ライフサイエンスコーパス: growth retardation

1 OR small for gestational age OR intrauterine growth retardation).

2 dysmorphism, cardiac defects, and postnatal growth retardation.

3 s with epithelial metastatic progression and growth retardation.

4 ions such as pre-eclampsia and intra-uterine growth retardation.

5 ith microcephaly, cerebellar hypoplasia, and growth retardation.

6 potrophy and insufficiency, leading to fetal growth retardation.

7 vation, a mechanism that could contribute to growth retardation.

8 s of the lower limbs, inability to walk, and growth retardation.

9 levated risk of cancer, telangiectasias, and growth retardation.

10 yond postnatal day 28, they exhibited marked growth retardation.

11 likely to have contributed directly to their growth retardation.

12 al deficits including seizures, tremors, and growth retardation.

13 lation, and lead to small fetuses with organ growth retardation.

14 f Hrpt2 after E8.5 resulted in apoptosis and growth retardation.

15 osed splotch embryos, probably via embryonic growth retardation.

16 ient embryos exhibit developmental delay and growth retardation.

17 LIG4 syndrome, showing immunodeficiency and growth retardation.

18 rylation of Erk in neural tissues and led to growth retardation.

19 rly embryogenesis can result in intrauterine growth retardation.

20 xhibits oral leukoplakia and blistering, and growth retardation.

21 volved in the BMI1-dependent cancer-specific growth retardation.

22 irth weight, preterm birth, and intrauterine growth retardation.

23 lar malformations, urogenital anomalies, and growth retardation.

24 ride content diarrhea, volume depletion, and growth retardation.

25 ) hazard villages suffered from intrauterine growth retardation.

26 ing human pregnancy failure and intrauterine growth retardation.

27 by approximately 25-40% and suffered severe growth retardation.

28 e genes lead to important, sometimes lethal, growth retardation.

29 postnatal mortality, as well as significant growth retardation.

30 mbryos that exhibit craniofacial defects and growth retardation.

31 Four of the 5 patients also had postnatal growth retardation.

32 se4 accumulation in rcy1Delta cells leads to growth retardation.

33 hy, which manifests as joint deformities and growth retardation.

34 erse health effects, including cretinism and growth retardation.

35 surviving animals exhibiting a lifelong 20% growth retardation.

36 ce results in pre-eclampsia and intrauterine growth retardation.

37 , and extracutaneous abnormalities including growth retardation.

38 PCNT) that lead to severe pre- and postnatal growth retardation.

39 poplasia, immunodeficiency, and intrauterine growth retardation.

40 with birth defects, mental disabilities and growth retardation.

41 n various human disorders, such as perinatal growth retardation.

42 bitor, 26B, triggered massive cell death and growth retardation.

43 tic architecture and show pre- and postnatal growth retardation.

44 getic dysfunctional phenotypes, including 1) growth retardation, 2) cold intolerance, 3) reduced exer

45 mice Lig4(R278H/R278H) (Lig4(R/R)) includes growth retardation, a decreased life span, a severe cell

46 ditional expression of RPS19R62W resulted in growth retardation, a mild anemia with reduced numbers o

47 Ectopic HAN expression causes growth retardation, aberrant cell division patterns, and

48 6 related patients with autosomal recessive growth retardation, adrenal insufficiency, and a selecti

49 FACC1KO mice showed prenatal growth retardation; after weaning, however, their weight

50 sing the CtIP(E157K) protein alone exhibited growth retardation, an increase in the G(1) population,

51 er NDT2 in HEK293 cells resulted in dramatic growth retardation and a metabolic shift from oxidative

52 These data indicate that the patients' growth retardation and adrenal insufficiency likely refl

53 We demonstrate that ART treatment induces growth retardation and an accumulation of ubiquitinated

54 They also display growth retardation and anemia.

55 isruption of these oncogenic pathways led to growth retardation and apoptotic cell death of the Tax2-

56 -deficient mice were found to display severe growth retardation and are unable to survive beyond post

57 ex3c homozygous mutant mice causes postnatal growth retardation and background-dependent perinatal le

58 tfr1b morphants exhibited growth retardation and brain necrosis, similar to the ce

59 r that is invariably characterized by severe growth retardation and cancer predisposition.

