Wire Marking Results in a Small but Significant Reduction in Avian Mortality at Power Lines: A BACI Designed Study

10 paginas, 4 figuras y 4 tablesBackground: Collision with electric power lines is a conservation problem for many bird species. Although the implementation of flight diverters is rapidly increasing, few well-designed studies supporting the effectiveness of this costly conservation measure have been published. Methodology/Principal Findings: We provide information on the largest worldwide marking experiment to date, including carcass searches at 35 (15 experimental, 20 control) power lines totalling 72.5 km, at both transmission (220 kV) and distribution (15 kV-45 kV) lines. We found carcasses of 45 species, 19 of conservation concern. Numbers of carcasses found were corrected to account for carcass losses due to removal by scavengers or being overlooked by researchers, resulting in an estimated collision rate of 8.2 collisions per km per month. We observed a small (9.6%) but significant decrease in the number of casualties after line marking compared to before line marking in experimental lines. This was not observed in control lines. We found no influence of either marker size (large vs. small spirals, sample of distribution lines only) or power line type (transmission vs. distribution, sample of large spirals only) on the collision rate when we analyzed all species together. However, great bustard mortality was slightly lower when lines were marked with large spirals and in transmission lines after marking. Conclusions: Our results confirm the overall effectiveness of wire marking as a way to reduce, but not eliminate, bird collisions with power lines. If raw field data are not corrected by carcass losses due to scavengers and missed observations, findings may be biased. The high cost of this conservation measure suggests a need for more studies to improve its application, including wire marking with non-visual devices. Our findings suggest that different species may respond differently to marking, implying that species-specific patterns should be explored, at least for species of conservation concern.We thank A. Garcıa Fernandez and M. Carrasco for their assistance during the field work. We also thank J. Camaño and J. Velasco of HENARSA, and the electric companies Iberdrola, Union Fenosa and Red Electrica de España for their cooperation. S. Young reviewed the English. RB was contracted within the project CGL2008-02567 of the Direccion General de Investigacion, Spanish Ministry of Science and Innovation and later supported by a postdoctoral grant from Junta de Comunidades de Castilla-La Mancha. C. Ponce, C. Palacın, CM and BM were supported by contracts CSICHENARSA. This study was carried out within the Preventive, corrective and compensatory measures to balance the impact of the M-50 and R-2 highways on the population of great bustards and other steppe-land birds in the Important Bird Area Talamanca-Camarma and the Site of Community Importance Cuenca de los rıos Jarama y Henares, supported by a contract HENARSA-CSIC. Additional financial support was provided by project GL2008-02567 of the Direccion General de Investigacion, Spanish Ministry of Science and Innovation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewe

Mammary epithelial cell transformation: insights from cell culture and mouse models

Normal human mammary epithelial cells (HMECs) have a finite life span and do not undergo spontaneous immortalization in culture. Critical to oncogenic transformation is the ability of cells to overcome the senescence checkpoints that define their replicative life span and to multiply indefinitely – a phenomenon referred to as immortalization. HMECs can be immortalized by exposing them to chemicals or radiation, or by causing them to overexpress certain cellular genes or viral oncogenes. However, the most efficient and reproducible model of HMEC immortalization remains expression of high-risk human papillomavirus (HPV) oncogenes E6 and E7. Cell culture models have defined the role of tumor suppressor proteins (pRb and p53), inhibitors of cyclin-dependent kinases (p16(INK4a), p21, p27 and p57), p14(ARF), telomerase, and small G proteins Rap, Rho and Ras in immortalization and transformation of HMECs. These cell culture models have also provided evidence that multiple epithelial cell subtypes with distinct patterns of susceptibility to oncogenesis exist in the normal mammary tissue. Coupled with information from distinct molecular portraits of primary breast cancers, these findings suggest that various subtypes of mammary cells may be precursors of different subtypes of breast cancers. Full oncogenic transformation of HMECs in culture requires the expression of multiple gene products, such as SV40 large T and small t, hTERT (catalytic subunit of human telomerase), Raf, phosphatidylinositol 3-kinase, and Ral-GEFs (Ral guanine nucleotide exchange factors). However, when implanted into nude mice these transformed cells typically produce poorly differentiated carcinomas and not adenocarcinomas. On the other hand, transgenic mouse models using ErbB2/neu, Ras, Myc, SV40 T or polyomavirus T develop adenocarcinomas, raising the possibility that the parental normal cell subtype may determine the pathological type of breast tumors. Availability of three-dimensional and mammosphere models has led to the identification of putative stem cells, but more studies are needed to define their biologic role and potential as precursor cells for distinct breast cancers. The combined use of transformation strategies in cell culture and mouse models together with molecular definition of human breast cancer subtypes should help to elucidate the nature of breast cancer diversity and to develop individualized therapies

Decreased cyclin B1 expression contributes to G2 delay in human brain tumor cells after treatment with camptothecin.

DNA damage produces delayed mitosis (G2/M delay) in proliferating cells, and shortening the delay sensitizes human malignant glioma and medulloblastoma cells to cytotoxic chemotherapy. Although activation of the cyclin-dependent kinase CDC2 mediates G2/M transition in all tumor cells studied to date, regulation of CDC2 varies between tumor types. Persistent hyperphosphorylation of kinase and reduced cyclin expression have been implicated as mediators of treatment-induced G2 delay in different tumor models. To evaluate regulation of G2/M transition in human brain tumors, we studied the expression and/or activity of CDC2 kinase and cyclins A and B1 in U-251 MG and DAOY medulloblastoma cells after their treatment with camptothecin (CPT). Synchronized cells were treated during S phase, then harvested at predetermined intervals for evaluation of cell cycle kinetics, kinase activity mRNA, and protein expression. CPT produced G2 delay associated with decreased CDC2 kinase activity and cyclin B1 expression. Kinase activity was associated with CDC2 bound to cyclin B1, not cyclin A, in both cell lines. Cyclin A mRNA and protein expression were reduced after CPT treatment; however, decreased protein expression was short lived and moderate in the glioma and primitive neuroectodermal tumor/medulloblastoma cells, respectively. We conclude that G2 delay is a common response of brain tumor cells to chemotherapy with topoisomerase I inhibitors and that a mechanism of this delay may be reduced expression of cyclin B1

Glial differentiation predicts poor clinical outcome in primitive neuroectodermal brain tumors.

Abstract Primitive neuroectodermal tumors (PNETs) of the central nervous system, including medulloblastomas (PNET/MB), are the most common malignant brain tumor of childhood. These tumors often express proteins characteristic of glial differentiation (glial fibrillary acidic protein, GFAP), neuronal differentiation (neurofilament proteins, NFPs), and/or photoreceptor differentiation (retinal-S antigen). To identify biological factors of prognostic significance in PNETs, the expression of glial, neuronal, or photoreceptor antigens was evaluated in the tumor specimens of 86 patients with PNETs by immunohistochemistry after microwave antigen enhancement. Patterns of differentiation were then compared with patient relapse-free survival. Multivariate analysis of PNET immunohistochemistry and clinical variables indicated GFAP expression conferred a 6.7-fold greater risk of relapse than tumors that did not express GFAP or NFPs. Increased risk of relapse was directly related to the amount of GFAP expression. Tumors exhibiting clumps or sheets of GFAP-staining cells were associated with a 3.0-fold increased risk of relapse compared with tumors that did not express GFAP, irrespective of immunohistochemical evidence of other differentiation, while scattered GFAP staining was not associated with increased risk of relapse. These findings indicate that expression of GFAP in PNETs has prognostic power comparable with the most significant clinical factors currently used to predict clinical outcome