ライフサイエンスコーパス: oedema

1 low, most probably as a result of developing oedema.

2 nic day (E)17.5, associated with generalized oedema.

3 on of intraretinal fluid, indicating macular oedema.

4 hoea, constipation, vomiting, and peripheral oedema.

5 who did not have another reason for macular oedema.

6 ith FTY-720 (fingolimod) may exhibit macular oedema.

7 ocyte velocity, and yolk sac and pericardium oedema.

8 of T regulatory cells and reduced pulmonary oedema.

9 ity in the absence and presence of vasogenic oedema.

10 rmacological prevention and/or resolution of oedema.

11 such as haematomas, contusions and cerebral oedema.

12 s including hypopigmentation and pericardial oedema.

13 case of RDD associated with cystoid macular oedema.

14 Os) led to bent body axes, hydrocephalus and oedema.

15 tients' cerebellar defects, microcephaly and oedema.

16 elates with Wallerian degeneration and nerve oedema.

17 which result in vascular leakage and retinal oedema.

18 NK(1) receptor in mediating NKB-induced skin oedema.

19 iferation or loss, gliosis, inflammation and oedema.

20 differs from that for cardiogenic pulmonary oedema.

21 d a chest radiograph showed severe pulmonary oedema.

22 ia, coagulopathy and peripheral and cerebral oedema.

23 died within 1 week of complete resolution of oedema.

24 s had intracranial hypertension and cerebral oedema.

25 al congestion, rhinorrhoea, ptosis or eyelid oedema.

26 nhibitor for prophylaxis of hereditary angio-oedema.

27 tina homeostasis thus preventing retina from oedema.

28 such as diffuse capillary leak and pulmonary oedema.

29 arge hemispheric stroke at risk for cerebral oedema.

30 erapy for the management of diabetic macular oedema.

31 or ACE inhibitor (ACE-I) treatment and angio-oedema.

32 tegrity, but also to inflammation-associated oedema.

33 small fibres polyneuropathy and lower limbs oedema.

34 nsferase, influenza, insomnia and peripheral oedema.

35 schaemia, paralleling the onset of cytotoxic oedema.

36 f swelling and low frequency of perilesional oedema (10%) at diagnosis, as compared with the PML-IRIS

37 ents after emactuzumab treatment were facial oedema (16 [64%] of 25 patients), asthenia (14 [56%]), a

38 29 [33%]), myalgia 21 [24%]), and peripheral oedema 20 [23%]).

39 hy (21 [39%] of 54 patients), and peripheral oedema (21 [39%] of 54 patients).

40 cytopenia in nine [11%] vs none), peripheral oedema (22 [27%] vs three [8%]), and venous thromboembol

41 pokalaemia (28 [1%]), and fluid retention or oedema (23 [1%]).

42 Most donor lungs had no or mild pulmonary oedema (24/29 [83%]), intact alveolar fluid clearance (1

43 [6%], respectively) and higher incidences of oedema (294 [64%] patients had any-grade oedema in the t

44 ue (six [18%] of 33 patients) and peripheral oedema (4 [12%]).

45 m the nifedipine group because of peripheral oedema (725 vs 518, p<0.0001), but serious adverse event

46 ents in the macitentan group were peripheral oedema (9 [23%] of 40 patients) and decreased haemoglobi

47 ogical department due to unilateral blepharo-oedema, abrupt pain and vision disturbances; in 5 cases,

48 Angio-oedema affecting the gastrointestinal tract or abdominal

49 t lung fluid clearance and formation of lung oedema after acute lung injury.

50 be a case of fatal non-cardiogenic pulmonary oedema, after use of iopamidol, a widely used, low osmol

51 multiple sclerosis with microcystic macular oedema also had higher Multiple Sclerosis Severity Score

52 episodes progressed to bilateral optic nerve oedema and a subsequent left sided optic neuropathy.

53 ive (inhaled epinephrine for early laryngeal oedema and an epinephrine injector for severe reactions)

54 nly used perioperatively to control cerebral oedema and are frequently continued throughout subsequen

55 l cancer, who developed bilateral optic disc oedema and associated left sided optic neuropathy is des

56 To report a case of bilateral optic disc oedema and associated optic neuropathy in the setting of

57 High lysine alone resulted in vasogenic oedema and blood-brain barrier breakdown within the stri

58 ic disorders, including especially pulmonary oedema and cardiorespiratory collapse.