60 revealed that caspase-2 deficiency enhanced growth retardation and caused synthetic perinatal lethal

61 of DBA, the disease is also characterized by growth retardation and congenital anomalies that are pre

62 of DBA, the disease is also characterized by growth retardation and congenital malformations, in part

63 Snx13-null embryos had significant overall growth retardation and defects in neural tube closure, b

64 addition, similar to patients, AT pigs show growth retardation and develop motor deficit phenotypes.

65 th preterm delivery, low birth weight, fetal growth retardation and developmental defects.

66 d IGFBP-1 mediates hypoxia-induced embryonic growth retardation and developmental delay by binding to

67 significantly alleviated the hypoxia-induced growth retardation and developmental delay.

68 , null mutant (Spca1(-/-)) embryos exhibited growth retardation and did not survive beyond gestation

69 ckout mice were born normally, but displayed growth retardation and died prematurely.

70 Kif3a deficiency caused cranial base growth retardation and dysmorphogenesis, which were evid

71 ibited synergistic phenotypes such as severe growth retardation and enhanced chromosome instability.

72 fish touchtone/nutria mutants exhibit severe growth retardation and gross alterations in skeletal dev

73 9.1(-/-) mouse embryos exhibit intra-uterine growth retardation and have small placentas due to a red

74 n in insulin-like growth factor 1, postnatal growth retardation and hepatic steatosis.

75 embryos survive gestation but exhibit severe growth retardation and impaired erythropoiesis, and loss

76 These mice have severe preweaning growth retardation and incomplete catch-up growth.

77 Early Ott1-deficient embryos show growth retardation and incomplete closure of the notocho

78 mice are marked by decreased survival rates, growth retardation and increased variability in body wei

79 Global Et2 knockout mice exhibited severe growth retardation and juvenile lethality.

80 Surviving mutants exhibited growth retardation and late-onset dilated cardiomyopathy

81 in 98% of cells, while resulting in similar growth retardation and lipoatrophy, caused diabetes with

82 highly sensitive to salinity stress causing growth retardation and loss in productivity.

83 holipid Abs have been shown to mediate fetal growth retardation and loss when injected into pregnant

84 he fetus including physical and intellectual growth retardation and malformations.

85 OB precursor cells (OPC) in mice results in growth retardation and markedly decreased bone mass with

86 sorder characterized by extreme intrauterine growth retardation and multiple organ abnormalities.

87 ally, GH supplementation was able to correct growth retardation and muscle weakness.

88 oral administration of taurine rescued their growth retardation and osteoporosis phenotypes.

89 genetic model results in severe postweaning growth retardation and osteoporosis, and the severity an

90 n factor involved in brain development, show growth retardation and other abnormalities consistent wi

91 ay an inflammatory phenotype associated with growth retardation and paw swelling.

92 Mpi(-/-) embryos showed growth retardation and placental hyperplasia.

93 Inactivation of tensin3 resulted in growth retardation and postnatal lethality in one third

94 lacking Fgf8a-containing spliceforms exhibit growth retardation and postnatal lethality, and the phen

95 family helicase BLM that is associated with growth retardation and predisposition to cancer.

96 expressing human TDP-43 in neurons exhibited growth retardation and premature death that are characte

97 consequently, neonatal Pgc-1(c) mice exhibit growth retardation and profound anemia.

98 fter E13.5, YB-1(-/-) embryos exhibit severe growth retardation and progressive mortality, revealing

99 ures with the human syndromes in its overall growth retardation and reduced brain size.

100 n of one-carbon-carrying folates, as well as growth retardation and reduced cellular proliferation.

101 ficiency caused condylar disorganization and growth retardation and reduced polymorphic cell layer pr

102 g adult mice by tamoxifen injections induced growth retardation and severe deformities in knee joints

103 They also exhibit growth retardation and severe postnatal osteopenia stemm

104 everity of anemia, abnormal iron metabolism, growth retardation and shortened lifespan.

105 t the decidual-placental interface and fetal growth retardation and subsequent demise.

106 th; however, soon after weaning they exhibit growth retardation and the adult mice are hypophagic, le

107 enotype, and correlated with the severity of growth retardation and the in vitro cellular phenotype.

108 ossly normal at 2 weeks of age but exhibited growth retardation and were significantly smaller than c

109 s, deafness, sterility, a profound postnatal growth retardation, and a propensity to sudden death.

