ライフサイエンスコーパス: edema

1 ratory mechanics, blood gases, and pulmonary edema.

2 nd acute RV dysfunction with flash pulmonary edema.

3 e observed in patients with diabetic macular edema.

4 injury and other diseases involving cerebral edema.

5 nto the parenchyma causes brain swelling and edema.

6 unded by hemorrhagic effusions and pulmonary edema.

7 ed mice die within days from acute pulmonary edema.

8 aluable for diagnosing reperfusion pulmonary edema.

9 by bilaterally symmetrical parieto-occipital edema.

10 nce tomography detection of diabetic macular edema.

11 been shown to prevent and resolve pulmonary edema.

12 noncalcium images for traumatic bone marrow edema.

13 protected against vascular permeability and edema.

14 ith development of prolonged hypotension and edema.

15 re nausea, fatigue, vomiting, and peripheral edema.

16 d in vivo pig model of hydrostatic pulmonary edema.

17 s initial bolus is to quickly treat cerebral edema.

18 morrhage transformation, infarct volume, and edema.

19 athy (DR) in the absence of diabetic macular edema.

20 ornea and regulate the resolution of corneal edema.

21 s a novel therapeutic approach for pulmonary edema.

22 ers, enhanced vascular leakage, and alveolar edema.

23 CSF pressure was elevated in those with edema.

24 imaging were done in view of diffuse corneal edema.

25 ted macular degeneration or diabetic macular edema.

26 GABAA receptor upregulation and inflammatory edema.

27 onspicuity of enthesopathic cysts and marrow edema.

28 ted macular degeneration or diabetic macular edema.

29 RVO patients receiving treatment for macular edema.

30 nic hyperpermeability causes damaging tissue edema.

31 ip was found between other measures and SHFP edema.

32 or the ability of the injured brain to clear edema.

33 therapeutic strategy for treating pulmonary edema.

34 al membrane (0.16/EY), and recurrent macular edema (0.09/EY).

35 nations (15 [23.8%] vs 1 [1.7%]), peripheral edema (15 [23.8%] vs 0), and dizziness (14 [22.2%] vs 0)

36 es analyzed, 60 (48.4%) had diabetic macular edema, 32 (25.8%) had neovascular age-related macular de

37 ea receptor-1 was higher in patients with CT edema (4.96 +/- 1.13 ng/mL vs 2.10 +/- 0.34 ng/mL; p = 0

38 vascular permeability contributes to macular edema, a leading cause of vision loss in eye pathologies

39 We conclude that cerebral edema, a previously unrecognized complication, may devel

40 educed neurodeficits and perihematomal brain edema after ICH induction by injection of either autolog

41 aluable for diagnosing reperfusion pulmonary edema after pulmonary endarterectomy and had prognostic

42 with C25; peripheral neuropathy, peripheral edema, alopecia, and nail disorders were more frequent w

43 reas high native T1 values are observed with edema, amyloid, and other conditions.

44 thickness due to delayed drainage of corneal edema and a trend towards prolonged corneal opacificatio

45 ted with normal visual acuity but optic disc edema and an enlarged blind spot in the right eye (oculu

46 cular permeability, T2-weighted MRI revealed edema and brain swelling.

47 immediately after ablation to predict acute edema and chronic lesion size.

48 nificantly associated with improved cerebral edema and clinical outcome.

49 gical examination revealed mild interstitial edema and closely packed seminiferous tubules in the lef

50 Optic disc edema and epiretinal membrane formation was found more f

51 cardiac abnormalities, including pericardial edema and heart failure.

52 luded diffuse alveolar damage with pulmonary edema and hyaline membrane formation associated with acc

53 We observed that VPC reduced brain edema and improved neurological function 24 h and 72 h a

54 inflammation, consequently attenuating brain edema and improving of neurological functions after ICH.

55 improves gas exchange, and reduces alveolar edema and inflammation in preclinical studies of lung in

56 ronic retinal diseases, results in vasogenic edema and neural tissue damage, causing vision loss.

57 controls, Anxa2(-/-) mice develop pulmonary edema and neutrophil infiltration in the lung parenchyma

58 in injury and is an informative biomarker of edema and outcome.

59 tastases to the liver as well as progressive edema and pain in the left leg, limiting ambulation.

