Simulated resilience of tropical rainforests to CO2-induced climate change

How tropical forest carbon stocks might alter in response to changes in climate and atmospheric composition is uncertain. However, assessing potential future carbon loss from tropical forests is important for evaluating the efficacy of programmes for reducing emissions from deforestation and degradation. Uncertainties are associated with different carbon stock responses in models with different representations of vegetation processes on the one hand 1, 2, 3, and differences in projected changes in temperature and precipitation patterns on the other hand 4, 5. Here we present a systematic exploration of these sources of uncertainty, along with uncertainty arising from different emissions scenarios for all three main tropical forest regions: the Americas (that is, Amazonia and Central America), Africa and Asia. Using simulations with 22 climate models and the MOSES–TRIFFID land surface scheme, we find that only in one 5 of the simulations are tropical forests projected to lose biomass by the end of the twenty-first century—and then only for the Americas. When comparing with alternative models of plant physiological processes 1, 2, we find that the largest uncertainties are associated with plant physiological responses, and then with future emissions scenarios. Uncertainties from differences in the climate projections are significantly smaller. Despite the considerable uncertainties, we conclude that there is evidence of forest resilience for all three regions

Targeting Mitochondrial Defects to Increase Longevity in Animal Models of Neurodegenerative Diseases

International audienceBioenergetic homeostasis is a vital process maintaining cellular health and has primary importance in neuronal cells due to their high energy demand markedly at synapses. Mitochondria, the metabolic hubs of the cells, are the organelles responsible for producing energy in the form of ATP by using nutrients and oxygen. Defects in mitochondrial homeostasis result in energy deprivation and can lead to disrupted neuronal functions. Mitochondrial defects adversely contribute to the pathogenesis of neurodegenerative diseases such as Alzheimer's (AD) and Parkinson's disease (PD). Mitochondrial defects not only include reduced ATP levels but also increased reactive oxygen species (ROS) leading to cellular damage. Here, we detail the mechanisms that lead to neuronal pathologies involving mitochondrial defects. Furthermore, we discuss how to target these mitochondrial defects in order to have beneficial effects as novel and complementary therapeutic avenues in neurodegenerative diseases. The critical evaluation of these strategies and their potential outcome can pave the way for finding novel therapies for neurodegenerative pathologies

Failed hypospadias in paediatric patients

Failed hypospadias refers to any hypospadias repair that leads to complications or causes patient dissatisfaction. The complication rate after hypospadias repairs ranges from 5-70%, but the actual incidence of failed hypospadias is unknown as complications can become apparent many years after surgery and series with lifelong follow-up data do not exist. Moreover, little is known about uncomplicated repairs that fail in terms of patient satisfaction. Risk factors for complications include factors related to the hypospadias (severity of the condition and characteristics of the urethral plate), the patient (age at surgery, endocrine environment, and wound healing impairment), the surgeon (technique selection and surgeon expertise), and the procedure (technical details and postoperative management). The most important factors for preventing complications are surgeon expertise (number of cases treated per year), interposition of a barrier layer between the urethroplasty and the skin, and postoperative urinary drainage. Major complications associated with failed hypospadias include residual curvature, healing complications (preputial dehiscence, glans dehiscence, fistula formation, and urethral breakdown), urethral obstruction (meatal stenosis, urethral stricture, and functional obstruction), urethral diverticula, hairy urethra, and penile skin deficiency