These data led us to conclude that small deletions involving KANK1 do not cause a highly-penetrant influence of large effect size and they are unlikely to contribute significantly to the aetiology of disease in patients with development delay, intellectual disability, autism or cerebral palsy.
A total of 182 children, 110 with ABI and 72 with CP and with Gross Motor Function Classification System (GMFCS) levels I-IV, were evaluated retrospectively.
After NSCs transplantation, the neurobehavioral status of CP rats was improved, the degree of brain pathological injury was alleviated, the apoptotic index of cells in cerebral cortex and hippocampus and the expression of the apoptotic protein (caspase-3 and Bax) were decreased, the expression of GFAP were significantly decreased.
DAS for 4 consecutive days before CP showed moderate positive immunohistochemically expression of the glial fibrillary acidic protein (GFAP) in the brain and kidney tissues comparable to CP-treated rats.
After NSCs transplantation, the neurobehavioral status of CP rats was improved, the degree of brain pathological injury was alleviated, the apoptotic index of cells in cerebral cortex and hippocampus and the expression of the apoptotic protein (caspase-3 and Bax) were decreased, the expression of GFAP were significantly decreased.
A total of 157 patients with nonambulatory CP (Gross Motor Function Classification System IV and V) with a minimum of 2-year follow-up after PSF were identified from a prospective multicenter registry.
A total of 157 patients with nonambulatory CP (Gross Motor Function Classification System IV and V) with a minimum of 2-year follow-up after PSF were identified from a prospective multicenter registry.
A total of 157 patients with nonambulatory CP (Gross Motor Function Classification System IV and V) with a minimum of 2-year follow-up after PSF were identified from a prospective multicenter registry.
After evaluation of our case series and reconsideration of the literature, we propose that KANK1 aberrations do not frequently cause CP but cannot exclude that they represent a risk factor for ASD, especially when the coding region of the shorter, alternate KANK1 transcript (termed "transcript 4" in the UCSC Genome Browser) is impacted.
In 23 patients molecular diagnosis was reached and included 5 hereditary spastic paraplegia genes (SPG) in spastic CP mimics; HPRT1, TH, QDPR, DDC in dystonic CP mimics; ADCY5 and NIKX2-1 in choreic CP mimics; CANA1A in ataxic CP mimics; and SPG, PDHA1, NIKX2-1, AT, SLC2A1 and SPR in mixed CP mimics.
In 23 patients molecular diagnosis was reached and included 5 hereditary spastic paraplegia genes (SPG) in spastic CP mimics; HPRT1, TH, QDPR, DDC in dystonic CP mimics; ADCY5 and NIKX2-1 in choreic CP mimics; CANA1A in ataxic CP mimics; and SPG, PDHA1, NIKX2-1, AT, SLC2A1 and SPR in mixed CP mimics.
In addition, in CP-treated rats, PGE treatment induced the recovery of white blood cell, neutrophil, and lymphocyte counts, along with mid-range absolute counts, and increased the serum levels of inflammatory cytokines (TNF-α, IFN-γ, IL-2, and IL-12) and immunoglobulins (IgG and IgA).
Fever and increased maternal interleukin-6 (IL-6) plasma levels in labor are associated with an increased risk of adverse events in offspring, including neonatal seizures, cerebral palsy, and low intelligence scores at school age.
One hundred and fifty-one individuals with CP aged 16 to 20 years were included (63% male, 37% female; Gross Motor Function Classification System [GMFCS] levels I-IV; without intellectual disability).
Children with CP (N=41; age range 5-18y, Gross Motor Function Classification System I-IV) were randomized to a control group (CG) (n=21, 2 dropouts) receiving conventional therapy or an intervention group (IG) (n=20) receiving hand-arm bimanual intensive therapy-including lower extremities (HABIT-ILE).
<b>Methods</b>: Cohort studies were included if the participants were children with cerebral palsy at Gross Motor Function Classification System (GMFCS) Level I-IV, initial measurement of walking by 13 years of age and follow-up measurement by 30 years of age.
One hundred and forty-six children with CP (mean age: 5.78 ± 1.72 years, male: 56.2%) presenting variable function (gross motor function classification system [GMFCS], levels I-IV) participated in this study.