ライフサイエンスコーパス: PFO

1 PFO binds both to sterols that tend to localize in order

2 PFO closure did not meet the primary endpoint of reducti

3 PFO closure seems as effective as medical therapy for se

4 PFO closure was associated with an increased risk of atr

5 PFO conformational behavior in asymmetric vesicles was f

6 PFO forms a multimeric barrel with many TM segments.

7 PFO is a potential route for embolic transit from the sy

8 PFO is believed to interact with liquid ordered lipid do

9 PFO is found more frequently in stroke patients than in

10 PFO presence was assessed by transthoracic echocardiogra

11 PFO prevalence was similar in 50 patients with COPD and

12 PFO size, degree of shunting, and a coexisting hypercoag

13 PFO was considered present if both studies were positive

14 PFO was present in 164 participants (14.9%).

15 PFO+ subjects had a higher oesophageal temperature (T(oe

16 (3) a residual pool that does not bind 125I-PFO* even after sphingomyelinase treatment.

17 lesterol: (1) a pool accessible to bind 125I-PFO*, a mutant form of bacterial Perfringolysin O, which

18 omyelin(SM)-sequestered pool that binds 125I-PFO* only after SM is destroyed by sphingomyelinase; and

19 Thirty well-matched males (15 PFO-, 8 large PFO+, 7 small PFO+) completed cycle ergome

20 point of stroke/TIA was met in 30/364 (8.2%) PFO versus 117/5711 (2.0%) non-PFO patients (hazard rati

21 Surgical closure was performed in 639 PFO patients (28%), and surgeons were more likely to clo

22 uently in patients more likely to have had a PFO-attributable stroke (n=637) compared with those less

23 7) compared with those less likely to have a PFO-attributable stroke (n=657).

24 cardiac implantable electronic devices; if a PFO is detected, PFO closure, anticoagulation, or nonvas

25 data suggest that the presence and size of a PFO are associated with T(oesoph) in healthy humans but

26 ts with endocardial leads, the presence of a PFO on routine echocardiography is associated with a sub

27 were screened for the presence and size of a PFO using saline contrast echocardiography.

28 a cryptogenic ischemic stroke, closure of a PFO was associated with a lower rate of recurrent ischem

29 eft shunts consistent with the presence of a PFO were randomized to transcatheter PFO closure with th

30 ngiography and TEE, both modalities showed a PFO shunt in seven.

31 We sought to determine whether a PFO increases the risk of stroke/transient ischemic atta

32 crease the stroke risk in individuals with a PFO and the results from randomized treatment trials com

33 Among patients with a PFO who had had a cryptogenic stroke, the risk of subseq

34 ultinational trial involving patients with a PFO who had had a cryptogenic stroke, we randomly assign

35 The stroke risk associated with a PFO, mainly considered of importance in younger patients

36 llation occurred in 29 patients (6.6%) after PFO closure.

37 During exercise breathing cold and dry air, PFO+ subjects achieved a higher T(oesoph) than PFO- subj

38 , Inc., Boston, Massachusetts] and Amplatzer PFO Occluder [disc occluder] [AGA Medical/St. Jude Medic

39 l therapy and PFO closure with the Amplatzer PFO Occluder device (St.

40 the patent foramen ovale with the Amplatzer PFO Occluder or to receive medical therapy.

41 ts With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Management [PREMIUM]; NCT0035505

42 ts With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Management) was a double-blind s

43 resence of atrial septal aneurysm (ASA), and PFO shunts were evaluated.

44 g toluene with the rigid polymers PFO-BT and PFO to suspend isolated nanotubes.

45 n of important toxins, such as CPA, CPB, and PFO, is controlled by the C. perfringens Agr-like (CpAL)

46 ache Reduction in Subjects With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Manageme

47 ache Reduction in Subjects With Migraine and PFO Using the AMPLATZER PFO Occluder to Medical Manageme

48 y explain the differing abilities of SLO and PFO to efficiently penetrate target cell membranes in th

49 unresolved issues related to PFO stroke and PFO migraine pathophysiology, and to identify the patien

50 ents each year have a cryptogenic stroke and PFO.

51 catheterization) versus medical therapy and PFO closure with the Amplatzer PFO Occluder device (St.

52 for the concerted action of alpha-toxin and PFO during C. perfringens pathogenesis.