59 the frequency of side-effects such as angio-oedema and cough remains to be established.

60 ation, production of oxidative stress, brain oedema and degenerating neurons.

61 ed sparse infiltration of mononuclear cells, oedema and demyelination.

62 sm presenting with life-threatening cerebral oedema and dysmyelination in affected individuals.

63 Both bone oedema and erosions on MRI have been confirmed as repres

64 on episodes were characterized by reversible oedema and erythema of the graft.

65 h multiple sclerosis for microcystic macular oedema and examined correlations between macular oedema

66 ad smaller infarcts and developed less brain oedema and fewer neurological deficits.

67 of infarcts showed well demarcated zones of oedema and hypoxic-ischaemic neuronal injury, consistent

68 Cerebral oedema and increased intracranial pressure can occur in

69 We report here the development of cerebral oedema and increased intracranial pressure in 12 patient

70 helial junctions, thereby suppressing tumour oedema and metastatic spread, may be preferable to full

71 grade 3-4 adverse events include generalised oedema and myalgia (each in two [1%] patients) in those

72 aetiology of neuroleptic associated cerebral oedema and neuroleptic malignant syndrome.

73 IL-1beta/IL-1R actions account for oedema and neutrophil recruitment to the lungs, leading

74 ic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular pe

75 Haemorrhaging, oedema and other severe vascular defects are a central a

76 itted to the Internal Diseases Clinic due to oedema and pain of the right shoulder joint.

77 m and alveolar epithelium, leads to alveolar oedema and pulmonary surfactant dysfunction.

78 Astrocytes were swollen indicating oedema and remained swollen during the next 24 h through

79 ups, except for a slight excess of pulmonary oedema and respiratory failure in the lower magnesium ta

80 arrived with deep vein thrombosis DVT, pain, oedema and rubor of right lower limb and drug abuse.

81 signal abnormalities suggestive of vasogenic oedema and sulcal effusions (ARIA-E) and microhaemorrhag

82 ors have a role in the formation of cerebral oedema and there is evidence that cGMP is an important s

83 onses resulting in tissue damage, intestinal oedema and thrombotic abnormalities.

84 tected against ALI and ameliorated pulmonary oedema and total protein in BALF.

85 is (one); pain associated with severe tongue oedema and trismus occurred twice; and non-cardiac chest

86 ma and examined correlations between macular oedema and visual and ambulatory disability in a cross-s

87 factors has been linked to haemorrhaging and oedema and we find widespread expression of VEGF-D, rigf

88 sis lesions include size >2 cm, mass effect, oedema and/or ring enhancement.

89 y with associated development of pericardial oedemas and cardiac damage.

90 tion of ionic oedema, formation of vasogenic oedema, and catastrophic failure with haemorrhagic conve

91 zures, optic nerve/cerebellar atrophy, pedal oedema, and early death.

92 , influenza, diarrhoea, headache, peripheral oedema, and wrong drug given.

93 nd glucose uptake, and supervening vasogenic oedema; and (3) a chronic stage of striatal atrophy.

94 ental hypoxia, hypertension, proteinuria and oedema are the principal clinical features of this disea

95 uch as haemorrhagic transformation and angio-oedema, are reviewed.

96 vents were reported, and no cases of macular oedema arose.

97 y and are strongly suggestive of hippocampal oedema as the abnormality in the initial investigations.

98 galy or splenomegaly (52/67), fever (33/64), oedema, ascites, anasarca, or a combination (29/37), ele

99 ver, the increased cellularity and vasogenic oedema associated with inflammation cannot be detected o

100 who had chronic heart failure, were free of oedema at baseline, and survived for at least 4 months a

101 reductions in frequency of hereditary angio-oedema attacks and was well tolerated.

102 hypernatraemia resulted in significant brain oedema because brain osmolality failed to decrease at th

103 t response to treatment and died of cerebral oedema before a transplant could be done.

