ライフサイエンスコーパス: inborn

1 umans learn to imitate; this capacity is not inborn.

2 n perceive children's food preferences to be inborn.

3 d stem cells are in clinical development for inborn and acquired liver diseases and could represent a

4 emerging field that is currently tested for inborn and acquired liver diseases.

5 ter to distinguish between immunity which is inborn and that which has been acquired" (The Inborn Fac

6 erythropoietic anemia type 1 (CDA-1), a rare inborn anemia characterized by abnormal chromatin ultras

7 l instability, for example, in patients with inborn aneuploidy.

8 disease (CHD) represents the most prevalent inborn anomaly.

9 the domestic chicken, to demonstrate that an inborn auditory perceptual predisposition is transferabl

10 All inborn babies with type 1 zone 1 ROP at the Neonatal Int

11 All inborn babies with type 1 zone I ROP at a single institu

12 Inborn brain differences in metabolic capacity were mapp

13 Here we show that the same mutations as inborn de novo mutations cause an early onset multisyste

14 Inborn defects in both kinds of cilia cause human ciliop

15 The phenotype was reminiscent of inborn defects in fatty acid oxidation and of fasted PPA

16 Multiple inborn defects in metabolic circuitries accelerate aging

17 etabolic byproducts that arise from specific inborn defects of tyrosine catabolism.

18 Interestingly, inborn deletion of thalamic reticular nucleus-enriched,

19 embers and X-ist, which potentially leads to inborn differences between males and females and their d

20 to Ace-K, highlighting a potential role for inborn differences in vulnerability to overconsumption o

21 imary immunodeficiencies are a rare group of inborn diseases characterized by a broad clinical and ge

22 , mutations in the corresponding genes cause inborn diseases of amino acid metabolism, most of which

23 elevance in hereditary pancreatitis, a human inborn disorder associated with mutations in the cationi

24 Although initially described as an inborn disorder of affective contact, information on aut

25 Severe congenital neutropenia (SCN) is an inborn disorder of granulopoiesis that in many cases is

26 Severe congenital neutropenia (SCN) is an inborn disorder of granulopoiesis.

27 Severe congenital neutropenia is an inborn disorder of granulopoiesis.

28 mophagocytic lymphohistiocytosis (HLH) is an inborn disorder of immune regulation caused by mutations

29 These findings suggest that inborn DNA methylation differences play important roles

30 Here, we describe a newly recognized inborn error due to the deficiency of P5CS in two siblin

31 se intolerance (HFI) is a potentially lethal inborn error in metabolism caused by mutations in the al

32 in CBS are known to cause homocystinuria, an inborn error in metabolism.

33 nt of vasculitis, drug removal, support from inborn error metabolism, multiorgan system failure, prim

34 erapies for phenylketonuria, the most common inborn error of amino acid metabolism.

35 ry cause of phenylketonuria, the most common inborn error of amino acid metabolism.

36 hese findings define a potentially treatable inborn error of bile acid biosynthesis caused by ACOX2 d

37 The most common inborn error of bile acid metabolism is 3beta-hydroxy-De

38 Lysinuric protein intolerance (LPI) is an inborn error of cationic amino acid (arginine, lysine, o

39 RSH/SLOS is due to an inborn error of cholesterol biosynthesis caused by mutat

40 Smith-Lemli-Opitz syndrome (SLOS) is an inborn error of cholesterol biosynthesis characterized b

41 The most common inborn error of cobalamin metabolism, combined methylmal

42 This is the second inborn error of coenzyme A biosynthesis to be implicated

43 rt for the first time an autosomal recessive inborn error of de novo purine synthesis (DNPS)-PAICS de

44 MCAD-deficiency is the most common inborn error of fatty acid oxidation now included in man

45 In conclusion, we describe an inborn error of glutamate metabolism caused by a GLS hyp

46 Fabry disease is an inborn error of glycosphingolipid catabolism, resulting

47 , cause Fabry disease, an X-linked recessive inborn error of glycosphingolipid catabolism.

