[Description of Influenza B in seasonal epidemics in Spain]. / Descripción de la gripe B en las epidemias estacionales de España.

OBJECTIVE: Seasonal influenza epidemics are a major public health concern. They are caused by the influenza A and B viruses; although the A virus is more prominent, influenza B virus infection causes a disease with similar characteristics. There are two phylogenetically distinct influenza B lineages (B/Victoria and B/Yamagata), only one of which is present in the trivalent vaccine formulated each season. METHODS: Epidemiological data from the Spanish Influenza Surveillance System for 2007 to 2017 were reviewed to establish the relative proportion of each type of virus and the characterization of the B lineages in relation to the composition of the trivalent vaccine. RESULTS: The median proportion of B (2007-2017) was 27.2% (0.7%-74.8%) vs. 16.3% (0.4%-98.6%) for A-H3 and 44.2% (0.1%-98.0%) for pandemic A-H1N1 (20092017). The B lineages co-circulated in 8/10 seasons and there was mismatch with the B vaccine strain in 4/10 seasons. The B virus was dominant in 2007/08 and 2012/13 throughout Spain. There was a combination of dominance/codominance of influenza B and mismatch with the vaccine lineage in at least one third of epidemic seasons reviewed. CONCLUSIONS: Epidemiological information on influenza B has been less compiled in comparison with data on the A virus. Influenza virus type B is responsible for a significant number of cases in almost all seasons. The predominant B lineage in each season is unpredictable, affecting the protection conferred by the seasonal vaccine. Spanish epidemiological data support the rationale for a quadrivalent vaccine with both B virus lineages similarly to data from other settings.

Progressive reduction of sleep time and quality in rats with hepatic encephalopathy caused by portacaval shunts.

Patients with liver cirrhosis show sleep disturbances. Insight into their relationship with hepatic encephalopathy (HE) can be obtained using animal models of HE. The aims of this work were to assess (1) whether rats with portacaval shunts (PCS), a model of HE, show alterations in sleep and if they are similar to those in patients with HE; (2) Whether hyperammonemia plays a role in these sleep alterations; and (3) the time course of sleep alterations in these animal models. Rats were subjected to PCS to induce HE. Another group of rats was fed an ammonium-containing diet to induce hyperammonemia. Polysomnographic recordings were acquired for 24 h and sleep architecture was analyzed in control, PCS, and hyperammonemic rats at 4, 7, and 11 weeks after surgery or diet, respectively. PCS rats show a significant reduction in rapid eye movement (REM) and non-rapid eye movement (NREM) sleep time and increased sleep fragmentation, whereas reduced sleep occurs at 4 weeks and worsens at 7 and 11 weeks, sleep fragmentation appears at 7 weeks and worsens at 11 weeks. Hyperammonemic rats show decreased REM sleep, starting at 7 weeks and worsening at 11 weeks, with no changes in NREM sleep or sleep fragmentation. Therefore, PCS rats are a good model to study sleep alterations in HE, their mechanisms, and potential treatment. Mild hyperammonemia mainly impacts mechanisms involved in REM generation and/or maintenance but does not seem to be involved in sleep fragmentation.

Developmental exposure to polychlorinated biphenyls or methylmercury, but not to its combination, impairs the glutamate-nitric oxide-cyclic GMP pathway and learning in 3-month-old rats.

Prenatal exposure to polychlorinated biphenyls (PCBs) or methylmercury (MeHg) contaminated food may affect brain development, leading to long-term alterations in cognitive function. Both types of contaminants, PCBs and MeHg, are often found together contaminating food, especially fish in some polluted areas. Exposure to combinations of neurotoxicants may exert different effects on the developing nervous system than exposure to individual contaminants. Developmental exposure (during pregnancy and lactation) to PCB126 or PCB153 impairs learning ability when the rats are 3 months old. Impairment of learning seems to be a consequence of impairment of the function of the glutamate-nitric oxide (NO)-cGMP pathway in brain in vivo. The aims of the present work were 1) to assess whether perinatal exposure to MeHg also affects the function of the glutamate-NO-cGMP pathway in brain in vivo analyzed by in vivo brain microdialysis and/or the ability to learn the Y maze task when the rats are 3 months old, and 2) to assess whether perinatal exposure to combinations of MeHg with PCB153 or PCB126 potentiates, decreases or does not modify the effects of the individual neurotoxicants. Perinatal exposure to PCB126, PCB153 or MeHg impaired the function of the glutamate-NO-cGMP pathway in cerebellum and learning ability. However, co-exposure to PCB126+MeHg or PCB153+MeHg inhibits the impairment of the pathway or learning ability. These results support that the function of this pathway modulates learning of the Y maze task. Moreover, they show that co-exposure to these PCBs and MeHg does not exacerbate, but reduces the effects on the ability to learn this task.