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).
Our results showed that incubation with CP significantly increases the percent of cell death, activities of caspase-3 and -9, level of TNF-α and also promotes the levels of biomarkers which play important role in oxidative stress.
Also, a significant increase in the risk of CP was observed to be associated with the interactions of TNF-αrs1799724 and MTHFR rs9651118 (OR 2.75, 95 % CI 1.23-6.13).
Factor 5, Factor 2, methylene tetrahydrofolate reductase, tumor necrosis factor-alpha, and other SNPs tested were not significantly associated with CP risk.
There is evidence that the amount of EPO in CP children is lower than in normal children, but the levels of proinflammatory cytokines, such as interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha, are higher in the CP children.
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.
Statistically significant association was also found in patients with cPVL between TNFα TC, CC, GG, GG -1031/-857/-308/-238 genotypes combination (OR, 4.107; p=0.024), as well as IL1β TT, CC -511/+3954 genotypes combination (OR, 7.333; p=0.005) and risk of CP.
We found a significant association between CP and IL-6 (rs1800795) [C vs G: odds ratio (OR) 1.79, 95% confidence interval (CI) 1.44-2.22, p<0.001; CC+GC vs GG: OR 1.72, 95% CI 1.29-2.29, p=0.002; CC vs GG+GC: OR 2.17, 95% CI 1.52-3.09, p<0.001], but no other genetic polymorphisms.
The aim of our study was to evaluate the possible association of four TNFα promoter single nucleotide polymorphisms (SNPs) (-1031 T/C, -857 C/T, -308 G/A and -238 G/A), two IL1β SNPs (-511 C/T and +3954 C/T) and one IL6 (-174 C/G) polymorphism with susceptibility to CP in very preterm infants.
The APOE epsilon2epsilon3 genotype was significantly more prevalent in the group with CP (11%) than the comparison group (5%) (odds ratio [OR] 2.8; 95% confidence interval [CI] 1.01-7.66).
Additional studies are warranted to establish the role of apolipoprotein E in specific pathogenetic pathways leading to cerebral palsy or poor neurologic outcomes after perinatal brain injury.
Our findings suggest that specific combinations of genes influence the structure and production of apoE differently and affect the clinical manifestations of CP.
Our findings suggest that genetic variations in one of the sequences regulating the expression of APOE, may be associated with worse clinical outcome in children with cerebral palsy.
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).
Inclusion: cerebral palsy or brain injury; age 4-15 years; Manual Abilities Classification System (MACS) I-IV; goals related to hand function; sufficient cognitive, language and behavioral ability to undertake CO-OP.
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.
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).