53 esophageal echocardiography features such as PFO size, associated hypermobile septum, and presence of

54 s patent at the entry into the right atrium (PFO) in 62 patients (61.4% of patients with flap valve,

55 The observed lack of association between PFO and migraine (with or without aura) was not modified

56 nt difference in all-cause mortality between PFO and non-PFO patients (hazard ratio, 0.91; 95% confid

57 This suggests a causal relationship between PFO and cryptogenic stroke.

58 The causal relationship between PFO and migraine remains uncertain, and the role of PFO

59 ll established, and the relationship between PFO and silent brain infarcts (SBI) is not known.

60 n, and data for percutaneous closure of both PFOs and ASDs.

61 ered by sphingomyelin and cannot be bound by PFO* unless the sphingomyelin is destroyed with sphingom

62 te that accessible cholesterol, as judged by PFO* or ALO-D4 binding, is not evenly distributed over t

63 ltiethnic, elderly, population-based cohort, PFO detected with transthoracic echocardiography and agi

64 In this community-based cohort, PFO was not associated with an increased risk of clinica

65 In an expanded COPD cohort, PFO prevalence was similar in 31 hypoxemic (Pao2 </= 7.3

66 a from completed randomized trials comparing PFO closure versus medical therapy in patients with cryp

67 ull mutants exhibited reduced levels of CPB, PFO, and CPA in their culture supernatants, and this eff

68 ocardiography was used to establish definite PFO and non-PFO cohorts.

69 Additional tools to describe PFOs may be useful in helping to determine whether an ob

70 le electronic devices; if a PFO is detected, PFO closure, anticoagulation, or nonvascular lead placem

71 , although the pathogenicity of a discovered PFO in the setting of CS is typically unclear.

72 s displaces it from rafts, does not displace PFO from ordered domains.

73 effect would be dependent upon the estimated PFO size and inspired air temperature.

74 ast to the 5% threshold previously found for PFO binding to endoplasmic reticulum membranes.

75 oup further improved the detection limit for PFO(-) to 1.7 x 10(-10) M (0.070 ppb).

76 of cholesterol required in the membrane for PFO binding and pore formation.

77 ction limits of 2.3 x 10(-9) M (1.0 ppb) for PFO(-) and 8.6 x 10(-10) M (0.43 ppb) for PFOS(-).

78 The adjusted hazard ratio for PFO and stroke was 1.10 (95% confidence interval [CI]: 0

79 women; mean age, 60 years) were reviewed for PFO morphologic features.

80 With their higher selectivity for PFO(-) over OH(-), membranes containing the alternative

81 These changes were much weaker for PFO(W165T) lipo where substantial stabilization was obse

82 his finding suggests a role of screening for PFOs in patients who require cardiac implantable electro

83 presenting risk of stroke would benefit from PFO closure or anticoagulation, as compared with antipla

84 patients who would most likely benefit from PFO closure.

85 Procedural complications from PFO closure occurred in 14 patients (5.9%).

86 scence resonance energy transfer (FRET) from PFO Trp to domain-localized acceptors indicated that PFO

87 he biochemical properties of the homodimeric PFO of C. reinhardtii expressed in Escherichia coli.

88 gned to antiplatelet therapy alone; however, PFO closure was associated with higher rates of device c

89 y relate cholesterol concentration to (125)I-PFO binding.

90 The (125)I-PFO probe also proved useful in monitoring the movement

91 ography and transcranial Doppler to identify PFO.

92 mpelling circumstantial evidence implicating PFO, the precise role of PFO in the pathogenesis of cryp

93 In PFO, the strongest changes accompanying binding to the m

94 y (MS), we have mapped structural changes in PFO and its variant bearing a point mutation during inco

95 postimplantation follow-up were compared in PFO versus non-PFO patients with the use of Cox proporti

96 There was no difference in PFO prevalence in those with migraine with aura and thos

97 represent an important intermediate stage in PFO pore formation.

98 An analysis reveals that, in PFO, there are complementary interactions between the mo

99 Incidental PFO is common in patients undergoing cardiothoracic surg

100 is usually a presumed diagnosis, incidental PFOs are common, and treatment options have not been wel

101 cholesterol concentration required to induce PFO binding, whereas phosphatidylethanolamine and phosph

102 Intraoperative PFO was diagnosed in 2277 patients in the study populati

103 rafts is poorly understood, we investigated PFO raft affinity in vesicles having coexisting ordered

104 th clinical features suggesting that a CS is PFO-attributable.

105 d CS by the probability that their stroke is PFO-attributable.