110 ing those of the heart and the renal tract), growth retardation, and a recognizable facial gestalt (i

111 pose tissue and brown adipose tissue, severe growth retardation, and bone defects.

112 clinically characterized by mild hypotonia, growth retardation, and delayed motor milestones.

113 3 and characterized by developmental delay, growth retardation, and dysmorphic features.

114 exhibited a reduced amount of WAT, postnatal growth retardation, and early death before weaning.

115 cal dysfunction, congenital lactic acidosis, growth retardation, and early death.

116 in mice lead to partial embryonic lethality, growth retardation, and elevated level of circulating pr

117 of normal vascular patterning, severe fetal growth retardation, and embryonic death at E9.5 to 10, a

118 exhibited dwarfism, as a result of in utero growth retardation, and had low serum insulin-like growt

119 inant form of mild syndromic ID with ptosis, growth retardation, and hypotonia, and we identified an

120 vation of supv311 caused liver degeneration, growth retardation, and juvenile lethality, a phenotype

121 t explains how Giardia infection can lead to growth retardation, and may offer insights that guide fu

122 or its murine homologue Fto result in severe growth retardation, and mice globally overexpressing FTO

123 lated disorders are macrocephaly, absence of growth retardation, and more variability in the degree o

124 edentulous (toothless), and exhibited severe growth retardation, and most of them died around the tim

125 increased prenatal and postnatal mortality, growth retardation, and multiple tissue abnormalities.

126 against death, progression of brain injury, growth retardation, and neurobehavioral deficits after a

127 o extend our understanding of diet-dependent growth retardation, and offers a potential mechanism to

128 efective RNR often led to cell cycle arrest, growth retardation, and p53-dependent apoptosis, whereas

129 rt shape, ventricular septal defects, severe growth retardation, and postnatal lethality with no upre

130 tions such as preterm delivery, intrauterine growth retardation, and preeclampsia; however, the molec

131 pilepsy, microcephaly, congenital cataracts, growth retardation, and spasticity.

132 The Pitx2-Cre/Dicer1 mutant mice demonstrate growth retardation, and the pituitaries are hypoplastic

133 astrulation, results in increased apoptosis, growth retardation, and, ultimately, embryonic death.

134 female, but not male, UGRP(-/-) mice exhibit growth retardation as do G6Pase(-/-) mice and patients w

135 e for up to several weeks although they show growth retardation as well as emphysema.

136 on of digits in a mitten-glove deformity and growth retardation associated with anemia.

137 istically significant effect on intrauterine growth retardation associated with any of the chlorine d

138 Only a few genetic studies of growth retardation associated with the KBD have been car

139 the short stature homeobox gene SHOX lead to growth retardation associated with Turner, Leri-Weill dy

140 alpha-Adducin-null mice show growth retardation at birth and throughout adulthood.

141 cking LBP-1a expression develop intrauterine growth retardation at embryonic day 10.5, culminating in

142 rowth suppression and of stress-induced leaf growth retardation both required the AUXIN-RESISTANT1 ge

143 ll mice display partial embryonic lethality, growth retardation, brain disorders, and maternal effect

144 xia treatment not only resulted in embryonic growth retardation but also caused significant delay in

145 tly after birth, and the other showed slight growth retardation but subsequently developed into a fer

146 ual disability with cataracts, epilepsy, and growth retardation but without rhizomelia.

147 a and vascular abnormalities, causing severe growth retardation by E9.5 and death by E10.5, early dev

148 are more sensitive than wild-type plants to growth retardation by nanomolar concentrations of MTX, a

149 utosomal recessive disorder characterized by growth retardation, cancer predisposition, and sterility

150 myopathy, neutropenia, organic aciduria, and growth retardation caused by mutations in tafazzin.

151 e show that Hsp90 inhibitors rescue the axon growth retardation caused by overexpression of the LRRK2

152 disease, including predisposition to cancer, growth retardation, cell-proliferation defects and infer

153 kindreds, all of whom displayed intrauterine growth retardation, chronic neutropenia, and NK cell def

154 and underlies intra-uterine (and postnatal) growth retardation, chronic neutropenia, and NK cell def

155 he association of CALM/PICALM mutations with growth retardation, cognitive defects, and Alzheimer's d

156 ty for ionizing radiation, microcephaly, and growth retardation comparable to mutations in LIG4 and X

157 chemical gradient, aha2 mutant plants show a growth retardation compared with wild-type plants.