104 s with chronic kidney disease was peripheral oedema (benazepril plus amlodipine, 189 of 561, 33.7%; b

105 odality of treatment for refractory cerebral oedema, but the only form of treatment known to improve

106 inhibitor deter attacks of hereditary angio-oedema, but the prophylactic effect of recombinant human

107 We detected cerebral oedema by computed axial tomography of the head and necr

108 onociception was assessed by aesthesiometry, oedema by plethysmometry, clinical severity by scoring,

109 12% of the angio-oedema cases were severe (1% of all patients treated wit

110 acute haemorrhage or massive posterior fossa oedema causing obstructive hydrocephalus or brainstem co

111 on of the alveolar epithelial function (lung oedema clearance), epithelial cell repair, innate immuni

112 study is to report a case of cystoid macular oedema (CME) associated with Rosai-Dorfman Disease (RDD)

113 To report the rate of cystoid macular oedema (CMO) as detected by spectral-domain optical cohe

114 evated intraocular pressure, cystoid macular oedema (CMO), cataract and posterior capsule opacificati

115 hypertension, but in most patients cerebral oedema contributes to death or places them at too high a

116 y was used in parallel as an alternative for oedema control.

117 Oedema develops quickly after trauma, raising intracrani

118 acular degeneration (nAMD), diabetic macular oedema (DME) or branch/central retinal vein occlusion (B

119 treatment for recalcitrant diabetic macular oedema (DMO).

120 of treating DR, focusing on diabetic macular oedema [DMO] after anti-vascular endothelial growth fact

121 pernatraemia over 4-24 h results in cerebral oedema, due primarily to failure of brain amino acids an

122 [6%]), fatigue (six [2%] vs 19 [5%]), brain oedema (eight [2%] vs 11 [3%]), seizure (nine [2%] vs ei

123 ated adverse events included arm swelling or oedema (eight [32%] patients), and vein hardening (seven

124 maging (MRI) for location, size, mass effect/oedema, enhancement, multifocality and fulfilment of Bar

125 Thrombin and TFLLR-amide produced no oedema (Evans Blue extravasation) in the spinal cord tha

126 erwise thought to be associated with macular oedema except in the context of comorbid clinical uveiti

127 vent in lesion pathogenesis, predisposing to oedema, excitotoxicity, and ingress of plasma proteins a

128 included nasal blockage, rhinorrhoea, eyelid oedema, facial sweating/flushing and ear flushing.

129 zymatically active Lethal Factor (LF) and/or Oedema Factor (EF) bound to Protective Antigen 63 (PA63)

130 ntities of the toxins lethal factor (LF) and oedema factor (EF), leading to widespread vascular leaka

131 tective antigen (PA), lethal factor (LF) and oedema factor (EF).

132 rates within the cytosol of mammalian cells: oedema factor (OF) is an adenylate cyclase that impairs

133 n catalytic moieties, lethal factor (LF) and oedema factor (OF), are internalized into the host-cell

134 wo enzyme components, lethal factor (LF) and oedema factor (OF).

135 eptamer that translocates the toxic enzymes, oedema factor and lethal factor, into the cytosol.

136 ive pore, and translocates lethal factor and oedema factor are not well defined without an atomic mod

137 tion and a 30 degrees rotation away from the oedema factor catalytic core, which stabilizes a disorde

138 Four discrete regions of oedema factor form a surface that recognizes an extended

139 On calmodulin binding, an oedema factor helical domain of relative molecular mass

140 es translocate the enzymes lethal factor and oedema factor into the cytosol of target cells.

141 Oedema factor is an adenylate cyclase that impairs host

142 Oedema factor shares no significant structural homology

143 Here we report the X-ray structures of oedema factor with and without bound calmodulin.

144 Oedema factor, a calmodulin-activated adenylyl cyclase,

145 ising protective antigen, lethal factor, and oedema factor, is the major virulence factor of Bacillus

146 in the placebo group), symptomatic cerebral oedema (five [2%] vs four [2%]), and major haemorrhage (

147 normalities may be associated with cytotoxic oedema following mechanical forces, resulting in changes

148 After freedom of oedema for more than 3 months after oedema resolved, end

149 were restudied again after remaining free of oedema for more than 3 months.

150 er cranial autonomic features include eyelid oedema, forehead/facial sweating, sense of aural fullnes

151 ed intradermally or intravenously, to induce oedema formation (assessed as plasma extravasation) was

152 induction, macrophage iNOS upregulation and oedema formation after GTN infusion, dural mast cells ex

153 cerebral capillary dysfunction, resulting in oedema formation and haemorrhagic conversion.

