ライフサイエンスコーパス: infantile

1 h from respiratory failure and infections in infantiles.

2 Study paediatricians collected data on infantile AD at repeated follow-up examinations during t

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

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

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

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

7 We propose that infantile amnesia reflects a developmental critical peri

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

9 Infantile amnesia, the inability of adults to recollect

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

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

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

13 cid position were found in both variant late infantile and Kufs disease.

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

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

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

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

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

32 described in patients presenting with fatal infantile cardiomyopathy and multiple oxidative phosphor

33 described patients with AARS2-related fatal infantile cardiomyopathy are united by either a homozygo

34 of two unrelated boys presenting with fatal infantile cardiomyopathy, lactic acidosis and respirator

35 Severe ocular alterations occur in infantile cases, whereas mild or no ocular alterations a

36 on for unilateral or bilateral congenital or infantile cataract in children younger than 2 years of a

37 ciated with profound developmental delay and infantile cataract.

38 mans, has been known to cause congenital and infantile cataracts.

39 rkably, is also responsible for variant late infantile ceroid lipofuscinosis.

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

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

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

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

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

48 that can cause hemolytic uremic syndrome and infantile diarrhea, respectively.

49 Only 6 patients with non-infantile disease (11%, all with end-stage renal disease

50 the MA ion channel TMEM63A that result in an infantile disorder resembling a hypomyelinating leukodys

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

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

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

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

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

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

57 Infantile encephalopathies are a group of clinically and

58 Early-infantile encephalopathies with epilepsy are devastating

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

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

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

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

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

64 ional and regional incidence of neonatal and infantile endogenous endophthalmitis and comorbidities a

65 risk factors for development of neonatal and infantile endogenous endophthalmitis.

66 In 2007, an estimated 291 total cases of infantile endophthalmitis were identified, in comparison

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

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

69 dystonia at 3 years, and L924P, with severe infantile epilepsy and profound impairment.

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

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

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

73 e promoter of CDKL5, a gene causative for an infantile epilepsy, from the silenced X-chromosomal alle

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

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

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

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

78 Early infantile epileptic encephalopathy (EIEE)-associated mut

79 ve mutation of TBC1D24 associated with early infantile epileptic encephalopathy (EIEE).

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

81 ion and present with developmental and early infantile epileptic encephalopathy that is far more seve

82 ated sodium channel gene are linked to early-infantile epileptic encephalopathy type 13, also known a

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

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

85 ed individuals with congenital microcephaly, infantile epileptic encephalopathy, and profound develop

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

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

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

89 SCN8A is a novel causal gene for early infantile epileptic encephalopathy.

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

91 Mutations in the SCN8A gene cause early infantile epileptic encephalopathy.

92 ts, often manifesting as treatment-resistant infantile epileptic encephalopathy.

93 Menkes is an infantile, fatal, hereditary copper-deficiency disorder

94 TRK3 with various partners are diagnostic of infantile fibrosarcoma and secretory carcinoma yet also

95 st universally harbor TRK fusions, including infantile fibrosarcoma, cellular congenital mesoblastic

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

97 Compared to the variant late infantile form, there was a lower proportion of variants

98 ilinear profiles, which are seen in the late infantile form, were not a feature.

99 One of the more severe infantile forms of the disease (INCL or CLN1 disease) is

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

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

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

103 inal muscular atrophy (SMA) is a devastating infantile genetic disorder caused by the loss of surviva

104 Infantile globoid cell leukodystrophy (GLD, Krabbe disea

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

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

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

108 Most infantile haemangiomas do not require therapy.

109 rdant regulation was also conserved in human infantile hearts.

110 (3 mg/kg/day) in the treatment of periocular infantile hemangioma (IH) based on clinical and radiolog

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

112 stly, in a patient-derived in vitro model of infantile hemangioma and pre-clinical model of HLTRS we

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

114 Infantile hemangioma is the most common benign vascular

115 220 parents/caregivers completed the 35-item Infantile Hemangioma Quality-of-Life (IH-QoL) instrument

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

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

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

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

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

121 mportant for cellular growth and survival of infantile hemangioma.

122 owth factor-D is a target of itraconazole in infantile hemangioma.

123 ergic blocker that is first line therapy for infantile hemangioma.

124 fungal agent, can clinically improve or cure infantile hemangioma; however, the underlying molecular

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

126 Infantile hemangiomas (IHs) are the most common benign t

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

128 Infantile hemangiomas are benign tumors of vascular endo

129 Infantile hemangiomas are the most common benign tumors

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

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

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

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

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

135 ar malformations, juvenile angiofibromas and infantile hemangiomas.

136 Infantile hepatic hemangiomas exhibit a diverse phenotyp

137 A proportion of infantile hepatic hemangiomas remain asymptomatic permit

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

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 diso

144 children with life-threatening perinatal or infantile hypophosphatasia showed 1 year safety and effi

145 Patients with perinatal or infantile hypophosphatasia treated with asfotase alfa fo

146 r younger with life-threatening perinatal or infantile hypophosphatasia were recruited from ten hospi

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

148 Symptoms include infantile hypotonia, global developmental delay, intelle

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

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

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 (ANM), a recessively inherited disease with infantile lethality.

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

158 associated pulmonary hypertension (PH) is an infantile lung disease characterized by aberrant angioge

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

160 rmation/maturation is necessary for creating infantile memories.

