Anti-HVA (Homovanillic acid) polyclonal antibody

Aim of the study: Neuroblastoma (NBL) is one of the most common extracranial tumours occurring in children with N-Myc gene amplification, acknowledged as a marker of poor prognosis. We assessed the frequency of N-Myc amplification and its impact on NBL markers and on the treatment outcome. Material and methods: Among 160 children with NBL treated from 1991 to 2015 in one centre 140 patients had known N-Myc gene status, and they were enrolled in the study. The analysed group was divided into two subgroups: with and without N-Myc amplification (25 and 115 children, respectively). Association of N-Myc amplification with stage of the disease, levels of biochemical parameters, overall survival (OS) and failure-free survival (FFS) were analysed. Results: The frequency of N-Myc amplification was 17.9%. Most children with N-Myc amplification (64%) were classified to stage 4 NBL The levels of biochemical markers of NBL: ferritin, dopamine, NSE, and LDH were significantly higher in the group with N-Myc amplification, whereas the levels of VMA and HVA were lower. OS and FFS were significantly lower in children with N-Myc amplification in comparison to children from the control group (OS 53% vs. 76%, p = 0.03; FFS 50% vs. 72%, p = 0.03). The impact of N-Myc amplification on the treatment outcome was significant in patients with stage 4 NBL and children under one year of age. Conclusions: N-Myc amplification is a crucial prognostic factor in neuroblastoma, which is associated with almost all features related with poor prognosis and a higher probability of unfavourable outcome.

The abnormal deposition of A beta amyloid deposits in the brain is a hallmark of Alzheimer's disease (AD). Based on this evidence, many current therapeutic approaches focus on the development of small molecules halting A beta aggregation. However, due to the temporary and elusive structures of amyloid assemblies, the rational design of aggregation inhibitors remains a challenging task. Here we combine ThT assays and MD simulations to study A beta aggregation in the presence of the natural compounds tyrosol (TY), 3-hydroxytyrosol (HDT), and 3-methoxytyrosol (homovanillyl alcohol - HVA). We show that albeit HDT is a potent inhibitor of amyloid growth, TY and HVA catalyze fibril formation. An inspection of MD simulations trajectories revealed that the different effects of these three molecules on A beta(1-40) aggregation are ascribable to their capacity to arrange H-bonds network between the ligand (position C-3) and the peptide (Glu22). We believe that our results may contribute to the design of more effective and safe small molecules able to contrast pathogenic amyloid aggregation