Event related potentials reveal that increasing perceptual load leads to increased responses for target stimuli and decreased responses for irrelevant stimuli

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Towards incorporation of blue carbon in Falkland Islands marine spatial planning: a multi-tiered approach

Ecosystem-based conservation that includes carbon sinks, alongside a linked carbon credit system, as part of a nature-based solution to combating climate change, could help reduce greenhouse gas levels and therefore the impact of their emissions. Blue carbon habitats and pathways can also facilitate biodiversity retention, aiding sustainable fisheries and island economies. However, robust blue carbon research is often limited at the scale of regional governance and management, lacking both incentives and facilitation of policy-integration. The remote and highly biodiverse coastal ecosystems and surrounding continental shelf can be used to better inform long-term ecosystem-based management in the vast South Atlantic Ocean and sub-Antarctic, to synergistically protect both unique biodiversity and inform on the magnitude of nature-based benefits they provide. Understanding key ecosystem information such as their location, extent, and condition of habitat types, will be critical in understanding carbon pathways to sequestration, threats to this, and vulnerability. This paper considers the current status of blue carbon data and information available, and what is still required before blue carbon can be used as a conservation management tool integrated in national Marine Spatial Planning (MSP) initiatives. Our research indicates that the data and information gathered has enabled baselines for a number of different blue carbon ecosystems, and indicated potential threats and vulnerability that need to be managed. However, significant knowledge gaps remain across habitats, such as salt marsh, mudflats and the mesophotic zones, which hinders meaningful progress on the ground where it is needed most

Aldosterone Antagonists in Monotherapy Are Protective against Streptozotocin-Induced Diabetic Nephropathy in Rats

Angiotensin converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARB) are the standard clinical therapy of diabetic nephropathy (DN), while aldosterone antagonists are only used as adjuncts. Previously in experimental DN we showed that Na/K ATPase (NKA) is mislocated and angiotensin II leads to superimposed renal progression. Here we investigated the monotherapeutic effect of aldosterone blockers on the progression of DN and renal NKA alteration in comparison to ACEi and ARBs. Streptozotocin-diabetic rats developing DN were treated with aldosterone antagonists; ACEi and ARB. Renal function, morphology, protein level and tubular localization of NKA were analyzed. To evaluate the effect of high glucose per se; HK-2 proximal tubular cells were cultured in normal or high concentration of glucose and treated with the same agents. Aldosterone antagonists were the most effective in ameliorating functional and structural kidney damage and they normalized diabetes induced bradycardia and weight loss. Aldosterone blockers also prevented hyperglycemia and diabetes induced increase in NKA protein level and enzyme mislocation. A monotherapy with aldosterone antagonists might be as, or more effective than ACEi or ARBs in the prevention of STZ-induced DN. Furthermore the alteration of the NKA could represent a novel pathophysiological feature of DN and might serve as an additional target of aldosterone blockers

Dysregulation of CXC motif ligand 10 during aging and association with cognitive performance

Chronic low-grade inflammation during aging (inflammaging) is associated with cognitive decline and neurodegeneration, however, the mechanisms underlying inflammaging are unclear. We studied a population (n = 361) of healthy young and old adults from the MyoAge cohort. Peripheral levels of C-X-C motif chemokine 10 (CXCL10) was found to be higher in older adults, compared with young, and negatively associated with working memory performance. This coincided with an age-related reduction in blood DNA methylation at specific CpGs within the CXCL10 gene promoter. In vitro analysis supported the role of DNA methylation in regulating CXCL10 transcription. A polymorphism (rs56061981) that altered methylation at one of these CpG sites further associated with working memory performance in two independent aging cohorts. Studying prefrontal cortex samples, we found higher CXCL10 protein levels in those with Alzheimer’s disease, compared to aged controls. These findings support the association of peripheral inflammation, as demonstrated by CXCL10, in aging and cognitive decline. We reveal age-related epigenetic and genetic factors which contribute to the dysregulation of CXCL10