106 Thirty well-matched males (15 PFO-, 8 large PFO+, 7 small PFO+) completed cycle ergometer exercise t

107 Subjects with a large PFO, but not those with a small PFO, had a higher T(oeso

108 ageal echocardiography risk markers of large PFO size, hypermobile septum, and presence of right-to-l

109 t shunts consistent with a moderate or large PFO.

110 h COPD with no shunt and patients with large PFO underwent cardiopulmonary exercise tests with contra

111 Both mutant and wild type length PFO exhibited cholesterol-dependent membrane insertion.

112 By using a non-lytic PFO derivative, we showed that the sensitivity of the pr

113 Maximal PFO-induced pore formation occurred in vesicles with wid

114 Moreover, PFO association with the membrane was inhibited by the a

115 30/364 (8.2%) PFO versus 117/5711 (2.0%) non-PFO patients (hazard ratio, 3.49; 95% confidence interva

116 y was used to establish definite PFO and non-PFO cohorts.

117 e in all-cause mortality between PFO and non-PFO patients (hazard ratio, 0.91; 95% confidence interva

118 on follow-up were compared in PFO versus non-PFO patients with the use of Cox proportional hazards mo

119 ype B strains also produce perfringolysin O (PFO) and beta2 toxin (CPB2).

120 and is globally similar to perfringolysin O (PFO) and intermedilysin (ILY), yet the highly conserved

121 cholesterol-binding CDCs, perfringolysin O (PFO) and streptolysin O (SLO), were found to exhibit str

122 sterol-dependent cytolysin Perfringolysin O (PFO) constitutes a powerful tool to detect cholesterol i

123 e structures at the tip of perfringolysin O (PFO) domain 4 reveals that a threonine-leucine pair medi

124 eraction with cholesterol, perfringolysin O (PFO) inserts into membranes and forms a rigid transmembr

125 Perfringolysin O (PFO) is a toxic protein that binds to cholesterol-contai

126 Perfringolysin O (PFO) is the prototype for the cholesterol-dependent cyto

127 The sterol-binding protein perfringolysin O (PFO) was used to test this hypothesis.

128 -labeled mutant version of Perfringolysin O (PFO), a cholesterol-binding protein, and use it to measu

129 s (rafts) was tested using perfringolysin O (PFO), a pore-forming cholesterol-dependent cytolysin.

130 the well-characterized CDC perfringolysin O (PFO), although the sequences in this region are identica

131 f the pore-forming protein Perfringolysin O (PFO), potent silencing was achieved in vitro with no det

132 rticularly alpha-toxin and perfringolysin O (PFO).

133 sterol-dependent cytolysin perfringolysin O (PFO).

134 d version of the cytolysin perfringolysin O (PFO*), whereas another pool is sequestered by sphingomye

135 in helping to determine whether an observed PFO is incidental or pathogenically related to CS.

136 It has been suggested that the ability of PFO to perforate the membrane of target cells is dictate

137 The association of PFO with stroke/TIA remained significant after multivari

138 Unfortunately, the benefit of PFO closure in patients with stroke has not been demonst

139 SIMS images revealed preferential binding of PFO* and ALO-D4 to microvilli on the plasma membrane; lo

140 d new insight into conformational changes of PFO associated with the membrane binding, oligomerizatio

141 The comparison of PFO closure plus antiplatelet therapy with antiplatelet

142 pecific compared to TTE for the detection of PFO in patients with cryptogenic cerebral ischemia.

143 c echocardiography (TTE) in the detection of PFO in patients with cryptogenic ischemic stroke or tran

144 f 13,092 patients without prior diagnosis of PFO or atrial septal defect undergoing surgery at the Cl

145 We investigated the effect of PFO closure combined with antiplatelet therapy versus an

146 We investigated the effects of PFO closure for migraine in a randomized, double-blind,

147 trials comparing the safety and efficacy of PFO closure with that of medical therapy.

148 d lipid domains, both TM and non-TM forms of PFO were found to concentrate in ordered domains in vesi

149 phospholipids vesicles results in a loss of PFO immunoreactivity with a corresponding increase in al

150 The pore-forming mechanism of PFO exhibits an absolute requirement for membrane choles

151 nt ferredoxin, is thus likely the partner of PFO in C. reinhardtii.

152 M form, demonstrating that the TM portion of PFO interacts unfavorably with rafts.

153 tween migraine headaches and the presence of PFO by use of a large case-control study.

154 tween migraine headaches and the presence of PFO in this large case-control study.

