ライフサイエンスコーパス: infantile

1 h from respiratory failure and infections in infantiles.

2 Unlike established AD, these patients with infantile AD did not have noticeably dysbiotic communiti

3 Like CF, DMD, SMA, and infantile AMD are inexorably debilitating and require li

4 It has been suggested that infantile amnesia is due to the underdevelopment of the

5 hat in rats an experience learned during the infantile amnesia period is stored as a latent memory tr

6 We propose that infantile amnesia reflects a developmental critical peri

7 re rapidly forgotten, a phenomenon known as 'infantile amnesia'.

8 Infantile amnesia, the inability of adults to recollect

9 ined in rats that illuminates the paradox of infantile amnesia.

10 ng BDNF or mGluR5 after training rescues the infantile amnesia.

11 Early onset (infantile and childhood) phenotypes likely represent dev

12 sidered as a differential diagnosis for both infantile- and juvenile-onset movement disorders, includ

13 Results of the Infantile Aphakia Treatment Study have concluded that pr

14 rate of adverse events than reported in the Infantile Aphakia Treatment Study.

15 nificantly more likely to have had recurrent infantile apnoeas (RR1.9; P < 0.005) than those with GLR

16 intake during pregnancy and breastfeeding to infantile asthma phenotypes and elevated IgE level.

17 After adjustment for infantile atopic dermatitis and preceding egg skin prick

18 Patients with persistent infantile atopic dermatitis are more likely to develop a

19 Of the 246 patients with infantile atopic dermatitis at 6 months of age, 48 patie

20 lowed until 6 years of age; 246 patients had infantile atopic dermatitis at 6 months of age.

21 Patients with persistent infantile atopic dermatitis had a higher risk of asthma

22 Risk factors associated with persistent infantile atopic dermatitis included egg white sensitiza

23 s of age were associated with the persistent infantile atopic dermatitis.

24 e risk factors related to the persistence of infantile atopic dermatitis.

25 tum was associated with an increased risk of infantile atopic eczema at age 12 months, but no signifi

26 Within the UK Southampton Women Survey, infantile atopic eczema at ages 6 and 12 months was asce

27 y (n = 497) and related to the odds ratio of infantile atopic eczema.

28 antile neuronal ceroid lipofuscinosis (INCL, Infantile Batten disease) is a neurodegenerative lysosom

29 fied fish sauce has the potential to prevent infantile beriberi in this population.

30 Importance: Infantile beriberi, a potentially fatal disease caused b

31 Monocular infantile blindness may be associated with bilateral hor

32 l virus (RSV) is the most important cause of infantile bronchiolitis and a major pathogen in elderly

33 al virus (RSV) is the most frequent cause of infantile bronchiolitis and pneumonia.

34 l virus (RSV) is the leading global cause of infantile bronchiolitis, which is associated with recurr

35 All patients with eyelid infantile capillary hemangiomas at risk of developing am

36 f treatment with oral propranolol for eyelid infantile capillary hemangiomas led to complete regressi

37 Of 17 patients with eyelid infantile capillary hemangiomas, 3 were excluded for ast

38 s, the risk for postoperative glaucoma after infantile cataract surgery appears to be influenced by t

39 Infantile cataract surgery bears a significant risk for

40 Patients and mutations were separated into infantile, childhood and adult-onset groups.

41 Patients were divided into classic infantile, childhood-onset, and adult-onset patients.

42 We found that (i) encephalopathies with infantile/childhood onset epilepsies (>/=3 months of age

43 Difference in the prevalence of infantile colic between children with and without a diag

44 questionnaire identified personal history of infantile colic for case and control participants, confi

45 Infantile colic is a common cause of inconsolable crying

46 igraine were more likely to have experienced infantile colic than those without migraine (72.6% vs 26

47 Infantile colic, gastroesophageal reflux, and constipati

48 kinesigenic dyskinesia (38.7%; n = 560) and infantile convulsions and choreoathetosis (14.3%; n = 20

49 nts with benign familial infantile epilepsy, infantile convulsions and choreoathetosis and paroxysmal

50 inesia (PKD), and their combination-known as infantile convulsions and paroxysmal choreoathetosis (IC

51 .Asp336Val, previously associated with fatal infantile COX deficiency, and c.1015C>T; p.Arg339Trp.

