Seasonal dynamic shifts in patch exploitation by parasitic wasps.

We developed and tested predictions of a dynamic life history model that is concerned with how temperate-zone parasitic wasps adjust patch residence time and tendency to superparasitize when expectation of life and habitat quality varies. The theory predicts that wasps with short life expectancy should continue to search longer and superparasitize more frequently than similar wasps with long life expectancy. Similarly, wasps with long life expectancy that forage in habitats where patches are already heavily exploited should continue to search longer and superparasitize more frequently than similar wasps foraging in habitats where patches are relatively unexploited. In contrast, the theory predicts that wasps with short life expectancy will be insensitive to habitat quality. We tested the predictions on Drosophila parasitoids (Lep-topilina heterotoma) by (1) rearing wasps under fall and summer photoperiod (i.e., short versus long life expectancy) and (2) giving wasps foraging experience on different quality patches (i.e., exploited versus unexploited habitats). Results of the experiments corroborated our predictions. We discuss how parasitic wasp behavior can be shaped by globally predictable and locally unpredictable events. [Behav Ecol 3:156-165 (1992)] Recent advances in the development of dy-namic life-history models (Houston e

Seasonal dynamic shifts in patch exploitation by a parasitic wasp

We developed and tested predictions of a dynamic life history model that is concerned with how temperate-zone parasitic wasps adjust patch residence time and tendency to superparasitize when expectation of life and habitat quality varies. The theory predicts that wasps with short life expectancy should continue to search longer and superparasitize more frequently than similar wasps with long life expectancy. Similarly, wasps with long life expectancy that forage in habitats where patches are already heavily exploited should continue to search longer and superparasitize more frequently than similar wasps foraging in habitats where patches are relatively unexploited. In contrast, the theory predicts that wasps with short life expectancy will be insensitive to habitat quality. We tested the predictions on Drosophila parasitoids (Lep-topilina heterotoma) by (1) rearing wasps under fall and summer photoperiod (i.e., short versus long life expectancy) and (2) giving wasps foraging experience on different quality patches (i.e., exploited versus unexploited habitats). Results of the experiments corroborated our predictions. We discuss how parasitic wasp behavior can be shaped by globally predictable and locally unpredictable events.

Cribriform and intraductal prostate cancer are associated with increased genomic instability and distinct genomic alterations

Background: Invasive cribriform and intraductal carcinoma (CR/IDC) is associated with adverse outcome of prostate cancer patients. The aim of this study was to determine the molecular aberrations associated with CR/IDC in primary prostate cancer, focusing on genomic instability and somatic copy number alterations (CNA). Methods: Whole-slide images of The Cancer Genome Atlas Project (TCGA, N = 260) and the Canadian Prostate Cancer Genome Network (CPC-GENE, N = 199) radical prostatectomy datasets were reviewed for Gleason score (GS) and presence of CR/IDC. Genomic instability was assessed by calculating the percentage of genome altered (PGA). Somatic copy number alterations (CNA) were determined using Fisher-Boschloo tests and logistic regression. Primary analysis were performed on TCGA (N = 260) as discovery and CPC-GENE (N = 199) as validation set. Results: CR/IDC growth was present in 80/260 (31%) TCGA and 76/199 (38%) CPC-GENE cases. Patients with CR/IDC and ≥ GS 7 had significantly higher PGA than men without this pattern in both TCGA (2.2 fold; p = 0.0003) and CPC-GENE (1.7 fold; p = 0.004) cohorts. CR/IDC growth was associated with deletions of 8p, 16q, 10q23, 13q22, 17p13, 21q22, and amplification of 8q24. CNAs comprised a total of 1299 gene deletions and 369 amplifications in the TCGA dataset, of which 474 and 328 events were independently validated, respectively. Several of the affected genes were known to be associated with aggressive prostate cancer such as loss of PTEN, CDH1, BCAR1 and gain of MYC. Point mutations in TP53, SPOP and FOXA1were also associated with CR/IDC, but occurred less frequently than CNAs. Conclusions: CR/IDC growth is associated with increased genomic instability clustering to genetic regions involved in aggressive prostate cancer. Therefore, CR/IDC is a pathologic substrate for progressive molecular tumour derangement