Managing multiple pressures for cetaceans’ conservation with an Ecosystem-Based Marine Spatial Planning approach

Despite the recognized important ecological role that cetaceans play in the marine environment, their protection is still scarcely enforced in the Mediterranean Sea even though this area is strongly threatened by local human pressures and climate change. The piecemeal of knowledge related to cetaceans' ecology and distribution in the basin undermines the capacity of addressing cetaceans' protection and identifying effective conservation strategies. In this study, an Ecosystem-Based Marine Spatial Planning (EB-MSP) approach is applied to assess human pressures on cetaceans and guide the designation of a conservation area in the Gulf of Taranto, Northern Ionian Sea (Central-eastern Mediterranean Sea). The Gulf of Taranto hosts different cetacean species that accomplish important phases of their life in the area. Despite this fact, the gulf does not fall within any area-based management tools (ABMTs) for cetacean conservation. We pin down the Gulf of Taranto being eligible for the designation of diverse ABMTs for conservation, both legally and non-legally binding. Through a risk-based approach, this study explores the cause-effect relationships that link any human activities and pressures exerted in the study area to potential effects on cetaceans, by identifying major drivers of potential impacts. These were found to be underwater noise, marine litter, ship collision, and competition and disturbance on preys. We draw some recommendations based on different sources of available knowledge produced so far in the area (i.e., empirical evidence, scientific and grey literature, and expert judgement) to boost cetaceans’ conservation. Finally, we stress the need of sectoral coordination for the management of human activities by applying an EB-MSP approach and valuing the establishment of an ABMT in the Gulf of Taranto

A 13-Gene DNA Methylation Analysis Using Oral Brushing Specimens as an Indicator of Oral Cancer Risk: A Descriptive Case Report

Analysis of genetic or epigenetic markers from saliva or brushing specimens has been proposed as a diagnostic aid to identify patients at risk of developing oral cancer. However, no reliable non-invasive molecular method for this purpose is commercially available. In the present report, we describe the potential application of a procedure based on a 13-gene DNA methylation analysis using oral brushing samples from a patient affected by oral leukoplakia who developed two metachronous oral carcinomas during the follow-up period. A positive or a negative score was calculated for each brushing sample based on a predefined cut-off value. In this patient, a positive score was detected in the oral leukoplakia diagnosed more than 2 years before the development of oral squamous cell carcinoma and subsequently in clinically healthy mucosa 8 months before the appearance of a secondary tumor. This suggests a potential role of our procedure as an indicator of oral cancer risk

Phylogenomics and systematics of botryllid ascidians, and implications for the evolution of allorecognition

Allorecognition, the ability of an organism to distinguish kin from non-kin, or self from non-self, has been studied extensively in a group of invertebrate chordates, the colonial ascidians called botryllids (Subphylum Tunicata, Class Ascidiacea, Family Styelidae). When two conspecific botryllid colonies come in contact, there are two potential outcomes to an allorecognition reaction: fusion or rejection. The rejection outcome of allorecognition varies by species, and has been classified by type (referred to as R-Type). R-Type is defined according to how far the fusion process progresses before the rejection begins, since the rejection reaction appears as an interference of the fusion process. Here, we map the evolution of R-Types onto an extended and robust phylogeny of the botryllids. In this study, we have reconstructed the largest phylogenomic tree of botryllids, including 97 samples and more than 40 different species, and mapped on it nine of the 13 species for which the R-Type is known. Based on the R-Type known in a single outgroup species (Symplegma reptans), we infer that at least R-Type B and E-like could be ancestral to the Botrylloides/Botryllus group. However, the application of ancestral character state reconstructions does not provide conclusive results since several clades show more than one equiparsimonious R-Type state. Notably, all R-Type A species are clustered together and certainly evolved later than other R-Types. Our phylogenomic tree has been built on 177 nuclear loci and nearly all clades are well supported. Moreover, our phylogenetic analyses also take into account the results of species delimitation analyses based on the mitochondrial COI gene and of careful morphological analyses of the samples. The implementation of this integrated taxonomic approach, combining morphological as well as nuclear and mitochondrial data, has allowed the description of six new species, and the identification of a number of putative unnamed taxa. Thus, our results also demonstrate the existence of an unexplored hidden diversity within botryllids

CD200 as a Potential New Player in Inflammation during Rotator Cuff Tendon Injury/Repair: An In Vitro Model

Rotator cuff tendon (RCT) disease results from multifactorial mechanisms, in which inflammation plays a key role. Pro-inflammatory cytokines and tendon stem cell/progenitor cells (TSPCs) have been shown to participate in the inflammatory response. However, the underlying molecular mechanism is still not clear. In this study, flow cytometry analyses of different subpopulations of RCT-derived TSPCs demonstrate that after three days of administration, TNFα alone or in combination with IFNγ significantly decreases the percentage of CD146+CD49d+ and CD146+CD49f+ but not CD146+CD109+ TSPCs populations. In parallel, the same pro-inflammatory cytokines upregulate the expression of CD200 in the CD146+ TSPCs population. Additionally, the TNFα/IFNγ combination modulates the protein expression of STAT1, STAT3, and MMP9, but not fibromodulin. At the gene level, IRF1, CAAT (CAAT/EBPbeta), and DOK2 but not NF-κb, TGRF2 (TGFBR2), and RAS-GAP are modulated. In conclusion, although our study has several important limitations, the results highlight a new potential role of CD200 in regulating inflammation during tendon injuries. In addition, the genes analyzed here might be new potential players in the inflammatory response of TSPCs

Bioinformatics in Italy : BITS 2012, the ninth annual meeting of the Italian Society of Bioinformatics

The BITS2012 meeting, held in Catania on May 2-4, 2012, brought together almost 100 Italian researchers working in the field of Bioinformatics, as well as students in the same or related disciplines. About 90 original research works were presented either as oral communication or as posters, representing a landscape of Italian current research in bioinformatics.This preface provides a brief overview of the meeting and introduces the manuscripts that were accepted for publication in this supplement, after a strict and careful peer-review by an International board of referees

Glufosinate constrains synchronous and metachronous metastasis by promoting anti-tumor macrophages

Abstract Glutamine synthetase (GS) generates glutamine from glutamate and controls the release of inflammatory mediators. In macrophages, GS activity, driven by IL10, associates to the acquisition of M2‐like functions. Conditional deletion of GS in macrophages inhibits metastasis by boosting the formation of anti‐tumor, M1‐like, tumor‐associated macrophages (TAMs). From this basis, we evaluated the pharmacological potential of GS inhibitors in targeting metastasis, identifying glufosinate as a specific human GS inhibitor. Glufosinate was tested in both cultured macrophages and on mice bearing metastatic lung, skin and breast cancer. We found that glufosinate rewires macrophages toward an M1‐like phenotype both at the primary tumor and metastatic site, countering immunosuppression and promoting vessel sprouting. This was also accompanied to a reduction in cancer cell intravasation and extravasation, leading to synchronous and metachronous metastasis growth inhibition, but no effects on primary tumor growth. Glufosinate treatment was well‐tolerated, without liver and brain toxicity, nor hematopoietic defects. These results identify GS as a druggable enzyme to rewire macrophage functions and highlight the potential of targeting metabolic checkpoints in macrophages to treat cancer metastasis