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1 somatic postzygotic genetic lesions in brain maldevelopment.
2 cs of ARS, including corneal and iris stroma maldevelopment.
3   Delayed repair causes permanent motion VEP maldevelopment.
4 atterns that are a consequence of visuomotor maldevelopment.
5 here are no means of directly assessing such maldevelopment.
6  focal cortical dysgenesis and may be due to maldevelopment.
7 entation, or a mixture of these two modes of maldevelopment.
8 d open defects (i.e., exencephaly) and gross maldevelopment.
9 lt from facial branchial motor neuron (FBMN) maldevelopment.
10 the potential of local knowledge to overcome maldevelopment.
11 s well as the sequelae associated with their maldevelopment.
12 deficiency, a disease with potential retinal maldevelopment.
13  is associated with increased risks of fetal maldevelopment and adverse metabolic conditions in postn
14 essing in cerebellar and spinal motor neuron maldevelopment and degeneration.
15 ocephaly complex with associated features of maldevelopment and examine the roles of OTX2 and PRRX1.
16 isualizes current knowledge informing kidney maldevelopment and genetic causes of CAKUT and facilitat
17 xtended window of susceptibility to vascular maldevelopment and maladaptation.
18 n the fetal genome and the risk of placental maldevelopment and preeclampsia, possibly due to impairm
19 layers of the retina and choroid demonstrate maldevelopment and varying degrees of malfunction.
20 f transcriptional dysregulation and cortical maldevelopment are reviewed, along with potential therap
21 ide the first detailed description of the V1 maldevelopments associated with unrepaired natural, infa
22  cerebral damage, and both overt lesions and maldevelopment can result.
23 er overactive BG, and a frontostriatoinsular maldevelopment in ASD with reduced structure and functio
24       In contrast with ret-/- embryos, renal maldevelopment in DbetaH-Ret(MEN2B)-transgenic embryos r
25 gs thus far suggest subtle prenatal neuronal maldevelopment in the cerebellum and certain limbic stru
26                 We discuss evidence of brain maldevelopment in the first years of life in autism and
27                                          The maldevelopment may be explained in large part by the pau
28  stereopsis recovery in patients with fusion maldevelopment nystagmus (FMN) and patients without nyst
29 al horizontal nystagmus, a subtype of fusion maldevelopment nystagmus syndrome (FMNS).
30 rabismus or anisometropia can develop fusion maldevelopment nystagmus syndrome (FMNS).
31 matically with PVL severity: latent ("fusion maldevelopment") nystagmus (20%, 47%, and 40%, respectiv
32            Initiation is often rooted in the maldevelopment of a maternal-placental blood supply capa
33 t aberrant FGF signalling contributes to the maldevelopment of joints and to the onset and progressio
34  of strabismus influences the development or maldevelopment of motion VEPs.
35 robiological discoveries pertaining to early maldevelopment of ocular motor control systems.
36                                              Maldevelopment of placental villous trees and their bloo
37 n of the two factors is necessary to trigger maldevelopment of prefrontal cortical and ventral striat
38                                              Maldevelopment of Schlemm canal (SC) and trabecular mesh
39 vere optical neuropathy that originates from maldevelopment of the anterior segment of the eye.
40 ted by biochemical perturbations rather than maldevelopment of the brain.
41 t is due to an absence of the hippocampus, a maldevelopment of the dorsolateral prefrontal cortex, or
42      Congenital heart diseases often involve maldevelopment of the evolutionarily recent right heart
43 velopmental disorder most commonly involving maldevelopment of the fingernails, kneecaps and elbow jo
44 ate that these disorders may result from the maldevelopment of the oculomotor (nIII), trochlear (nIV)
45                                              Maldevelopment of the pharyngeal endoderm, an embryonic
46                                              Maldevelopment of the pulmonary vasculature contributes
47 esis syndrome (TDS) hypothesis proposes that maldevelopment of the testis, irrespective of cause, lea
48  in humans and the monkey is associated with maldevelopment of visual motion responsiveness, one mani
49 al disorder associated with early injury and maldevelopment of visual processing pathways and areas.
50 arge-angle infantile esotropia have striking maldevelopments of binocular (disparity-driven) converge
51 This work indicates that a preexisting brain maldevelopment predisposes to a secondary autoimmune res
52 exosc3 in zebrafish embryos caused embryonic maldevelopment, resulting in small brain size and poor m
53 e actin dysregulation in vivo and glomerular maldevelopment that is rescued by WT-DAAM2 mRNA.
54                               However, renal maldevelopment was not recapitulated in kidneys that wer
55 nically relevant imaging markers of cerebral maldevelopment, which offer new insights into the nature
56 vivo evidence in humans for possible retinal maldevelopment with a predilection for retinal GCL loss