60 ound that 0.5% PVI can attenuate congestion, edema and pain induced by pressure sores.

61 F in the vascular compartment, which reduces edema and permeation.

62 jury, absent in controls, correlated with CT-edema and preceded peak intracranial pressure.

63 nificantly declined for treatment of macular edema and proliferative retinopathy.

64 y reveals soft tissue changes such as muscle edema and scapulothoracic bursitis.

65 y reveals soft tissue changes such as muscle edema and scapulothoracic bursitis.

66 two common clinical sequela of brain injury: edema and seizures.

67 search terms diabetic retinopathy OR macular edema AND stroke OR cerebrovascular disease OR coronary

68 anism by which dexamethasone implants reduce edema and suggest that additional study is needed to inv

69 in blinding diseases associated with corneal edema and transparency loss.

70 beneficial role in the regulation of corneal edema and transparency.

71 he lung tissues revealed extensive pulmonary edema and vascular damage following infection, a finding

72 rmore, through small-animal MRI, we analyzed edema and vascular leakage.

73 f NDPK-C in zebrafish embryos caused cardiac edema and ventricular dysfunction.

74 rejection, and CT findings of peripancreatic edema and/or inflammatory change were significant risk f

75 Injection in Patients With Diabetic Macular Edema) and VIVID (Intravitreal Aflibercept Injection in

76 ng the brain (hydrocephalus), heart (cardiac edema), and kidney (disordered and shorter cilia).

77 l pressure measurements, therapies targeting edema, and 3-month Glasgow Outcome Scale score.

78 den, fungal epithelial invasion, swimbladder edema, and epithelial extrusion events serve as predicti

79 ch as angle closure glaucoma, cystic macular edema, and exudative retinal detachment.

80 characterized by fever, myalgia, periorbital edema, and fatigue.

81 planchnic circulation congestion, bowel wall edema, and impaired intestinal barrier function are thou

82 infarct volume, neuronal apoptosis, cerebral edema, and improved neurological scores.

83 scavenging ROS, decreasing inflammation and edema, and improving recovery after SCI.

84 proportion of patients with resolved macular edema, and leakage on fluorescein angiography.

85 respiratory failure, reintubation, pulmonary edema, and pneumonia) within 3 days of surgery.

86 by patient characteristics such as obesity, edema, and tenderness., Arterial PI can be used as a com

87 e to prohibitively high vascular resistance, edema, and worsening compliance.

88 acoresistant seizures and cytotoxic cerebral edema are serious complications of ischemic and traumati

89 of decreased vision attributable to macular edema associated with central retinal vein occlusion (CR

90 synechiae, bilateral papilledema and macular edema associated with serous retinal detachment in the l

91 CLO also induced immobilization and edema at high concentrations.

92 Visual analysis of the presence of edema at standard T2-weighted cardiac MR imaging resulte

93 here were no deaths or instances of cerebral edema attributable to product toxicity.

94 T2-mapping was used to quantify the edema-based AAR (% of left ventricle) following ischemic

95 ch has been shown to accurately quantify the edema-based area-at-risk (AAR) in ST-segment elevation m

96 the integrity of the BRB and prevent retinal edema, became gliotic and expressed increased levels of

97 eatment, but longer mean duration of macular edema before randomization (18 months vs. 1 month for th

98 ent group showed significantly reduced brain edema, blood-brain barrier disruption, lesion volume, an

99 etinopathy or clinically significant macular edema, both of which require timely intervention to pres

100 BF compared to CMS patients without cerebral edema; but what triggers this complication is unknown.

101 luding enhancing the resolution of pulmonary edema by up-regulating sodium-dependent alveolar fluid c

102 Subsequent edema can hinder cerebrospinal fluid efflux and can lead

103 ar magnetic resonance (T2-CMR) of myocardial edema can quantify the area-at-risk (AAR) following acut

104 ide a novel treatment option to prevent lung edema caused by S. aureus alpha-toxin.

105 ous haze score of >/=1.5+ or cystoid macular edema (CME) of >300 mum were enrolled.

106 ty (VA) in eyes with uveitic cystoid macular edema (CME).

107 ure (IOP) increase (n = 12), cystoid macular edema (CME; n = 3), and nonarteritic anterior ischemic o

108 f 55 letters or better); (2) cystoid macular edema (CMO), foveal thickness, and macular volume; (3) d

109 r ischemia, and has a higher risk of macular edema compared to eyes with no vasculitis.

