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1 n postulated that LMNB1 variants could cause microcephaly.
2 ral diseases including birth defects such as microcephaly.
3 ations affecting centriole duplication cause microcephaly.
4 ic encephalopathy and primary or progressive microcephaly.
5 ously reported that Lin28a deletion leads to microcephaly.
6 lls with somatic genome damage, thus causing microcephaly.
7 ut the immunopathogenesis of ZIKV-associated microcephaly.
8 itosis, with MCPH1 mutations causing primary microcephaly.
9 order, schizophrenia, and Zika virus induced microcephaly.
10 cause of its global transmission and link to microcephaly.
11 scribed to RTTN mutations, including primary microcephaly.
12 on of neuronal progenitors often observed in microcephaly.
13 ading to smaller organoids characteristic of microcephaly.
14 nomalies such as Guillain-Barre syndrome and microcephaly.
15 e its loss reveals a pathogenic mechanism in microcephaly.
16 re finding in patients with genetic forms of microcephaly.
17 polymicrogyria, can occur in the absence of microcephaly.
18 set steroid-resistant nephrotic syndrome and microcephaly.
19 BubR1 in mouse cerebral cortex recapitulates microcephaly.
20 assembly, disruption of which contributes to microcephaly.
21 re- and peri-implantation ZIKV infection and microcephaly.
22 tion that a ZIKV mutation is responsible for microcephaly.
23 initial insights into the cellular basis of microcephaly.
24 lls (NPCs) during brain development, causing microcephaly.
25 he mitotic checkpoint in the pathogenesis of microcephaly.
26 st common genetic alteration associated with microcephaly.
27 ranscription PCR, including one neonate with microcephaly.
28 variants in the PH-domain of WDFY3 leads to microcephaly.
29 icas, bringing unusual complications such as microcephaly.
30 f ZIKV-positive pregnant women with neonatal microcephaly.
31 e larvicide pyriproxyfen was associated with microcephaly.
32 nd prevent ZIKV-associated outcomes, such as microcephaly.
33 ficiency of DYRK1A is associated with severe microcephaly.
34 derate to severe intellectual disability and microcephaly.
35 severe intellectual disability, epilepsy and microcephaly.
36 ge genome stability and parallels with human microcephaly.
37 ypes of obesity/underweight and macrocephaly/microcephaly.
38 including corpus callosum agenesis (ACC) and microcephaly.
39 ain have been employed to model ZIKV-induced microcephaly.
40 individuals with autosomal recessive primary microcephaly.
41 ttention to links between Zika infection and microcephaly.
42 th neurologic disorders including autism and microcephaly.
43 particular, is distinctively associated with microcephaly.
44 enlargement of the cerebral ventricles, and microcephaly.
45 Its mutation causes microcephaly.
46 cluding neurodevelopmental abnormalities and microcephaly.
47 neonate at birth is strongly associated with microcephaly.
48 e HIV-exposed but uninfected with or without microcephaly.
49 and congenital brain abnormalities including microcephaly.
50 genital Zika syndrome (CZS), including fetal microcephaly.
51 ation defects may contribute to the onset of microcephaly.
52 ional to the disease severity hallmarks ZIKV microcephaly.
53 th GEFD1 variants, who display milder ID and microcephaly.
54 d from normal to decreased gyral folding and microcephaly.
55 etus is a key mechanism by which ZIKV causes microcephaly.
56 d pathogenesis and may underlie ZIKV-related microcephaly.
57 t infects neural tissues, causing congenital microcephaly.
58 odevelopmental impairment than those without microcephaly.
59 use developmental defects, including primary microcephaly.
60 pair, triggering p53-dependent apoptosis and microcephaly.
61 ead of ZIKV within the Americas has unveiled microcephaly (1) and Guillain-Barre syndrome(2,3) as ZIK
62 a virus infection, 76 infants with suspected microcephaly, 24 mothers of infants with suspected micro
63 ephaly, 24 mothers of infants with suspected microcephaly, 336 patients with suspected dengue virus o
64 mean age: 16.1 +/- 9.8 years, SD); postnatal microcephaly (83%); foot deformities (69%); and epilepsy
65 from a region of Brazil with high levels of microcephaly (abnormally small head circumference) produ
66 retinal hypovascularization with or without microcephaly and (2) multi-organ syndromes characterized
67 tations in WD repeat domain 62 (WDR62) cause microcephaly and a wide spectrum of severe brain malform
68 MCM2 develop ciliopathy-phenotypes including microcephaly and aberrant heart looping due to malformed
69 done on a child with microcephaly to confirm microcephaly and assess previous Zika virus infection.