52 pinal cord motor neurons, muscle atrophy and infantile death or severe disability.

53 disease that is the leading genetic cause of infantile death.

54 opper dysregulation is associated with fatal infantile disease, liver, and cardiac dysfunction, neuro

55 e autosomal recessive later-onset and severe infantile disorders, respectively, which result from the

56 pamine transporter (DAT) cause a syndrome of infantile dystonia/parkinsonism.

57 presynaptic membrane-fusion machinery, cause infantile early epileptic encephalopathy (Ohtahara syndr

58 multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 popu

59 logy 'childhood eczema', 'flexural eczema', 'infantile eczema', 'atopic neurodermatitis', or 'Besnier

60 ion was associated with an increased risk of infantile eczema, childhood wheeze/asthma, eczema and al

61 show that probiotic supplementation prevents infantile eczema, thus suggesting a new potential indica

62 iciency due ACAD9 mutations spans from fatal infantile encephalocardiomyopathy to mild encephalomyopa

63 deficiency are usually associated with fatal infantile encephalomyopathy.

64 Infantile encephalopathies are a group of clinically and

65 rs that comprise approximately 10% of static infantile encephalopathies.

66 affected by a remarkably similar phenotype (infantile encephalopathy and largely normal brain MRI) t

67 We identified two additional patients with infantile encephalopathy and partially overlapping clini

68 (4 acute necrotizing encephalopathy, 1 acute infantile encephalopathy predominantly affecting the fro

69 cluding the recently described NALCN-related infantile encephalopathy, is increasingly recognized.

70 y normal brain MRI) to that of NALCN-related infantile encephalopathy, we identified a locus on 2q34

71 on or seizure freedom in children with early infantile epilepsies (<3 months), whereas other antiepil

72 Benign familial infantile epilepsy (41.7%; n = 602), paroxysmal kinesige

73 ction mutations in KCC2 are a known cause of infantile epilepsy in humans and KCC2 dysfunction is pre

74 suggest that mutations associated with early infantile epilepsy result in increased sodium channel ac

75 Infantile spasms constitutes a severe infantile epilepsy syndrome that is difficult to treat a

76 he majority of patients with benign familial infantile epilepsy, infantile convulsions and choreoathe

77 Patients with early infantile epileptic encephalopathy (EIEE) are at increas

78 Patients with early infantile epileptic encephalopathy (EIEE) experience sev

79 defects and epileptic phenotypes, including infantile epileptic encephalopathy (EIEE), suggestive of

80 Early infantile epileptic encephalopathy (EIEE)-associated mut

81 SCN8A encephalopathy, or early infantile epileptic encephalopathy 13 (EIEE13), is cause

82 etic testing for other currently known early infantile epileptic encephalopathy genes (including PLCB

83 owth endothelial cells (BOECs) from an early infantile epileptic encephalopathy type 4 (EIEE4) patien

84 uals described here, however, cause a severe infantile epileptic encephalopathy with a central myelin

85 th migrating focal seizures, is a rare early infantile epileptic encephalopathy with poor prognosis,

86 HO-like, and there is an overlap with 'early infantile epileptic encephalopathy'.

87 ngs and an unrelated individual) with severe infantile epileptic encephalopathy, clubfoot, absent dee

88 behavioural disorders, and 14 patients with infantile epileptic encephalopathy, of which 13 had seve

89 deficiency leads to potentially fatal early infantile epileptic encephalopathy, severe developmental

90 ndrome, autism spectrum disorders, and early infantile epileptic encephalopathy.

91 ng was performed in 7 patients with isolated infantile esotropia (5 untreated and 2 previously treate

92 on surgery for the correction of large-angle infantile esotropia may be associated with a favorable l

93 2 previously treated) and in 3 patients with infantile esotropia syndrome associated with mild neurol

94 bismus surgery in infant eyes with essential infantile esotropia.

95 optokinetic asymmetry seen in patients with infantile esotropia.

96 ranching enzyme deficiency includes a severe infantile form and a late-onset variant known as adult p

97 osomal recessive ataxia type-1 (SPARCA1), an infantile form of ataxia with cognitive impairment.

98 A significant subset of the infantile form of the disease is due to missense mutatio

99 of rectal bleeding in infants, while classic infantile FPE is rarely diagnosed.