110 nal vasculitis had twice the risk of macular edema compared to the non-vasculitis group.

111 anges, including choroidal folds, optic disc edema, cotton-wool spots, globe flattening, and refracti

112 detection of clinically significant macular edema (CSME).

113 rative DR, or clinically significant macular edema (CSME).

114 ive DR [PDR], clinically significant macular edema [CSME], or both who had evidence of retinal scatte

115 d a heart failure phenotype with pericardial edema, decreased ventricular systolic function, and embr

116 mice led to blood-filled lymphatic vessels, edema, defective lymphovenous valve morphogenesis, impro

117 anial pressure greater than 20 mm Hg, use of edema-directed therapies, decompressive craniotomy, or 3

118 Patients with diabetic macular edema (DME) are at high risk of vascular complications,

119 terization of patients with diabetic macular edema (DME) are important for individualizing treatment

120 2 or worse) center-involved diabetic macular edema (DME) at baseline were required to receive ranibiz

121 rcept injections (IAIs) for diabetic macular edema (DME) during the phase III VISTA DME trial were ma

122 tor (anti-VEGF) therapy for diabetic macular edema (DME) favorably affects diabetic retinopathy (DR)

123 ethasone implant therapy in diabetic macular edema (DME) is associated with long-term outcome.

124 s photographs, we evaluated diabetic macular edema (DME) progression and DR progression.

125 ore (DRSS) in patients with diabetic macular edema (DME) treated with intravitreal ranibizumab.

126 Patients with diabetic macular edema (DME) who received sham control or FAc 0.2 or 0.5

127 haracteristics in eyes with diabetic macular edema (DME) with subfoveal neuroretinal detachment (SND+

128 factor therapy in eyes with diabetic macular edema (DME) with vision loss after macular laser photoco

129 DR (NPDR), 51 with NPDR and diabetic macular edema (DME), and 18 with proliferative DR (PDR)-and 64 a

130 macular degeneration (AMD), diabetic macular edema (DME), and retinal vein occlusion (RVO) were evalu

131 g severity, with or without diabetic macular edema (DME), using en face Doppler OCT.

132 Diabetic retinopathy, diabetic macular edema (DME), vision-threatening diabetic retinopathy (VT

133 of diabetic retinopathy and diabetic macular edema (DME).

134 retinopathy (DR), including diabetic macular edema (DME).

135 tients with center-involved diabetic macular edema (DME).

136 lation for center-involving diabetic macular edema (DME).

137 ithout concomitant baseline diabetic macular edema (DME).

138 egeneration (AMD, n = 400), diabetic macular edema (DME, n = 400), or retinal vein occlusion (RVO, n

139 es and severe stages of DR (diabetic macular edema [DME] and proliferative diabetic retinopathy [PDR]

140 be treated with ketorolac and PA qid, but if edema does not resolve after 12 weeks, a switch to ketor

141 ted macular degeneration or diabetic macular edema does not respond to an initial anti-vascular endot

142 atremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical emergency

143 Among patients with macular edema due to central retinal or hemiretinal vein occlusi

144 ates, and included 362 patients with macular edema due to central retinal or hemiretinal vein occlusi

145 of aflibercept for the treatment of macular edema due to central retinal vein occlusion.

146 hy with primary intestinal lymphangiectasia, edema due to hypoproteinemia, malabsorption, and less fr

147 le suspension (CLS-TA), in eyes with macular edema due to retinal vein occlusion (RVO).

148 vitreal Aflibercept in Subjects with Macular Edema Due to Retinal Vein Occlusion (TANZANITE) study wh

149 ter choroidal thickness in eyes with macular edema due to RVO, but may result in expansion of the SCS

150 of 38 treatment-naive patients with macular edema due to RVO, enrolled in the prospective Suprachoro

151 ctable in the cornea of a patient with acute edema due to spontaneous Descemet s (basement) membrane

152 the ability of CD8 T cells to initiate brain edema during ECM.

153 y by CD8 T cells was required to cause fatal edema during ECM.