154 y reduces infarct size, neuronal cell death, oedema formation and neutrophil infiltration in H/I mice

155 e of Starling's principle, which states that oedema formation is determined by the driving force and

156 atic vessel function and thereby exacerbates oedema formation is unknown.

157 ponse resulting in increased vasoreactivity, oedema formation, and microvascular obstruction.

158 laries into three phases: formation of ionic oedema, formation of vasogenic oedema, and catastrophic

159 umonitis (four [8%] and none, respectively), oedema (four [8%] and none, respectively), dyspnoea (thr

160 risks of retinal detachment, cystoid macular oedema, glare, halos and posterior capsule opacification

161 n sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mechanisms, a

162 multiple sclerosis with microcystic macular oedema had significantly worse disability [median Expand

163 Hereditary angio-oedema (HAE) with normal C1 inhibitor is associated with

164 Oedema, haemodilution, and weight gain occurred in a dos

165 e Pdgfrb-Cre transgenic mouse line, leads to oedema, haemorrhage and increased levels of embryonic le

166 alveolitis associated with massive pulmonary oedema, haemorrhage and rapid destruction of the respira

167 of the blood-brain barrier, which can cause oedema, haemorrhage, and cell death.

168 n sickness (AMS) and high-altitude pulmonary oedema (HAPE) were diagnosed using clinical questionnair

169 for treatment of uveitis and uveitic macular oedema has a limited duration of action and is associate

170 pathways, and patients with hereditary angio-oedema have intermittent cutaneous or mucosal swellings

171 Adverse events were peripheral oedema, hypotension, or orthostatic hypotension.

172 Progressive encephalopathy with oedema, hypsarrhythmia and optic atrophy (PEHO) syndrome

173 Progressive encephalopathy with oedema, hypsarrhythmia, and optic atrophy (PEHO) syndrom

174 F) mice display reduced vascular leakage and oedema, improved response to chemotherapy and, important

175 lesions demonstrated mass effect in 45% and oedema in 77%.

176 jections of bevacizumab to treat the macular oedema in a case of arteriovenous malformation.

177 mmation-associated cellularity and vasogenic oedema in addition to accounting for partial volume effe

178 t it is responsible for preventing embryonic oedema in birds, a role previously thought to be played

179 287 significantly inhibited hyperalgesia and oedema in both models.

180 ges in infants and interstitial white matter oedema in children and adults.

181 agents may play a role in wealing and tissue oedema in CSU so representing novel targets in therapy.

182 elial growth factor antagonists for managing oedema in glioblastoma patients.

183 The patient developed oedema in her right leg, which was treated successfully.

184 The presence of microcystic macular oedema in multiple sclerosis suggests that there may be

185 24%) in the placebo group, including macular oedema in six (2%) versus six (1%), and basal-cell carci

186 ween groups, but more patients had pulmonary oedema in the intervention group (94 [11%] of 840) than

187 ncrease in striatal water content, vasogenic oedema in the perihaematomal region presented as increas

188 lated; two resulted in death (from pulmonary oedema in the placebo group and a pre-existing unspecifi

189 nduced significant ulceration, bleeding, and oedema in the stomach or small intestine of wild-type (W

190 of oedema (294 [64%] patients had any-grade oedema in the trebananib group vs 127 [28%] patients in

191 ied by light microscopy, and we estimated an oedema index and a fibre degeneration index.

192 activities of EDP were assessed in mouse paw oedema induced by lambda-carrageenan (Carr).

193 ed Fisher scale, rebleeding, global cerebral oedema, intracranial pressure crisis, pneumonia and seps

194 Cerebral oedema is a cause of morbidity and mortality in fulminan

195 Orolingual angio-oedema is a recognised complication of tissue plasminoge

196 Hereditary angio-oedema is a recurrent, oedematous disorder caused by def

197 ises pre-eclampsia, a condition where tissue oedema is also observed.

