ライフサイエンスコーパス: PGD

1 PGD and fertilization cycles resulted in detection of 6

2 PGD remains a frequent early complication of HTx and is

3 PGD remains a threat to the 2 primary aims of lung trans

4 PGD scores were significantly higher in the C1-INH-group

5 PGD was defined as PaO2/FiO2 less than or equal to 200 w

6 PGD was significantly associated with 90-day (relative r

7 PGD(2) activates its receptor DP1 and excites downstream

8 PGD(2) binding to CRTH2 induced ILC2 migration and produ

9 PGD(2) exerts a number of proinflammatory responses thro

10 PGD(2) induced concentration-dependent Th2 cytokine prod

11 PGD(2) is an important and potent activator of ILC2s thr

12 PGD(2) produced by ILC2s is, in a paracrine/autocrine ma

13 PGD(2), which is generated by hematopoietic prostaglandi

14 search suggests that the prostaglandin D(2) (PGD(2) ) receptor 2 (DP(2) ) is a principal regulator in

15 ukotrienes (cys-LTs) and prostaglandin D(2) (PGD(2) ) was assessed as was expression of the activatio

16 hibited recycling of the prostaglandin D(2) (PGD(2)) DP1 receptor (DP1) to the cell surface after ago

17 e show that increases in prostaglandin D(2) (PGD(2)) expression in mouse lungs upon aging correlate w

18 ls of the lipid mediator prostaglandin D(2) (PGD(2)) in the respiratory tract with age and could be p

19 Prostaglandin D(2) (PGD(2)) is known to have antipruritic activity by suppre

20 n Th2 cells (CRTH2) is a prostaglandin D(2) (PGD(2)) receptor, expressed by Th2 cells and other infla

21 lism of sex hormones and prostaglandin D(2) (PGD(2)), a lipid mediator that promotes skin inflammatio

22 (CRTH2), a receptor for prostaglandin D(2) (PGD(2)), is expressed by human ILC2s.

23 Prostaglandin D(2) (PGD(2)), mainly produced by mast cells, promotes orbital

24 for the bioactive lipid prostaglandin D(2) (PGD(2)).

25 veolar lavage (BAL) fluid prostaglandin D(2)(PGD(2)) levels are increased in patients with severe, po

26 ne, norepinephrine, prostaglandin (PG) E(2), PGD(2), and adenosine strongly inhibit integrin activati

27 dy was to verify ARMS-qPCR in a cohort of 20 PGD cycles with a diverse group of SGDs (15 couples at r

28 y for Heart and Lung Transplantation grade 3 PGD at 48 or 72 hours post-transplant.

29 FiO2 ratios were early predictors of grade 3 PGD at or beyond 6 hours and may trigger early therapeut

30 e primary outcome was development of grade 3 PGD in the first 72 hours.

31 Significant predictors of grade 3 PGD included (1) EVLWi (optimal cutoff, 13.7 mL/kg; AUC,

32 We identified grade 3 PGD risk factors, several of which are potentially modif

33 k factors, EVLWi and biomarkers with grade 3 PGD was analyzed under the Bayesian paradigm, using logi

34 Grade 3 PGD was defined according to the International Society f

35 y for Heart and Lung Transplantation grade 3 PGD within 72 hours of transplantation.

36 In 47 LT recipients, 10 developed grade 3 PGD, which was obvious at H6 in 8 cases.

37 lled; 211 subjects (16.8%) developed grade 3 PGD.

38 both forms) were not associated with grade 3 PGD.

39 n-1 were correlated with severe (grades 2-3) PGD at 72 hours posttransplant (5982 [3016-17191] versus

40 ere treated with the COX-2 inhibitor NS-398, PGD(2), or vehicle and stimulated with cytokines.

41 , yet increased production of pro- (LTE(4) , PGD(2) and 11-dehydro-TBX(2) ) was balanced by anti-infl

42 33 potently liberates AA and elicits LTC(4), PGD(2), and thromboxane A(2) production by bone marrow-d

43 There were 40 PGD subjects and 79 non-PGD subjects included for analys

44 (U-46619), TXB(2), PGH(2) mimetic (U-51605), PGD(2,) PGJ(2), and PGF(2alpha).

45 a metabolic adaptation that stably activates PGD to reprogram metastatic chromatin.

46 effects by boosting the antipruritic agent, PGD(2), by the activation of the p38-MAPK pathway.

47 ent in response to endotoxin and ameliorated PGD.