48 Acute intermittent porphyria (AIP) is an inborn error of heme biosynthesis due to the deficiency

49 hepatic porphyria, is an autosomal dominant inborn error of heme biosynthesis due to the half-normal

50 hropoietic porphyria, an autosomal recessive inborn error of heme biosynthesis, results from the mark

51 genital erythropoietic porphyria (CEP) is an inborn error of heme synthesis resulting from uroporphyr

52 CD137 deficiency is a novel inborn error of human immunity characterized by lymphocy

53 tosomal dominant STAT4 deficiency as a novel inborn error of IL-12-dependent IFN-gamma immunity assoc

54 identified NF-kappaB1-related disease as an inborn error of immunity with immune dysregulation, rath

55 homolog (DEF6) as the molecular cause of an inborn error of immunity with systemic autoimmunity.

56 hat the patient may have had a novel type of inborn error of immunity.

57 et of rapamycin pathway and underlie a novel inborn error of immunity.

58 Thus, human MDA5 deficiency is a novel inborn error of innate and/or intrinsic immunity that ca

59 balamin C (cblC) deficiency, the most common inborn error of intracellular cobalamin metabolism, is c

60 Hereditary hemochromatosis (HH) is a common inborn error of iron metabolism characterized by excess

61 Isovaleric acidemia (IVA) is an inborn error of leucine metabolism that can cause signif

62 Glutaric aciduria type 1 (GA1) is an inborn error of lysine degradation characterized by a sp

63 Phenylketonuria is a flagship inborn error of metabolism and has been at the forefront

64 An inborn error of metabolism associated with mutations in

65 ionic acidemia is a rare autosomal recessive inborn error of metabolism caused by a deficiency of pro

66 We report an inborn error of metabolism caused by an expansion of a G

67 ylmalonic acidemia is an autosomal recessive inborn error of metabolism caused by defective activity

68 Glycogen storage disease (GSD) type 1a is an inborn error of metabolism caused by defective glucose-6

69 Propionic acidemia (PA) is an inborn error of metabolism caused by the genetic deficie

70 We report an inborn error of metabolism caused by TKFC deficiency in

71 ase kinase has also been implicated in a new inborn error of metabolism characterized by autism, inte

72 eta-synthase (CBS) deficiency is a recessive inborn error of metabolism characterized by elevated ser

73 deficiency (MoCD) is an autosomal recessive inborn error of metabolism characterized by neurodegener

74 s enzyme as the cause of PGM1 deficiency, an inborn error of metabolism classified as both a glycogen

75 Mutations in the TNAP gene result in the inborn error of metabolism known as hypophosphatasia, ch

76 sor of 7-ketocholesterol has relevance to an inborn error of metabolism known as Smith-Lemli-Opitz sy

77 Creatine Transporter Deficiency (CTD) is an inborn error of metabolism presenting with intellectual

78 Primary hyperoxaluria type 1 (PH1) is an inborn error of metabolism resulting from a deficiency o

79 aB, MMAA, lead to methylmalonic aciduria, an inborn error of metabolism that can be fatal.

80 in ALPL result in hypophosphatasia (HPP), an inborn error of metabolism that causes defective skeleta

81 Our data reveal a potentially frequent inborn error of metabolism that results from MTO deficie

82 ch transcriptional dysregulation leads to an inborn error of metabolism with a complex clinical pheno

83 e identification of NTCP deficiency as a new inborn error of metabolism with a relatively mild clinic

84 cerol kinase deficiency (GKD) is an X-linked inborn error of metabolism with metabolic and neurologic

85 U, phenylalanine hydroxylase deficiency), an inborn error of metabolism, can be detected through newb

86 dividuals from two families with a recessive inborn error of metabolism, characterized by megaloblast

87 represents the first reported case of a new inborn error of metabolism, DMGDH deficiency.

88 Phenylketonuria is an inborn error of metabolism, involving, in most cases, a

89 athionine beta-synthase (CBS) deficiency, an inborn error of metabolism.

90 of MeaB result in methylmalonic aciduria, an inborn error of metabolism.

91 1, result in ethylmalonic encephalopathy, an inborn error of metabolism.

92 aB, MMAA, lead to methylmalonic aciduria, an inborn error of metabolism.

93 Homocystinuria is an inborn error of methionine metabolism that results in ra

94 o acid decarboxylase (AADC) deficiency is an inborn error of monoamine neurotransmitter synthesis, wh

95 at NLS represents the extreme end of a known inborn error of serine metabolism and highlights the pow

96 Classical homocystinuria (HCU) is an inborn error of sulfur amino acid metabolism caused by d

97 stinuria (HCU) is a serious life-threatening inborn error of sulfur metabolism with poorly understood

98 t homocystinuria (HCU) is a life-threatening inborn error of sulfur metabolism.