100 ated sweat chloride, recurrent hyponatremia, infantile FTT and lung disease identified deleterious va

101 , two children with elevated sweat chloride, infantile FTT, and recurrent hyponatremia were homozygou

102 D), retinal vascular tortuosity, and primary infantile glaucoma.

103 al characteristics resembling those noted in infantile GM2 gangliosidosis has been described.

104 dications for treatment are life-threatening infantile haemangioma (causing heart failure or respirat

105 With a prevalence of 4.5%, infantile haemangiomas are the most common benign tumour

106 Most infantile haemangiomas do not require therapy.

107 rdant regulation was also conserved in human infantile hearts.

108 (3 mg/kg/day) in the treatment of periocular infantile hemangioma (IH) based on clinical and radiolog

109 Infantile hemangioma (IH) is the most common tumor of in

110 es of these lesions are shared with those of infantile hemangioma and tufted angioma of children, but

111 as wet age-related macular degeneration and infantile hemangioma are more common in light-skinned in

112 220 parents/caregivers completed the 35-item Infantile Hemangioma Quality-of-Life (IH-QoL) instrument

113 hat EndMT induced by M1 macrophages promotes infantile hemangioma regression and may lead to novel th

114 ants 1 to 5 months of age with proliferating infantile hemangioma requiring systemic therapy.

115 Human placenta and infantile hemangioma samples highly express ECSCR protei

116 common, predominantly benign complication in infantile hemangioma, little is known about the prognosi

117 e pathogenic C482R VEGFR-2 mutant, linked to infantile hemangioma, promotes ligand-independent signal

118 ram per day for 6 months in the treatment of infantile hemangioma.

119 clinical evaluation and treatment of CMN and infantile hemangioma.

120 Infantile hemangiomas (IH) are common tumors for which t

121 Infantile hemangiomas (IHs) are common benign tumors of

122 Objectives: To describe the sequelae left by infantile hemangiomas after natural involution and to id

123 Infantile hemangiomas are benign tumors of vascular endo

124 Congenital melanocytic nevi (CMN) and infantile hemangiomas are commonly encountered in newbor

125 Infantile hemangiomas are the most common benign tumors

126 Although most CMN and infantile hemangiomas do not require active intervention

127 nign vascular tumors that differ from common infantile hemangiomas in that they grow in utero and are

128 Importance: Infantile hemangiomas involute to some extent, but they

129 etrospective cohort study of images from 187 infantile hemangiomas that had not received systemic tre

130 Most are benign infantile hemangiomas that typically regress by 5 years

131 opranolol has been used to treat complicated infantile hemangiomas, although data from randomized, co

132 evolutionized the treatment of proliferating infantile hemangiomas, laser and/or surgical excision ar

133 ar malformations, juvenile angiofibromas and infantile hemangiomas.

134 treatment of benign vascular tumors such as infantile hemangiomas.

135 romise for the treatment of certain types of infantile hemangiomas.

136 Universal infantile hepatitis B (HB) vaccination is very efficacio

137 Two of the individuals had infantile hepatopathy with fibrosis and steatosis, leadi

138 lasmic mt-tRNA(Glu) mutation, and reversible infantile hepatopathy, due to tRNA 5-methylaminomethyl-2

139 ockout (Alpl (-/-)) mouse phenocopies severe infantile HPP, including profound skeletal and dental de

140 racteristic of the Alpl(-/-) model of severe infantile HPP.

141 Idiopathic infantile hypercalcemia (IIH) is characterized by severe

142 amino acid conversions associated with fatal infantile hypertrophic cardiomyopathy and the neurologic

143 Infantile hypertrophic pyloric stenosis (IHPS) is a seri

144 Infantile hypertrophic pyloric stenosis shows strong fam

145 on of genetic variation with the presence of infantile hypertrophic pyloric stenosis.

146 Loss-of-function mutations of NALCN cause infantile hypotonia with psychomotor retardation and cha

147 Symptoms include infantile hypotonia, global developmental delay, intelle

148 prenatal acetaminophen intake and increased infantile IgEs related to aeroallergens was statisticall

149 ansporter (hDAT, SLC6A3) cause a syndrome of infantile/juvenile dystonia and parkinsonism.

150 the E130K missense mutation in patients with infantile Krabbe disease.

