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Septicemia is the main cause of neonatal mortality. The early-onset neonatal sepsis is usually related to maternal factor risks including recto-vaginal colonization. In the late-onset neonatal septicemia it is more difficult to establish the etiology because the majority of the cases are nosocomial or community related. The Streptococcus agalactiae (beta-hemolytic Streptococcus) is the most frequent germ associated with neonatal sepsis in developed countries. The late-onset form usually occurs with septic symptoms and meningitis and, in a few cases, with osteoarticular, skin and soft tissue infection. Adenitis-cellulitis syndrome is rarely seen, and its main cause is Staphylococcus aureus, followed by Streptococcus agalactiae. We report two cases of group B Streptococcus late-onset neonatal septicemia, both of them with adenitis-cellulitis syndrome. Patients recovered uneventfully after an adequate antibiotic therapy.

Medical records of children14 years with CAMP were retrospectively reviewed from January 2010 to December 2015. Patients with radiological evidence of pneumonia and microbiological confirmation of MP (PCR from nasopharyngeal swab and/or serum specific IgM) were considered CAMP.One hundred and sixty two children were diagnosed with CAMP; median age 6 years (IQR: 4-9). The positive MP test rate among children with CAP progressively increased with age as did the empirical use of macrolides. There were two peaks of cases in 2011 and in 2015, being July, August, November and December the seasons with the higher number of cases. The most frequent radiological pattern was segmental infiltrate (62.3%) and 22 (13.6%) children had pleural effusion. It was noteworthy the mild symptomatology and low levels of inflammatory parameters that children with CAMP had. A macrolide was empirically initiated in 68.5% of cases. Hospital admission rate was inversely proportional to patient's age.According to this study, older, less symptomatic patients and with lower inflammatory parameters had the greatest rate of MP infection among children with CAP and thus they could benefit of empiric macrolide therapy. Therefore, knowing the epidemiology of a geographical area may be important for the management of CAP in children.Se revisaron retrospectivamente las historias clínicas de los niños 14 años con NACM entre enero de 2010 y diciembre de 2015. Los pacientes con evidencia radiológica de neumonía y confirmación microbiológica de MP (PCR de exudado nasofaríngeo y/o anticuerpos IgM específicos frente a MP) se consideraron NACM.Un total de 162 pacientes se diagnosticaron de NACM; mediana de edad de 6 años (rango intercuartílico: 4-9 años). La proporción de pruebas positivas para MP en pacientes con NAC, así como el uso empírico de macrólidos, aumentó progresivamente con la edad. Hubo un pico de casos en 2011 y en 2015, con un máximo de casos en julio, agosto, noviembre y diciembre. El patrón radiológico más frecuente fue el infiltrado segmentario (62,3%), mientras que 22 (13,6%) presentaron derrame pleural. Los niños con NACM desarrollaron una clínica leve, con poca elevación de parámetros inflamatorios. Se inició tratamiento empírico con un macrólido en el 68,5% de los casos. La necesidad de ingreso hospitalario fue inversamente proporcional a la edad del paciente.Según este estudio, los niños con NAC de mayor edad tuvieron la mayor proporción de infección por MP, siendo poco sintomáticos y con escasa elevación de parámetros inflamatorios, pudiéndose beneficiar del tratamiento empírico con macrólidos. Por consiguiente, conocer la epidemiología de un área geográfica podría ser importante para el abordaje de las NAC en niños.

Common single-nucleotide polymorphisms (SNPs) account for a large proportion of the heritability of obsessive-compulsive disorder (OCD). Co-ocurrence of OCD and schizophrenia is commoner than expected based on their respective prevalences, complicating the clinical management of patients. This study addresses two main objectives: to identify particular genes associated with OCD by SNP-based and gene-based tests; and to test the existence of a polygenic risk shared with schizophrenia. The primary analysis was an exon-focused genome-wide association study of 370 OCD cases and 443 controls from Spain. A polygenic risk model based on the Psychiatric Genetics Consortium schizophrenia data set (PGC-SCZ2) was tested in our OCD data. A polygenic risk model based on our OCD data was tested on previous data of schizophrenia from our group. The most significant association at the gene-based test was found at DNM3 (P=7.9 × 10(-5)), a gene involved in synaptic vesicle endocytosis. The polygenic risk model from PGC-SCZ2 data was strongly associated with disease status in our OCD sample, reaching its most significant value after removal of the major histocompatibility complex region (lowest P=2.3 × 10(-6), explaining 3.7% of the variance). The shared polygenic risk was confirmed in our schizophrenia data. In conclusion, DNM3 may be involved in risk to OCD. The shared polygenic risk between schizophrenia and OCD may be partially responsible for the frequent comorbidity of both disorders, explaining epidemiological data on cross-disorder risk. This common etiology may have clinical implications. The study was supported by Fundación María José Jove, Fondo Europeo de Desarrollo Regional (FEDER), Xunta de Galicia; and by grants from the Instituto de Salud Carlos III FIS PI13/01136 to AC, CP11/00163 to JC, PI13/00918 to JMM, PI14/00413 to PA; the Generalitat de Catalunya AGAUR 2014 SGR-1138; the Spanish MINIECO SAF2013-49108- R Plan Estatal; and the European Commission 7th Framework Program, Project N. 262055 (ESGI) to XE. LD is supported by a Severo Ochoa fellowship of the Spanish MINIECO.

Altres ajuts: Fundació La Marato-TV3(TV3201428-10), AFM-Telethon (Nrg14ALS) Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive degeneration of motoneurons, which is preceded by loss of neuromuscular connections in a "dying back" process. Neuregulin-1 (Nrg1) is a neurotrophic factor essential for the development and maintenance of neuromuscular junctions, and Nrg1 receptor ErbB4 loss-of-function mutations have been reported as causative for ALS. Our main goal was to investigate the role of Nrg1 type I (Nrg1-I) in SOD1G93A mice muscles. We overexpressed Nrg1-I by means of an adeno-associated viral (AAV) vector, and investigated its effect by means of neurophysiological techniques assessing neuromuscular function, as well as molecular approaches (RT-PCR, western blot, immunohistochemistry, ELISA) to determine the mechanisms underlying Nrg1-I action. AAV-Nrg1-I intramuscular administration promoted motor axon collateral sprouting by acting on terminal Schwann cells, preventing denervation of the injected muscles through Akt and ERK1/2 pathways. We further used a model of muscle partial denervation by transecting the L4 spinal nerve. AAV-Nrg1-I intramuscular injection enhanced muscle reinnervation by collateral sprouting, whereas administration of lapatinib (ErbB receptor inhibitor) completely blocked it. We demonstrated that Nrg1-I plays a crucial role in the collateral reinnervation process, opening a new window for developing novel ALS therapies for functional recovery rather than preservation.