99 iency is a rare disorder characterized by an inborn error of the catabolism of the inhibitory neurotr

100 identify the cause of a relatively frequent inborn error, pseudoxanthoma elasticum (PXE), a disorder

101 etic porphyria (CEP), an autosomal recessive inborn error, results from the deficient but not absent

102 iseases reflect a relatively new category of inborn error.

103 EBP can cause Conradi-Hunermann syndrome, an inborn error.

104 t of PGM3 function leads to a novel primary (inborn) error of development and immunity because bialle

105 than T and B cells, but a growing number of inborn errors affect cells other than circulating and ti

106 iciency of PLP in the brain can be caused by inborn errors affecting B6 vitamer metabolism or by inac

107 olving information on a new group of genetic inborn errors affecting ubiquitination and proteasomal d

108 Ever since Garrod deduced the existence of inborn errors in 1901, a vast array of metabolic disease

109 rspective, we discuss emerging evidence that inborn errors in immunity constitute real-life models th

110 s, the study of genetic defects arising from inborn errors in immunity has resulted in the discovery

111 The ability to incriminate single-gene inborn errors in immunodeficient patients results from t

112 Our findings may help explain human inborn errors in propionate metabolism.

113 ata indicate a potentially causal link among inborn errors in SETX, susceptibility to infection and t

114 However, inborn errors in STAT4, which controls interleukin-12 (I

115 We propose that inborn errors in the human ATR gene identified here resu

116 Such deficiencies can result from inborn errors in the MCM structural gene or from mutatio

117 Inborn errors in Toll-like receptor 3 (TLR3)-IFN type I

118 of malignant brain tumours in patients with inborn errors of 2HG metabolism.

119 in MMACHC represent the most common cause of inborn errors of B(12) metabolism, and our results expla

120 absorption in children and adolescents with inborn errors of bile acid metabolism due to amidation d

121 Inborn errors of bile acid metabolism may present as neo

122 Inborn errors of Cacna1a, the P/Q-type voltage-gated cal

123 Inborn errors of CACNA1A-encoded P/Q-type calcium channe

124 ronic mucocutaneous candidiasis (CMC), while inborn errors of caspase recruitment domain-containing p

125 Inborn errors of cholesterol synthesis are associated wi

126 Inborn errors of cholesterol synthesis cause human malfo

127 Inborn errors of cholesterol synthesis underlie a group

128 and ichthyosis are laminopathies rather than inborn errors of cholesterol synthesis.

129 se and that HEM dysplasia and ichthyosis are inborn errors of cholesterol synthesis.

130 malformation syndromes, which are caused by inborn errors of cholesterol synthesis.

131 ynthase and is impaired in the cblC group of inborn errors of cobalamin disorders.

132 ken together, our results expand the list of inborn errors of copper metabolism.

133 tions has been clarified by the discovery of inborn errors of cytokines, hormones, and their receptor

134 Inborn errors of DNA repair or replication underlie a va

135 Primary hyperoxalurias (PH) are inborn errors of glyoxylate metabolism characterized by

136 The inborn errors of heme biosynthesis, the porphyrias, are

137 iPSCs to screen for potential treatments for inborn errors of hepatic metabolism and suggest that car

138 Inborn errors of human interferon gamma (IFN-gamma) immu

139 ctious diseases has led to the definition of inborn errors of human STAT1 immunity of four types, inc

140 Combined immunodeficiency (CID) refers to inborn errors of human T cells that also affect B cells

141 illustrated by the discovery of single-gene inborn errors of IFN-gamma immunity underlying severe ca

142 ich trigger mycobacterial diseases and mimic inborn errors of IFN-gamma immunity, is genetically dete

143 D) and X-linked agammaglobulinemia (XLA) are inborn errors of immune function that require prompt dia

144 he discovery and characterization of several inborn errors of immune-related genes that underlie inhe

145 RS-CoV-2) infection in individuals with rare inborn errors of immunity (IEI), a population at risk of

146 m prognosis of children and adolescents with inborn errors of immunity (IEIs).

