A complex species complex: The controversial role of ecology and biogeography in the evolutionary history of Syllis gracilis Grube, 1840 (Annelida,Syllidae)

The cryptic diversity in the polychaete Syllis gracilis Grube, 1840, in the Mediterranean Sea was examined with an integrative morpho-molecular approach. Individuals of S. gracilis were collected at eleven Mediterranean localities to provide an insight into the role of brackish environments in inducing cryptic speciation. The examination of morphological features combined with a molecular genetic analysis based on a partial sequence of the 16S rRNA gene highlighted discrepancies between morphological and molecular diversity. Morphological data allowed to identify a morphotype with short appendages occurring in coralline algae communities and another one with long appendages observed in brackish-water environments and Sabellaria reefs. Multivariate analyses showed that sampling localities were the greatest source of morphological divergence, suggesting that phenotypic plasticity may play a role in local adaptations of S. gracilis populations. Molecular data showed the occurrence of four divergent lineages not corresponding to morphological clusters. Different species delimitation tests gave conflicting results, retrieving, however, at least four separated entities. Some lineages occurred in sympatry and were equally distributed in marine and brackish-water environments, excluding a biogeographic or ecological explanation of the observed pattern and suggesting instead ancient separation between lineages and secondary contact. The co-occurrence of different lineages hindered the identification of the lineage corresponding to S. gracilis sensu stricto. The discrepancy between morphological and molecular diversity suggests that different environmental and biogeographic features may interact in a complex and unpredictable way in shaping diversity patterns. An integrative approach is needed to provide a satisfactory insight on evolutionary processes in marine invertebrates.     

The mode of action of Aescin and the release of prostaglandins

The horse-chestnut saponin Aescin, an anti-exudative compound, induces contraction of isolated portal vein of rat and rabbit. This effect appears to be mediated by Prostaglandins of F_α type.The ability of Aescin to stimulate generation and release of Prostaglandins has been demonstrated in isolated lung of the rat. Mass-fragmentographic analysis of the lung effluent indicate that when Aescin is perfused through this organ the release of PGF_2α is increased. The capability of Aescin to generate Prostaglandins is discussed in connection with its anti-exudative activity.     

Spatial genetic patterns of Octopus vulgaris Mediterranean populations support the hypothesis of a transitional zone across the Siculo-Tunisian Strait

Hydrobiologia - Recent research hypothesised that the Siculo-Tunisian Strait might fit, at least for some species, the picture of a genetic transitional zone instead of a sharp genetic break...     

Phylogeography of Aphanius fasciatus (Osteichthyes: Aphaniidae) in the Mediterranean Sea,with a focus on its conservation in Cyprus

Hydrobiologia - Aphanius fasciatus is a small fish occurring in Mediterranean brackish environments. In Cyprus it is known from three localities separated by long stretches of coast. The genetic...     

New echocardiographic techniques in the evaluation of left ventricular function in obesity

Objective:

Obesity has reached global epidemic proportions and is associated with numerous comorbidities, including major cardiovascular (CV) diseases.

Design and Methods:

It has many adverse effects on hemodynamics and CV structure and function: it increases total blood volume and cardiac output, and the cardiac workload is greater. Typically, obese patients have a higher cardiac output but a lower level of total peripheral resistance at any given level of arterial pressure. Most of the increase in cardiac output in obesity is caused by stroke volume, although heart rate typically mildly increases also due to enhanced sympathetic activation.

Results:

Over the last few years, experimental investigations have unraveled some important pathogenetic mechanisms that may underlie a specific form of “obesity cardiomyopathy.” Bariatric surgery represents an effective alternative to treat obesity when nonsurgical weight loss programs (diet + behavior modifications + regular exercise) have failed. A great numbers of questions are still open in the global comprehension of the pathophysiological interactions between obesity and heart.

Conclusion:

Conventional two‐dimensional Doppler echocardiography, integrated by relative new technological ultrasonic approaches, represents the reference technique to study and possibly clarify both the very complex hemodynamic changes induced by obesity and those relative to obesity treatment.     

Cigarette smoke metabolically promotes cancer,via autophagy and premature aging in the host stromal microenvironment

Cigarette smoke has been directly implicated in the disease pathogenesis of a plethora of different human cancer subtypes, including breast cancers. The prevailing view is that cigarette smoke acts as a mutagen and DNA damaging agent in normal epithelial cells, driving tumor initiation. However, its potential negative metabolic effects on the normal stromal microenvironment have been largely ignored. Here, we propose a new mechanism by which carcinogen-rich cigarette smoke may promote cancer growth, by metabolically “fertilizing” the host microenvironment. More specifically, we show that cigarette smoke exposure is indeed sufficient to drive the onset of the cancer-associated fibroblast phenotype via the induction of DNA damage, autophagy and mitophagy in the tumor stroma. In turn, cigarette smoke exposure induces premature aging and mitochondrial dysfunction in stromal fibroblasts, leading to the secretion of high-energy mitochondrial fuels, such as L-lactate and ketone bodies. Hence, cigarette smoke induces catabolism in the local microenvironment, directly fueling oxidative mitochondrial metabolism (OXPHOS) in neighboring epithelial cancer cells, actively promoting anabolic tumor growth. Remarkably, these autophagic-senescent fibroblasts increased breast cancer tumor growth in vivo by up to 4-fold. Importantly, we show that cigarette smoke-induced metabolic reprogramming of the fibroblastic stroma occurs independently of tumor neo-angiogenesis. We discuss the possible implications of our current findings for the prevention of aging-associated human diseases and, especially, common epithelial cancers, as we show that cigarette smoke can systemically accelerate aging in the host microenvironment. Finally, our current findings are consistent with the idea that cigarette smoke induces the “reverse Warburg effect,” thereby fueling “two-compartment tumor metabolism” and oxidative mitochondrial metabolism in epithelial cancer cells.     

Genetic determinants of glutamine synthetase inDrosophila melanogaster: A gene for glutamine synthetase I resides in the 21B3-6 region

Recombinational and deletion mapping of electrophoretic variants of the glutamine synthetase I isozyme (GSI) in Drosophila melanogaster locates the gene in the 21B region on the second chromosome. We have conducted a genetic analysis of the region extending cytologically from 21A to 21B4-6. Recessive lethal mutations were generated by ethyl methanesulfonate (EMS) and ethyl nitrosourea (ENU) mutagenesis and by hybrid dysgenesis (HD). These lethals fall into seven functional groups, which were partially ordered by complementation with cytologically defined deficiencies of this region generated by hybrid dysgenesis. Two of the EMS- and two of the ENU-induced lethals fulfill biochemical criteria expected for null alleles of the GSI gene.