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 is not available for all haematologic mutations, is

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

4 PGD to exclude embryos carrying serious haematologic dis

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) binding to CRTH2 induced ILC2 migration and produ

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

9 PGD(2) has been implicated in both the development and r

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

11 PGD(2) is an eicosanoid primarily synthesized by mast ce

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

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

14 PGD-H is more diagnostically and ethically challenging,

15 tected by mRNA analysis and Western blot; 2) PGD(2) inhibits cytotoxicity, chemotaxis, and type 1 cyt

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

17 hat accurately measures prostaglandins D(2) (PGD(2)) and E(2) (PGE(2)) in cell culture supernatants a

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

19 2 expression and causing prostaglandin D(2) (PGD(2)) generation.

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

21 Prostaglandin D(2) (PGD(2)) is a cyclooxygenase (COX) product of arachidonic

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

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

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

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

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

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

28 sing brain levels of prostaglandin (PG)E(2), PGD(2), PGF(2alpha), and thromboxane B(2), as well as th

29 -series compounds were observed with PGHS-2, PGD synthases, microsomal PGE synthase-1 and EP1, EP2, E

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

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

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

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

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

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

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

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

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

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

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

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

42 human NK cells via signaling through DP; 3) PGD(2) signaling via DP elevates intracellular cAMP leve

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

44 y effects on NK cells are cAMP dependent; 4) PGD(2) binding to DP suppresses Ca(2+) mobilization trig

45 Both d(4)-PGE(2) and d(4)-PGD(2) were used as surrogate standards to control for d

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

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

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

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 heir nonelectrophilic precursors, PGE(2) and PGD(2), or PGB(2), which differs from PGA(2) only in tha

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

53 genase and cyclooxygenase to form LTC(4) and PGD(2), respectively.

54 regulate the generation of ROS, LTC(4), and PGD(2) by contributing to the necessary Ca(2+) signal fo

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

56 Because PGE(2) is antiasthmatic and PGD(2) is proasthmatic, we speculate that the balance of

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

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

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

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

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

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

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

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

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

71 tion of the nuclear factor-kappaB cascade by PGD(2) metabolites.

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

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

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

75 the recruitment and activation of Th2 cells, PGD(2) may also impede the resolution of allergic inflam

76 n the lung in both experimental and clinical PGD.

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

78 The Protein Geometry Database (PGD) enables biologists to easily and flexibly query inf

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

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

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

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

83 gnificantly attenuated FcepsilonRI-dependent PGD(2), LTC(4), and ROS production in bone marrow-derive

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Primary graft dysfunction (PGD) is a major complication following lung transplantat

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

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

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

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

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

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

107 the incidence of primary graft dysfunction (PGD).

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

109 cells are a major source of the eicosanoids PGD(2) and leukotriene C(4) (LTC(4)), which contribute t

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

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

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

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

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

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

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

117 ors, but a role for biosynthetic enzymes for PGD(2) in tumor development has not been studied.

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

119 the gene encoding PTX3 are risk factors for PGD.

120 ecipient, and perioperative risk factors for PGD.

121 bout whether exposure therapy is optimal for PGD.

122 studies have yielded conflicting results for PGD risk factors.

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

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

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

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

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

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

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

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

131 unohistochemistry, we detected hematopoietic PGD synthase mainly in macrophages and monocytes of the

132 hat disruption of the gene for hematopoietic PGD synthase in Apc(Min/+) mice led to approximately 50%

133 /+) mice with transgenic human hematopoietic PGD synthase tended to have 80% fewer intestinal adenoma

134 support an interpretation that hematopoietic PGD synthase controls an inhibitory effect on intestinal

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

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

137 tion of either lipocalin-type or hemopoietic PGD synthase enzymes decreased urinary tetranor PGDM.

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

139 role for the candidate mediators histamine, PGD(2), LTB(4), CXCL10, or IL-16, each of which can be p

140 O(2)/FiO(2), an index of lung dysfunction in PGD.

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

142 jor role for anti-col(V) humoral immunity in PGD, and identifies the airway epithelium as a target in

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

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

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

146 t component to achieve optimal reductions in PGD severity.

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

148 nti-col(V) Abs and their potential target in PGD are unknown.

149 ntifies the airway epithelium as a target in PGD.

150 t NETs are a promising therapeutic target in PGD.

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

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

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 LTE(4)-mediated COX-2 induction, PGD(2) generation, and ERK phosphorylation were all sens

164 mass spectrometry as a metabolite of infused PGD(2) that is detectable in mouse and human urine.