48 the synthesis of anti-aggregatory PGI(2) and PGD(2) at non-platelet sites leading to predicted thromb

49 r data show that LPS induced both PGE(2) and PGD(2) production, which was evident by approximately 8

50 The two major PGs, PGE(2) and PGD(2), are synthesized by the prostanoid isomerases, PG

51 e complex interactions between the IL-33 and PGD(2)-CRTH2 pathways that regulate ILC2 population size

52 Cysteinyl leukotrienes D(4) and E(4) and PGD(2) also induced these effects.

53 also had greater production of both IL-6 and PGD(2) as well as ERK phosphorylation, which is known to

54 Seven patients developed PGD (38.9%), and PGD development was associated with selective reduction

55 ule expressed on TH2 lymphocytes (CRTH2) and PGD(2) receptor 1 (DP1).

56 rdomain interactions among the VSD, CTD, and PGD are altered by the beta subunits to affect channel a

57 The association between E/e and PGD was assessed with multivariable logistic regression.

58 al urinary levels of both leukotriene E4 and PGD-M.

59 eal-time PCR/immunohistochemistry [IHC]) and PGD(2) (ELISA/liquid chromatography mass spectrometry) i

60 associated with neutrophil infiltration and PGD.

61 ociation of angiopoietin-2 plasma levels and PGD was evaluated using generalized estimating equations

62 stanoid isomerases, PGE synthases (PGES) and PGD synthases (PGDS), respectively.

63 We observed increased PTGDS protein and PGD(2) in female mouse DRG.

64 -rich plasma, where formation of both Tx and PGD(2) was increased, spreading was not as pronounced an

65 on, its expression and activity (measured as PGD(2) reduction to 9alpha,11beta-PGF(2) by ELISA) were

66 B(4), LTC(4), LTD(4), and LTE(4), as well as PGD(2), stimulated goblet cell secretion in rat goblet c

67 mote the release of histamine, and augmented PGD(2) production in mast cells and macrophages.

68 The association between PGD and each SNP was evaluated by logistic regression, a

69 25%) of whom developed left or biventricular PGD requiring VA-ECMO.

70 25%) of whom developed left or biventricular PGD requiring VA-ECMO.

71 he DP1 antagonist MK-0524 completely blocked PGD(2)-induced HA synthesis.

72 Blocking PGD(2) function with small-molecule antagonists enhanced

73 completely prevented the generation of both PGD(2) and LTC(4) in a model of AERD in which MC activat

74 ponse of Th2 cells to the levels produced by PGD(2) alone.

75 ant isoform responsible for HA production by PGD(2).

76 e proposed a clinical definition for cardiac PGD comprising severely impaired systolic function affec

77 n the lung in both experimental and clinical PGD.

78 Consequently, PGD(2) and its metabolites can be detected in ILC2 super

79 In contrast, PGD-M levels increased dramatically in group II (61.3 +/

80 he enzyme that synthesizes prostaglandin D2 (PGD(2)), we further explored its role in thermoregulatio

81 EUK-134, or catalase significantly decreased PGD(2) production, whereas coincubation with H(2)O(2) si

82 (G6PD) and 6-phosphogluconate dehydrogenase (PGD) in the pentose phosphate pathway (PPP) were found t

83 ization of 6-phosphogluconate dehydrogenase (PGD) isoforms of Arabidopsis (Arabidopsis thaliana).

84 izing enzyme phosphogluconate dehydrogenase (PGD).

85 t is conjugated to a polyglycerol dendrimer (PGD).

86 ed that niacin evoked platelet COX-1-derived PGD(2) biosynthesis.

87 Mast cell-derived PGD(2) increased HA production via activation of DP1.

88 We report here that mast cell-derived PGD(2) is a key factor that promotes HA biosynthesis by

89 oduction and inhibition of mast cell-derived PGD(2) prevented HA synthesis.

90 251 lung transplant recipients, 50 developed PGD Grade 3.

91 Seven patients developed PGD (38.9%), and PGD development was associated with sel

92 Ninety-four of 290 transplants developed PGD (32.4%).

93 t case of preimplantation genetic diagnosis (PGD) and in vitro fertilization (IVF) performed for the

94 ations of preimplantation genetic diagnosis (PGD) for haematologic disease to enable clinicians to of

95 lable for preimplantation genetic diagnosis (PGD) of in vitro fertilized (IVF) embryos do not detect

96 ndard for preimplantation genetic diagnosis (PGD) of single-gene disorders (SGD), this approach can b

97 Prolonged grief disorder (PGD) is a potentially disabling condition that affects a

98 fic agonist 13,14-dihydro-15-keto-PGD(2) (DK-PGD(2) ) and measuring IL-4 and IL-13 by intracellular s

99 more IL-4 and IL-13 expression following DK-PGD(2) stimulation (P < 0.05).

