequencing or a

175 t children and adults with specific forms of PID, such as severe combined immunodeficiency, for over

176 A history of PID was associated with an increased risk of borderline

177 OSoxy) with H4B to elucidate the kinetics of PID binding to the iNOS monomer and dimer.

178 a limited role in root development; loss of PID activity alters auxin transport and gravitropism wit

179 of concurrently screening a large number of PID genes.

180 The PEFs of PID due to C. trachomatis decline steeply with age by a

181 ecific population excess fractions (PEFs) of PID due to C. trachomatis, using routine data, surveys,

182 our preferred estimates of the proportion of PID cases caused by C. trachomatis are 35% (95% credible

183 t risk factor for PID, but the proportion of PID cases caused by C. trachomatis is unclear.

184 cial for identifying a certain proportion of PID phenotypes and genotypes among descriptive diagnoses

185 nvestigated the possibility that the rate of PID due to CT is greater during the period immediately f

186 However, the rate of PID progression in the general, asymptomatic population

187 p3r2-deficient mice displayed a reduction of PID frequency and overall PID burden and showed increase

188 There is heterogeneity in the risk of PID after a chlamydia infection.

189 tested for chlamydia to estimate the risk of PID diagnosed in a primary care, outpatient, or inpatien

190 The increased risk of PID from reinfection was highest in younger individuals

191 gnosis of chlamydia had an increased risk of PID over their reproductive lifetime compared with those

192 result of calcium-dependent sequestration of PID by the calcium-binding protein TOUCH3 (TCH3).

193 iagnosis of PID, the incidence and timing of PID and long-term sequelae from an untreated chlamydial

194 n is highly suggestive of a specific type of PID.

195 ly reported on the updated classification of PIDs.

196 oimmunity and inflammation in the context of PIDs, with a view to accurately assessing these risks an

197 ectly related to the laboratory diagnosis of PIDs.

198 us diseases specialists in the management of PIDs and improving the outcome of patients with PIDs.

199 In the management of PIDs, refinement of indication and strategies to hematop

200 An increasing number of PIDs are being shown to underlie fungal infectious disea

201 The development of an ontology of PIDs is therefore a central step toward developing infor

202 The prevalence of PIDs increases as researchers discover novel immunodefic

203 The proportion of PIDs was much higher in children aged >2 years than in y

204 ble alternative for children with a range of PIDs.

205 nce in clinical recognition and treatment of PIDs in children.

206 or gene therapy where effective treatment of PIDs is achieved without serious risk for patients.

207 targeting technologies for the treatment of PIDs.

208 Twenty-five patients with 12 types of PIDs received 26 HSCTs.

209 Remarkably, all types of PIDs were associated with a risk of autoimmune and infla

210 However, because of the variety of PIDs and pathogens involved, and because evidence is sca

211 On PID 21, rats were tested for spatial learning in a Morri

212 Immunological Societies Expert Committee on PIDs recently reported on the updated classification of

213 yed a reduction of PID frequency and overall PID burden and showed increased neuronal survival after

214 Compared to overall PID maximums, overall intereye differences in EEG monkey

215 For each normal animal and each parameter, PID was calculated (both overall and regionally) by conv

216 o other databases: Reactome, BioCarta, Pfam, PID and SMART, finding additional hits in ErbB and EPHA

217 While PINIOD (PID) kinase is directly involved in the phosphorylation

218 ated by D6 PROTEIN KINASE (D6PK) and PINOID (PID)/WAG kinases of the Arabidopsis AGCVIII kinase famil

219 INASE (D6PK) and the BFA-insensitive PINOID (PID) phosphorylate and activate PIN1 through phosphoryla

220 The protein kinase PINOID (PID) is involved in regulating PIN phosphorylation, and

221 the serine/threonine protein kinase PINOID (PID), which regulates auxin transport in Arabidopsis.

222 PIDTC analyze outcomes of treatment for rare PIDs in multicenter longitudinal retrospective, prospect

223 The rarer PID patients without chronic granulomatous disease (CGD)

224 ents in stroke and brain injury would reduce PID incidence and their adverse impact on outcome.

225 Our data suggest that reduced PID kinase function inhibits gravitropism and basipetal

226 prevent 61% (95% CrI: 55, 67) of CT-related PID in women who became infected with CT.

227 TRAP150's PID directly inhibits the interaction of PSF RRMs with R

228 to safe and effective treatments for several PIDs, including forms of severe combined immune deficien

229 ffective in young adult patients with severe PID and should be considered the treatment of choice whe

230 ng success rates for some of the most severe PIDs.

231 therapies (such as gene therapy) to specific PID disorders.

232 boratory parameters associated with specific PID and should improve the time required to attain an ac

233 erstanding of optimal therapies for specific PIDs.

234 views of new information related to specific PIDs including new tests, new genetic associations and n

235 can American women with clinically suspected PID from the PID Evaluation and Clinical Health Study.