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

166 t effects being on PGHS-1 pathways involving PGD, PGE, and PGF.

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

168 elective CRTH2 agonist 13,14-dihydro-15-keto-PGD(2), inhibited by the CRTH2 antagonists ramatroban an

169 ation time should be less than 8h to measure PGD(2) accurately, whereas preparation time did not affe

170 Although LTE(4)-mediated PGD(2) production was also sensitive to MK571, an antago

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

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

173 As an application of the method, PGD(2) and PGE(2) were measured in culture supernatants

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

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

176 line A549 was found to produce PGE(2) but no PGD(2), whereas the murine macrophage cell line RAW 264.

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

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

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

180 granulation and cytokine production, but not PGD(2) production.

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

182 material, and may enable the application of PGD to the less common haematological mutations, and the

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

184 ase the diagnostic scope and availability of PGD in the future, but certain limitations will remain.

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

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

187 rine that reflects modulated biosynthesis of PGD(2) in humans and mice.

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

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

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

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

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

193 vels would be associated with development of PGD.

194 unction may contribute to the development of PGD.

195 I3K inhibitor LY294002 blocked the effect of PGD(2) both on the signaling events and on the apoptotic

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

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

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

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

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

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

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

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

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

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

206 ary PGE-M, whereas it augmented excretion of PGD(2) and PGI(2) metabolites, reflecting rediversion of

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

208 otein production and decreased generation of PGD(2), and this was correlated with decreased binding o

209 Despite recent advancements, incidence of PGD remains high.

210 The incidence of PGD was 29%.

211 Infusion of PGD(2) dose dependently increased urinary tetranor PGDM

212 Similarly, intratracheal instillation of PGD(2) enhanced removal of Pseudomonas from the lung in

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

214 ression in macrophages blunted a majority of PGD(2) produced after LPS treatment.

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

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

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

218 The pathogenesis of PGD involves ischemia-reperfusion injury.

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

220 ssion can lead to differential production of PGD(2) and PGE(2) by epithelial cells and macrophages.

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

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

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

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

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

226 in terms of degranulation and production of PGD(2), GM-CSF, IL-6, IL-13, and TNF-alpha.

227 closely associated with local production of PGD(2).

228 8 were associated with an increased risk of PGD (E/e odds ratio, 1.93; 95% confidence interval, 1.02

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

230 cular diastolic function reduces the risk of PGD.

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

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

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

234 -dihydro-15d-PGJ(2), PGE(2), PGF(2alpha), or PGD(2) that lack the reactive alpha,beta-unsaturated ket

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

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

237 rine macrophage cell line RAW 264.7 produced PGD(2) and only trace amounts of PGE(2).

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

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

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

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

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

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

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

245 Within the immune system, PGD(2) binding to DP generally leads to suppression of c

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

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

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

249 xperiments 20 to 30 years ago suggested that PGD(2) may suppress tumors, but a role for biosynthetic

250 The PGD server is available at http://pgd.science.oregonstat

251 ith monoclonal antibodies (mAbs) against the PGD(2) receptor, CRTH2, the best selective Th2-cell surf

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

253 The capabilities the PGD provides are valuable for assessing the uniqueness o

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

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

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

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

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

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

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

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

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

263 Consistent with this prediction, the PGD(2) metabolite 15-deoxy-Delta(12,14)-prostaglandin J(

264 etranor PGDM was much more abundant than the PGD(2) metabolites, 11beta-PGF(2alpha) and 2,3-dinor-11b

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

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

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

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

269 dentified as a possible mechanism leading to PGD.

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

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

272 expressed in neuronal cells, lipocalin-type PGD synthase (L-PGDS) is detected in the macrophages inf

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

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

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

276 hese data uncover a novel mechanism by which PGD(2) functions through DP to suppress type 1 and cytol

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

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

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

280 nti-col(V) Abs were strongly associated with PGD development.

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

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

283 T cell immunity was strongly associated with PGD.

284 to assess their independent association with PGD.

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

286 cells all induced pathology consistent with PGD within 4 days posttransfer; up-regulated IFN-gamma,

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

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

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

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

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

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 igation was not suppressed by treatment with PGD(2), illustrating that activation of CRTH2 only inhib

298 om lung transplant patients with and without PGD.

299 tion of plasma from patients with or without PGD revealed that higher levels of preformed anti-col(V)

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