151 An infant presented with fatal infantile lactic acidosis and cardiomyopathy, and was fo

152 ciated with a clinical spectrum ranging from infantile lactic acidosis to childhood (cardio)myopathy

153 eta subunit (SCS A-beta) is linked to lethal infantile Leigh or leigh-like syndrome.

154 the ubiquitin adaptor protein PLAA cause an infantile-lethal neurodysfunction syndrome with seizures

155 ical outcomes to a more severe spectrum with infantile lethality (p.Val112Glu).

156 mend NBAS analysis in individuals with acute infantile liver failure, especially if triggered by feve

157 , including younger age at onset, history of infantile liver involvement, and subacute and remitting

158 ng the question of which mechanisms underlie infantile memories and amnesia.

159 Infantile mice exposed to alpha-, gamma-, or CM-HBCD dem

160 ts have been characterized as causing severe infantile mitochondrial neurodegeneration.

161 Infantile myofibromatosis (IM) is the most common benign

162 mutations in PDGFRB have been shown to cause infantile myofibromatosis, idiopathic basal ganglia calc

163 th mutations in CLN1 primarily manifest with infantile NCL (INCL or Haltia-Santavuori disease), which

164 underlie various types of NCLs, of which the infantile NCL (INCL) and congenital NCL (CNCL) are the m

165 e two most common NCL subtypes: classic late-infantile NCL, caused by TPP1(CLN2) mutation, and juveni

166 for 52.3% of all disease causing alleles in infantile NCL, the most common of which worldwide is the

167 ow that, in an ovine model of a variant late-infantile NCL, there is abnormal expression of sleep hom

168 r DAP-component-encoding gene, as a cause of infantile nephronophthisis associated with central nervo

169 have been associated with disorders such as infantile neuroaxonal dystrophy, neurodegeneration with

170 nts from two unrelated families each with an infantile neurodegenerative disorder characterized by lo

171 the neurodegenerative lysosomal disease late-infantile neuronal ceroid lipofuscinosis (CLN2 disease).

172 The Finnish variant of late infantile neuronal ceroid lipofuscinosis (CLN5 disease)

173 Infantile neuronal ceroid lipofuscinosis (INCL) is a dev

174 Infantile neuronal ceroid lipofuscinosis (INCL) is an in

175 Infantile neuronal ceroid lipofuscinosis (INCL, Infantil

176 Infantile neuronal ceroid lipofuscinosis (INCL, or CLN1

177 tated in the lysosomal storage disorder Late Infantile Neuronal Ceroid Lipofuscinosis (LINCL).

178 neurologic features typical for variant late-infantile neuronal ceroid lipofuscinosis (vLINCL), a sev

179 ompared with the reported natural history of infantile neuronal ceroid lipofuscinosis and that of aff

180 Infantile neuronal ceroid lipofuscinosis is a devastatin

181 port of the natural history of patients with infantile neuronal ceroid lipofuscinosis provides a guid

182 tion of the novel Cln1(R151X) mouse model of infantile neuronal ceroid lipofuscinosis that we have ge

183 ren between 6 months and 3 years of age with infantile neuronal ceroid lipofuscinosis with any two of

184 quences for the CLN2 gene implicated in late infantile neuronal ceroid lipofuscinosis with iodine-124

185 LN2 disease, late infantile (or classic late infantile neuronal ceroid lipofuscinosis), a paediatric

186 une 30, 2012, we recruited ten children with infantile neuronal ceroid lipofuscinosis; one child was

187 Children with idiopathic infantile nystagmus (IIN) exhibit visual acuity deficits

188 Idiopathic infantile nystagmus (IIN) is a genetically heterogeneous

189 Idiopathic infantile nystagmus (IIN) is a genetically heterogeneous

190 e way to achieving a much clearer picture of infantile nystagmus aetiology in the future.

191 Mechanisms underlying infantile nystagmus are unclear.

192 ommon mechanisms that could underlie various infantile nystagmus subtypes are also highlighted.

193 d phenotypical characterization of all these infantile nystagmus subtypes has been achieved recently

194 This study was conducted on patients with infantile nystagmus syndrome and myopia equal to or more

195 PRK in patients with infantile nystagmus syndrome and myopia improved monocul

196 lts from the control group with unassociated infantile nystagmus was used to relate fixation stabilit

197 of opinion regarding the mechanisms causing infantile nystagmus, identification of new genes and det

198 rs (95% confidence interval [CI], 5.15-8.28) Infantile nystagmus, onset by 6 months, comprised 62 (87

199 derstanding mechanisms underlying idiopathic infantile nystagmus, which has progressed through determ

200 of 93 age-similar children with unassociated infantile nystagmus.

