Overexpression of the nonpancreatic secretory group II PLA2 messenger RNA and protein in colorectal adenomas from familial adenomatous polyposis patients

The synovial fluid or group II secretory phospholipase A2 (sPLA2) has been implicated in various inflammatory processes and has been shown to release arachidonic acid for prostaglandin biosynthesis. In human colorectal cancer, both arachidonic acid and eicosanoid levels are elevated. Recently, sPLA2 has been identified as a candidate gene that modifies the Apc gene in the Min mouse, a murine model for familial adenomatous polyposis (FAP). Loss of sPLA2 gene function results in susceptibility to the Min phenotype and the formation of multiple intestinal polyps, whereas mice expressing an active sPLA2 gene are resistant to polyp formation. Therefore, there are two potentially contrasting roles for sPLA2 in colon cancer; one is protection against polyp formation, and the other, the release of arachidonic acid for prostaglandin production and subsequent tumor promotion. To investigate these contrasting dual roles of sPLA2, we have examined the expression and sequence of the sPLA2 mRNA in normal mucosa and duodenal and colorectal polyps from FAP patients. In 11 of 14 patients, there was a significant increase in sPLA2 mRNA levels in the adenoma over the normal tissue. In some cases, there was over 100-fold increase in mRNA levels in the adenoma compared with normal tissue. Analysis of multiple adenomatous polyps from individual patients revealed that not all polyps contained elevated levels of sPLA2 mRNA. Immunoblot analysis also showed that sPLA2 protein expression was elevated in adenoma over normal tissue in five of six FAP patients analyzed. Furthermore, sequence analysis of sPLA2 mRNA present in these samples did not reveal mutations in the coding region. The implications of the up-regulation of sPLA2 in FAP is not clear, but unlike the Min mouse model, it does not seem to have a significant effect on polyp formation. In contrast, the high level of sPLA2 expression is more likely contributing to the elevated levels of arachidonic acid found in colorectal cancer and, in conjunction with the elevated expression of cyclooxygenase-2, could be another factor in tumor formation

First documentation of leopard seal predation of South Georgia pintail duck

Leopard seals are regular winter visitors to Bird Island, South Georgia, where they mostly prey on fur seals and penguins, and to a lesser extent on Antarctic krill and fish. Leopard seals can exploit many different species, but there are no records of predation on flying shorebirds in the wild. On 4 October 2008, an individually identified juvenile leopard seal female was observed killing and eating a South Georgia Pintail duck. It also preyed on Antarctic fur seals and gentoo and macaroni penguins during its 2-month temporary residency around the island. The varied diet of this seal exemplifies the generalist prey utilization typical of its species. Long-term diet studies at Bird Island and the published record suggest that predation on ducks is a rather exceptional finding; individual ducks are more likely to escape leopard seal attacks than penguins and provide a far less substantial ration. This note documents the first observation of this species of duck in the diet of leopard seals

Scarring patterns and relative mortality rates of Indian Ocean whale sharks

This study recorded the scarring rate and severity for whale sharks Rhincodon typus from three Indian Ocean aggregations (Australia, Seychelles and Mozambique), and examined whether scarring (mostly attributed to boat strikes and predator attacks) influences apparent survival rates using photo-identification libraries. Identifications were based on spot-and-stripe patterns that are unique to individual whale sharks. Scarring was most prevalent in the Seychelles aggregation (67% of individuals). Predator bites were the most frequent source of scarring (aside from minor nicks and abrasions) and 27% of individuals had scars consistent with predator attacks. A similar proportion of whale sharks had blunt trauma, laceration and amputation scars, the majority of which appeared to be caused by ship collisions. Predator bites were more common (44% of individuals) and scars from ship collisions were less common at Ningaloo Reef than at the other two locations (probability of among-site differences occurring randomly = 0.0007 based on a randomized multinomial contingency analysis). In all aggregations, scars occurred most often on the caudal fin, which may result from the fin being the body part closest to the surface when boats pass over, or they may provide a large target for predator attack. No evidence was found for an effect of scarring on apparent survival (φ; mean ± s.e.) for the Ningaloo (not scarred φ = 0.858 ± 0.033; scarred φ = 0.929 ± 0.033) or Seychelles populations (not scarred φ = 0.502 ± 0.060; scarred φ = 0.538 ± 0.070). The lower apparent survival of the Seychelles population may be attributed to a high number of transient whale sharks in this aggregation that might bias estimates. This study indicates that while scarring from natural predators and smaller vessels appears to be unrelated to whale shark survival, the effect of deaths related to ship strike need to be quantified to assist in future management of this species. © 2008 The Authors

Family history characteristics, tumor microsatellite instability and germline MSH2 and MLH1 mutations in hereditary colorectal cancer

Recent characterization of the molecular genetic basis of hereditary nonpolyposis colorectal cancer provides an important opportunity for identification of individuals and their families with germline mutations in mismatch repair genes. Cancer family history criteria that accurately define hereditary colorectal cancer are necessary for cost-effective testing for germline mutations in mismatch repair genes. The present report describes the results of analysis of 33 colorectal cancer cases/families that satisfy our modified family history criteria (Mount Sinai criteria) for colorectal cancer. Fourteen of these families met the more stringent Amsterdam criteria. Germline MSH2 and MLH1 mutations were identified by the reverse transcription-polymerase chain reaction and the protein truncation test, and confirmed by sequencing. Microsatellite instability analysis was performed on available tumors from affected patients. MSH2 or MLH1 mutations were detected in 8 of 14 Amsterdam criteria families and in 5 of the remaining 19 cases/families that only satisfied the Mount Sinai criteria. Three of the latter families had features of the Muir-Torre syndrome. A high level of microsatellite instability (MSI-H) was detected in almost all (16/18) colorectal cancers from individuals with MSH2 and MLH1 mutations, and infrequently (1/21) in colorectal cancer specimens from cases without detectable mutations. Families with germline MSH2 and MLH1 mutations tended to have individuals affected at younger ages and with multiple tumors. The Amsterdam criteria are useful, but not sufficient, for detecting hereditary colorectal cancer families with germline MSH2 and MLH1 mutations, since a proportion of cases and families with mutations in mismatch repair genes will be missed. Further development of cancer family history criteria are needed, using unbiased prospectively collected cases, to define more accurately those who will benefit from MSH2 and MLH1 mutation analysis