100 olic domain (CTD), and the pore gate domain (PGD) of the Slo1 alpha-subunit, and is further regulated

101 cell carcinoma of the preputial gland duct (PGD).

102 Primary allograft dysfunction (PGD) is reported in up to 40% of transplants and is asso

103 he development of primary graft dysfunction (PGD) after lung transplantation.

104 Primary graft dysfunction (PGD) continues to be a potentially life-threatening earl

105 fatal syndrome of primary graft dysfunction (PGD) following lung transplantation.

106 Primary graft dysfunction (PGD) is a significant cause of early morbidity and morta

107 Primary graft dysfunction (PGD) is a significant contributor to early morbidity and

108 Severe primary graft dysfunction (PGD) is the leading cause of early death following cardi

109 Rationale: Primary graft dysfunction (PGD) is the leading cause of early morbidity and mortali

110 Primary graft dysfunction (PGD) is the main cause of early morbidity and mortality

111 Primary graft dysfunction (PGD) is the most important cause of early morbidity and

112 tion of grade 3 pulmonary graft dysfunction (PGD) remains a research gap for clinicians.

113 ents with Grade 3 primary graft dysfunction (PGD) were frequency matched with controls based on donor

114 t to determine if primary graft dysfunction (PGD), a syndrome of acute lung injury, attenuates improv

115 plant and risk of primary graft dysfunction (PGD).

116 the incidence of primary graft dysfunction (PGD).

117 come [absence of primary graft dysfunction- (PGD) grade 3]; (II) PGD3: bilateral transplantation with

118 2) in Th2 cells without affecting endogenous PGD(2) production or CRTH2 receptor expression.

119 conducted a retrospective study to evaluate PGD incidence, trends, and associated risk factors by an

120 Addition of exogenous PGD(2) abrogated compound 48/80-induced degranulation by

121 In experimental PGD, NET formation is platelet-dependent, and disruption

122 Confirming previous results, BAL fluid PGD(2) levels were highest in patients with severe asthm

123 ly (2011) devised a novel in-house assay for PGD of aromatic L-amino acid decarboxylase deficiency, b

124 dition at follow-up (14.8%) met criteria for PGD than those in the CBT condition (37.9%) (odds ratio,

125 (ISHLT) established diagnostic criteria for PGD.

126 ariable models, independent risk factors for PGD were any history of donor smoking (odds ratio [OR],

127 ecipient, and perioperative risk factors for PGD.

128 the gene encoding PTX3 are risk factors for PGD.

129 bout whether exposure therapy is optimal for PGD.

130 studies have yielded conflicting results for PGD risk factors.

131 Although treatments for PGD have focused on exposure therapy, much debate remain

132 ly represent a functional signaling unit for PGD(2) but also a potential target for the development o

133 precursor required for 15d-PGJ(2) formation, PGD(2), was also significantly reduced in COX-2-deficien

134 Twenty-four PGD subjects (40%) and 47 non-PGD subjects (59%) receive

135 Furthermore, PGD(2) attenuated cytokine-induced hyperpermeability and

136 indicating that CBT/exposure led to greater PGD reductions than CBT alone.

137 Patients were categorized as having PGD using the International Society for Heart & Lung Tra

138 We further found that both hematopoietic PGD synthase (H-PGDS) siRNA and its inhibitor HQL-79, bu

139 lveolar macrophages along with hematopoietic PGD synthase, the rate-limiting enzyme of PGD2 synthesis

140 increase in the expression of hematopoietic-PGD(2) synthase (H-PGDS) by selenium and a corresponding

141 High PGD catalysis prevents transcriptional up-regulation of

142 ammatory markers were associated with higher PGD(2), HPGDS, and CRTH2 levels.

143 The greatest diagnostic hurdle in PGD is the paucity of molecular material in the single e

144 cted the observed age-dependent increases in PGD(2) expression.

145 ar traps (NETs) contribute to lung injury in PGD in a platelet-dependent manner.

146 andin E2 synthetic and signaling pathways in PGD is warranted.

