Voltage-gated potassium currents within the dorsal vagal nucleus: inhibition by BDS toxin

Voltage-gated potassium (Kv) channels are essential components of neuronal excitability. The Kv3.4 channel protein is widely distributed throughout the central nervous system (CNS), where it can form heteromeric or homomeric Kv3 channels. Electrophysiological studies reported here highlight a functional role for this channel protein within neurons of the dorsal vagal nucleus (DVN). Current clamp experiments revealed that blood depressing substance (BDS) and intracellular dialysis of an anti-Kv3.4 antibody prolonged the action potential duration. In addition, a BDS sensitive, voltage-dependent, slowly inactivating outward current was observed in voltage clamp recordings from DVN neurons. Electrical stimulation of the solitary tract evoked EPSPs and IPSPs in DVN neurons and BDS increased the average amplitude and decreased the paired pulse ratio, consistent with a presynaptic site of action. This presynaptic modulation was action potential dependent as revealed by ongoing synaptic activity. Given the role of the Kv3 proteins in shaping neuronal excitability, these data highlight a role for homomeric Kv3.4 channels in spike timing and neurotransmitter release in low frequency firing neurons of the DVN.

On the voltage and distance across the low latitude boundary layer

A pass of the AMPTE-UKS satellite through the low-latitude boundary layer (LLBL) at 8:30 MLT is studied in detail. The magnetosheath field is predominantly northward. It is shown that multiple transitions through part or all of the layer of antisunward flow lead to overestimation of both the voltage across this layer and its width. The voltage is estimated to be only about 3 kV and this implies that the full LLBL is about 1200 km thick, consistent with previous studies.

The role of root exuded low molecular weight organic anions in facilitating petroleum hydrocarbon degradation: current knowledge and future directions

Rhizoremediation is a bioremediation technique whereby enhanced microbial degradation of organic contaminants occurs within the plant root zone (rhizosphere). It is considered an effective and affordable ‘green technology’ for remediating soils contaminated with petroleum hydrocarbons (PHCs). This paper critically reviews the potential role of root exuded compounds in rhizoremediation, with emphasis on commonly exuded low molecular weight aliphatic organic acid anions (carboxylates). The extent to which remediation is achieved shows wide disparity among plant species. Therefore, plant selection is crucial for the advancement and widespread adoption of this technology. Root exudation is speculated to be one of the predominant factors leading to microbial changes in the rhizosphere and thus the potential driver behind enhanced petroleum biodegradation. Carboxylates can form a significant component of the root exudate mixture and are hypothesised to enhance petroleum biodegradation by: i) providing an easily degradable energy source; ii) increasing phosphorus supply; and/or iii) enhancing the contaminant bioavailability. These differing hypotheses, which are not mutually exclusive, require further investigation to progress our understanding of plant–microbe interactions with the aim to improve plant species selection and the efficacy of rhizoremediation.

Low-grade inflammation, diet composition and health: current research evidence and its translation

The importance of chronic low-grade inflammation in the pathology of numerous age-related chronic conditions is now clear. An unresolved inflammatory response is likely to be involved from the early stages of disease development. The present position paper is the most recent in a series produced by the International Life Sciences Institute's European Branch (ILSI Europe). It is co-authored by the speakers from a 2013 workshop led by the Obesity and Diabetes Task Force entitled ‘Low-grade inflammation, a high-grade challenge: biomarkers and modulation by dietary strategies’. The latest research in the areas of acute and chronic inflammation and cardiometabolic, gut and cognitive health is presented along with the cellular and molecular mechanisms underlying inflammation–health/disease associations. The evidence relating diet composition and early-life nutrition to inflammatory status is reviewed. Human epidemiological and intervention data are thus far heavily reliant on the measurement of inflammatory markers in the circulation, and in particular cytokines in the fasting state, which are recognised as an insensitive and highly variable index of tissue inflammation. Potential novel kinetic and integrated approaches to capture inflammatory status in humans are discussed. Such approaches are likely to provide a more discriminating means of quantifying inflammation–health/disease associations, and the ability of diet to positively modulate inflammation and provide the much needed evidence to develop research portfolios that will inform new product development and associated health claims.