Family functioning but not social capital is associated with better mental health in adolescents affected by violence and displacement by armed conflict in Colombia

Background: The effect of the Colombian armed conflict on the mental health of adolescents is still poorly understood. Aims: Given social interventions are most likely to inform policy, we tested whether two potential intervention targets, family functioning and social capital, were associated with mental health in Colombian adolescents, and whether this was moderated by experience of violence and displacement. Methods: We examined the cross-sectional association between family functioning, cognitive social capital, structural social capital and 12-month prevalence of Composite International Diagnostic Interview (CIDI) diagnosed psychiatric disorder, using data on 12 to 17-year-old adolescents (N = 1,754) from the 2015 National Mental Health Survey of Colombia, a nationally representative epidemiological study. We tested whether associations survived cumulative adjustment for demographic confounders, experience of non-specific violence and harm and displacement by armed conflict. Results: Neither structural nor cognitive social capital were associated with better mental health. Better family functioning was associated with reduced risk of poor mental health in an unadjusted analysis (OR 0.90 [0.85–0.96]), and after cumulative adjustments for demographic confounders (OR 0.91 [0.86–0.97]), non-specific violence and harm (OR 0.91 [0.86–0.97]) and social capital variables (OR 0.91 [0.85–0.97]). In the final model, each additional point on the family APGAR scale was associated with a 9% reduced odds of any CIDI diagnosed disorder in the last 12 months. Conclusions: Better family functioning was associated with better mental health outcomes for all adolescents. This effect remained present in those affected by the armed conflict even after accounting for potential confounders

Association of the mtDNA m.4171C>A/MT-ND1 mutation with both optic neuropathy and bilateral brainstem lesions

Background: An increasing number of mitochondrial DNA (mtDNA) mutations, mainly in complex I genes, have been associated with variably overlapping phenotypes of Leber’s hereditary optic neuropathy (LHON), mitochondrial encephalomyopathy with stroke-like episodes (MELAS) and Leigh syndrome (LS). We here describe the first case in which the m.4171C>A/MT-ND1 mutation, previously reported only in association with LHON, leads also to a Leigh-like phenotype. Case presentation: A 16-year-old male suffered subacute visual loss and recurrent vomiting and vertigo associated with bilateral brainstem lesions affecting the vestibular nuclei. His mother and one sister also presented subacute visual loss compatible with LHON. Sequencing of the entire mtDNA revealed the homoplasmic m.4171C>A/MT-ND1 mutation, previously associated with pure LHON, on a haplogroup H background. Three additional non-synonymous homoplasmic transitions affecting ND2 (m.4705T>C/MT-ND2 and m.5263C>T/MT-ND2) and ND6 (m.14180T>C/MT-ND6) subunits, well recognized as polymorphisms in other mtDNA haplogroups but never found on the haplogroup H background, were also present. Conclusion: This case widens the phenotypic expression of the rare m.4171C>A/MT-ND1 LHON mutation, which may also lead to Leigh-like brainstem lesions, and indicates that the co-occurrence of other ND non-synonymous variants, found outside of their usual mtDNA backgrounds, may have increased the pathogenic potential of the primary LHON mutation

High accuracy 234U(n,f) cross section in the resonance energy region

New results are presented of the 234U neutron-induced fission cross section, obtained with high accuracy in the resonance region by means of two methods using the 235U(n,f) as reference. The recent evaluation of the 235U(n,f) obtained with SAMMY by L. C. Leal et al. (these Proceedings), based on previous n-TOF data [1], has been used to calculate the 234U(n,f) cross section through the 234U/235U ratio, being here compared with the results obtained by using the n-TOF neutron flux

Toxicidad hematológica asociada al tratamiento con sulfonamidas y pirimetamina en pacientes VIH positivos y toxoplasmosis cerebral en un hospital de tercer nivel en Colombia

Objective. To determine the frequency of hematologic adverse effects associated with treatment for cerebral toxoplasmosis in HIV / AIDS patients. Design: Retrospective case series. Location: University Hospital Hernando Moncaleano Perdomo (HMP), Neiva, Colombia. Population. Patients with cerebral toxoplasmosis and HIV / AIDS treated at the infection service unit between 2006 and 2009. Población. Pacientes con toxoplasmosis cerebral y VIH/SIDA atendidos en el servicio de infectología entre 2006-2009. Results. 51 patients were evaluated during the study period. 40 (78%) were men. The average age was 33 years. 25 patients had cerebral toxoplasmosis as the first marker of HIV infection. 60.7% of cases had hematologic toxicity. 42% of patients had anemia before treatment. The peak onset of bone marrow toxicity was the sixth day of the start of treatment schedule. The anti-toxoplasma scheme that was most commonly associated with myelotoxicity was the combination of pyrimethamine/sulfadoxine, trimethoprim-sulfamethoxazole and clindamycin in 48% of cases. Objetivo. Determinar la frecuencia efectos adversos hematológicos asociados al tratamiento para toxoplasmosis cerebral en pacientes VIH/SIDA. Diseño. Serie de casos retrospectiva. Lugar. Hospital Universitario Hernando Moncaleano Perdomo (HMP), Neiva- Colombia. Población. Pacientes con toxoplasmosis cerebral y VIH/SIDA atendidos en el servicio de Infectología entre 2006-2009. Resultados. 51 pacientes fueron evaluados durante el periodo de estudio. 40 (78%) fueron hombres. El promedio de edad fue 33 años. 25 pacientes presentaban toxoplasmosis cerebral como primer marcador de Infección VIH. El 60,7% de los casos presentaron toxicidad hematológica. 42% de los pacientes presentaron anemia previa al tratamiento. El pico de aparición de toxicidad medular fue al sexto día de inicio del esquema de tratamiento. El esquema antitoxoplasma que más comúnmente fue asociado a mielotoxicidad fue la combinación de pirimetamina/sulfadoxina, trimetoprimsulfametoxazol y clindamicina en 48% de los casos