147 Insights from study of inborn errors of immunity and multi-omics profiling toge

148 Here we consider inborn errors of immunity arising from mutations in eith

149 Molecular dissection of inborn errors of immunity can help to elucidate the nonr

150 inically overlapping, heterogeneous group of inborn errors of immunity characterized by elevated seru

151 Furthermore, some individuals with defined inborn errors of immunity exhibit extreme susceptibility

152 d by July 1, 2020, 60 with PID, 7 with other inborn errors of immunity including autoinflammatory dis

153 Human inborn errors of immunity mediated by the cytokines inte

154 We suggest that the group of Mendelian inborn errors of immunity referred to as the type I inte

155 e absence of overt risk factors, single-gene inborn errors of immunity should be sought in children a

156 ral killer cell deficiency (NKD) arises from inborn errors of immunity that lead to impaired NK cell

157 We hypothesized that rare single-gene inborn errors of immunity to HHV-8 may underlie classic

158 We hypothesized that inborn errors of immunity to HHV-8 might underlie the ex

159 portance of the recently described monogenic inborn errors of immunity underlying resistance or susce

160 ctions may also result from hitherto unknown inborn errors of immunity, at least in some patients wit

161 ation and understanding of this novel set of inborn errors of immunity, the human type I interferonop

162 medicine, particularly the growing field of inborn errors of immunity.

163 genetic diagnosis of patients with monogenic inborn errors of immunity.

164 severe influenza may result from single-gene inborn errors of immunity.

165 g adults have been attributed to single-gene inborn errors of immunity.

166 to search for the corresponding single-gene inborn errors of immunity.

167 Human inborn errors of innate immunity often underlie infectio

168 Here we review inborn errors of innate immunity that have been recently

169 Most known inborn errors of innate immunity to infection disrupt th

170 underlie mucocutaneous candidiasis, whereas inborn errors of interferon-gamma (IFN-gamma) immunity u

171 More rarely, inborn errors of interferon-gamma immunity underlie ende

172 Inborn errors of interleukin-17 immunity have recently b

173 Patients with inborn errors of interleukin-17F (IL-17F) or IL-17RA dis

174 estigations suggest that CD may be caused by inborn errors of macrophages.

175 rt (n = 87) included patients with confirmed inborn errors of metabolism (IEM) and genetic syndromes;

176 nd accurate quantification of biomarkers for inborn errors of metabolism (IEM) from dried blood spots

177 For many inborn errors of metabolism (IEM), allogeneic hematopoie

178 polysaccharidoses (MPS), patients with other inborn errors of metabolism (IEM), patients with neuroge

179 been made in the treatment of patients with inborn errors of metabolism (IEM),(1) resulting in incre

180 Inborn errors of metabolism (IEMs) are a large class of

181 used to screen newborns for a panel of rare inborn errors of metabolism (IEMs)(1-4).

182 ng T cell immunometabolism in the context of inborn errors of metabolism allows one to define essenti

183 Mutations in many CYP genes cause inborn errors of metabolism and contribute to many clini

184 MMA concentrations are a hallmark of several inborn errors of metabolism and indicators of cobalamin

185 Children with HCM associated with inborn errors of metabolism and malformation syndromes h

186 RASopathies) (30% of the genetic diagnoses); inborn errors of metabolism and musculoskeletal disorder

187 erlap with known loci for complex disorders, inborn errors of metabolism and pharmacological targets.

188 ned a gene panel targeting 614 genes causing inborn errors of metabolism and tested its diagnostic ef

189 ral role in the pathophysiology of both rare inborn errors of metabolism and the more common multifac

190 tabolic abnormalities, storage diseases, and inborn errors of metabolism are described.

191 Inborn errors of metabolism are genetic conditions that

192 drial disorders are among the most prevalent inborn errors of metabolism but largely lack treatments

193 ers of autophagy' as an emerging subclass of inborn errors of metabolism by using the examples of six

194 ficiencies in these enzyme activities due to inborn errors of metabolism cause neuronal ceroid lipofu

195 mucopolysaccharidoses (MPSs) are a class of inborn errors of metabolism caused by deficiency of each

196 Urea cycle disorders (UCD) are inborn errors of metabolism caused by deficiency of enzy

197 Fatty acid oxidation (FAO) defects are inborn errors of metabolism clinically associated with c

198 Inborn errors of metabolism highlight the importance of

199 ting insulin or insulin-like molecules or by inborn errors of metabolism impairing liver glucose prod

