Marine alien species in Greek Seas: Additions and amendments by 2010

An update of the inventory of alien marine species from the coastal and offshore waters of Greece is presented. Records were compiled based on the existing scientific and grey literature, including the HCMR database of Greek alien species (ELNAIS), technical reports, scientific congresses, academic dissertations, websites, and unpublished/personal observations. 47 species were added to the inventory, including 34 invertebrates, one vertebrate (fish), three plants, eight protozoa, and one cyanobacterium. With the new records, the inventory of alien marine species of Greece now includes a total of 237 species (33 macrophytes, 131 invertebrates, 42 vertebrates, two bacteria and 29 protozoans). Among these, the presence of the gastropodHypselodoris infucata, the bivalvesDendrostrea frons and Septifer forskaliand the chondrichthyan Rhizoprionodon acutus is reported here for the first time. Based on molecular analysis, the occurrence of Bulla arabica in Greek waters is confirmed, and the suggestion that previous records of Bulla ampulla in the Mediterranean should be considered as misidentification of B. arabica is further supported. The acclimitization status of earlier records was revised in the light of new data, and thus the fishEnchelycore anatina, Seriola fasciata andTylerius spinosissimus, the red algaeHypnea cornuta and Sarconema scinaioides, the scyphomedusaCassiopea andromeda, the cephalopodSepioteuthis lessoniana, the nudibranchChromodoris annulata and the bivalvesGastrochaena cymbium andPseudochama corbieri were upgraded from casual records to established populations. The increased rate of introductions of warm water species confirms previous findings, which link the rate of introduction in the eastern Mediterranean to climate change

Assessment of goods and services, vulnerability, and conservation status of European seabed biotopes: a stepping stone towards ecosystem-based marine spatial management

The goal of ecosystem-based marine spatial management is to maintain marine ecosystems in a healthy, productive and resilient condition; hence, they can sustainably provide the needed goods and services for human welfare. However, the increasing pressures upon the marine realm threaten marine ecosystems, especially seabed biotopes, and thus a well-planned approach of managing use of marine space is essential to achieve sustainability. The relative value of seabed biotopes, evaluated on the basis of goods and services, is an important starting point for the spatial management of marine areas. Herein, 56 types of European seabed biotopes and their related goods, services, sensitivity issues, and conservation status were compiled, the latter referring to management and protection tools which currently apply for these biotopes at European or international level. Fishing activities, especially by benthic trawls, and marine pollution are the main threats to European seabed biotopes. Increased seawater turbidity, dredged sediment disposal, coastal constructions, biological invasions, mining, extraction of raw materials, shipping-related activities, tourism, hydrocarbon exploration, and even some practices of scientific research, also exert substantial pressure. Although some first steps have been taken to protect the European sea beds through international agreements and European and national legislation, a finer scale of classification and assessment of marine biotopes is considered crucial in shaping sound priorities and management guidelines towards the effective conservation and sustainability of European marine resources

Upregulation of p16INK4A and Bax in p53 wild/p53-overexpressing crypts in ulcerative colitis-associated tumours

In ulcerative colitis (UC)-associated tumours, p53 gene mutations and p53 protein overexpression are frequently found in early stages, but the two types of alteration do not always coincide. To clarify this discrepancy, p53 mutations and expression of p53-associated molecules were analysed in UC-associated dysplasias by a combination of microdissection, polymerase chain reaction-direct sequencing and immunohistochemistry at the single crypt level. Mismatch of p53 protein overexpression (+)/mutation (−) or p53 overexpression (−)/gene mutation (+) was found in nine crypts in regenerative mucosa (19 crypts), in 27 in low-grade dysplasia (41), in one in high-grade dysplasia (5) and in 12 in invasive carcinomas (17). Regarding these mismatched crypts of the first type, significant increase in p16INK4A and Bax expression was found. The Ki-67 labelling index was depressed in such p53-diffusely positive lesions with the wild-type p53 gene, compared to their p53-diffusely positive and mutant type counterparts. p16INK4A was upregulated indirectly as part of the negative feedback, and increase in Bax, directly controlled by wild-type p53, indicates upregulation of apoptosis. No significant relation with p53-related gene products was detected with the p53 protein overexpression (−)/p53 mutation (+) mismatch. Therefore, a tumorigenesis pathway independent of p53 dysfunction appears to exist in association with ulcerative colitis

Chemopreventive potential of β-Sitosterol in experimental colon cancer model - an In vitro and In vivo study