198 Hereditary angio-oedema is caused by a heterozygous deficiency of C1 inhi

199 Perilesional oedema is common and associated with episodic seizure ac

200 Transient perilesional brain oedema is seen around the calcified foci but its importa

201 contrast-induced, non-cardiogenic pulmonary oedema is unclear, and treatment differs from that for c

202 The commonest side-effect, peripheral oedema, is attributed to a larger arterial than venous d

203 of NPSLE brains reveals presence of cerebral oedema, loss of neurons and myelinated axons, microglial

204 Five serious adverse events (periorbital oedema, lupus erythematosus [occurring twice], erythema,

205 non-restricted isotropic diffusion fraction (oedema marker) correlated with magnetization transfer ra

206 Microcystic macular oedema may also contribute to visual dysfunction beyond

207 Angio-oedema may be delayed and progress to life-threatening a

208 c heart failure with recent-onset peripheral oedema (mean age 64 years [SD 10], New York Heart Associ

209 le range 3-6)] than patients without macular oedema [median Expanded Disability Score Scale 2 (interq

210 e of disease progression, than those without oedema [median of 6.47 (interquartile range 4.96-7.98) v

211 modal MRI, and that perihaematomal vasogenic oedema might be attributable to microglial activation, i

212 Microcystic macular oedema (MMO) of the retinal inner nuclear layer (INL) ha

213 agas' disease, amyloidosis, alcoholism, myxo-oedema, multiple sclerosis, idiopathic pseudo-obstructio

214 g loss of aquaporin-4 expression, glial cell oedema, myelin breakdown and axonal injury, but little i

215 y-tract infection (n=17, 10%) and peripheral oedema (n=13, 8%) were the most frequent events with pio

216 roup were dizziness (n=10 [12%]), peripheral oedema (n=9 [11%]), urinary tract infections (n=9 [11%])

217 as the number of attacks of hereditary angio-oedema observed in each 4 week treatment period.

218 Microcystic macular oedema occurred more commonly in eyes with prior optic n

219 perpigmentation, pain, hypopigmentation, and oedema) occurred in 943 (93%) of 1015 participants in th

220 Angio-oedema occurs more frequently than previously reported a

221 a significant independent predictor of angio-oedema (odds ratio (OR) 2.3; 95% CI 1.1 to 4.7).

222 ce values, the presence of bilateral pitting oedema of nutritional origin, or a mid-upper-arm circumf

223 ncephalopathy syndrome predominantly causing oedema of the white matter of the parietal and occipital

224 ateral infiltrates consistent with pulmonary oedema on frontal chest radiograph.

225 P) acutely above 25 mmHg (to cause pulmonary oedema) on RARs was also investigated.

226 the five serious adverse events-periorbital oedema (one [4%]), lupus erythematosus (one [4%]), and d

227 with diabetic retinopathy, diabetic macular oedema or age-related macular degeneration.

228 (BHs) on MRIs may represent either areas of oedema or axonal loss in patients with multiple sclerosi

229 sease characterized by pruritic weals, angio-oedema or both occurring for at least 6 weeks.

230 raphically might show few areas of vasogenic oedema or even normal brain imaging in some rare cases.

231 Oedema or fluid retention occurred in 67 (27%) patients

232 Neurological complications, such as brain oedema or haemorrhagic transformation, occur earlier tha

233 he search terms "neurogenic" with "pulmonary oedema" or "pulmonary edema," "experimental neurogenic p

234 cumented intracranial hypertension, cerebral oedema, or both.

235 for patients presenting with osteomyelitis, oedema, or multifocal or large lesions.

236 Presentation with oedema, osteomyelitis, or large (>/=15 cm in diameter),

237 e mean number of attacks of hereditary angio-oedema over 4 weeks was significantly reduced with recom

238 ion size, and presence of mass effect and/or oedema (P < 0.001).

239 In addition to orofacial angio-oedema, painless swellings affect peripheries, which cau

240 of four or more attacks of hereditary angio-oedema per month for at least 3 months before study init

241 ll unknown whether subsequent perihaematomal oedema (PHE) formation further increases the odds of an

242 The oedema phenotype is effectively lethal and resembles tha

243 stemic reaction that culminates in pulmonary oedema, potentially leading to death.

244 The microcystic oedema predominantly involved the inner nuclear layer of

245 rrelated with occurrence of diffuse cerebral oedema, presence of subdural and extradural hematoma; ho

246 The patient's symptoms and oedema regressed with discontinuation of chemotherapy.

247 Hepatic encephalopathy and cerebral oedema remain important and life-threatening complicatio

248 ; two patients in each group developed brain oedema requiring osmotherapy.