158 showed increased levels of serum glucose and growth retardation consistent with a severe diabetic sta

159 The developmental timing of palatal growth retardation correlates exactly with the spatiotem

160 Significant cell growth retardation could be observed for pathogenic bact

161 en entails metabolic costs and the resulting growth retardation could generally increase tolerance ag

162 RBS) is an autosomal recessive disorder with growth retardation, craniofacial abnormalities and limb

163 The rc mice show growth retardation, cyclic and progressive hair loss, hy

164 hat knockout of p21 can partially rescue the growth retardation defect of Ola1(-/-) embryos but fails

165 pe in developing zebrafish, characterized by growth retardation, delayed hindbrain formation, and emb

166 sitivity, microcephaly, facial dysmorphisms, growth retardation, developmental delay, and a variable

167 terized by bone marrow failure, intrauterine growth retardation, developmental delay, microcephaly, c

168 ild with classic features of hypothyroidism (growth retardation, developmental retardation, skeletal

169 enotypes observed in ACH patients, including growth retardation, disproportionate shortening of the l

170 Severe growth retardation, distorted branches and up-curled lea

171 aternal smoke exposure results in fetal lung growth retardation due to dysregulation in various signa

172 useful therapeutic approach to intrauterine growth retardation due to placental vascular hypofunctio

173 These mice exhibited growth retardation due to reduced intestinal length as w

174 sirtuin 6 (Sirt6) in mice leads to postnatal growth retardation due to somatotropic attenuation throu

175 for a slightly elevated risk of intrauterine growth retardation during the second and third trimester

176 pofacial (CSCF) syndrome is characterized by growth retardation, dysmorphic facial features, brachyda

177 l expression during embryogenesis results in growth retardation, eye malformations, multiorgan pathol

178 rized by ID, ASD, microcephaly, intrauterine growth retardation, febrile seizures in infancy, impaire

179 ernal cobalamin may be associated with fetal growth retardation, fetal insulin resistance, and excess

180 printing of Gsalpha, resulting in preweaning growth retardation followed by catch-up growth.

181 the tgd1-1 mutant background causes serious growth retardation, gametophytic defects and premature c

182 ar coloboma, heart defects, choanal atresia, growth retardation, genital abnormalities, and ear abnor

183 for 53BP1 modestly exacerbates phenotypes of growth retardation, genomic instability, and organismal

184 larly speech delay), microcephaly, postnatal growth retardation, heart defects, and hand, foot, and l

185 ch is characterized in part by hypoglycemia, growth retardation, hypertriglyceridemia, hypercholester

186 hyperthermia, hypogonadotropic hypogonadism, growth retardation, hypoglycemia, myopathy, dilated card

187 ouble-knockout (Smad1/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicu

188 at the age of 5 weeks, HGPS mutant mice show growth retardation, imbalanced gait and spontaneous frac

189 neck cancers, whereas BS is characterized by growth retardation, immunodeficiency, and a wide spectru

190 These defects result in severe growth retardation in a proportion of Tgif null embryos

191 ns are associated with diabetes mellitus and growth retardation in both rodents and humans.

192 Treatment with the TF:FVIIa inhibitor led to growth retardation in breast tumor models.

193 l as look at evidence for this phenomenon in growth retardation in certain groups of these individual

194 years, coinciding with the period of linear growth retardation in deprived children.

195 related to an increased risk of intrauterine growth retardation in four regions of a Maryland county

196 the fetal ovine pancreatic islets, and that growth retardation in hypothyroid fetal sheep is associa

197 cantly increased p53 protein levels and cell growth retardation in multiple cell lines.

198 n some animals and axial skeletal defects or growth retardation in others.

199 Growth retardation in recombinant PEDV carrying uncleava

200 utants, suggesting that ABA is implicated in growth retardation in such nutritional stress.

201 xic milk" causes inflammation, alopecia, and growth retardation in the nursing neonates.

202 Growth retardation in utero leading to small-for-gestati

203 PEDVAVCT12 harboring uncleavable N displayed growth retardation in Vero E6-APN cells compared to the

204 more, P. yoelii Deltamif parasites exhibited growth retardation in vivo.

205 ed that miR-494 induces a significant cancer growth retardation in vivo.