200 ect multiple compounds diagnostic of diverse inborn errors of metabolism in neonatal dried blood spec

201 olase deficiency is one of a growing list of inborn errors of metabolism in the non-oxidative part of

202 variants as a cause of potentially treatable inborn errors of metabolism manifesting with MADD and sh

203 N-methyl-d-aspartate-encephalitis or inborn errors of metabolism may present after birth with

204 ps of de novo purine synthesis lead to human inborn errors of metabolism often characterized by menta

205 Thirteen of the 17 genes are associated with inborn errors of metabolism or other pediatric genetic c

206 t for those who presented as infants or with inborn errors of metabolism or with mixed hypertrophic a

207 ations between defective autophagy and other inborn errors of metabolism such as lysosomal storage di

208 olesterol biosynthesis dysfunction and other inborn errors of metabolism such as: mucolipidosis type

209 be included in the differential diagnosis of inborn errors of metabolism that cause cerebral malforma

210 f human conditions, ranging from devastating inborn errors of metabolism to aging.

211 ctrum of human disorders, ranging from rare, inborn errors of metabolism to common, age-associated di

212 trum of human conditions, ranging from rare, inborn errors of metabolism to the aging process.

213 s as well as in urine from patients with the inborn errors of metabolism tyrosinemia type II, arginin

214 t before coming to our outpatient clinic for inborn errors of metabolism was worried that isolated AS

215 will be specifically directed toward various inborn errors of metabolism which may be helpful for ans

216 Novel inborn errors of metabolism with informative amino acid

217 s <18 years of age with HCM, 8.7% (n=74) had inborn errors of metabolism, 9.0% (n=77) had malformatio

218 Inborn errors of metabolism, a class of diseases first n

219 g Parkinson's disease, Huntington's disease, inborn errors of metabolism, and cancer.

220 tant therapy for hematological malignancies, inborn errors of metabolism, and immunodeficiency disord

221 lems when used in patients with a variety of inborn errors of metabolism, but effects of nitrous oxid

222 Heritable mutations, known as inborn errors of metabolism, cause numerous devastating

223 n with pure hypertrophic cardiomyopathy with inborn errors of metabolism, for whom the estimated rate

224 ne hepatitis, n = 14; Wilson disease, n = 6; inborn errors of metabolism, n = 2) and 34 with ALF (par

225 However, the exception is inborn errors of metabolism, since many of these disorde

226 Lysosomal storage diseases are inborn errors of metabolism, the hallmark of which is th

227 r the genetic basis of potentially treatable inborn errors of metabolism, we combined deep clinical p

228 malities, congenital immunodeficiencies, and inborn errors of metabolism, were identified.

229 been reported in other riboflavin-responsive inborn errors of metabolism.

230 ting novel coding variants that may underlie inborn errors of metabolism.

231 in the general population that may underlie inborn errors of metabolism.

232 sented for the population level screening of inborn errors of metabolism.

233 pothesized by Archibald Garrod in 1908 to be inborn errors of metabolism.

234 f FAO and OXPHOS are among the most frequent inborn errors of metabolism.

235 iciency of the PDH complex and perhaps other inborn errors of metabolism.

236 and neuropathology, including their related inborn errors of metabolism.

237 lantation of more than 2 dozen hepatic-based inborn errors of metabolism.

238 preventive medicine in children with diverse inborn errors of metabolism.

239 ients, animal models, and in vitro models of inborn errors of metabolism.

240 s and follow-up of neuroendocrine tumors and inborn errors of metabolism.

241 luding other primary immune deficiencies and inborn errors of metabolism.

242 s with a collection of symptoms secondary to inborn errors of metabolism.

243 ri syndrome, hepatitis B virus reactivation, inborn errors of metabolism.

244 old a great promise as a diagnostic tool for inborn errors of metabolisms (IEMs) in the near future.

245 cur when compounds accumulate as a result of inborn errors of other pathways or when small molecules

246 Inborn errors of OXPHOS function are termed primary mito

247 istic basis for the pathophysiology of human inborn errors of purine nucleotide metabolism.

