The effects of temperature and dispersal on species diversity in natural microbial metacommunities

Dispersal is key for maintaining biodiversity at local- and regional scales in metacommunities. However, little is known about the combined effects of dispersal and climate change on biodiversity. Theory predicts that alpha-diversity is maximized at intermediate dispersal rates, resulting in a hump-shaped diversity-dispersal relationship. This relationship is predicted to flatten when competition increases. We anticipate that this same flattening will occur with increased temperature because, in the rising part of the temperature performance curve, interspecific competition is predicted to increase. We explored this question using aquatic communities of Sarracenia purpurea from early- and late-successional stages, in which we simulated four levels of dispersal and four temperature scenarios. With increased dispersal, the hump shape was observed consistently in late successional communities, but only in higher temperature treatments in early succession. Increased temperature did not flatten the hump-shape relationship, but decreased the level of alpha- and gamma- diversity. Interestingly, higher temperatures negatively impacted small-bodied species. These metacommunity-level extinctions likely relaxed interspecific competition, which could explain the absence of flattening of the diversity-dispersal relationship. Our findings suggest that climate change will cause extinctions both at local- and global- scales and emphasize the importance of intermediate levels of dispersal as an insurance for local diversity

Increased temperature disrupts the biodiversity–ecosystem functioning relationship

Gaining knowledge of how ecosystems provide essential services to humans is of primary importance, especially with the current threat of climate change. Yet little is known about how increased temperature will impact the biodiversity–ecosystem functioning (BEF) relationship. We tackled this subject theoretically and experimentally. We developed a BEF theory based on mechanistic population dynamic models, which allows the inclusion of the effect of temperature. Using experimentally established relationships between attack rate and temperature, the model predicts that temperature increase will intensify competition, and consequently the BEF relationship will flatten or even become negative. We conducted a laboratory experiment with natural microbial microcosms, and the results were in agreement with the model predictions. The experimental results also revealed that an increase in both temperature average and variation had a more intense effect than an increase in temperature average alone. Our results indicate that under climate change, high diversity may not guarantee high ecosystem functioning

Treatment of primary headache in children: a multicenter hospital-based study in France

The aim of this 6-month, prospective, multicenter study of 398 children and adolescents with primary headaches was to collect data on headache treatment in neuropediatric departments. Treatments were compared before and after consultation. Prior to consultation, the acute treatments that had been prescribed most frequently were paracetamol (82.2% of children) and non-steroidal anti-inflammatory drugs treatment (53.5%); 10.3% had received a prophylactic treatment. No differences in either acute or prophylactic treatment with respect to headache diagnosis were observed. After the neuropediatric consultation, paracetamol was replaced by a non-steroidal anti-inflammatory drug in about three-quarters of cases and by triptan in about one-quarter of cases. The number of children prescribed a prophylactic treatment nearly doubled, whereas there was a 5-fold and 23-fold increase in psychotherapy and relaxation training, respectively, between pre-referral and referral. We conclude that specific treatments were underused for primary headache

The ongoing pursuit of neuroprotective therapies in Parkinson disease

Many agents developed for neuroprotective treatment of Parkinson disease (PD) have shown great promise in the laboratory, but none have translated to positive results in patients with PD. Potential neuroprotective drugs, such as ubiquinone, creatine and PYM50028, have failed to show any clinical benefits in recent high-profile clinical trials. This 'failure to translate' is likely to be related primarily to our incomplete understanding of the pathogenic mechanisms underlying PD, and excessive reliance on data from toxin-based animal models to judge which agents should be selected for clinical trials. Restricted resources inevitably mean that difficult compromises must be made in terms of trial design, and reliable estimation of efficacy is further hampered by the absence of validated biomarkers of disease progression. Drug development in PD dementia has been mostly unsuccessful; however, emerging biochemical, genetic and pathological evidence suggests a link between tau and amyloid-β deposition and cognitive decline in PD, potentially opening up new possibilities for therapeutic intervention. This Review discusses the most important 'druggable' disease mechanisms in PD, as well as the most-promising drugs that are being evaluated for their potential efficiency in treatment of motor and cognitive impairments in PD

Data and R codes for the analyses

The file "data.xlsx" contains a description of the variables (sheet "metadata") and data used for the analyses (sheet "data"). The analyses can be performed using the R code provided in the zip file, starting with the R file "data_extraction.R"