70 were reported(13,14) together with cases of microcephaly and associated developmental problems in in
71 ay lead to adverse infant outcomes including microcephaly and being small for gestational age (SGA).
72 cephaly and no reported neuroimaging, 14 had microcephaly and brain abnormalities, and 4 had brain ab
74 enes implicated in severe autosomal-dominant microcephaly and broadens the phenotypic spectrum of the
85 trimesters of pregnancy, is associated with microcephaly and less frequently with other birth defect
89 tudies that linked the virus to the cases of microcephaly and neurological complications have reveale
90 Of the 26 affected fetuses or infants, 4 had microcephaly and no reported neuroimaging, 14 had microc
91 ber 2016) and the most cases associated with microcephaly and other birth defects (2,366 confirmed by
92 discovery that Zika virus (ZIKV) could cause microcephaly and other birth defects, we have scrambled
95 infection with Zika virus (ZIKV) can lead to microcephaly and other congenital abnormalities of the f
97 orbidity, including Guillain-Barre syndrome, microcephaly and other fetal developmental defects(1,2).
99 osquito-transmitted flavivirus, is linked to microcephaly and other neurological defects in neonates
100 a serious threat to pregnant women, causing microcephaly and other neuropathies in developing fetuse
102 neurodevelopmental abnormalities, including microcephaly and reduced intra- and inter-hemispheric co
103 hich encodes an amino acid transporter cause microcephaly and seizures, yet the mechanisms responsibl
105 ight potential issues with classification of microcephaly and show how some infants affected by conge
107 band presented with an opposing phenotype of microcephaly and the only missense-variant located in th
108 ds ratio was 73.1 (95% CI 13.0-infinity) for microcephaly and Zika virus infection after adjustments.
110 irus is only one of the infectious causes of microcephaly and, although the contexts in which they oc
111 mutations in some spliceosome proteins cause microcephaly and/or growth retardation, phenotypes that
113 of congenital brain abnormalities including microcephaly, and (b) the most likely explanation of ava
115 elevant phenotypes, such as renal anomalies, microcephaly, and concomitant increases in apoptosis and
116 inked to Guillain-Barre syndrome, congenital microcephaly, and devastating ophthalmologic and neurolo
123 elated with central nervous system findings, microcephaly, and the timing of maternal infection.
124 intellectual disability, growth retardation, microcephaly, and variable craniofacial dysmorphism.
125 were segregating with moderate to severe ID, microcephaly, and various facial dysmorphisms, in an aut
128 ated with Guillain-Barre syndrome, and fetal microcephaly as well as other neurological complications
129 sis in the etiology of primary and syndromic microcephaly, as has been proposed by recent findings on
131 ls and that ablation of this gene results in microcephaly-associated vasculopathy in mice and humans.
132 lammatory biomarkers from newborns with ZIKV microcephaly, asymptomatic ZKV infection, or uninfected
133 abnormalities in infants that do not display microcephaly at birth, and the full impact of these more
134 sures were associated with increased risk of microcephaly based on long-term follow-up of infants and
135 ponse to alarming statistics of infants with microcephaly being born to women who were infected with
136 e-damaged cells are not cleared, alleviating microcephaly, but paradoxically leading to total pre-wea
137 is of cortical NSCs accounts for most of the microcephaly, but that there is a significant apoptosis-
138 posed) was associated with increased risk of microcephaly by both Nellhaus standards (adjusted RR 2.0
139 ose that mutations in centrosome genes cause microcephaly by delaying mitosis and pathologically acti
143 ollowed by a striking increase in congenital microcephaly cases, triggering a declaration of an inter
147 ng antibodies in 28 mothers of children with microcephaly (cases) and 122 controls from northeastern
149 outcomes, ranging from mental retardation to microcephaly, caused by congenital HCMV infection can be
150 congenital brain abnormalities, particularly microcephaly, caused by Zika virus (ZIKV) infection duri
151 nd designated the viral outbreak and related microcephaly clusters as a long-term program of work.
