Pro-/antiinflammatory dysregulation in early psychosis: Results from a 1-year follow-Up study

Background: Previous studies indicated a systemic deregulation of the pro-/antiinflammatory balance in subjects after 6 months of a first psychotic episode. This disruption was reexamined 12 months after diagnosis to identify potential risk/ protective factors and associations with symptom severity. Methods: Eighty-five subjects were followed during 12 months and the determination of the same pro-/antiinflammatory mediators was carried out in plasma and peripheral blood mononuclear cells. Multivariate logistic regression analyses were used to identify risk/protective factors. Multiple linear regression models were performed to detect the change of each biological marker during follow-up in relation to clinical characteristics and confounding factors. Results: This study suggests a more severe systemic pro-/antiinflammatory deregulation than in earlier pathological stages in first psychotic episode, because not only were intracellular components of the inflammatory response increased but also the majority of soluble elements. Nitrite plasma levels and cyclooxygenase-2 expression in peripheral blood mononuclear cells are reliable potential risk factors and 15d-prostaglandin-J2 plasma levels a protection biomarker. An interesting relationship exists between antipsychotic dose and the levels of prostaglandin-E2 (inverse) and 15d-prostaglandin-J2 (direct). An inverse relationship between the Global Assessment of Functioning scale and lipid peroxidation is also present. Conclusions: Summing up, pro-/antiinflammatory mediators can be used as risk/protection biomarkers. The inverse association between oxidative/nitrosative damage and the Global Assessment of Functioning scale, and the possibility that one of the targets of antipsychotics could be the restoration of the pro-/antiinflammatory balance support the use of antiinflammatory drugs as coadjuvant to antipsychotics

Prácticas alimentarias de los adolescentes de Cantabria

Objetivo. Analizar determinadas prácticas alimentarias en adolescentes escolarizados en centros de educación pública de Cantabria, participantes en el Proyecto "Promoción de Hábitos Saludables en Adolescentes desde el Ámbito Educativo". Sujetos. Se realizó un estudio transversal, analizando una muestra de 1.101 adolescentes: 568 (51,6%) varones y 533 (48,4%) mujeres, de edades comprendidas entre los 10 y los 17 años, escolarizados en dieciséis centros de enseñanza primaria y secundaria, mediante un cuestionario autocumplimentado. Resultados. Los adolescentes suelen realizar entre cuatro (41,5%) y cinco (31,6%) ingestas diarias. Durante los días de colegio, el 34% emplea entre diez y quince minutos en desayunar, y entre 30 y 35 minutos en comer (33,5%) y cenar (23%). Un elevado porcentaje (49,4%) de adolescentes desayunaba en soledad durante los días lectivos. Las principales ingestas alimenticias se realizan en el hogar. Las bebidas no alcohólicas (53,6%) y los dulces (42%) son los principales destinos de su dinero de bolsillo. En la casi totalidad de los hogares, es la madre la que se encarga de la compra de los alimentos, de la preparación de las comidas y de decidir tanto el almuerzo como la merienda. La pizza (72,6%) y las patatas fritas (70,8%) son los alimentos considerados más ricos entre los analizados, mientras que el perrito caliente (49,4%) y la hamburguesa (48,5%) son considerados como los menos sanos. El 58,6% de los encuestados cena viendo la televisión. Conclusión. En el estudio del comportamiento alimentario es necesario analizar la influencia de otros factores que, en muchas ocasiones, están detrás de las recomendaciones dietéticas y que casi siempre son ignorados. Prácticas alimentarias como las analizadas en el presente estudio, permiten, cuando estas se desarrollan de forma adecuada, una mejora sustancial en la salud alimentaria y nutricional de las personas

Extracellular signal‐regulated kinase activation in the chronic constriction injury model of neuropathic pain in anaesthetized rats

Abstract Background The role of extracellular signal‐regulated kinases ( ERKs ) in nociception has been explored in the last years. While in spinal cord their activation is frequently correlated with pain or acute noxious stimuli, supraspinally, this association is not so evident and remains unclear. This study aims to evaluate ERK 1/2 activation in the spinal cord and brainstem nuclei upon neuropathy and/or an additional mechanical stimulus. Methods Acute noxious mechanical stimulation was applied in the left hindpaw of anaesthetized SHAM ‐operated and chronic constriction injured ( CCI , neuropathic pain model) rats. Other SHAM or CCI rats did not receive any stimulus. Immunohistochemistry against the phosphorylated isoforms of ERK 1/2 ( pERK 1/2) was performed in lumbar spinal cord and brainstem sections to assess ERK 1/2 activation. Results In the spinal cord, stimulation promoted an increase in pERK 1/2 expression in the superficial dorsal horn of SHAM rats. No significant effects were caused by CCI alone. At supraspinal level, changes in ERK 1/2 activation induced by CCI were observed in A5 , locus coeruleus ( LC ), raphe obscurus ( ROb ), raphe magnus, dorsal raphe ( DRN ), lateral reticular and paragigantocellularis nucleus. CCI increased pERK 1/2 expression in all these nuclei, with exception of LC , where a significant decrease was verified. Mechanical noxious stimulation of CCI rats decreased pERK 1/2 expression in ROb and DRN , but no further changes were detected in either SHAM ‐ or CCI ‐stimulated animals. Conclusion ERK 1/2 are differentially activated in the spinal cord and in selected brainstem nuclei implicated in nociception, in response to an acute noxious stimulus and/or to a neuropathic pain condition

Involvement of 5-HT1A/1B receptors in the antinociceptive effect of paracetamol in the rat formalin test

The mechanism of analgesic action of paracetamol (acetominophen) remains still unknown. However, a relationship between serotonergic system and the effect of paracetamol has been previously demonstrated. The serotonin activity in the brainstem is primarily under the control of 5-HT1A somatodendritic receptors, although some data also suggest the involvement of 5-HT1B receptors. To determine whether the 5-HT1A and 5-HT1B receptors are involved in the antinociceptive effect of paracetamol, we evaluated the effect of paracetamol (0.125–1 g/kg i.p.) followed by different antagonists [WAY 100,635 (0.8 mg/kg s.c.) and SB 216,641 (0.8 mg/kg s.c.)] or agonists [8-OH-DPAT (0.125 mg/kg s.c.) and CP 93,129 (0.125 mg/kg s.c.)] of 5-HT1A and 5-HT1B receptors, respectively, in the rat model of formalin-induced pain. We demonstrated that paracetamol administration showed a dose-dependent antinociceptive effect in the formalin test. WAY 100,635 (5-HT1A antagonist) induced an increase in the antinociceptive effect of paracetamol at 250 mg/kg doses. Conversely, 8-OH-DPAT (5-HT1A agonist) decreased the antinociceptive effect of paracetamol at 500–1000 mg/kg doses. However, SB216641 (5-HT1B antagonist) modified weakly the antinociceptive effect of paracetamol at 250 mg/kg doses and CP 93,129 (5-HT1B agonist) not produce a clear effect in the antinociceptive effect of paracetamol. These results suggest that the antinociceptive effect of paracetamol can be enhanced mainly by compounds having 5-HT1A antagonist properties in the formalin test and maybe by 5-HT1B receptors antagonists. Keywords: Paracetamol, Formalin test, 5-HT1A receptors, 5-HT1B receptors, Antinociceptive effec