155 The presence of PFO was assessed by transthoracic echocardiography.

156 Presence of PFO was determined by transthoracic echocardiogram with

157 se-control study to assess the prevalence of PFO in subjects with and without migraine.

158 The prevalence of PFO was not significantly different between subjects who

159 In the matched analysis, the prevalence of PFO was similar in case and control subjects (26.4% vers

160 with COPD do not have a higher prevalence of PFO.

161 The properties of PFO mutants with lengthened or shortened TM segments wer

162 migraine remains uncertain, and the role of PFO closure among unselected patients with migraine rema

163 vidence implicating PFO, the precise role of PFO in the pathogenesis of cryptogenic stroke is not yet

164 This can be explained by shielding of PFO-bound cholesterol from water.

165 s pertaining to the clinical significance of PFO.

166 tened TM segments were compared with that of PFO with wild type TM sequences.

167 ect cholesterol in membranes, and the use of PFO-based probes has flourished in recent years.

168 at lipid vesicles catalyze the conversion of PFOs into APFs.

169 Incubation of PFOs with phospholipids vesicles results in a loss of PF

170 eneric epitope that is distinct from that of PFOs and amyloid fibrils.

171 ts exist as follows: prefibrillar oligomers (PFOs), fibrillar oligomers (FOs), and annular protofibri

172 years of age who had a patent foramen ovale (PFO) and had had a cryptogenic ischemic stroke to underg

173 l relationship between patent foramen ovale (PFO) and migraine has been hypothesized, and improvement

174 olism in patients with patent foramen ovale (PFO) and otherwise unexplained ischemic stroke, in a pro

175 presumably related to patent foramen ovale (PFO) are at risk for recurrent cerebrovascular events.

176 The role of a patent foramen ovale (PFO) as a risk factor for ischemic stroke has been estab

177 Patent foramen ovale (PFO) can be detected in up to 43% of patients with crypt

178 ose for catheter-based patent foramen ovale (PFO) closure are still evolving.

179 Trials of patent foramen ovale (PFO) closure to prevent recurrent stroke have been incon

180 Patent foramen ovale (PFO) has been associated with migraine, but its role in

181 ficacy of closure of a patent foramen ovale (PFO) in the prevention of recurrent stroke after cryptog

182 The patent foramen ovale (PFO) is a normal interatrial communication during fetal

183 Patent foramen ovale (PFO) is associated with cryptogenic stroke (CS), althoug

184 Patent foramen ovale (PFO) is prevalent in patients with migraine with aura.

185 A patent foramen ovale (PFO) may permit arterial embolization of thrombi that ac

186 ercutaneous closure of patent foramen ovale (PFO) plus medical therapy versus medical therapy alone f

187 d blood flow through a patent foramen ovale (PFO) would not be cooled.

188 oms in patients with a patent foramen ovale (PFO), both of which conditions are highly prevalent, hav

189 e relationship between patent foramen ovale (PFO), ischemic stroke, and subclinical cerebrovascular d

190 surrounds the issue of patent foramen ovale (PFO), stroke, and secondary prevention strategies.

191 ncidentally discovered patent foramen ovale (PFO).

192 The prevalence of patent foramena ovale (PFOs) in the general population is around 25%, but it is

193 ists) is pyruvate:ferredoxin oxidoreductase (PFO), which decarboxylates pyruvate and forms acetyl-coe

194 ne frequency and severity after percutaneous PFO closure has been reported.

195 related to PFO underwent either percutaneous PFO closure (150 patients) or medical treatment (158 pat

196 g Adults), who underwent either percutaneous PFO closure or medical therapy for comparative analysis.

197 study examined the efficacy of percutaneous PFO closure as a therapy for migraine with or without au

198 trials question the benefit of percutaneous PFO closure, but concern has also been raised about the

199 propensity score-matched study, percutaneous PFO closure was more effective than medical treatment fo

200 pairs of patients who underwent percutaneous PFO closure or medical treatment.

201 red in 15 patients treated with percutaneous PFO closure (7.3%) versus 33 patients medically treated

202 nvestigated among patients with percutaneous PFO closure and those who received medical treatment.

203 entiometric detection of perfluorooctanoate (PFO(-)) and perfluorooctanesulfonate (PFOS(-)) were deve

204 chemic stroke to undergo closure of the PFO (PFO closure group) or to receive medical therapy alone (

205 served using toluene with the rigid polymers PFO-BT and PFO to suspend isolated nanotubes.