236 ng to the largest studies, after symptomatic PID of any cause has occurred, up to 18% of women may de

237 ctive studies assessing rates of symptomatic PID, subclinical tubal damage, and long-term reproductiv

238 Our data suggest that PID plays a limited role in root development; loss of PI

239 model of focal ischemia to demonstrate that PIDs are associated with a strong increase of intracellu

240 It is known that PIDs can also predispose to cancer and immune diseases,

241 The PID-LSK demonstrated decreased phosphorylation of extrac

242 BRD4 domains, the second bromodomain and the PID, bind P-TEFb and are required for full transcription

243 women with clinically suspected PID from the PID Evaluation and Clinical Health Study.

244 ontain HEXIM1 and 7SK snRNA, implicating the PID in the liberation of P-TEFb from the 7SK small nucle

245 Overexpression of the PID alone in cells dissociates HEXIM1 and 7SK snRNA from

246 ne regions of the amino acid sequence of the PID and engineer a highly soluble mutant that preserves

247 For all parameters the PID maximums were relatively small overall.

248 overall and regionally were compared to the PID and PIPD maximums.

249 the same molecular defect that underlies the PID, such as syndromes of DNA repair deficiency or immun

250 as a therapeutic tool, particularly for the PIDs.

251 Therefore, PIDs are triggered upon supply-demand mismatch transient

252 However, a systematic search for these PIDs has never been carried out in children presenting w

253 Studies of these PIDs have revealed a pivotal role for the actin cytoskel

254 However, in contrast to PID overexpression studies, we observed wild-type asymme

255 Describing the progression to PID in mathematical models as an average rate may be an

256 one marrow and altered cell shape similar to PID-LSK cells in vitro and are completely defective in H

257 lation days (PID) 1 to 3 and continued up to PID 16 (1 x 10(5) to 2 x 10(7) GE/ml).

258 that mismatch predisposes stroke patients to PIDs as well.

259 related to local CBF changes in response to PIDs.

260 uggest that further improvements in treating PID with SCT are possible with a greater understanding o

261 Factors triggering PIDs are unknown.

262 y activation of peri-infarct cortex triggers PIDs when the activated cortex is within a critical rang

263 ia or hypotension also reproducibly triggers PIDs.

264 in patients with previously uncharacterized PIDs has opened up the potential for targeted therapy di

265 ry analyses aimed at defining the underlying PID.

266 However, the cellular pathways underlying PIDs have remained unclear.

267 n mutations and 26 patients with undiagnosed PIDs.

268 hatase holoenzyme acts antagonistically with PID to direct auxin transport polarity and plant develop

269 ted chlamydial infection was associated with PID and other reproductive sequelae, although it was dif

270 icated a histotype-specific association with PID, the association of PID with ovarian cancer risk is

271 reatment modalities offered to patients with PID is leading to a better understanding of optimal ther

272 Women with PID who carried the TLR4 rs1927911 CC genotype had signi

273 Among women with PID, TLR variants that increase inflammation are associa

274 Among African American women with PID, variants in the TLR1 and TLR4 genes, which may incr

275 Adults with PIDs diagnosed during childhood experienced a heavy burd

276 d with the French normal values, adults with PIDs scored significantly lower for all HRQoL domains.

277 f gain-of-function mutations associated with PIDs has become well recognized and adds a new dimension

278 ined expectations for many infants born with PIDs.

279 stem cell source of choice in children with PIDs undergoing transplantation with Flu/Melph RIC from

280 iven in conditioned (except 3) children with PIDs.

281 be the clinical use of VSTs in patients with PIDs at 4 centers.

282 ce in recognizing and managing patients with PIDs caused by CBM complex mutations.

283 h makes a genetic diagnosis in patients with PIDs complex and laborious.

284 and pattern of malignancies in patients with PIDs do not reflect an increased tumor immune escape per

285 f malignancy predisposition in patients with PIDs has been determined.

286 s and risks of malignancies in patients with PIDs in light of current tumor immune therapies.

287 art of tumor predisposition in patients with PIDs is derived from the same molecular defect as the im

288 f significant research done in patients with PIDs that has accelerated the quality of care of these p

289 Patients with PIDs who have received VST therapy on previous or curren

290 netic changes in the DNA of 41 patients with PIDs with known mutations and 26 patients with undiagnos

291 ting new treatment options for patients with PIDs, and advances are sure to continue.

292 toimmunity and inflammation in patients with PIDs.

293 s and improving the outcome of patients with PIDs.

294 eatment of viral infections in patients with PIDs.

295 first-line molecular assay in patients with PIDs.

296 eatment of viral infections in patients with PIDs.

297 the Xist RNA Polycomb Interaction Domain (XR-PID), a 600 nt sequence encompassing the Xist B-repeat e

298 ally tethering hnRNPK to Xist RNA lacking XR-PID is sufficient for Xist-dependent Polycomb recruitmen

299 Deletion of XR-PID abolishes Xist-dependent Polycomb recruitment, in tu

300 A-binding protein hnRNPK as the principal XR-PID binding factor required to recruit PCGF3/5-PRC1.