154 ents (84%) experienced reperfusion pulmonary edema during the first 72 hours after pulmonary endarter

155 actoferrin administration results in reduced edema, enhanced hematoma clearance, and improved neurolo

156 drug-induced LQT3 model, acute interstitial edema exacerbated action potential duration prolongation

157 To reproduce the lung injury and edema examined in the Webb and Tierney study and to inve

158 Consequently, edema extent measured by T2-weighted short-tau triple in

159 ), necessary for host cell toxin uptake, and edema factor (EF), the toxic moiety which increases host

160 ective antigen (PA), lethal factor (LF), and edema factor (EF).

161 d to establish lethal infection, whereas its edema factor modulates progression and dissemination of

162 h the two catalytic parts (lethal factor and edema factor) or other proteins can be transported into

163 rate proteins, called lethal factor (LF) and edema factor.

164 e Fluocinolone Acetonide in Diabetic Macular Edema (FAME) A and B Phase III clinical trials.

165 Edema formation followed a bimodal pattern in all 40-min

166 f regional contractility was associated with edema formation on CMR and increases in inflammation and

167 tive effects by reducing necrotic injury and edema formation via adenosine-dependent mechanisms.

168 cterized by alveolar epithelial cell injury, edema formation, and intraalveolar contact phase activat

169 included unilateral and bilateral optic disc edema, globe flattening, choroidal and retinal folds, hy

170 grade 1 to 2, 35%; grade 3, 10%), peripheral edema (grade 1 to 2, 37%; grade 3, 2%), and fatigue (gra

171 amic changes in post-ST-segment-elevation MI edema highlight the need for standardization of CMR timi

172 {CI}, 2.15-4.35], P < .001), cystoid macular edema (HR = 2.87 [95% CI, 1.41-5.82], P = .004), posteri

173 cular magnetic resonance included imaging of edema, hyperemia, necrosis, and fibrosis using semiquant

174 (late gadolinium enhancement and T2-weighted edema imaging) immediately after ablation and after 1, 2

175 D5423) displayed a potent inhibition of lung edema in a rat model of allergic airway inflammation fol

176 isolated pig lung lobes ex vivo and reduced edema in a volume overload in vivo pig model of hydrosta

177 h an increase in macrophage infiltration and edema in and around the depot region and was correlated

178 upregulated only after brain injury, causing edema in animal studies.

179 nd nontumoral uveitis complicated by macular edema in at least 1 eye.

180 ommonly used glucocorticoid to prevent brain edema in GBM patients, suppressed the observed inflammat

181 Moreover, the cytotoxin induced edema in isolated lungs.

182 s to life-threatening high-altitude cerebral edema in less than 1% of patients.

183 Post-MI edema in patients follows a bimodal pattern that affects

184 etinopathy or clinically significant macular edema in patients with various initial retinopathy level

185 nique for detection of traumatic bone marrow edema in patients with vertebral compression fractures.

186 Cystoid macular edema in retinal vein occlusion occurred in relation to

187 ) disruption due to SBI can exacerbate brain edema in the post-operative period.

188 lation-provoking compound 48/80 induced less edema in the skin of GF mice than in conventional mice.

189 formance for assessing traumatic bone marrow edema in vertebral compression fractures.

190 To model hydrostatic pressure-induced edema in vitro, we developed a method of applied pressur

191 tight junctions in the lung and causes lung edema in vivo, which is prevented by genetic deficiency

192 ionate) and prolonged the inhibition of lung edema, indicating potential for once-daily treatment.

193 SCs) can significantly reduce the pancreatic edema, infiltration, hemorrhage, necrosis, the release o

194 , attenuated glutamate uptake, intramyelinic edema, interleukin-6 release, complement activation, inf

195 associated with the development of cerebral edema, intracranial hypertension, and secondary neuronal

196 Outcomes included CT edema, intracranial pressure measurements, therapies tar

197 Cerebral edema is a key poor prognosticator in traumatic brain in

198 Reperfusion pulmonary edema is a specific complication of pulmonary endarterec

199 n monthly and PRN dosing, when recurrence of edema is anticipated in many patients, CRT appears stron

200 Pseudophakic cystoid macular edema is common after phacoemulsification cataract surge

201 Diabetic macular edema is one of the leading causes of vision loss among

202 Macular edema is the leading cause of vision loss in bilateral c

203 e to manage a wide range of ailments such as edema, jaundice, and gonorrhea.