206 abilize lipid bilayers, unlike the precursor PFOs.

207 detected more often in those with a probable PFO-attributable stroke (OR, 0.80; P=0.45; OR, 1.15; P=0

208 re frequently seen among those with probable PFO-attributable strokes (odds ratio [OR], 0.92; P=0.53)

209 (15)N-labeled cholesterol-binding proteins (PFO* and ALO-D4, a modified anthrolysin O), to generate

210 Many physicians recommend PFO closure, an intuitively attractive mechanical soluti

211 Patients with repaired PFO demonstrated a 2.47-times greater odds (95% confiden

212 fter a short lag, it also increases the ER's PFO-accessible regulatory pool.

213 es: first, it is unclear whether a patient's PFO is causally related to the event ('pathogenic') or n

214 holesterol leaves lysosomes, it expands PM's PFO-accessible pool and, after a short lag, it also incr

215 atched males (15 PFO-, 8 large PFO+, 7 small PFO+) completed cycle ergometer exercise trials on three

216 with a large PFO, but not those with a small PFO, had a higher T(oesoph) than PFO- subjects (P < 0.05

217 lyzes phosphatidylcholine and sphingomyelin, PFO forms large transmembrane pores on cholesterol-conta

218 In the MRI subcohort, PFO was not associated with SBI (adjusted odds ratio: 1.

219 geal temperature (T(oesoph)) (P < 0.05) than PFO- subjects on Trial 1.

220 ith a small PFO, had a higher T(oesoph) than PFO- subjects (P < 0.05) during Trial 1 and increased T(

221 O+ subjects achieved a higher T(oesoph) than PFO- subjects (P < 0.05).

222 ts would have a higher core temperature than PFO- subjects due, in part, to absence of respiratory sy

223 n interaction at multiple labeled sites than PFOs and are more structurally similar to fibrils.

224 in giant unilamellar vesicles confirmed that PFO exhibits intermediate raft affinity, and showed that

225 Long-term analysis demonstrated that PFO repair was associated with no survival difference (P

226 Accordingly, we hypothesized that PFO+ subjects would have a higher core temperature than

227 to domain-localized acceptors indicated that PFO generally has a raft affinity between that of LW pep

228 Taken together, our studies reveal that PFO binding to membranes is triggered when the concentra

229 Herein we show that PFO binding to the bilayer and the initiation of the seq

230 Finally, FRET showed that PFO affinity for ordered domains was higher in its non-T

231 action on membrane bilayers facilitates the PFO-cholesterol interaction as evidenced by a reduction

232 However, the PFO-related stroke risk in the general population is not

233 e was no difference in responder rate in the PFO closure (45 of 117) versus control (33 of 103) group

234 occurred in 6 of 441 patients (1.4%) in the PFO closure group and in 12 of 223 patients (5.4%) in th

235 ermined cause occurred in 10 patients in the PFO closure group and in 23 patients in the medical-ther

236 nts occurred in 23.1% of the patients in the PFO closure group and in 27.8% of the patients in the an

237 chemic stroke occurred in 18 patients in the PFO closure group and in 28 patients in the medical-ther

238 Subjects in the PFO closure group had a significantly greater reduction

239 n infarctions was significantly lower in the PFO closure group than in the antiplatelet-only group (2

240 ate of atrial fibrillation was higher in the PFO closure group than in the antiplatelet-only group (4

241 deep-vein thrombosis) was more common in the PFO closure group than in the medical-therapy group.

242 milar in the 2 treatment groups (6.3% in the PFO closure group versus 10.2% in the medically treated

243 roups was unequal (3141 patient-years in the PFO closure group vs. 2669 patient-years in the medical-

244 events occurred in 6 patients (1.4%) in the PFO closure group, and atrial fibrillation occurred in 2

245 troke occurred among the 238 patients in the PFO closure group, whereas stroke occurred in 14 of the

246 roke was 10.1% (standard error: 2.5%) in the PFO+ and 10.4% (standard error: 1.1%) in the PFO- group

247 c strokes occurred (10.1%), 15 (9.2%) in the PFO+ and 96 (10.3%) in the PFO- groups.

248 PFO+ and 10.4% (standard error: 1.1%) in the PFO- group (p = 0.46).

249 15 (9.2%) in the PFO+ and 96 (10.3%) in the PFO- groups.

