Breast Cancer Survivor Advocacy at a University Hospital: Development of a Peer Support Program with Evaluation by Patients, Advocates, and Clinicians.

Peer-to-peer support programs provide unique psychosocial and educational support for breast cancer patients. A Patient Survivor Advocacy (PSA) program was developed by the University of Wisconsin Breast Center (UWBC) to provide support for newly diagnosed patients from peers who had completed primary treatment. In this study, we evaluated patient, advocate, and clinician experience with the PSA program. A program matching volunteer peer advocates at least 1 year removed from primary treatment with newly diagnosed patients was developed. Peer advocates were recruited from the practices of UWBC clinicians and received in-person training on six dimensions of peer advocacy. Trained advocates were then paired based on demographic and medical history with new patients referred to the program. Survey assessment tools were distributed to assess peer advocate and patient satisfaction, as well as clinician experience. Forty patients have been matched with seven advocates, with contact largely by email (53 %) or phone (36 %). Patients and peer advocates reported satisfaction with the program. The majority of patients (92.9 %) reported that the program was "helpful" and that they would recommend the PSA program to another woman with breast cancer. All peer advocates (100 %) responded with a sense of achievement in their advocate roles. Clinicians noted challenges in referral to the program. Peer advocates can provide key emotional and psychosocial support to newly diagnosed breast cancer patients. The peer advocate, patient, and clinician feedback collected in this study will inform the future development of this program at our and peer institutions.

Effects of antioxidants coenzyme Q10 and lipoic acid on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets.

During the development of the autoimmune disease, insulin-dependent diabetes mellitus (IDDM) islet cell death is thought to be mediated in part by oxygen and nitrogen free radicals and interleukin 1beta (IL-1beta), secreted by activated macrophages. Free radicals disrupt the homeostasis of biological systems by damaging major constituent molecules such as lipids, proteins, and DNA. Islet cells are quite susceptible to oxidative damage due to low levels of antioxidant enzymes involved in free radical consumption. If IDDM is associated with an imbalance of oxidative stresses and antioxidant responses in islet cells, then it may be possible to ameliorate disease by supplementating antioxidant defenses. In this study, the antioxidants coenzyme Q10 and lipoic acid were able to block IL-1beta-mediated inhibition of glucose-stimulated insulin secretion from islet cells at 10(-12) M and 10(-9) M, respectively.