206 els resulted in reduced cell division rates, growth retardation, increased G:F actin ratios and letha

207 e characterized by severe pre- and postnatal growth retardation, indicating that CUL7 is closely asso

208 We conclude that intrauterine growth retardation induced by uteroplacental insufficien

209 lated individuals with severe prenatal-onset growth retardation, intellectual disability, and muscula

210 Growth retardation is a major adverse long-term outcome

211 udies suggest that celiac disease-associated growth retardation is becoming a tangible health problem

212 x plants have more starch compared to wt and growth retardation is partially rescued by sucrose.

213 lacental insufficiency leads to intrauterine growth retardation (IUGR) and adult onset insulin resist

214 o 90 days of gestation leads to intrauterine growth retardation (IUGR) and increased prepubertal grow

215 Intrauterine growth retardation (IUGR) has been linked to the develop

216 Intrauterine growth retardation (IUGR) has been linked to the onset o

217 s this, we developed a model of intrauterine growth retardation (IUGR) in the rat that leads to diabe

218 Six2-KL(-/-) mice exhibited severe growth retardation, kyphosis, and premature death, close

219 in approximately 80% of cells caused extreme growth retardation, lipoatrophy, and hypoglycemia, a cli

220 d many phenotypes of H2AX-/- mice, including growth retardation, male infertility, immune defects, ch

221 ependent lethality, severe developmental and growth retardation, marked bradycardia and pericardial e

222 ) is a malformation syndrome associated with growth retardation, mental retardation, and immunodefici

223 a stark phenotype characterized by postnatal growth retardation, metabolic dysfunction, and lethality

224 iation (IR) and are variably associated with growth retardation, microcephaly, and neurodevelopmental

225 a rare recessive condition characterized by growth retardation, microcephaly, childhood cancer and c

226 ur individuals share several major features (growth retardation, microcephaly, digital abnormalities,

227 disorder, with dysmorphic facial appearance, growth retardation, microcephaly, mental retardation, va

228 c-met receptor (betamet-/-) displayed slight growth retardation, mild hyperglycemia, and decreased se

229 RAD21 have been identified in children with growth retardation, minor skeletal anomalies and facial

230 athy." Children with RAD21 mutations display growth retardation, minor skeletal anomalies, and facial

231 e to inadequate sun exposure and resulted in growth retardation, muscle weakness, skeletal deformitie

232 exhibited a wide range of defects, including growth retardation, neurodegeneration, muscular atrophy,

233 We hypothesize that the embryonic growth retardation observed in Cited2 null embryos is du

234 , which explains the perinatal lethality and growth retardation observed in MEX3C-deficient mice.

235 is, insulin resistance, severe diabetes, and growth retardation observed in mice carrying N-ethyl-N-n

236 PSI photo damage, thus explaining the marked growth retardation observed in these conditions.

237 mma (or RARbeta and RARgamma) exhibit severe growth retardation obvious by about 3 weeks postnatally.

238 We proceed to show that growth retardation occurs through the induction of trans

239 The growth retardation of CMS relative to the wild type was

240 a catalytically inactive MetAP2 resulted in growth retardation of HT1080 tumor cells, suggesting a d

241 t ORC1-H4K20me2-binding mutants, rescues the growth retardation of orc1 morphants.

242 ion of ROP results in repression of AOXI and growth retardation of P. pastoris cultured in YPM medium

243 In addition, KDM5C knockdown resulted in growth retardation of prostate cancer cells in vitro and

244 Thus, while the growth retardation of the cPGES/p23(-/-) pups and decrea

245 y gene underlying both joint destruction and growth retardation of the KBD.

246 embrane domain of LRP4 (LRP4 ECD) results in growth retardation of the NMJ, and these defects are mar

247 The severe growth retardation of vte6 mutants was partially rescued

248 status of the neonate without indications of growth retardation or impaired neurologic function at bi

249 al anemia accompanied by either intrauterine growth retardation or neutropenia.

250 erized by neuropathology, immune deficiency, growth retardation or predisposition to cancer.

251 OR = 2.7, 95% CI: 1.2, 5.7) and intrauterine growth retardation (OR = 3.3, 95% CI: 1.2, 9.4).

252 nutrient malab-sorption such as weight loss, growth retardation, or diarrhea.