147 t component to achieve optimal reductions in PGD severity.

148 mediated by PTX3 release, may play a role in PGD pathogenesis.

149 t NETs are a promising therapeutic target in PGD.

150 f the role of recipient genetic variation in PGD has thus far been limited to single, candidate gene

151 nd the mutant biosensor with the inactivated PGD downward arrowL(50) cleavage site (L50D mutant) and

152 f Ptgds-expressing neurons so as to increase PGD(2) production.

153 bation with H(2)O(2) significantly increased PGD(2) production.

154 gly long and stable emission from individual PGD-BODIPY probes, even in the absence of anti-fading ag

155 ate a promising approach to topically induce PGD(2) for improving pruritus.

156 However, agents that can topically induce PGD(2) for itch relief are not well established.

157 H-PGDS, but not L-PGDS, mediates LPS-induced PGD(2) production in BMDM.

158 cal role of NOX-generated ROS in LPS-induced PGD(2) production in BMDM.

159 AT-56, significantly attenuated LPS-induced PGD(2) production, suggesting that H-PGDS, but not L-PGD

160 cient mouse BMDM also attenuated LPS-induced PGD(2), but not PGE(2) production, suggesting the critic

161 Conversely LPS-induced PGD(2), but not PGE(2), production, was potentiated with

162 ulation, but also attenuated the LPS-induced PGD(2), but not PGE(2), production.

163 Our results suggest that inhibiting PGD(2) function may be a useful approach to enhance T ce

164 CRTh2-specific agonist 13,14-dihydro-15-keto-PGD(2) (DK-PGD(2) ) and measuring IL-4 and IL-13 by intr

165 TXNIP normalizes glucose consumption, lowers PGD catalysis, reverses hyperacetylation, represses mali

166 observation that the AD-associated mediator, PGD(2), upregulated AKR1C3 expression in PHKs, we used i

167 Basal prostaglandin D2 metabolite (PGD-M; 13.6 +/- 2.7 vs 7.0 +/- 0.8 pmol/mg creatinine [C

168 backcrosses of pgd2-1 suggested that missing PGD activity in peroxisomes primarily affects the male g

169 Two experimental murine PGD models were studied: hilar clamp and orthotopic lung

170 Twenty-four PGD subjects (40%) and 47 non-PGD subjects (59%) received a transplant for the diagnos

171 There were 40 PGD subjects and 79 non-PGD subjects included for analysis.

172 compared the clinical outcome of PGD and non-PGD cases.

173 ations were compared between the PGD and non-PGD groups using the ISHLT definition.

174 to compare the expression and activation of PGD(2) pathway elements in bronchoscopically obtained sa

175 PK, SB203580, resulted in the attenuation of PGD(2) levels.

176 Neurologists should be aware of PGD to be able to better consult at-risk families on the

177 is known about the cardiovascular biology of PGD(2).

178 d could be partially reversed by blockade of PGD(2) synthesis or action.

179 In conclusion, our definition of PGD could be applied in a national multicenter study, an

180 ificantly associated with the development of PGD after lung transplantation.

181 hways as key mediators of the development of PGD in lung transplant patients.

182 ietin-2 plasma levels and the development of PGD in the subset of patients transplanted for chronic o

183 vels would be associated with development of PGD.

184 dicts organ acceptability and development of PGD.

185 unction may contribute to the development of PGD.

186 The effect of PGD(2) on HA production was mimicked by the selective DP

187 f CRTH2 in mediating an inhibitory effect of PGD(2) on the apoptosis of human Th2 cells induced by cy

188 ad any effect on the antiapoptotic effect of PGD(2).

189 eptor in mediating the biological effects of PGD(2) in patients with allergic inflammation has remain

190 The effects of PGD(2) on ILC2s could be mimicked by the supernatant fro

191 not play a role in mediating the effects of PGD(2) on the apoptosis of Th2 cells because neither the

192 The effects of PGD(2) under physiologic conditions were evaluated by us

193 The effects of PGD(2), IL-25, and IL-33 on the cell migration, cytokine

194 Although contrasting effects of PGD(2), PGE(2), and PGI(2) on ILC2 responses have been p

195 ere isolated and used to test the effects of PGD(2), prostaglandin J(2), as well as prostaglandin D r

196 iator release from mast cells, especially of PGD(2), than hitherto appreciated and this could be impo

197 ng results from COX-1-dependent formation of PGD(2) and PGE(2) followed by COX-2-dependent production

198 if interventions can mitigate the impact of PGD on patient-reported outcomes.