250 ic ischemic stroke to undergo closure of the PFO (PFO closure group) or to receive medical therapy al

251 ay between the structural arrangement of the PFO C-terminal domain and the distribution of cholestero

252 th the increased binding and affinity of the PFO L3 mutant, suggesting that selection of a compatible

253 he length and diameter of the opening of the PFO tunnel, presence of atrial septal aneurysm (ASA), an

254 morphologic features, and shunt grade of the PFO.

255 lity of paradoxical embolization through the PFO has made some progress and holds promises of allowin

256 dergo PFO closure plus antiplatelet therapy (PFO closure group) or to receive antiplatelet therapy al

257 closure plus long-term antiplatelet therapy (PFO closure group), antiplatelet therapy alone (antiplat

258 known whether right-to-left shunting through PFO increases during exercise impairing exercise perform

259 nity, and showed that TM PFO (but not non-TM PFO) concentrated at the edges of liquid ordered domains

260 termediate raft affinity, and showed that TM PFO (but not non-TM PFO) concentrated at the edges of li

261 mic stroke was lower among those assigned to PFO closure combined with antiplatelet therapy than amon

262 recurrence was lower among those assigned to PFO closure combined with antiplatelet therapy than amon

263 ad a recent cryptogenic stroke attributed to PFO with an associated atrial septal aneurysm or large i

264 ge who had had a recent stroke attributed to PFO, with an associated atrial septal aneurysm or large

265 ne in a manner that makes it inaccessible to PFO until its concentration exceeds a threshold of 35 mo

266 th contraindications to anticoagulants or to PFO closure were randomly assigned to the alternative no

267 address several unresolved issues related to PFO stroke and PFO migraine pathophysiology, and to iden

268 cerebrovascular events presumably related to PFO underwent either percutaneous PFO closure (150 patie

269 te outcome occurred in 11 patients slated to PFO closure (11%) and 22 patients slated to medical trea

270 p conferred the binding properties of SLO to PFO and vice versa.

271 Several randomized trials of transcatheter PFO closure versus medical management are ongoing.

272 e available on the efficacy of transcatheter PFO closure.

273 th antithrombotic treatment or transcatheter PFO closure being favored by different clinicians.

274 or large interatrial shunt, to transcatheter PFO closure plus long-term antiplatelet therapy (PFO clo

275 ce of a PFO were randomized to transcatheter PFO closure with the STARFlex implant or to a sham proce

276 he amount of cholesterol required to trigger PFO binding.

277 with the lipid environment both in wild-type PFO, thus providing new experimental constraints for mol

278 ssigned patients, in a 2:1 ratio, to undergo PFO closure plus antiplatelet therapy (PFO closure group

279 tion) occurred in 205 subjects who underwent PFO closure.

280 e stroke compared with those with unrepaired PFO (2.8% vs 1.2%, P = .04).

281 the barrier function of C2BBE cells, whereas PFO domain 4 cannot substitute for this role.

282 Thus far, it has been unclear whether PFO* and related cholesterol-binding proteins bind unifo

283 We analyzed 6075 patients (364 with PFO) followed for a mean 4.7 +/- 3.1 years.

284 evaluated the risk of stroke associated with PFO after adjusting for established stroke risk factors

285 Patients with COPD with PFO do not perform less well either on a 6-minute walk o

286 d during exercise in patients with COPD with PFO.

287 gent-resistant domains do not correlate with PFO binding.

288 ition of molecules that do not interact with PFO, but intercalate into the membrane and displace chol

289 2max was 574 (178) seconds for patients with PFO and 534 (279) seconds for those without (P = ns).

290 Among patients with PFO and cryptogenic stroke, closure reduced recurrent st

291 roimaging features to stratify patients with PFO and CS by the probability that their stroke is PFO-a

292 The approach to patients with PFO and ischemic stroke has been better defined in recen

293 nting had lower Pao2 than both patients with PFO and those with no right-to-left shunt (7.7 vs. 8.6 v

294 ed with the comparator groups, patients with PFO demonstrated similar rates of in-hospital death (3.4

295 t cerebrovascular events among patients with PFO-related transient ischemic attack or stroke.

296 tient-years, respectively (hazard ratio with PFO closure vs. medical therapy, 0.55; 95% confidence in

297 ment trials comparing medical treatment with PFO closure are needed to further advance the field.

298 mic stroke patients aged 18 to 45 years with PFO and no other cause of brain ischemia, as part of the

299 s of having SBI among those with and without PFO.

300 ke were similar in patients with and without PFO.