Objectives: Oncology providers are often confronted by patients who use complementary or alternative therapies, but have limited knowledge or confidence on how to advise patients on appropriate use. Despite this, there are few opportunities for oncology providers to learn about complementary or alternative therapies, while at the same time there is a high demand for integrative oncology (IO) training. To address a gap in IO educational opportunities, and particularly for nonphysicians, we created the Integrative Oncology Scholars (IOS) Program. The program's goal is to train 100 IO leaders and facilitate partnerships between them and complementary practitioners. Design: Four iterations of a year-long National Cancer Institute-funded educational program that combines in-person team-based learning and eLearning to teach the evidence, application, and philosophy supporting IO. Settings: In-person sessions take place at the University of Michigan, and eLearning is implemented using a Canvas website (Instructure, Inc., Salt Lake City, UT). Subjects: Nurses, social workers, physician assistants, psychologists, physicians, pharmacists, and physical/ occupational therapists with active oncology practices. Educational intervention: Four cohorts of 25 oncology providers per year will learn the evidence base for complementary and alternative approaches to a wide number of oncology topics, including symptom control, dietary supplements commonly used by cancer patients, diet, and the utility of specific integrative approaches for common oncology side-effects such as fatigue. Outcome measures: A mixed methods approach will be used to evaluate overall IOS Program progress and individual scholar's impact on IO research, education, and clinical endeavors. Results: The first cohort of 25 IOS has been recruited and their education will begin in Summer 2018. Scholars come from 13 states and represent 23 different healthcare systems. Conclusions: The IOS Program has the potential to increase the number of trained IO providers, educators, and researchers in the United States.

The mechanistic target of rapamycin (mTORC1) is a nutrient responsive protein kinase complex that helps co-ordinate anabolic processes across all tissues. There is evidence that signaling through mTORC1 in skeletal muscle may be a determinant of energy expenditure and aging and therefore components downstream of mTORC1 signaling may be potential targets for treating obesity and ageassociated metabolic disease. Here, we generated mice with Ckmm-Cre driven ablation of Tsc1, which confers constitutive activation of mTORC1 in skeletal muscle and performed unbiased transcriptional analyses to identify pathways and candidate genes that may explain how skeletal muscle mTORC1 activity regulates energy balance and aging. Activation of skeletal muscle mTORC1 produced a striking resistance to diet-and age-induced obesity without inducing systemic insulin resistance. We found that increases in energy expenditure following a high fat diet were mTORC1-dependent and that elevated energy expenditure caused by ablation of Tsc1 coincided with the upregulation of skeletal musclespecific thermogenic mechanisms that involve sarcolipin-driven futile cycling of Ca 2+ through SERCA2.Additionally, we report that constitutive activation of mTORC1 in skeletal muscle reduces lifespan.These findings support the hypothesis that activation of mTORC1 and its downstream targets, specifically in skeletal muscle, may play a role in nutrient-dependent thermogenesis and aging.Skeletal muscle is the major site of postprandial glucose disposal and the primary determinant of resting energy expenditure in mammals [18,19]. Constitutive activation of mTORC1, via musclespecific deletion of its negative regulator Tsc1, results in age-related myoatrophy, dysregulation of autophagy induction and increased expression of mitochondrial enzymes [6,20,21]. Consistent with the latter, cell culture models implicate mTORC1 as a positive regulator of mitochondrial biogenesis and aerobic ATP production [22][23][24]. During the aging process, skeletal muscle exhibits a fiber-type transformation towards a more oxidative phenotype, concomitant with increased mTORC1 activity. In line with these observations, several studies have implicated mTORC1 inhibition as a mechanism of organismal lifespan extension in yeast, worms and mammals [25][26][27]; however, the tissue or tissues that link mTORC1 activity to lifespan have not yet been identified.Skeletal muscle is an important tissue for understanding aging, insulin sensitivity and changes in energy metabolism, as functional differences in muscle strength predict lifespan in humans [28][29][30][31][32][33].Furthermore, mTORC1 regulates several important metabolic processes in muscle; including oxidative stress, the unfolded protein response, autophagy and lipid metabolism [20,34,35]. Here, we have performed unbiased transcriptional analyses to identify pathways and candidate genes that may explain how skeletal muscle mTORC1 activity regulates energy balance and aging. We show that chronic mTORC1 activation in skeletal muscle (...

An iterative procedure for obtaining two-carrier d.c. solutions in regions of rapidly varying carrier concentration is presented. The procedure uses an analytic solution for the carrier concentrations in a region of linear spatial electric field variation. Field-dependent diffusion and field-dependent velocities are assumed. A single-carrier small-signal model for a drift region with a spatially varying field and field-dependent transport properties is presented. When applied to a BARITT device, results consistent with published experimental data are obtained. The importance of momentum relaxation effects in Si BARITT drift regions is discussed.

The timing of food intake is a novel dietary component that can impact health. Time-restricted feeding (TRF), a form of intermittent fasting, manipulates food timing. During pregnancy, one may experience disruptions to food intake for diverse reasons (e.g. nausea and vomiting of pregnancy, food insecurity, desire to manage gestational weight gain, disordered eating behaviors, changes in taste and food preferences, etc) and therefore may experience periods of intentional or unintentional fasting similar to TRF protocols. Because interest in TRF is gaining popularity and feeding may be interrupted in those who are pregnant, it is important to understand the long-term effects of TRF during pregnancy on the resultant offspring. Using a mouse model, we tested the effects of gestational exposure to early TRF (eTRF) over the life course of both male and female offspring. Offspring body composition was similar between experimental groups in both males and females from weaning (day 21) to adulthood (day 70), with minor increases in food intake in eTRF females and improved glucose tolerance in males. After 10 weeks of high fat, high sucrose diet feeding, male eTRF offspring were more sensitive to insulin but developed glucose intolerance with impaired insulin secretion. As such, gestational eTRF causes sex-specific deleterious effects on glucose homeostasis after chronic high fat, high sucrose diet feeding in male offspring. Further studies are needed to determine the effect gestational eTRF has on the male pancreas as well as to elucidate the mechanisms that protect females from this metabolic dysfunction.