204 r, IPC, but not CsA, also reduced myocardial edema leading to an underestimation of the AAR by T2-map

205 However, some of these therapies may reduce edema, leading to an underestimation of the AAR by T2-CM

206 e neuroinflammatory process, and/or cerebral edema may predict better functional outcome.

207 variables were: patients (%) in whom macular edema (ME) developed (>/=30% increase from preoperative

208 Macular edema (ME) is the leading cause of decreased visual acui

209 c alternatives for the management of macular edema (ME) secondary to branch retinal vein occlusion (B

210 vein occlusion (BRVO) complicated by macular edema (ME).

211 nt topical steroids for postsurgical macular edema (ME).

212 the retina [i.e., the development of macular edema, (ME)].

213 Edema, microvascular obstruction, and enhanced volumes w

214 hydroethanolic extract of fruit reduced the edema, migration of polymorphonuclear leukocytes into th

215 scopic examination features included macular edema, mild intraretinal pigment migration, and widespre

216 Our main findings are as follows: brain edema mimicking hypoosmotic conditions stimulates the fo

217 lated with significant improvements in brain edema, motor coordination, and working memory, and abrog

218 rization, including assessment of myocardial edema, myocardial siderosis, myocardial perfusion, and d

219 aging techniques and protocols for assessing edema, myocardium at risk, infarct size, salvage, intram

220 rfusion (I/R) myocardial tissue composition (edema, myocardium at risk, infarct size, salvage, intram

221 r presence of clinically significant macular edema; n = 95) using the modified Airlie House classific

222 cal to recognize the early signs of cerebral edema (nausea, vomiting, and headache) and intervene wit

223 In hypoosmotic conditions, which elicit cell edema, OAP formation was considerably enhanced by overex

224 losely associated with reperfusion pulmonary edema occurrence in the next 48 hours (area under the re

225 f the right scapula that was associated with edema of the serratus anterior muscle at the scapulothor

226 ogical deterioration showed diffuse cerebral edema on imaging and more deranged cerebral hemodynamics

227 hology to superolateral Hoffa fat pad (SHFP) edema on magnetic resonance (MR) images in older adults

228 alta were significantly associated with SHFP edema on MR images in subjects with or at risk for osteo

229 d with visual and quantitative assessment of edema on T2-weighted cardiac magnetic resonance (MR) ima

230 he myocardium (T2 mapping) and the extent of edema on T2-weighted short-tau triple inversion-recovery

231 inhibitor deficiency and patients with bowel edema only were excluded.

232 oreover, mice lacking NAAA failed to develop edema or scratching behavior after challenge with DNFB,

233 : 0.47; 95% CI: 0.25 to 0.87), and pulmonary edema (OR: 3.41; 95% CI: 1.53 to 7.60).

234 of decreased vision attributable to macular edema owing to CRVO or HRVO.

235 fferent in vertebral bodies with and without edema (P < .001).

236 inal detachments (P = 0.76), cystoid macular edema (P = 0.83), or timing of complications between the

237 atible with cortical vasogenic and cytotoxic edema, partial contrast enhancement, and hyperperfusion.

238 e prevention of pseudophakic cystoid macular edema (PCME) using a prospective, randomized, double-mas

239 The prevalence of pedal edema (PE) and its associations with abnormal cardiac st

240 The transient development of perilesional edema (PE) around >/=1 calcification (defined as 1 episo

241 these cases are associated with perilesional edema (PE), likely due to host inflammation.

242 ormations including hydrocephaly and cardiac edema, phenotypes associated with vitamin A deficiency.

243 lted in renal tubule defects and pericardial edema, phenotypes typically induced by kidney dysfunctio

244 s) on the incidence of postoperative macular edema (PME) after cataract surgery.

245 risk factor for ventilator-induced pulmonary edema, possibly because it amplifies lung viscoelastic b

246 orrected visual acuity, incidence of macular edema, posterior capsular opacification, epiretinal memb

247 atment successfully dampened PMA-induced ear edema, proinflammatory cytokine production, reactive oxy

248 Collectively, these changes enhanced edema, prolonged hemorrhage, and impaired forelimb funct

249 Here, we evaluated the time course of edema reaction in patients with ST-segment-elevation MI

250 Changes in BCVA and CRT associated with edema recurrence upon transition from monthly to pro re

251 Correlation of edema reduction with reduction in the PPFs angiopoietin-

252 I: 4.7, 16.9) times more likely to show SHFP edema, respectively.

253 ly after contrast injection accurately shows edema resulting from radiofrequency ablation.