152 , intrauterine growth restriction, and fetal microcephaly, collectively known as congenital Zika synd
153 nalytical cohort of 115 infants born without microcephaly, comprising 56 infants with qRT-PCR confirm
154 tbreaks, ZIKV infections have been linked to microcephaly, congenital disease, and Guillain-Barre syn
155 With severe disease manifestations including microcephaly, congenital malformation, and Guillain-Barr
156 ern Hemisphere is associated with reports of microcephaly, congenital malformations, and Guillain-Bar
157 rol study evaluating the potential causes of microcephaly: congenital Zika virus infection, vaccines,
158 nrelated families presenting with congenital microcephaly, cortical polymicrogyria, and other migrati
159 uses intrauterine growth restriction, severe microcephaly, craniofacial anomalies, skeletal dysplasia
160 In the het CKO model, Mpp5 depletion led to microcephaly, decreased cerebellar volume and cortical t
161 families with complex syndromes that include microcephaly, developmental delay, and brittle hair and
162 ed during pregnancy, ZIKV has been linked to microcephaly, developmental delays, or other congenital
164 he genetic cause of a congenital syndrome of microcephaly, epilepsy, and neonatal/early-onset diabete
165 nclude growth failure, feeding difficulties, microcephaly, facial dysmorphism, and various other cong
166 xposure to 9 known or hypothesized causes of microcephaly for every pregnancy nationwide since the be
168 tory biomarkers could discriminate ZIKV with microcephaly from those with ZIKV without microcephaly o
169 We demonstrate that Pogz deficient mice show microcephaly, growth impairment, increased sociability,
170 dren who are HIV-exposed but uninfected with microcephaly had lower mean scores on neurodevelopmental
171 l relationship between Zika virus (ZIKV) and microcephaly has been established, it remains unclear wh
172 me and fetal neurological defects, including microcephaly, has prompted intense efforts aimed at the
174 e reported in two unrelated individuals with microcephaly, hearing loss, and overlapping dysmorphic f
175 s are strikingly similar: severe disability, microcephaly, hearing loss, spasticity, and characterist
176 ecting the brain (hypothalamic hamartoma and microcephaly), heart (atrioventricular septal defect), s
177 mal cysts, intracerebral calcifications, and microcephaly; however, the Zika virus is intensely neuro
178 impaired Tcf4 function results in consistent microcephaly, hyperactivity, reduced anxiety, and defici
179 ient with severe global developmental delay, microcephaly, hypotonia, epilepsy, cortical vision impai
180 -gestational-age, and fetal death as well as microcephaly (i.e., overall and disproportionate) in the
182 s conducted to investigate how ZIKV leads to microcephaly in a novel experimental model that mimics e
183 We reasoned that by elucidating the basis of microcephaly in AS, a highly penetrant syndromic feature
186 and severe clinical manifestations including microcephaly in fetuses of infected pregnant women and G
187 ka virus (ZIKV) infection is associated with microcephaly in fetuses, but the pathogenesis of ZIKV-re
188 at biallelic variants in METTL5 cause ID and microcephaly in humans and highlights the essential role
189 at loss of Ankle2, a protein associated with microcephaly in humans and known to interact with Zika p
191 indings begin to uncover the pathogenesis of microcephaly in LIG4 syndrome and open avenues to more f
192 esult in severe disease in humans, including microcephaly in newborns and Guillain-Barre syndrome in
193 causing severe disease in humans, including microcephaly in newborns and Guillain-Barre syndrome in
196 of eight children, development of secondary microcephaly in two other children and autism spectrum d
198 dence of a previously rare clinical outcome, microcephaly, in newborns from mothers who were infected
199 a) congenital brain abnormalities, including microcephaly, in the foetuses and offspring of pregnant
200 er rate of neurodevelopmental disorders like microcephaly, induced much weaker and delayed innate imm
201 related affected individuals with congenital microcephaly, infantile epileptic encephalopathy, and pr
202 nts had fewer adverse outcomes compared with microcephaly infants, notable adverse outcomes were obse
203 Growth rates by Z-score, particularly for microcephaly infants, were initially poor after birth bu
204 Growth rates by z score, particularly for microcephaly infants, were poor after birth but showed i
205 ed individuals show brain abnormalities with microcephaly, intellectual disability and delayed gross
206 ng ADAR2, in four unrelated individuals with microcephaly, intellectual disability, and epilepsy.