199 We studied the incidence of PGD across the United Kingdom.

200 Despite recent advancements, incidence of PGD remains high.

201 The incidence of PGD was 29%.

202 is now well established that interaction of PGD(2) with chemoattractant receptor- homologous molecul

203 Measures of PGD by clinical interview and self-reported measures of

204 We compared the clinical outcome of PGD and non-PGD cases.

205 ial cell permeability in the pathogenesis of PGD are indicated.

206 The pathogenesis of PGD involves ischemia-reperfusion injury.

207 The pathogenesis of PGD is unclear, although both neutrophils and activated

208 Selectively targeting the production of PGD(2) and/or activation of DP1 may prevent pathological

209 in (PG) synthases favoring the production of PGD(2) metabolites, Delta(12)-PGJ(2) and 15d-PGJ(2).

210 ng of AA metabolism toward the production of PGD(2) metabolites, which may have clinical implications

211 phase (16-24 hrs); whereas the production of PGD(2) remained at a stable level from 12 to 24 hrs post

212 regulates the H-PGDS-mediated production of PGD(2), but not PGE(2), in mouse BMDM.

213 Early recovery of PGD on VA-ECMO support negates its negative impact on sh

214 Early recovery of PGD on VA-ECMO support negates its negative impact on sh

215 Regardless of PGD severity, participants had improvements in disabilit

216 8 were associated with an increased risk of PGD (E/e odds ratio, 1.93; 95% confidence interval, 1.02

217 s that are responsible for increased risk of PGD using a two-phase large-scale genotyping approach.

218 cular diastolic function reduces the risk of PGD.

219 We sought to determine the role of PGD(2) and CRTH2 in human ILC2s and compare it with that

220 FiO2 ratio of less than 100 as early sign of PGD at first measurement in the OR were immediately trea

221 to examine the incidence and significance of PGD after HTx using the ISHLT definition.

222 cose consumption rates to rise in support of PGD, while simultaneously facilitating epigenetic reprog

223 Short- and long-term survival of PGD supported with VA-ECMO was better than previously de

224 Short and long-term survival of PGD supported with VA-ECMO was better than previously de

225 Treatment of PGD with C1-INH led to acceptable outcome.

226 ercentage of ILC subsets with reperfusion or PGD (grade 3 within 72 h) were assessed.Measurements and

227 he history and ethics involved in performing PGD together with human leukocyte antigen (HLA) testing

228 Human mast cells (HMC-1) produced PGD(2).

229 We reveal that endogenously produced PGD(2) is essential in cytokine-induced ILC2 activation

230 atment of donor bacterial pneumonia promotes PGD through ischemia/reperfusion-primed donor TRAMs.

231 The messenger RNA encodes the prostaglandin PGD(2) synthesizing enzyme.

232 iae induced the generation of prostaglandins PGD(2) and PGE(2) from RAW264.7 cells and thromboxane B(

233 sely, treatment with Cox-derived prostanoids PGD(2) or 15-deoxy-Delta(12,14)-PGJ(2) induced hBD3 or h

234 Aspirin increased 15 R-PGD(2) but not 15 R-PGE(2) in isolated human leukocytes

235 15 R-PGD(2) inhibited human platelet aggregation induced by t

236 During aspirin reactions, PGD-M levels remained unchanged, whereas TX-M levels (0.

237 ata suggest that ROS differentially regulate PGD(2) and PGE(2) production in BMDM.

238 This renders PGD constitutively activated and enables metaboloepigene

239 subgroup of recipients that developed severe PGD (PGD3-group) within 72 hours after LTX but did not r

240 LTX-recipients showing early signs of severe PGD would attenuate the condition.

241 g/mL) was even more effective at stimulating PGD(2) generation as almost all preparations generated s

242 Surprisingly, PGD catalysis was constitutively elevated without activa

243 with human leukocyte antigen (HLA) testing (PGD-H) to create matched siblings suitable for haematopo

244 ne production but were much less active than PGD(2).

245 We propose that PGD-driven suppression of TXNIP allows pancreatic cancer

246 Here, we show that PGD(2) biosynthesis is augmented during platelet activat

247 The IL-33-ST2 and the PGD(2)-CRTH2 pathways have both been implicated in promo

248 domain undergoes intradomain cleavage at the PGD downward arrow L(50) site followed by the release of

249 lant complications were compared between the PGD and non-PGD groups using the ISHLT definition.