201 tory activity of the eyes that characterizes infantile nystagmus.

202 e visual acuity in achiasma or patients with infantile nystagmus.

203 as used to determine the underlying cause of infantile nystagmus.

204 significantly advanced our understanding of infantile nystagmus.

205 velopments in understanding the aetiology of infantile nystagmus.

206 the diagnosis of conditions associated with infantile nystagmus.

207 occur almost as often as those with an early infantile onset (<3 months), and are thus more frequent

208 Patients presented with early infantile onset encephalopathy characterized by progress

209 yelination with spastic quadriplegia, and an infantile onset encephalopathy, suggesting multiple cell

210 nd in a single patient with a severe form of infantile onset encephalopathy.

211 ied a small family with autosomal recessive, infantile onset epilepsy and intellectual disability.

212 The infantile onset group had higher Charcot-Marie-Tooth dis

213 ng in a novel phenotype that includes severe infantile onset myoclonus, hypotonia, optic nerve abnorm

214 Clinically, infantile onset neurological regression with partial rec

215 Half of the infantile onset patients then required ambulation aids o

216 We report two siblings with infantile onset seizures, severe developmental delay and

217 (MLC) is a genetic disease characterized by infantile onset white matter edema and delayed onset neu

218 isease is hypothesised to be between that of infantile-onset (ie, <6 years old) and adult-onset disea

219 -onset disease is typically more severe than infantile-onset and adult-onset disease, long-term morbi

220 n early-onset amyotrophic lateral sclerosis, infantile-onset ascending hereditary spastic paraplegia

221 The patient had an infantile-onset but slowly progressive encephalomyopathy

222 f-function allele in UBA5 underlies a severe infantile-onset encephalopathy.

223 e we describe two unrelated individuals with infantile-onset epilepsy and abnormalities of brain morp

224 his gene has been previously associated with infantile-onset epilepsy syndromes in two other cohorts.

225 Infantile-onset inflammatory bowel disease (IO IBD) is a

226 Dravet syndrome (DS) is an infantile-onset intractable epilepsy caused by heterozyg

227 We describe a disease encompassing infantile-onset movement disorder (including severe park

228 biallelic mutation in the PTRH2 gene causes infantile-onset multisystem disease with progressive mus

229 In parallel, infantile-onset mutant GALCs showed reduced trafficking

230 t siblings of consanguineous parents with an infantile-onset neurodegenerative disorder manifesting a

231 Many GLD patients develop infantile-onset of progressive neurologic deterioration

232 ients in the cohort presented with classical infantile-onset parkinsonism dystonia, with one survivin

233 SLC12A5 mutations in patients with a severe infantile-onset pharmacoresistant epilepsy syndrome, epi

234 Infantile-onset Pompe disease is an autosomal recessive

235 reprogrammed fibroblasts from patients with infantile-onset Pompe disease to generate induced plurip

236 ibed, with a classical presentation of early infantile-onset progressive parkinsonism dystonia.

237 cted in dopamine transporter mutants causing infantile-onset rather than juvenile-onset disease.

238 neurodevelopmental delay and an intractable infantile-onset seizure disorder.

239 uNAc; sialic acid), in nine individuals with infantile-onset severe developmental delay and skeletal

240 ates meaningful change in clinical trials in infantile-onset SMA.

241 Infantile-onset spinal muscular atrophy (SMA) is the mos

242 and 12 mg dose equivalents) in patients with infantile-onset spinal muscular atrophy.

243 led, phase 3 clinical study of nusinersen in infantile-onset spinal muscular atrophy.

244 ved in the O-mannosylation pathway result in infantile-onset, severe developmental defects involving

245 APOPT1 mutations are responsible for infantile or childhood-onset mitochondrial disease, hall

246 Here, we study mutations that cause infantile or later-onset GLD, and show that GALC activit

247 (TPP1) deficiency causes CLN2 disease, late infantile (or classic late infantile neuronal ceroid lip

248 unrelated hematopoietic transplantation for infantile osteopetrosis in 193 patients.

