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Neutron peripheral contamination in patients undergoing high-energy photon radiotherapy is considered as a risk factor for secondary cancer induction. Organ-specific neutron-equivalent dose estimation is therefore essential for a reasonable assessment of these associated risks. This work aimed to develop a method to estimate neutron-equivalent doses in multiple organs of radiotherapy patients. The method involved the convolution, at 16 reference points in an anthropomorphic phantom, of the normalized Monte Carlo neutron fluence energy spectra with the kerma and energy-dependent radiation weighting factor. This was then scaled with the total neutron fluence measured with passive detectors, at the same reference points, in order to obtain the equivalent doses in organs. The latter were correlated with the readings of a neutron digital detector located inside the treatment room during phantom irradiation. This digital detector, designed and developed by our group, integrates the thermal neutron fluence. The correlation model, applied to the digital detector readings during patient irradiation, enables the online estimation of neutron-equivalent doses in organs. The model takes into account the specific irradiation site, the field parameters (energy, field size, angle incidence, etc) and the installation (linac and bunker geometry). This method, which is suitable for routine clinical use, will help to systematically generate the dosimetric data essential for the improvement of current risk-estimation models.

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INTRODUCTION: The rate of epilepsy in autism is higher than in other developmental disorders and estimates point to a frequency range of between 7% and 42%. Between 40% and 47% of autistic children suffer from clinical epilepsy. Onset of epilepsy may occur at any age. DEVELOPMENT: During the ontogenesis of the nervous system, if the maturing process is upset by some epileptogenic phenomenon, the consequences on the consolidation of the emerging cognitive functions can be severe. Epileptiform discharges can occur although clinical seizures are absent, but nevertheless they still have an effect on the maturing process. Between 10% and 50% of autistic children undergo a regression of acquired behaviour following a period of normal development. The absence of clinical seizures during regression does not rule out the epileptogenic origin of the regressive process. CONCLUSIONS: The relation between pervasive developmental disorders and epilepsy, epileptiform activity and subclinical seizures can be explained from a neurobiological point of view, on the one hand, by an imbalance between the excitatory system -glutamate- and the inhibitory system -gamma-aminobutyric acid (GABA)- in key points in the cerebral cortex and, on the other, by means of molecular genetic studies and studies of candidate genes (FOXP2, WNT2, subunits of GABA receptors, neuroligins, ARX, SCN1A, SCN2A, MECP2, CDKL5 and DLX5).

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Introducción. La tasa de epilepsia en el autismo es mayor que en otros trastornos del desarrollo, y se estima en un rango de frecuencia del 7 al 42%. Entre el 40 y el 47% de los niños autistas sufre epilepsia clínica. El inicio de la epilepsia puede darse a cualquier edad. Desarrollo. Durante la ontogénesis del sistema nervioso, si el proceso madurativo se ve interferido por un fenómeno epileptógeno, las consecuencias pueden ser graves para la consolidación de las funciones cognitivas emergentes. Las descargas epileptiformes pueden darse en ausencia de crisis clínicas, pero afectando de igual manera al proceso madurativo. Entre el 10 y el 50% de los niños autistas sufre una regresión de la conducta adquirida después de un período de desarrollo normal. La ausencia de crisis clínicas durante la regresión no descarta el origen epileptogénico del proceso regresivo. Conclusiones. Se puede explicar la relación entre los trastornos generalizados del desarrollo y la epilepsia, la actividad epileptiforme y las crisis subclínicas desde un punto de vista neurobiológico, por un lado, mediante un desequilibrio entre el sistema excitador –glutamato– y el sistema inhibidor –ácido gamma-aminobutírico (GABA)– en puntos claves del córtex cerebral y, por otro lado, mediante los estudios de genética molecular y estudio de genes candidatos (FOXP2, WNT2, subunidades de los receptores GABA, neuroliginas, ARX, SCN1A, SCN2A, MECP2, CDKL5 y DLX5) (AU)

Introduction. The rate of epilepsy in autism is higher than in other developmental disorders and estimates point to a frequency range of between 7% and 42%. Between 40% and 47% of autistic children suffer from clinical epilepsy. Onset of epilepsy may occur at any age. Development. During the ontogenesis of the nervous system, if the maturing process is upset by some epileptogenic phenomenon, the consequences on the consolidation of the emerging cognitive functions can be severe. Epileptiform discharges can occur although clinical seizures are absent, but nevertheless they still have an effect on the maturing process. Between 10% and 50% of autistic children undergo a regression of acquired behaviour following a period of normal development. The absence of clinical seizures during regression does not rule out the epileptogenic origin of the regressive process. Conclusions. The relation between pervasive developmental disorders and epilepsy, epileptiform activity and subclinical seizures can be explained from a neurobiological point of view, on the one hand, by an imbalance between the excitatory system –glutamate– and the inhibitory system –gamma-aminobutyric acid (GABA)– in key points in the cerebral cortex and, on the other, by means of molecular genetic studies and studies of candidate genes (FOXP2, WNT2, subunits of GABA receptors, neuroligins, ARX, SCN1A, SCN2A, MECP2, CDKL5 and DLX5) (AU)

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OBJECTIVES: To evaluate the efficacy in vitro and in vivo of a new antibacterial suture (PGAB) compared with a traditional braided suture (PG). Our primary goals were to study microbiological effectiveness and impact on wound healing of PGAB vs PG. Secondary goal was to analyze influence on inflammatory response. METHODS: In vitro study: clinical samples of Staphylococcus epidermidis, Staphylococcus aureus, S. hominis, Staphylococcus haemolyticus, Staphylococcus auricularis, Enterococcus faecalis, Corynebacterium spp. and Escherichia coli were studied. We also implanted a flat mesh in 10 minipigs, four incisions each (two PG and two PGAB) two contaminated with S. epidermidis and two not contaminated. Finally, we performed four colic anastomosis in each of 10 minipigs, two contaminated with E. coli and two not contaminated (two PG and two PGAB). We studied the inflammatory and wound healing processes in both models. RESULTS: We observed a bactericidal efficacy of PGAB against grampositive, and bacteriostatic effect against E. coli. Mesh study: recovered CFU were lower in the group PGAB vs PG. In the group PGAB, inflammatory mediators' concentrations were lower. In the group PGAB, concentrations of wound healing mediators were normal. Colic anastomosis: recovered CFU were lower in the group PGAB vs the group PG. In the group PGAB we observed a reduction of inflammatory mediators. In the group PGAB we observed normalized concentrations of wound healing mediators. CONCLUSIONS: This study demonstrates microbiological efficacy of PGAB, that normalizes wound healing process, and an anti-inflammatory effect.

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Se estudia la composición del crudo de sapogeninas del jugo de henequén, así como la evaluación de sus componentes principales: tigogenina y hecogenina, mediante el método de cromatografía gaseosa. Además de las dos sapogeninas principales, fueron detectadas, mediante CCD, otras cuatro manchas bien definidas: una de ellas correspondió, por comparación con patrones, a las 9-11 dehidrohecogenina dada a conocer por primera vez en el Agave fourcroydes que crece en Cuba. Se establecieron las condiciones para separar cualitativamente, por cromatografía gaseosa, la 9-11 dehidrohecogenina de la hecogenina(AU)

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