253 g neonates suffer from alopecia, anaemia and growth retardation owing to elevated levels of pro-infla

254 tal insufficiency can result in intrauterine growth retardation, perinatal death and spontaneous abor

255 rprisingly, FACC1KO mice manifested skeletal growth retardation phenotype accompanied by decreased ch

256 All Hpse2 mutants have a growth retardation phenotype and die within a month afte

257 We observed a temperature sensitive growth retardation phenotype and specific decrease of he

258 ve oxidase content/activity, and displayed a growth retardation phenotype similar to that of the nduf

259 e exhibited a maternal-specific intrauterine growth retardation phenotype that resulted in a 33% redu

260 A growth retardation phenotype, a reduction in the amount

261 se mice are viable and fertile but display a growth retardation phenotype.

262 cient embryos exhibited embryonic lethality, growth retardation, polyhydramnios, cardiac ventricular

263 eloid specific Flip-deficient mice exhibited growth retardation, premature death, and splenomegaly wi

264 Mis-specification and growth retardation rather than cell death most likely ac

265 RNA interference of delta resulted in growth retardation, reduced ATP synthase amounts, and in

266 eted disruption of the Cacna2d2 gene exhibit growth retardation, reduced life span, ataxic gait with

267 /- mice exhibited severe metabolic acidosis, growth retardation, reduced plasma Na+, hyperal-dosteron

268 How mutated SHP2 induces growth retardation remains poorly understood.

269 Fancd2/Mlh1 double-mutant embryos displayed growth retardation resulting in embryonic lethality and

270 ult in the pathological consequences such as growth retardation seen in VGV mice.

271 ia, congenital cataracts, profound postnatal growth retardation, severe intellectual disability, and

272 opy both JATD and SRP type III by exhibiting growth retardation, shortening of the long bones, constr

273 y recapitulates the human pathology, showing growth retardation, skeletal and facial abnormalities, i

274 0-knockout mice died postnatally with severe growth retardation, skeletal defects, and kidney and lun

275 ously unidentified syndrome characterized by growth retardation, spine malformation, facial dysmorphi

276 g csCSF-1, both failed to completely correct growth retardation, suggesting a role for csCSF-1 in the

277 mutated in a mutually exclusive manner in 3M growth retardation syndrome and function in microtubule

278 Silver-Russell syndrome (SRS) is a growth retardation syndrome in which loss of methylation

279 a mutually exclusive manner in 3M and other growth retardation syndromes.

280 ing A(1)ARs (A(1)AR-/-) had much more severe growth retardation than A(1)AR+/+ or +/- embryos.

281 Double mutant animals show a more severe growth retardation than ob/ob mice with similar levels o

282 r perinatal respiratory failure or exhibited growth retardation that was not due to the renal disease

283 d that its up-regulation induces cancer cell growth retardation through multiple targets involved in

284 splays early-onset severe tonic seizures and growth retardation, thus recapitulating the human phenot

285 adulthood, thereby potentially linking fetal growth retardation to cardiovascular disease and diabete

286 antitumor activity, ranging from pronounced growth retardation to complete tumor regression.

287 and the grik1-1 grik2-1 double mutant shows growth retardation under regular growth conditions.

288 s4(fky/fky) mice include temporary fur loss, growth retardation, unsteady gait, and abnormal body pos

289 The growth retardation was associated with a greater than 60

290 The cancer-specific growth retardation was mediated by an increased level of

291 luding exencephalia, anophthalmia and severe growth retardation were noted in heterozygous embryos, a

292 ntribute to microcephaly, pre- and postnatal growth retardation, which constitute the core clinical f

293 ry low birth weight infant with intrauterine growth retardation who did not respond to phototherapy.

294 These mice displayed growth retardation with a significant reduction of body

295 deficiency results in a genetic syndrome of growth retardation with adrenal insufficiency and select

296 Null embryos at 3.5 d.p.c. reveal growth retardation with cells in mitotic disarray manife

297 o thrive within 2 weeks, displaying profound growth retardation with communicating hydrocephalus and

298 e mutants survive into adulthood and display growth retardation with no apparent brain or behavioral

299 e map65-1 map65-2 mutants showed significant growth retardation with no obvious cell swelling, twisti

300 lay, microcephaly, absent speech, hypotonia, growth retardation with prenatal onset, feeding difficul