Faculty Bibliography

Senior housestaff and junior faculty are often expected to perform clinical research, yet may not always have the requisite knowledge and skills to do so successfully. Formal degree programs provide such knowledge, but require a significant commitment of time and money. Short-term training programs (days to weeks) provide alternative ways to accrue essential information and acquire fundamental methodological skills. Unfortunately, published information about short-term programs is sparse. To encourage discussion and exchange of ideas regarding such programs, we here share our experience developing and implementing INtensive Training in Research Statistics, Ethics, and Protocol Informatics and Design (INTREPID), a 24-day immersion training program in clinical research methodologies. Designing, planning, and offering INTREPID was feasible, and required significant faculty commitment, support personnel and infrastructure, as well as committed trainees. Clin Trans Sci 2014; Volume #: 1-7.

PURPOSE OF REVIEW: Clinically identified myopathies are frequently a consequence of medication toxicities. However, recognizing drug-induced myopathies is sometimes difficult. Developing a greater understanding of the underlying mechanisms of drug-induced muscle toxicity will promote enhanced awareness and recognition, and improved management of these syndromes. RECENT FINDINGS: The adverse impact of certain drugs on muscle metabolism, muscle cell atrophy, and myocyte apoptosis is increasingly clear. Glucocorticoids impair glucose handling and directly promote protein catabolism. Statins impair mitochondrial function and alter intracellular signaling proteins, which can lead to myocyte apoptosis. Alternatively, statins can induce an autoimmune necrotizing myositis. Several medications impair autophagy, thus limiting access to the needed glycogen stores. SUMMARY: This review provides an overview of the main underlying mechanisms of drug-induced myopathies. These myopathies will most often be related to a drug's ability to alter metabolism and protein balance, induce necrosis, or impair autophagy.

The prevalence of gout and hyperuricemia has increased dramatically during the last several decades, to the point that gout is the most common inflammatory arthritis in the United States, affecting approximately 8 million Americans. Patients with gout frequently have multiple comorbidities, including hypertension, chronic kidney disease, cardiovascular disease, obesity, diabetes, and hyperlipidemia, all of which have significant adverse impact on public health. In some cases (eg, chronic kidney disease) it is clear that the presence of the comorbidity contributes to the progression of hyperuricemia and/or gout. Conversely, the question of whether gout/hyperuricemia themselves contribute to the pathogenesis of gout comorbidities is an area of intensifying investigation. In vitro and animal models, large epidemiologic studies, and small clinical trials suggest that gout and/or hyperuricemia may contribute to hypertension, chronic kidney disease, and cardiovascular disease. More limited hypothesis-generating studies suggest a potential role for diabetes and obesity. Given that available drugs can lower serum urate levels and manage gout, it would be important to know whether not only gout and/or hyperuricemia can contribute to comorbidities but also better gout/hyperuricemic control can ameliorate some or all of these related conditions. We review the clinical associations between gout and its common comorbid conditions and the evidence supporting a causal relation between them. The evidence that gout and hyperuricemia contribute to the pathogenesis of their comorbidities creates greater urgency for appropriate gout management.