Electron cooling rates characterization at Fermilab's Recycler

A 0.1 A, 4.3 MeV DC electron beam is routinely used to cool 8 GeV antiprotons in Fermilab's Recycler storage ring [1]. The primary function of the electron cooler is to increase the longitudinal phase-space density of the antiprotons for storing and preparing high-density bunches for injection into the Tevatron. The longitudinal cooling rate is found to significantly depend on the transverse emittance of the antiproton beam. The paper presents the measured rates and compares them with calculations based on drag force data

Status of high energy electron cooling in FNAL's Recycler Ring

Electron cooling of 8 GeV antiprotons at Fermilab's Recycler storage ring is now routinely used in the collider operation. It requires a 0.1-0.5 A, 4.3 MeV DC electron beam to increase the longitudinal phase-space density of the circulating antiproton beam. This paper discusses the latest status of the electron cooler and its mode of operation within the context of Fermilab's accelerator complex. In addition, we will show preliminary results that demonstrate electron cooling of the transverse phase-space of the antiproton beam

Damaged DNA Binding Protein 2 Plays a Role in Breast Cancer Cell Growth

The Damaged DNA binding protein 2 (DDB2), is involved in nucleotide excision repair as well as in other biological processes in normal cells, including transcription and cell cycle regulation. Loss of DDB2 function may be related to tumor susceptibility. However, hypothesis of this study was that DDB2 could play a role in breast cancer cell growth, resulting in its well known interaction with the proliferative marker E2F1 in breast neoplasia. DDB2 gene was overexpressed in estrogen receptor (ER)-positive (MCF-7 and T47D), but not in ER-negative breast cancer (MDA-MB231 and SKBR3) or normal mammary epithelial cell lines. In addition, DDB2 expression was significantly (3.0-fold) higher in ER-positive than in ER-negative tumor samples (P = 0.0208) from 16 patients with breast carcinoma. Knockdown of DDB2 by small interfering RNA in MCF-7 cells caused a decrease in cancer cell growth and colony formation. Inversely, introduction of the DDB2 gene into MDA-MB231 cells stimulated growth and colony formation. Cell cycle distribution and 5 Bromodeoxyuridine incorporation by flow cytometry analysis showed that the growth-inhibiting effect of DDB2 knockdown was the consequence of a delayed G1/S transition and a slowed progression through the S phase of MCF-7 cells. These results were supported by a strong decrease in the expression of S phase markers (Proliferating Cell Nuclear Antigen, cyclin E and dihydrofolate reductase). These findings demonstrate for the first time that DDB2 can play a role as oncogene and may become a promising candidate as a predictive marker in breast cancer