Ecosystem processes: litter breakdown patterns in Mediterranean and Black Sea transitional waters

1 - Leaf litter decomposition rates, in aquatic ecosystems, are known to be related to many different abiotic and biotic factors. 2 - Here, we focus on the influence of abiotic factors, searching for patterns of reed litter decay rates on gradient of physiographic, hydrological and physico-chemical components of transitional water ecosystems. 3 - Field experiments were carried out in 16 water ecosystems in the Eastern Mediterranean and Black Sea in spring 2005. 4 - Significant differences of leaf litter decomposition were observed among ecosystems along univariate gradient of tidal range, index of sinuosity, water temperature and salinity. At least 71% of variance in the litter breakdown rate was explained by the considered abiotic factors. 5 - It is concluded that, at the macro-ecological scale of study, some key abiotic factors, such as tidal range and salinity, are suggested to play a major role as drivers of plant detritus decomposition processes. 6 - The relevance of the described abiotic drivers as descriptor of the most commonly used classification schemes for transitional water ecosystems (i.e., Confinement and Venice System classifications), is a further support to their role as environmental forcing factors

Rabphilin 3A: A novel target for the treatment of levodopa-induced dyskinesias

N-methyl-d-aspartate receptor (NMDAR) subunit composition strictly commands receptor function and pharmacological responses. Changes in NMDAR subunit composition have been documented in brain disorders such as Parkinson's disease (PD) and levodopa (L-DOPA)-induced dyskinesias (LIDs), where an increase of NMDAR GluN2A/GluN2B subunit ratio at striatal synapses has been observed. A therapeutic approach aimed at rebalancing NMDAR synaptic composition represents a valuable strategy for PD and LIDs. To this, the comprehension of the molecular mechanisms regulating the synaptic localization of different NMDAR subtypes is required. We have recently demonstrated that Rabphilin 3A (Rph3A) is a new binding partner of NMDARs containing the GluN2A subunit and that it plays a crucial function in the synaptic stabilization of these receptors. Considering that protein-protein interactions govern the synaptic retention of NMDARs, the purpose of this work was to analyse the role of Rph3A and Rph3A/NMDAR complex in PD and LIDs, and to modulate Rph3A/GluN2A interaction to counteract the aberrant motor behaviour associated to chronic L-DOPA administration. Thus, an array of biochemical, immunohistochemical and pharmacological tools together with electron microscopy were applied in this study. Here we found that Rph3A is localized at the striatal postsynaptic density where it interacts with GluN2A. Notably, Rph3A expression at the synapse and its interaction with GluN2A-containing NMDARs were increased in parkinsonian rats displaying a dyskinetic profile. Acute treatment of dyskinetic animals with a cell-permeable peptide able to interfere with Rph3A/GluN2A binding significantly reduced their abnormal motor behaviour. Altogether, our findings indicate that Rph3A activity is linked to the aberrant synaptic localization of GluN2A-expressing NMDARs characterizing LIDs. Thus, we suggest that Rph3A/GluN2A complex could represent an innovative therapeutic target for those pathological conditions where NMDAR composition is significantly altered

Sonographic assessment of abdominal fat distribution in infancy

There is growing evidence that not only the total amount of fat, but also the distribution of body fat determines risks for metabolic and cardiovascular disease. Developmental studies on factors influencing body fat distribution have been hampered by a lack of appropriate techniques for measuring intraabdominal fat in early life. Sonography, which is an established method for assessing abdominal fat distribution in adults, has not yet been evaluated in infants. To adapt the sonographic measurement of abdominal fat distribution to infants and study its reliability. The Generation R study, a population-based prospective cohort study. We included 212 one- and 227 two-year old Dutch infants in the present analysis. Sixty-two infants underwent replicate measurements to assess reproducibility. We developed a standardized protocol to measure the thickness of (1) subcutaneous and (2) preperitoneal fat in the upper abdomen of infants. To this end we defined infancy specific measurement areas to quantify fat thickness. Reproducibility of fat measurements was good to excellent with intraclass correlation coefficients of 0.93–0.97 for intra-observer agreement and of 0.89–0.95 for inter-observer agreement. We observed a pronounced increase in preperitoneal fat thickness in the second year of life while subcutaneous fat thickness increased only slightly, resulting in an altered body fat distribution. Gender did not significantly influence fat distribution in the first two years of life. Our age specific protocol for the sonographic measurement of central subcutaneous and preperitoneal fat is a reproducible method that can be instrumental for investigating fat distribution in early life

Cannabinoid receptor gene detection by electrochemical genosensor

This paper describes the investigation of two aspects which play a fundamental role in the development of an enzyme-linked electrochemical genosensor: the labelling step and the electrode surface. Biotinylated locked nucleic acid (LNA) signalling probes were investigated in order to design a sandwich hybridisation format able to detect PCR amplified samples with high specificity. After labelling the biotinylated hybrid with a streptavidin-enzyme conjugate, the electrochemical detection of the enzymatic product was performed onto the surface of disposable carbon nanotube-modified electrode. In this way, the sensor coupled the high stability and specificity of LNA with the unique electrical properties of carbon nanotubes (high surface area, fast heterogeneous electron transfer, chemical stability, and ease of miniaturisation). After characterisation, the sensor was applied to the detection of PCR amplicons related to a region of the CB2 cannabinoid receptor gene (CNR2), which is relevant for the study of a mutation suspected to account for altered receptor activity. To our knowledge, this is the first example of recognition of this particular gene in real samples, using a LNA-based electrochemical genosensor. A linear response was obtained over a wide concentration range (0-100 nmol/L) and a detection limit of 0.4 nmol/L was achieved (RDS = 9%)

Differences in circulating microRNA signature in prader\u2013willi syndrome and non-syndromic obesity

Prader\u2013Willi syndrome (PWS) represents the most common genetic-derived obesity disorder caused by the loss of expression of genes located on the paternal chromosome 15q11.2-q13. The PWS phenotype shows peculiar physical, endocrine and metabolic characteristics compared to those observed in non-syndromic essential obesity. Since miRNAs have now a well-established role in many molecular pathways, including regulatory networks related to obesity, this pilot study was aimed to characterize the expression of circulating miRNAs in PWS compared to essential obesity. The circulating miRNome of 10 PWS and 10 obese subjects, adequately matched for age, BMI and sex, was profiled throughout Genechip miRNA 4.0 microarray analysis. We identified 362 out of 2578 mature miRNAs to be expressed in serum of the studied population. The circulating miRNA signature significantly characterising the two populations include 34 differently expressed RNAs. Among them, miR-24-3p, miR-122 and miR-23a-3p highly differ between the two groups with a FC >10 in obese compared to PWS. In the obese subjects, miR-7107-5p, miR-6880-3p, miR-6793-3p and miR-4258 were associated to the presence of steatosis. A different signature of miRNAs significantly distinguished PWS with steatosis from PWS without steatosis, involving miR-619-5p, miR-4507, miR-4656, miR-7847-3p and miR-6782-5p. The miRNA target GO enrichment analysis showed the different pathway involved in these two different forms of obesity. Although the rarity of PWS actually represents a limitation to the availability of large series, the present study provides novel hints on the molecular pathogenesis of syndromic and non-syndromic obesity