Neonatal hydrocephalus is a result of a block in folate handling and metabolism involving 10-formyltetrahydrofolate dehydrogenase.

Folate is vital in a range of biological processes and folate deficiency is associated with neurodevelopmental disorders such as neural tube defects and hydrocephalus (HC). 10-formyl-tetrahydrofolate-dehydrogenase (FDH) is a key regulator for folate availability and metabolic interconversion for the supply of 1-carbon groups. In previous studies, we found a deficiency of FDH in CSF associated with the developmental deficit in congenital and neonatal HC. In this study, we therefore aimed to investigate the role of FDH in folate transport and metabolism during the brain development of the congenital hydrocephalic Texas (H-Tx) rat and normal (Sprague-Dawley) rats. We show that at embryonic (E) stage E18 and E20, FDH-positive cells and/or vesicles derived from the cortex can bind methyl-folate similarly to folate receptor alpha, the main folate transporter. Hydrocephalic rats expressed diminished nuclear FDH in both liver and brain at all postnatal (P) ages tested (P5, P15, and P20) together with a parallel increase in hepatic nuclear methyl-folate at P5 and cerebral methylfolate at P15 and P20. A similar relationship was found between FDH and 5-methyl cytosine, the main marker for DNA methylation. The data indicated that FDH binds and transports methylfolate in the brain and that decreased liver and brain nuclear expression of FDH is linked with decreased DNA methylation which could be a key factor in the developmental deficits associated with congenital and neonatal HC. Folate deficiency is associated with neurodevelopmental disorders such as neural tube defects and hydrocephalus. 10-formyl-tetrahydrofolate-dehydrogenase (FDH) is a key regulator for folate availability and metabolic interconversion. We show that FDH binds and transports methylfolate in the brain. Moreover, we found that a deficiency of FDH in the nucleus of brain and liver is linked with decreased DNA methylation which could be a key factor in the developmental deficits associated with congenital and neonatal hydrocephalus cells.

Mapping the knowledge of the main diseases affecting sea bass and sea bream in Mediterranean.

Good knowledge on the disease situation and its impact on production is a base mechanism for designing health surveillance, risk analysis and biosecurity systems. Mediterranean marine fish farming, as any aquaculture production, is affected by various infectious diseases. However, seabass and seabream, the main produced species, are not listed as susceptible host species for the notifiable pathogens listed in the current EU legislation, which generates a lack of systematic reporting. The results presented in this study come from a survey directly to fish farms (50 hatchery and on-growing units from 10 Mediterranean countries), with data from 2015 to 2017, conducted by the H2020 project MedAID. Seabass showed a higher survival rate (85%) through a production cycle than seabream (80%) in spite of equal mortality due to pathogen infections (10%). The differences in survival may be explained by mortality 'of other causes'. Seabream and seabass have different disease profiles, and the profile is slightly different between geographical regions. Among the most important diseases, tenacibaculosis and vibriosis were identified in seabass and Sparicotyle chrysophrii (a gill fluke) and nodavirus in seabream. Correlating mortality data to management variables showed that increasing density, buying fingerlings from external sources and treatments due to disease are factors that negatively influence mortality rate. Most of the surveyed farms did not keep sufficient quality data to implement good health status reports and perform detailed impact studies, which shows the necessity of updating the current legislative framework to provide the basis for better reporting of relevant pathogens in the Mediterranean basin.