Assessment of nutritional status and bone health in neurologically impaired children: a challenge in pediatric clinical practice

NTRODUCTION: neurologically impaired children frequently experience nutritional disorders and bone health complications. Our aim was firstly to analyze a method to interpret bone mineral density (BMD) accurately in neurologically impaired children. Secondly, to determine its relationship with the nutritional status and micronutrient levels in order to identify which factors are associated with low BMD. METHODS: a observational multicenter study was conducted in children with moderate-to-severe neurological impairment. Data collected included: medical records, anthropometric measures, hematologic and biochemical evaluation. BMD was measured with Dual-energy X-ray absorptiometry and z-scores were calculated adjusting for sex and chronological age. Secondly, BMD z-scores were calculated applying height age (age at which the child's height would be in 2nd percentile) instead of chronological age. RESULTS: fifty-two children were included (aged 4-16 years). Seventeen patients (32.7%) received feeding by gastrostomy tube. Height and BMI z-score were below 2SD in 64% and 31% of patients respectively, with normal mid upper arm circumference and skinfold thickness measurements. Low vitamin-D levels were found in 42% of cases. 50% of patients evidenced low BMD when calculated for chronological age, whereas only 34.5% showed BMD z-score <-2 when calculated for height age. No correlation was observed between BMD and vitamin-D levels, weight and height z-scores or age when BMD was calculated applying height age. CONCLUSIONS: the prevalence of low BMD is high in neurologically impaired children, and it is probably multifactorial. In these children, we suggest adjusting BMD for height age, in order not to over diagnose low BMD

Plp38MAPK activity in embryogenesis, morphogenesis and stress response: an indicator of perfect health?

P38 conveys a variety of signals, including conventional growth, migratory and death signals, as well as responding to environmental and mechanical stimuli. These signals induce phosphorylation of p38, which triggers both its translocation to the nucleus and the activation of its catalytic function. In Paracentrotus lividus we have shown that for a correct cilia re-generation the p38 activation is essential; we also showed, by time course Western blotting, two activation peaks during development (morula and early gastrula stages) with a precise localization of activated p38 in micromere and micromere derived cells (Nichel treatment higlighted this feature), and in the oral apical region. These results suggest that, like in Lytechinus variegatus, p38 activation/inactivation is involved in O-A axis specification, in gastrulation and in skeletogenesis. We found, in fact, that inhibiting (with SB203580) the p38 activation during cleavage (up to the morula stage) anomalies were observed in gastrulation (exogastrulae); later inhibition treatment (morula/blastula transition) impaired skeleton formation. Finally we was also able to demonstrate that in P. lividus are present four p38 isoforms differentially involved in different stress responses. All these features driven us to analyze if p38 activation is involved in high density population response in the “Ustica Island” MPA

A Survey on Tubulin and Arginine Methyltransferase Families Sheds Light on <i>P. lividus</i> Embryo as Model System for Antiproliferative Drug Development

Tubulins and microtubules (MTs) represent targets for taxane-based chemotherapy. To date, several lines of evidence suggest that effectiveness of compounds binding tubulin often relies on different post-translational modifications on tubulins. Among them, methylation was recently associated to drug resistance mechanisms impairing taxanes binding. The sea urchin is recognized as a research model in several fields including fertilization, embryo development and toxicology. To date, some &#945;- and &#946;-tubulin genes have been identified in P. lividus, while no data are available in echinoderms for arginine methyl transferases (PRMT). To evaluate the exploiting of the sea urchin embryo in the field of antiproliferative drug development, we carried out a survey of the expressed &#945;- and &#946;-tubulin gene sets, together with a comprehensive analysis of the PRMT gene family and of the methylable arginine residues in P. lividus tubulins. Because of their specificities, the sea urchin embryo may represent an interesting tool for dissecting mechanisms of tubulin targeting drug action. Therefore, results herein reported provide evidences supporting the P. lividus embryo as animal system for testing antiproliferative drugs

Sea urchin deciliation induces thermoresistance and activates the p38 mitogen-activated protein kinase pathway

In this study, we demonstrate by a variety of approaches (ie, morphological analysis, Western blots, immunolocalization, and the use of specific antibodies) that hyperosmotic deciliation stress of sea urchin embryos induces a thermotolerant response. Deciliation is also able to activate a phosphorylation signaling cascade the effector of which might be the p38 stress-activated protein kinase because we found that the administration of the p38 inhibitor SB203580 to sea urchin deciliated gastrula embryos makes the hyperosmotic deciliation stress lethal