207 loss-of-function variants in DYRK1A exhibit microcephaly, intellectual disability, developmental del
209 ed to NSNM infants.Zika-exposed infants with microcephaly, irrespective of being proportional or disp
216 l human telomere disorder syndromes, but how microcephaly is linked to dysfunctional telomeres is not
217 hough epidemiological evidence suggests that microcephaly is not associated with the original, Africa
219 eaks of Zika virus infection and clusters of microcephaly is that Zika virus infection during pregnan
224 g of intellectual disability, short stature, microcephaly, lissencephaly, periventricular heterotopia
228 inked to TP53-mediated cell death in several microcephaly models, how TP53 is activated remains uncle
229 irus in 2014 and subsequent association with microcephaly, much work has focused on the development o
230 ndividuals from 21 families, presenting with microcephaly, neurodevelopmental delay, seizures, periph
231 erences between groups regarding the rate of microcephaly, neuroimaging abnormalities, neurological s
232 affected by unmeasured confounding causes of microcephaly not available in routinely collected survei
233 s of adverse outcomes compared to those with microcephaly, notable adverse outcomes were observed in
237 nts with a developmental encephalopathy with microcephaly, often associated with early-onset epilepsy
239 screening eye examinations for infants with microcephaly or laboratory-confirmed Zika virus infectio
241 Description of eye findings, presence of microcephaly or other central nervous system abnormaliti
244 alternative non-ZIKV causes of the 2015-2017 microcephaly outbreak, nor that concurrent exposure to a
246 ve infants had a five-fold increased risk of microcephaly overall (RR 5.1, 95% CI 1.2-22.5) and a ten
247 typic features of Kabuki Syndrome, including microcephaly, palate defects, abnormal ear development,
252 e spread of Zika virus (ZIKV) and associated microcephaly present an urgent need for sensitive and sp
254 ZIKV-exposed infants with a diagnosis of microcephaly (proportional [PM] or disproportional [DM])
256 V-exposed infants with either a diagnosis of microcephaly [proportional (PM) or disproportional (DM)]
258 in seven individuals with pronounced primary microcephaly (ranging from -3.6 to -12 SD) associated wi
259 rnative causes for geographic differences in microcephaly rate leads us to hypothesize that the North
266 ities, and 4 had brain abnormalities without microcephaly; reported brain abnormalities included intr
267 n that Lig4(R/R) mice develop nonprogressive microcephaly, resulting primarily from apoptotic death o
269 f early-onset seizures, developmental delay, microcephaly, sensorineural deafness, spastic quadripare
270 h three affected individuals presenting with microcephaly, severe intellectual disability, simplifica
271 se who are small for gestational age without microcephaly should be closely followed, particularly th
272 se who are small for gestational age without microcephaly should be closely followed, particularly th
273 en from 12 unrelated families presented with microcephaly, simplified gyral pattern of the cortex, hy
274 nting at ages 2 to 4 months with progressive microcephaly, spastic quadriparesis, and global developm
275 RT (MCPH1/BRIT1) protein, mutated in primary microcephaly, specifically interacts with the TRFH domai
276 catastrophic fetal abnormalities, including microcephaly, spontaneous abortion, and intrauterine gro
277 between in utero antiretroviral exposure and microcephaly status, adjusted for potential confounders.
278 humans result in intellectual disability and microcephaly suggest that KATNAL1 may play a prominent r
279 how major structural brain defects or severe microcephaly, suggesting that defective proliferation an
280 ction probably causes an autosomal-recessive microcephaly syndrome and highlight further the critical
281 inflammatory signature associated with ZIKV microcephaly that suggested an increased inflammation.
282 niofacial dysmorphisms, including congenital microcephaly, that were strikingly different from those
284 serological assays were done on a child with microcephaly to confirm microcephaly and assess previous
287 microcephalin 1 (MCPH1), mutated in primary microcephaly, to the decatenation checkpoint, a less-und
288 at pathogenic PH-domain variants can lead to microcephaly via canonical Wnt-pathway upregulation.
291 MARTT criteria); an alternate definition for microcephaly was based on applying Nellhaus standards ac
294 s (10 families) with a diagnosis of FEVR and microcephaly were ascertained from pediatric genetic eye
295 problems, musculoskeletal abnormalities, and microcephaly were present in the majority of cases.
297 with severe developmental delay, progressive microcephaly with brachycephaly, optic atrophy, seizures
299 nging from neurodevelopmental dysfunction in microcephaly with early onset seizures (MCSZ) to neurode