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Methane (CH4) strongly contributes to observed global warming. As natural CH4 emissions mainly originate from wet ecosystems, it is important to unravel how climate change may affect these emissions. This is especially true for ebullition (bubble flux from sediments), a pathway that has long been underestimated but generally dominates emissions. Here we show a remarkably strong relationship between CH4 ebullition and temperature across a wide range of freshwater ecosystems on different continents using multi-seasonal CH4 ebullition data from the literature. As these temperature–ebullition relationships may have been affected by seasonal variation in organic matter availability, we also conducted a controlled year-round mesocosm experiment. Here 4 °C warming led to 51% higher total annual CH4 ebullition, while diffusion was not affected. Our combined findings suggest that global warming will strongly enhance freshwater CH4 emissions through a disproportional increase in ebullition (6–20% per 1 °C increase), contributing to global warming., The impacts of climate change on natural methane (CH4) emissions via ebullition are unclear. Here, using published and experimental multi-seasonal CH4 ebullition data, the authors find a strong relationship between CH4 ebullition and temperature across a wide range of freshwater ecosystems globally.

Introduction: Tumours with chest wall invasion form a distinct sub-entity in the heterogeneuous group of locally advanced NSCLC. Despite some available evidence, the best sequence of recommended multimodal therapeutic approaches continues to be subjet of clinical research in view of the improved possibilities of radiation and systemic therapies. Material and Methods: In our mono-centric, retrospective observational study, all NSCLC pts. with chest wall infiltration or pancoast tumour (N0-2, M0), diagnosed between 01/2009 and 12/2013, were analyzed using our hospital information system and cancer registry. Clinical, radiological, tumour biological, therapeutic and follow-up data were recorded for this study. Results: In the 5 year period, 81 pts. were detected with chest wall invasion and pancoast in 72 and 9 pts., respectively. Mean age was 66.4 yrs. (45.7-84,7 yrs.). Histology was dominated by squamous cell (53.1%) and adenocarcinoma (32.1%), followed by large cell carc. (6.2%). Theraputic regimes were: 1. neoadjuvant Tx.+resection (22 pts., 27.2%), 2. planned neoadj. Tx. with change to definite chemoradiotherapy due to progression (13. pts., 16.0%), 3. resection+adjuv. Tx (25 pts., 30.8%), 4. primary definite chemoradiotherapy (19 pts., 23.5%) and 5. best-supportive care only (2 pts., 2.5%). Best median 5-year overall survival was seen in the cohort with neoadjuvant Tx.+resection (11.6-153.4 months) (fig. 1). Discussion: Our retrospective data underline the prognostic significance of neoadjuvant tx followed by resection as treatment regimen in NSCLC with chest wall invasion. However, patient and tumour characteristics havinfluence the choice of treatment.

Knowledge on pediatric herpes simplex virus encephalitis is limited. Here we summarize 6 neonates and 32 children diagnosed by polymerase chain reaction (n = 37) or serological studies (n = 1), respectively. Diagnosis was difficult, as only 15 patients presented neurologic symptoms. Moreover, cerebrospinal fluid glucose, protein, and leukocytes were normal in 6 patients. Subsequently, all but 2 showed neurologic symptoms. Diffusion-weighted neuroimaging was the most sensitive early imaging method. Despite acyclovir treatment, 8 patients experienced early relapses, showing movement abnormalities, impaired vigilance, and seizures. Diffuse white matter changes, found in 3 of 5 relapse patients on neuroimaging, and a negative cerebrospinal fluid herpes simplex virus polymerase chain reaction suggested inflammatory processes. All relapse patients were again treated with acyclovir, and 3 responded to additional corticosteroid treatment. Whereas outcome after relapses was poor, overall outcome was good. No child died; 14 were asymptomatic at discharge, and neuroimaging remained normal in 7 of 30 patients studied.

Pendrin (SLC26A4, PDS) is an electroneutral anion exchanger transporting I(-), Cl(-), HCO(3)(-), OH(-), SCN(-) and formate. In the thyroid, pendrin is expressed at the apical membrane of the follicular epithelium and may be involved in mediating apical iodide efflux into the follicle; in the inner ear, it plays a crucial role in the conditioning of the pH and ion composition of the endolymph; in the kidney, it may exert a role in pH homeostasis and regulation of blood pressure. Mutations of the pendrin gene can lead to syndromic and non-syndromic hearing loss with EVA (enlarged vestibular aqueduct). Functional tests of mutated pendrin allelic variants found in patients with Pendred syndrome or non-syndromic EVA (ns-EVA) revealed that the pathological phenotype is due to the reduction or loss of function of the ion transport activity. The diagnosis of Pendred syndrome and ns-EVA can be difficult because of the presence of phenocopies of Pendred syndrome and benign polymorphisms occurring in the general population. As a consequence, defining whether or not an allelic variant is pathogenic is crucial. Recently, we found that the two parameters used so far to assess the pathogenic potential of a mutation, i.e. low incidence in the control population, and substitution of evolutionary conserved amino acids, are not always reliable for predicting the functionality of pendrin allelic variants; actually, we identified mutations occurring with the same frequency in the cohort of hearing impaired patients and in the control group of normal hearing individuals. Moreover, we identified functional polymorphisms affecting highly conserved amino acids. As a general rule however, we observed a complete loss of function for all truncations and amino acid substitutions involving a proline. In this view, clinical and radiological studies should be combined with genetic and molecular studies for a definitive diagnosis. In performing genetic studies, the possibility that the mutation could affect regions other than the pendrin coding region, such as its promoter region and/or the coding regions of functionally related genes (FOXI1, KCNJ10), should be taken into account. The presence of benign polymorphisms in the population suggests that genetic studies should be corroborated by functional studies; in this context, the existence of hypo-functional variants and possible differences between the I(-)/Cl(-) and Cl(-)/HCO(3)(-) exchange activities should be carefully evaluated.