248 nd Combined immunodeficiencies are marked by inborn errors of T-cell immunity in which the T cells th

249 Inborn errors of the genes encoding two of the four huma

250 Inborn errors of the phagocyte NADPH oxidase complex (ch

251 Surprisingly, the known human patients with inborn errors of the TLR3 pathway have remained healthy

252 cephalitis (HSE) may result from single-gene inborn errors of TLR3 immunity.

253 Inborn errors of TLR3- and DBR1-mediated central nervous

254 Inborn errors of TLR3- and IRF7-dependent type I IFN imm

255 erpes simplex virus 1 (HSV-1), children with inborn errors of toll-like receptor 3 (TLR3) immunity ar

256 nectome useful for the genetic dissection of inborn errors of Toll-like receptor 3 immunity.

257 ere illness by MMR vaccines can be caused by inborn errors of type I and/or III interferon (IFN) immu

258 A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-t

259 tosis, is an emerging phenotype accompanying inborn errors of type I interferon immunity.

260 y become critically ill because of monogenic inborn errors that disrupt protective immunity to SARS-C

261 nciple that FVH can be caused by single-gene inborn errors that selectively disrupt liver-specific im

262 Immunodeficiency due to inborn errors, infections, autoimmune diseases and the t

263 ients can decipher the genetic basis of rare inborn errors.

264 ell's inherent DNA repair systems to correct inborn errors.

265 Mutations causing inborn ether phospholipid deficiency, a very severe gene

266 nborn and that which has been acquired" (The Inborn Factors in Disease).

267 oimmunity is often familial, suggesting that inborn genetic variations might underlie its development

268 into clinical practice through prediction of inborn health risks(1), a strategy to utilize genetics t

269 insight into mutations in DHCR7 and LBR for inborn human diseases.

270 alent, although very heterogeneous, group of inborn immunodeficiencies, with a puzzling complexity of

271 On the basis of the hypothesis of a rare inborn immunodeficiency of autosomal recessive inheritan

272 Inborn infants at 29 weeks 0 days to 36 weeks 6 days of

273 Hospital databases and charts of all preterm inborn infants at the University of North Carolina from

274 ort study of data collected prospectively on inborn infants with a birth weight between 401 g and 100

275 ring more than 3 days after birth among VLBW inborn infants.

276 cal patterns of dysfunction, replicating the inborn loss-of-function phenotypes and, therefore demons

277 novel mutants with phenotypes related to the inborn metabolic defect sialuria and metastatic tumor ce

278 A number of inborn metabolic diseases are associated with CDP, inclu

279 Studies of rare, inborn metabolic diseases establish that the phenotypes

280 lain manifesting heterozygous cases in other inborn metabolic diseases.

281 Fabry disease is an X-linked recessive inborn metabolic disorder characterized by systemic and

282 analysis of selected amino acids (related to inborn metabolic disorders) in the unknown DBS was compa

283 es (LSDs) represent a significant portion of inborn metabolic disorders.

284 They also targeted inborn metabolic errors (e.g., familial hyperlipoprotein

285 osomal storage diseases are a group of rare, inborn, metabolic errors characterized by deficiencies i

286 Unexpectedly, unlike the inborn model, the adult-onset pattern of excitability ch

287 egative phenotypes reminiscent of human DRP1 inborn mutations, while interrupting the TBK1-DRP1 conne

288 The respective influences of exposure and inborn neural networks on conspecific and nonconspecific

289 Inborn olfactory loss, or congenital anosmia (CA), is re

290 t data have argued that muscle synergies are inborn or determined early in life, but development of t

291 raceae have been isolated from patients with inborn or iatrogenic immunodeficiencies.

292 with a history of olfactory experiences), or inborn (patients without olfactory experiences/life-long

293 that some obesity-prone individuals have an inborn reduction in their ability to sense and respond t

294 limbic-midbrain circuit mediates some of the inborn risk for developing anxiety and depression.

295 the specific neural systems that mediate the inborn risk for these debilitating disorders remain unkn

296 Inborn species' perceptual preferences are thought to se

297 Omnivores, including humans, have an inborn tendency to avoid noxious or unfamiliar foods.

298 selectively bred for low or high intrinsic (inborn) treadmill running capacity.

299 human genetic theory of infectious diseases, inborn variants underlie life-threatening infectious dis

300 ETTING, AND PATIENTS: Cohort study of 72,235 inborn VLBW infants weighing 501 to 1500 g born in 558 V