Nest initiation and flooding in response to season and semi-lunar spring tides in a ground-nesting shorebird.

Background: Marine and intertidal organisms face the rhythmic environmental changes induced by tides. The large amplitude of spring tides that occur around full and new moon may threaten nests of ground-nesting birds. These birds face a trade-off between ensuring nest safety from tidal flooding and nesting near the waterline to provide their newly hatched offspring with suitable foraging opportunities.

CyclinD1 and interleukin-1 receptor antagonist polymorphisms are associated with prognosis in neoadjuvant-treated gastric carcinoma.

Purpose: We evaluated DNA polymorphisms in genes related to DNA repair, cell-cycle control and tumour microenvironment to determine possible associations with response and survival in neoadjuvant-treated gastric cancer patients.

Patients And Methods: One hundred and seventy eight patients who received platinum/5FU-based chemotherapy were genotyped for 10 polymorphisms in nine genes (ERCC1: Asn118Asn, C > T; ERCC1: 8092C > A; TP53: Arg72Pro, G < C; cyclinD1: Pro241Pro, G > A; STK15: Phe31Ile, A > T; VEGF: 936C > T; TNF-alpha: -308G > A; interleukin-1b (IL-1B): -511C >T; IL-1 receptor antagonist (IL-1RN): variable tandem repeat; IL-8: -251T>A). Genotypes were correlated with histopathological and clinical response and overall (OS) and progression-free survival (PFS).

Desmoglein 2 is expressed abnormally rather than mutated in familial and sporadic gastric cancer.

Alterations of the cell adhesion molecule E-cadherin have been demonstrated in sporadic and hereditary gastric carcinomas. A cell adhesion molecule with functional similarity to E-cadherin is desmoglein 2 (Dsg2), a major component of the desmosomes. In this study, we investigated whether alterations of Dsg2 are involved in gastric carcinogenesis and whether germline mutations contribute to a genetic predisposition in familial gastric cancer patients with no germline mutations in the E-cadherin gene.

Relationship between E-cadherin gene mutation and p53 gene mutation, p53 accumulation, Bcl-2 expression and Ki-67 staining in diffuse-type gastric carcinoma.

E-cadherin mutations are found in 50% of diffuse-type gastric carcinoma, but not in intestinal gastric carcinoma. Because cell-cell adhesion mediated by E-cadherin plays an important role in epithelial cell survival, E-cadherin mutations could alter the apoptotic behavior of tumor cells. p53 and Bcl-2 family members are also important regulators of cellular apoptosis.