249 sease with severity ranging from progressive infantile paralysis and premature death (type I) to limi

250 ering a debilitating and often fatal form of infantile Parkinsonism known as AADC deficiency.

251 d in several DA-related disorders, including infantile parkinsonism, attention-deficit/hyperactivity

252 edict which infants are at high risk for the infantile phenotype while distinguishing other children

253 In individuals with infantile regression and this pattern of MRI abnormaliti

254 However, reversible infantile respiratory chain deficiency (RIRCD), due to a

255 Infantile SCA7, which is often paternally transmitted, c

256 Benign familial infantile seizures (BFIS), paroxysmal kinesigenic dyskin

257 Variants observed in infantile seizures are predominantly missense, leading t

258 rum disorder (ASD), developmental delay, and infantile seizures.

259 h pontocerebellar hypoplasia (SMA-PCH) is an infantile SMA variant with additional manifestations, pa

260 Infantile spasms (IS) and Lennox-Gastaut syndrome (LGS)

261 Infantile spasms (IS) is an early-onset epileptic enceph

262 thies (EEs) Lennox-Gastaut syndrome (LGS) or infantile spasms (IS).

263 al 5'-phosphate (n = 6); (ii) a patient with infantile spasms (onset 5 months) responsive to pyridoxa

264 lled infants who had a clinical diagnosis of infantile spasms and a hypsarrhythmic (or similar) EEG n

265 irst case of a child with ISOD who developed infantile spasms and hyperekplexia.

266 approved drug (Sabril) for the treatment of infantile spasms and refractory adult epilepsy.

267 Infantile spasms are seizures associated with a severe e

268 The National Infantile Spasms Consortium established a multicenter, p

269 Infantile spasms constitutes a severe infantile epilepsy

270 nt screening of 47 patients with unexplained infantile spasms did not reveal additional de novo mutat

271 ovel therapeutic target for the treatment of infantile spasms in DS.

272 an autism plus developmental syndrome after infantile spasms in others.

273 is necessary for the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse and may repre

274 in Ts brain upon the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse model of DS.

275 n-Q also rescued the GABAB R agonist-induced infantile spasms phenotype in Ts mutants.

276 is necessary for the GABAB R agonist-induced infantile spasms phenotype in Ts.

277 syndrome (DS) is exquisitely sensitive to an infantile spasms phenotype induced by gamma-aminobutyric

278 Ts mice rescued the GABAB R agonist-induced infantile spasms phenotype.

279 is significantly more effective at stopping infantile spasms than hormonal therapy alone.

280 is significantly more effective at stopping infantile spasms than hormonal therapy alone.

281 ildren with ISOD; however, to our knowledge, infantile spasms with a corresponding hypsarrhythmia pat

282 hat presented with cranial asymmetry, severe infantile spasms with hypsarrhythmia, and dysproportiona

283 es including hypsarrhythmia (associated with infantile spasms) and burst suppression.

284 hould be considered as initial treatment for infantile spasms, including those with impaired developm

285 bility, cataracts, severe epilepsy including infantile spasms, irritability, failure to thrive, and s

286 lonic encephalopathy, Ohtahara syndrome, and infantile spasms.

287 gnature in patients with a recent history of infantile spasms.

288 the hypsarrhythmia pattern characteristic of infantile spasms.

289 c-clonic, complex partial, focal clonic, and infantile spasms.

290 base enrolling infants with new diagnosis of infantile spasms.

291 first case to date of maternally transmitted infantile spinocerebellar ataxia type 7 (SCA7), in which

292 ardiomyopathy; the paradigmatic examples are infantile tafazzinopathies.

293 governs increased GnRH expression during the infantile-to-juvenile transition and that impairing micr

294 his report presents a 22-month-old girl with infantile type Sandhoff disease that was hospitalized fo

295 es, nine consecutive patients with FMNS with infantile unilateral visual loss underwent strabismus su

296 te a tailored surgical approach in FMNS with infantile unilateral visual loss.

297 surgical outcome of patients with FMNS with infantile unilateral visual loss.

298 that GALC activity is significantly lower in infantile versus later-onset mutants when measured in th

299 Infantile wheezing is a common problem, but there are no

300 Although infantile wheezing is common, there is a paucity of evid