250 olizing CYP1B1 in the PSI and CYP3A59 in the PGD are the most likely candidates to participate in tum

251 (P < 0.001) were significantly longer in the PGD cohort.

252 Inotrope use (score) was higher in the PGD group at 24, 48, and 72 hours after transplantation

253 In the PGD group, there was a greater requirement for, intra-ao

254 the study period, there was no change in the PGD incidence; however, there was an increase in the rec

255 strated that the intradomain cleavage of the PGD downward arrow L(50) sequence of the prodomain is es

256 A could be used in the future as part of the PGD process to maximize comprehensiveness in detecting d

257 y identifies coordinated upregulation of the PGD(2) pathway in patients with severe, poorly controlle

258 niacin is combined with an antagonist of the PGD(2) receptor DP1.

259 strated that the intradomain cleavage of the PGD/L(50) site initiates the MT1-MMP activation, whereas

260 These PGD(2) pathway markers were then compared with asthma se

261 Thus, PGD(2), like PGI(2), may function as a homeostatic respo

262 to the enzymatic transformation of PGH(2) to PGD(2).

263 modulate the response of human Th2 cells to PGD(2).

264 dentified as a possible mechanism leading to PGD.

265 increased neutrophil recruitment, and led to PGD, which was independent of donor NCMs.

266 enhanced calcium mobilization in response to PGD(2) in Th2 cells without affecting endogenous PGD(2)

267 ) has been shown to be effective in treating PGD.

268 il and basophil levels increased and urinary PGD-M levels (2.2 +/- 0.8 pmol/mg Cr, P < .001) decrease

269 Left ventricular PGD, right ventricular PGD, or both, were observed in 99

270 Left ventricular PGD, right ventricular PGD, or both, were observed in 99 patients (31%).

271 en examined.Objectives: To determine whether PGD in chronic obstructive pulmonary disease or intersti

272 The mechanism by which PGD(2) influences orbital fibroblasts and their synthesi

273 s2120243 and rs2305619, were associated with PGD (odds ratio, 1.5; 95% confidence interval, 1.1 to 1.

274 Genetic variants of PTX3 are associated with PGD after lung transplantation, and are associated with

275 ved lung ILC populations are associated with PGD development has never been examined.Objectives: To d

276 allograft reperfusion and is associated with PGD development, suggesting that ILCs may be involved in

277 donor syndecan-1 levels were associated with PGD in recipients (3142 [1575-4829] versus 6229 [4009-80

278 Risk factors independently associated with PGD included ischemic time, recipient African American r

279 pient, and operative factors associated with PGD were recipient diabetes mellitus (P = 0.031), recipi

280 variants were significantly associated with PGD, four of which were in the prostaglandin E2 family o

281 to assess their independent association with PGD.

282 However, when combined with PGD(2), cysLTs caused a greater than additive enhancemen

283 Levels were correlated with PGD severity and intubation time.

284 e association of potential risk factors with PGD was analyzed using multivariable conditional logisti

285 Treatment of human orbital fibroblasts with PGD(2) and PGJ(2) increased HA synthesis and HAS mRNA.

286 IVF with PGD is a viable option for couples who wish to avoid pas

287 Participants with PGD Grade 3 had a lower magnitude of improvement in gene

288 Among participants with PGD Grade 3, prolonged mechanical ventilation was associ

289 andomized clinical trial of 80 patients with PGD attending the outpatient University of New South Wal

290 chniques in therapies to treat patients with PGD is needed.

291 Perioperatively, patients with PGD received more blood products (P < 0.001).

292 ts, NETs were more abundant in patients with PGD.

293 ive care stay was longer for recipients with PGD (median 14 vs 5 days, P < 0.01) and early mortality

294 ity was significantly elevated in those with PGD versus those without PGD (6.06% vs 0.92%, P = .01).

295 ]; (II) PGD3: bilateral transplantation with PGD grade 3 anytime within 72 hours; (III) Declined: lun

296 Treatment with PGD(2) induced phosphorylation of Akt and BAD, prevented

297 ll-cause mortality in those with and without PGD was 31 (19%) versus 13 (4.5%) (P = 0.0001).

298 om lung transplant patients with and without PGD.

299 Conversely, patients without PGD exhibited significantly higher ILC1 frequencies befo

300 vated in those with PGD versus those without PGD (6.06% vs 0.92%, P = .01).