254 worsening of visual acuity, cystoid macular edema, retroprosthetic membrane formation, persistent ep

255 ity (BCVA) in retinal vein occlusion macular edema (RVO-ME).

256 tients with visual impairment due to macular edema secondary to branch retinal vein occlusion (BRVO).

257 to aflibercept for the treatment of macular edema secondary to central retinal or hemiretinal vein o

258 naire (NEI VFQ-25), in patients with macular edema secondary to central retinal vein occlusion (CRVO)

259 mities for larval exposures included cardiac edema, spinal malformation, and craniofacial deformities

260 er function, with development of pericardial edema, suggesting an important role of THSD7A in glomeru

261 onance (MR) imaging of transient bone marrow edema syndrome (TBMES) and avascular osteonecrosis.

262 and minor adverse events (eg, pigmentation, edema, telangiectatic matting, and hematomas).

263 First, vDeltaK1L induced slightly less edema than vK1L, as revealed by histopathology and nonin

264 Five patients (9%) developed transient edema that required short courses of dexamethasone.

265 nteresting novel target for diabetic macular edema therapy.

266 ht to define the mechanism controlling brain edema through the use of the murine experimental cerebra

267 n number of months from diagnosis of macular edema to randomization was 6 (range, 0-104 months).

268 Bacillus anthracis edema toxin (ET) consists of protective antigen (PA), ne

269 Edema toxin has renal effects that could contribute to e

270 tial for the transport of anthrax lethal and edema toxins into human cells.

271 led to demonstrate hypoxia-induced pulmonary edema under the same conditions.

272 Sixteen patients with NPDR without macular edema underwent SDOCT and OCTA.

273 The edema volume in late gadolinium enhancement correlated w

274 gadolinium enhancement correlated well with edema volume in T2-weighted MRI with an R(2) of 0.99.

275 etinopathy or clinically significant macular edema was 1.0% over 5 years among patients with a glycat

276 en 60 minutes after contrast administration, edema was 8.7+/-3.31 times and the enhanced area 6.14+/-

277 In all groups, CMR-measured edema was barely detectable at 24 hours postreperfusion.

278 Pulmonary edema was due to increased permeability, which was augme

279 Hydrostatic pulmonary edema was induced in pigs by acute volume overload.

280 Macular edema was less likely to resolve in eyes that received a

281 etinopathy or clinically significant macular edema was limited to approximately 5% between retinal sc

282 Resolution of macular edema was more common in patients with DRSS improvement:

283 fatigue, and peripheral neuropathy, whereas edema was more frequent after DC.

284 Macular edema was observed in 224 eyes (40.7%) and was associate

285 , and a reduced progression of perihematomal edema was observed in the presence of severe spleen shri

286 In 45/0, pulmonary edema was overt and rapid, with survival less than 30 mi

287 Results SHFP edema was present in 152 (13.4%) of the 1134 knees that

288 Postcataract surgery edema was the predominant indication in North America (2

289 METHODS AND Acute interstitial edema was used to increase intercellular cleft width in

290 ostreperfusion, coinciding with the deferred edema wave, were similar to values measured by reference

291 r inclination, and trochlear angle) and SHFP edema were assessed on MR images of the knee.

292 after which group 2 subjects with persistent edema were crossed over to PA q1hWA.

293 Improvements in RCH-associated retinal edema were observed in two patients.

294 thematous base with surrounding swelling and edema were observed.

295 30 eyes (20 patients) with diabetic macular edema were obtained.

296 d hypersusceptibility to develop pericardial edema when challenged by crowding stress or exposed to e

297 monstrated that SEB mediated lung damage and edema, which were absent after treatment with abatacept.

298 2), except in 1 patient with cystoid macular edema whose vision was 20/60(-) and 20/70(+1).

299 nment and morphology to the presence of SHFP edema, with adjustments for age, sex, and body mass inde

300 outcome measure was the diagnosis of macular edema within 90 days of cataract surgery.

301 eovascular disease to reduce VEGF165-induced edema without compromising vessel growth.