249 ew inflammatory activity from the effects on oedema resolution and lesion repair.

250 eedom of oedema for more than 3 months after oedema resolved, endotoxin concentrations remained uncha

251 Macular oedema responded to intravitreal treatment with triamcin

252 ctions VEGF causes vascular permeability and oedema, resulting in extensive injury to ischaemic tissu

253 ions (misapposition, granuloma, haemorrhage, oedema, retraction or necrosis), and postoperative sympt

254 toxaemia would be increased in patients with oedema secondary to congestive heart failure.

255 Macular oedema secondary to retinal vein occlusion (RVO) can cau

256 cacies of widely used treatments for macular oedema secondary to RVO and the feasibility of conductin

257 orehead/facial sweating, itching eye, eyelid oedema, sense of aural fullness and periaural swelling,

258 (eight [17%]; all grade 1-2), and peripheral oedema (seven [15%] grade 1-2, one [2%] grade 3).

259 luded seizure (18 [5%] vs 22 [6%]) and brain oedema (seven [2%] vs 12 [3%]).

260 with diseases with BRB breakdown and macular oedema such as diabetic retinopathy (DR).

261 at could account for the presence of macular oedema, such as uveitis, diabetes or other retinal disea

262 data are strongly suggestive of hippocampal oedema that is resolving within 5 days of a PFC, but do

263 e bilateral regions of subcortical vasogenic oedema that resolve within days or weeks.

264 [3%] patients vs two [1%] patients), macular oedema (three [1%] vs two [1%]), infections (11 [3%] vs

265 asymmetry could represent return (post-acute oedema) to a pre-existing hippocampal abnormality simila

266 two exotoxins: anthrax lethal toxin (LT) and oedema toxin (ET).

267 Here we demonstrate that oedema toxin (PA + OF) induces an increase in ANTXR expr

268 ce of resistance to anthrax lethal toxin and oedema toxin action.

269 Macular oedema typically results from blood-retinal barrier disr

270 We unexpectedly observed microcystic macular oedema using spectral domain optical coherence tomograph

271 veloped to determine the effect of admission oedema volume on outcome.

272 a nested case-control substudy, perilesional oedema was assessed by MRI at the time of seizure in sym

273 No macular oedema was identified in 52 healthy controls assessed ov

274 Although oedema was increased, typical anti-VEGF associated adver

275 Mild-to-moderate pulmonary oedema was more common in patients given albumin than in

276 patients with chronic kidney disease, angio-oedema was more frequent in the benazepril plus amlodipi

277 Orolingual angio-oedema was observed in 42 patients (7.9%; 95% CI 5.5% to

278 reas peripapillary retinal nerve fibre layer oedema was observed in affected eyes (P = 0.008) and sub

279 A microcystic pattern of macular oedema was observed on optical coherence tomography in 1

280 Angio-oedema was retrospectively classified as mild, moderate

281 ion within 5 days of the event; perilesional oedema was seen in 12 patients (50%) compared with two (

282 s had congestive heart failure, frequency of oedema was similar to placebo (one case at 50 mug, two a

283 Erythema and oedema were more frequent with avotermin than with place

284 breast shrinkage, telangiectasia, and breast oedema were significantly less common normal tissue effe

285 reast induration, telangiectasia, and breast oedema were significantly less common normal tissue effe

286 with dysarthria, fatigue, paraesthesias, and oedema, whereas gait problems, disequilibrium, dyskinesi

287 l abnormalities, consistent with hippocampal oedema, whilst non-febrile status epilepticus is not.

288 atment, there was complete regression of the oedema with a significant improvement in visual acuity t

289 include haematoma expansion, perihaematomal oedema with increased intracranial pressure, intraventri

290 cording to parental origin, a gross neonatal oedema with microcardia and a postnatal growth retardati

291 se events were skin rash (five patients) and oedema with weight gain (six).

292 iagnosis, and management of hereditary angio-oedema, with specific emphasis on the new treatments ava

293 Cases were defined as those developing angio-oedema within 24 h of initiation of tPA.

294 motor regression, characterized by cytotoxic oedema within the basal ganglia, cerebral oligemia, and

295 e urticarias, idiopathic histaminergic angio-oedema without weals as a presentation of CU and omalizu