161 s both AMPA receptor response maturation and infantile memory, indicating that the synapse formation/

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

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

164 ve disorder and the leading genetic cause of infantile mortality.

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

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

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

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

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

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

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

172 Krabbe's disease is an infantile neurodegenerative disease, which is affected b

173 Here, we report an infantile neurodegenerative disorder associated with enh

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

175 nd blinding lysosomal storage disorder: late infantile neuronal ceroid lipofucinosis, also known as "

176 lmitoyl-protein thioesterase 1 (PPT1) causes infantile neuronal ceroid lipofuscinosis (CLN1), a pedia

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

178 Infantile neuronal ceroid lipofuscinosis (INCL, Infantil

179 Infantile neuronal ceroid lipofuscinosis (INCL, or CLN1

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

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

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

183 The Finnish-variant late infantile neuronal ceroid lipofuscinosis, also known as

184 Forty-two patients with infantile nystagmus (19 with albinism, 17 with idiopathi

185 herited disorder in humans, characterized by infantile nystagmus and foveal hypoplasia.

186 We imaged 81 eyes from 42 patients with infantile nystagmus of mean age 19.8 months (range, 0.9-

187 management of head position associated with infantile nystagmus syndrome (INS) when strabismus coexi

188 abnormal head position (AHP) associated with infantile nystagmus syndrome (INS).

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

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

191 tagmus (19 with albinism, 17 with idiopathic infantile nystagmus, and 6 with achromatopsia) were exam

192 de a high diagnostic yield for patients with infantile nystagmus, enabling access to disease specific

193 children affected by foveal hypoplasia with infantile nystagmus, following an autosomal recessive mo

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

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

196 Handheld OCT can predict future VA in infantile nystagmus.

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

198 Patients presented with early infantile onset encephalopathy characterized by progress

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

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

201 eptic encephalopathy, characterized by early-infantile onset epilepsy and hypotonia with additional v

202 l loss of function, and with the neonatal or infantile onset epileptic encephalopathies due to KCNQ2

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

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

205 Clinically, infantile onset neurological regression with partial rec

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

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

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

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

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

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

212 emonstrate that FHF2 variants are a cause of infantile-onset developmental and epileptic encephalopat

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

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

215 in-containing protein, is affected in a late infantile-onset form of NCL.

216 complex encoding gene, in an individual with infantile-onset generalized dystonia.

217 splantation (HSCT) is the only treatment for infantile-onset GLD; however, clinical outcomes of HSCT

218 lopmental syndrome characterized by profound infantile-onset hypotonia and developmental delay throug

219 ith a severe phenotype dominated by profound infantile-onset hypotonia and developmental delay.

220 nt stem cells (iPSCs) were generated from an infantile-onset IBD patient lacking a functional IL10RB

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

222 neuron (SMN) protein triggers the oft-fatal infantile-onset motor neuron disorder, spinal muscular a

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

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

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

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

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

228 Infantile-onset Pompe Disease (IOPD), caused by mutation

229 Infantile-onset Pompe disease is an autosomal recessive

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

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

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

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

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

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

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

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

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

239 , which results in muscle weakness and often infantile or childhood mortality.

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

241 unrelated hematopoietic transplantation for infantile osteopetrosis in 193 patients.

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

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

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

245 at included seizure onset in the prenatal or infantile period and severe verbal and ambulatory comorb

246 ast, all eyes (n = 112) of patients with non-infantile PH1 had a BCVA in the normal range (median, 20

247 All eyes (n = 24) of infantile PH1 patients revealed severe retinal alteratio

248 or no ocular alterations are typical in non-infantile PH1 patients.

249 Infantile PH1 was diagnosed in 12 patients, and non-infa

250 le PH1 was diagnosed in 12 patients, and non-infantile PH1 was diagnosed in 56 patients (17 with end-

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

252 hthalmitis declined in both the neonatal and infantile population from 2007 through 2014.

253 The rate of decline in the infantile population was 7% from 2007 through 2014.

254 lial cells of mouse hemangioma cell line and infantile primary hemangioma endothelial cell.

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

256 Reversible infantile respiratory chain deficiency (RIRCD) is a rare

257 Infantile SCA7, which is often paternally transmitted, c

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

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

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

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

262 DNA methylation profiles of infantile sonic hedgehog-activated medulloblastoma (SHH-

263 preceding spasms, which was also observed in infantile spasm patients.

264 Comparisons were made to recordings from infantile spasm patients.

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

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

267 sistant epilepsy (OR = 0.23, p = 0.022), and infantile spasms (OR = 0, p < 0.001).

268 abnormalities, recurrent fever episodes, and infantile spasms .

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

270 that p.Glu200Ala, previously associated with infantile spasms and microcephaly, is also pathogenic.

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

272 are associated with intellectual disability, infantile spasms and seizures.

273 Infantile spasms are seizures associated with a severe e

274 The National Infantile Spasms Consortium established a multicenter, p

275 Infantile spasms constitutes a severe infantile epilepsy

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

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

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

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

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

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

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

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

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

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

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

287 Lennox-Gastaut syndrome, Dravet syndrome and infantile spasms with intellectual disability as well as

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

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

290 2 gene are associated with schizophrenia and infantile spasms, respectively.

291 base enrolling infants with new diagnosis of infantile spasms.

292 lonic encephalopathy, Ohtahara syndrome, and infantile spasms.

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

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

295 ardiomyopathy; the paradigmatic examples are infantile tafazzinopathies.

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

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

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