Although Asian Americans generally have the lowest cancer incidence rates and mortality rates, cancer is the leading cause of death among Asian Americans. The goal of this pilot study was to engage Chinese American cancer survivors (CACS) in systematic changes toward desired health behaviors through a healthy lifestyle intervention delivered by a community-based organization. The Reach out to ENhanceE Wellness (RENEW) program workbook was translated into Mandarin Chinese with additional physical activity (PA) and dietary information that are culturally appropriate (RENEW-C). Fifty-five Chinese cancer survivors were recruited from the greater Houston area to participate in this 50-week program and 50 of them completed both the baseline and postintervention surveys in 2013 and 2014, respectively. Paired sample t tests were used to assess changes in 5 groups of outcomes: (1) patient knowledge (measured by Health Education Impact Questionnaire [heiQ]), (2) dietary intake (Automated Self-Administered 24-Hour [ASA24] Dietary Assessment Tool), (3) PA (Community Healthy Activities Model Program for Seniors [CHAMPS]), (4) body mass index, and (5) quality of life (36-item Short-Form Survey [SF-36]). Compared with the baseline, participants reported significantly higher consumption of vegetables and higher frequency of PAs at the postintervention survey. They also showed improved mental health and lower limitation in doing their work or other activities due to physical health or emotional problems. Despite the small sample size, this pilot study demonstrated the effectiveness of using a community-based participatory approach in a healthy lifestyle intervention tailored for CACS.

Electrochemical treatment (EChT) with direct current delivered through implanted electrodes has been used for local control of solid tumors in humans. This study tested the hypothesis that rat breast cancer responses to EChT are dependent on electrode spacing and dose, and explored suitable parameters for treating breast cancers with EChT. Rat breast cancers were initiated by injecting 1 Â 10 6 MTF-7 cells to the right mammary gland fat pad of Fisher 344 female rats. The rats were randomly divided into designated experimental groups when the tumors grew to approximately 2 Â 2 Â 2 cm. One hundred and thirty rats were used for a survival study and 129 for a pathology study. A 4-channel EChT machine was used to administer coulometric doses. The survival study indicated that local tumor control rate is less than 40% in the 40 coulomb (C) and 60 C groups and more than 70% in the 80 and 100 C groups. Sixty six rats died of primary tumors, including all 10 rats in the control group. Once a rat's primary tumor was controlled, no recurrence was found. The main reason for terminating the primary tumor-free rats (51) was lymph node metastasis. Thirteen tumor-free rats survived for more than 6 months. The pathology study showed a signi®cant dose effect on EChT induced tumor necrosis. At 10, 20, 40, and 80 C, the fraction showing necrosis were 39.7, 52.3, 62, and 77.7%, respectively (P 0.001). Electrodes spacing was not an important factor within a given range. At 5, 10, and 15 mm spacing, the fraction showing the necrosis were 54.1, 60.4, and 59.2%, respectively (P 0.552). The overlap rate of necroses was similar in the 5 and 10 mm groups (82.5 and 85%) and lower in the 15 mm group (65%). We conclude that the tumor responses to EChT, local control, survival rates, and necrosis percentages were signi®cantly increased with increasing dose. The changes in electrode spacing (3, 5, and 10 mm) did not signi®cantly affect the tumor responses to EChT within the same dose. For a diameter of 2.0± 2.5 cm rat breast cancer, EChT should be applied with 5±10 mm spacing and a minimum dosage of 80 C.

Chronic inflammation may contribute to insulin resistance via molecular cross-talk between pathways for pro-inflammatory and insulin signaling. Interleukin 1 receptor-associated kinase 1 (IRAK-1) mediates pro-inflammatory signaling via IL-1 receptor/Toll-like receptors, which may contribute to insulin resistance, but this hypothesis is untested. Here, we used male null (k/o) mice to investigate the metabolic role of IRAK-1. C57BL/6 wild-type (WT) and k/o mice had comparable body weights on low-fat and high-fat diets (LFD and HFD, respectively). After 12 weeks on LFD (but not HFD), k/o mice ( WT) had substantially improved glucose tolerance (assessed by the intraperitoneal glucose tolerance test (IPGTT)). As assessed with the hyperinsulinemic euglycemic glucose clamp technique, insulin sensitivity was 30% higher in the k/o mice on chow diet, but the deletion did not affect IPGTT outcomes in mice on HFD, suggesting that the deletion did not overcome the impact of obesity on glucose tolerance. Moreover, insulin-stimulated glucose-disposal rates were higher in the k/o mice, but we detected no significant difference in hepatic glucose production rates (± insulin infusion). Positron emission/computed tomography scans indicated higher insulin-stimulated glucose uptake in muscle, but not liver, in k/o mice Moreover, insulin-stimulated phosphorylation of Akt was higher in muscle, but not in liver, from k/o mice In conclusion, deletion improved muscle insulin sensitivity, with the effect being most apparent in LFD mice.

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