<p>Abstract</p> <p>Background</p> <p><it>Asclepias curassavica </it>Linn. is a traditional medicinal plant used by tribal people in the western ghats, India, to treat piles, gonorrhoea, roundworm infestation and abdominal tumours. We have determined the protective effect of β-sitosterol isolated from <it>A. curassavica </it>in colon cancer, using <it>in vitro </it>and <it>in vivo </it>models.</p> <p>Methods</p> <p>The active molecule was isolated, based upon bioassay guided fractionation, and identified as β-sitosterol on spectral evidence. The ability to induce apoptosis was determined by its <it>in vitro </it>antiradical activity, cytotoxic studies using human colon adenocarcinoma and normal monkey kidney cell lines, and the expression of β-catenin and proliferating cell nuclear antigen (PCNA) in human colon cancer cell lines (COLO 320 DM). The chemopreventive potential of β-sitosterol in colon carcinogenesis was assessed by injecting 1,2-dimethylhydrazine (DMH, 20 mg/kg b.w.) into male Wistar rats and supplementing this with β-sitosterol throughout the experimental period of 16 weeks at 5, 10, and 20 mg/kg b.w.</p> <p>Results</p> <p>β-sitosterol induced significant dose-dependent growth inhibition of COLO 320 DM cells (IC₅₀266.2 μM), induced apoptosis by scavenging reactive oxygen species, and suppressed the expression of β-catenin and PCNA antigens in human colon cancer cells. β-sitosterol supplementation reduced the number of aberrant crypt and crypt multiplicity in DMH-initiated rats in a dose-dependent manner with no toxic effects.</p> <p>Conclusion</p> <p>We found doses of 10-20 mg/kg b.w. β-sitosterol to be effective for future <it>in vivo </it>studies. β-sitosterol had chemopreventive potential by virtue of its radical quenching ability <it>in vitro</it>, with minimal toxicity to normal cells. It also attenuated β-catenin and PCNA expression, making it a potential anticancer drug for colon carcinogenesis.</p

A limited role for p53 in modulating the immediate phenotype of Apc loss in the intestine

Background: p53 is an important tumour suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated. Methods: We have conditionally deleted the Adenomatous Polyposis coli gene (Apc) from the adult murine intestine in wild type and p53 deficient environments and subsequently compared the phenotype and transcriptome profiles in both genotypes. Results: Expression of p53 was shown to be elevated following the conditional deletion of Apc in the adult small intestine. Furthermore, p53 status was shown to impact on the transcription profile observed following Apc loss. A number of key Wnt pathway components and targets were altered in the p53 deficient environment. However, the aberrant phenotype observed following loss of Apc (rapid nuclear localisation of β-catenin, increased levels of DNA damage, nuclear atypia, perturbed cell death, proliferation, differentiation and migration) was not significantly altered by the absence of p53. Conclusion: p53 related feedback mechanisms regulating Wnt signalling activity are present in the intestine, and become activated following loss of Apc. However, the physiological Wnt pathway regulation by p53 appears to be overwhelmed by Apc loss and consequently the activity of these regulatory mechanisms is not sufficient to modulate the immediate phenotypes seen following Apc loss. Thus we are able to provide an explanation to the apparent contradiction that, despite having a Wnt regulatory capacity, p53 loss is not associated with early lesion development

Csnk1a1 inhibition has p53-dependent therapeutic efficacy in acute myeloid leukemia

Despite extensive insights into the underlying genetics and biology of acute myeloid leukemia (AML), overall survival remains poor and new therapies are needed. We found that casein kinase 1 α (Csnk1a1), a serine-threonine kinase, is essential for AML cell survival in vivo. Normal hematopoietic stem and progenitor cells (HSPCs) were relatively less affected by shRNA-mediated knockdown of Csnk1a1. To identify downstream mediators of Csnk1a1 critical for leukemia cells, we performed an in vivo pooled shRNA screen and gene expression profiling. We found that Csnk1a1 knockdown results in decreased Rps6 phosphorylation, increased p53 activity, and myeloid differentiation. Consistent with these observations, p53-null leukemias were insensitive to Csnk1a1 knockdown. We further evaluated whether D4476, a casein kinase 1 inhibitor, would exhibit selective antileukemic effects. Treatment of leukemia stem cells (LSCs) with D4476 showed highly selective killing of LSCs over normal HSPCs. In summary, these findings demonstrate that Csnk1a1 inhibition causes reduced Rps6 phosphorylation and activation of p53, resulting in selective elimination of leukemia cells, revealing Csnk1a1 as a potential therapeutic target for the treatment of AML