Trends and patterns in annually burned forest areas and fire weather across the European boreal zone in the 20th and early 21st centuries

Fire remains one of the main natural disturbance factors in the European boreal zone and understanding climatic forcing on fire activity is important for projecting effects of climate change on ecosystem services in this region. We analyzed records of annually burned areas in 16 administrative regions of the European boreal zone (countries or administrative units within countries) and fire weather variability to test for their spatio-temporal patterns over the 1901-2017 period.Over the 1992-2017 period, the region exhibited large variability in forest fire activity with the fire cycles varying from similar to 1600 (St. Petersburg region) to similar to 37000 years (Finland). The clustering of administrative units in respect to their burned area, suggested the presence of sub-regions with synchronous annual variability in burned areas. Large fire years (LFYs) in each of the clusters were associated with the development of the high pressure cell over or in immediate proximity of the regions in question in July, indicating climatic forcing of LFYs. Contingency analysis indicated that there was no long-term trend in the synchrony of LFYs observed simultaneously in several administrative units. We documented a trend towards higher values of Monthly Drought Code (MDC) for the months of April and May in the western (April) and northern (April and May) sections. The significant positive correlation between biome-wide fire activity index and June SNAO (Summer North Atlantic Oscillation) (r = 0.53) pointed to the importance of large-scale atmospheric circulation, in particular the summer European blocking pattern, in controlling forest fires across EBZ. The forest fire activity of the European boreal zone remains strongly connected to the annual climate variability. Higher frequency of strongly positive SNAO states in the future will likely synchronize years with a large area burned across the European boreal zone

The role of inflammation in epilepsy.

Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the approximately 30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators-released by brain cells and peripheral immune cells-in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis

The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia : design, results and future prospects

The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.Peer reviewe