Teaching about the Wild: A Survival Course as a Novel Resident Educational Experience.

Audience: Emergency medicine residents. Introduction: Wilderness medicine (WM) is the practice of resource-limited medicine under austere conditions. Emergency physicians in training should gain additional exposure to wilderness medicine knowledge and outdoor skills to allow for the development of problem solving and improvisation abilities. However, there is limited data on the instruction of general survival skills to residents interested in WM. Educational Objectives: By the end of the session the learner will be able to: 1) differentiate at least three different methods for water purification 2) describe how to erect a temporary survival shelter 3) construct a survival pack for personal use emphasizing multi-use items 4) demonstrate how to make a fire without a direct flame supply. Educational Methods: A small group of resident learners progressed through five survival stations designed to allow for an emphasis on select skills, wilderness medicine knowledge, and improvisation. Resident instructors led the discussion and skills demonstration. Research Methods: Participants completed a six item before and after questionnaire. Each item was ranked from 0 for "strongly disagree" to 10 for "strongly agree." Total mean scores before and after were compared. Results: Twelve individuals participated. The total mean score for the six-item analysis increased following the workshop (39.1 before versus 51.0 after, p = 0.0008). Discussion: General survival skills are traditionally acquired through time-intensive experiences; however, this is often unfeasible during residency training. We developed an alternative, more efficient mechanism for incorporating wilderness medicine skills into residency training that appears to improve understanding and confidence of participants, as well as to provide a teaching opportunity for new resident educators. Topics: Wilderness medicine, survival skills, emergency medicine, graduate medical education.

Decreased insulin sensitivity and increased oxidative damage in wasting adipose tissue depots of wild-type mice.

Unintentional weight loss (wasting) in the elderly is a major health concern as it leads to increased mortality. Several studies have focused on muscle loss, but little is known about the mechanisms giving rise to loss of fat mass at old ages. To investigate potential mechanisms, white adipose tissue (WAT) characteristics and proteomic profiles were compared between adult (10-12-month-old) and aged (22-24-month-old) wild-type mice. Four individual WAT depots were analyzed to account for possible depot-specific differences. Proteomic profiles of WAT depots, along with body weights and compositions, plasma levels of insulin, leptin and adiponectin, insulin tolerance, adipocyte sizes, and products of oxidative damage in each WAT depot were determined. We found that lean mass remained constant while fat mass and insulin tolerance were decreased in old age, as were adipocyte sizes in the WAT depots. Proteomic results showed increased levels of enolase, pyruvate dehydrogenase E1ß, NAD(+)-dependent isocitrate dehydrogenase α, and ATP synthase subunit ß, and decreased levels of carbonic anhydrase 3 in WAT of aged mice. These data suggest increased aerobic glucose oxidation in wasting WAT, consistent with decreased insulin signaling. Also, Cu/Zn superoxide dismutase and two chaperones were increased in aged WAT depots, indicating higher stress resistance. In agreement, lipid peroxidation (HNE-His adducts) increased in old age, although protein oxidation (carbonyl groups) showed no increase. In conclusion, features of wasting WAT were similar in the four depots, including decreased adipocyte sizes and alterations in protein expression profiles that indicated decreased insulin sensitivity and increased lipid peroxidation.

Heterogeneity among white adipose tissue depots in male C57BL/6J mice.

The widespread prevalence of obesity has lead to extensive research on white adipose tissue (WAT), which frequently uses the C57BL/6J mouse strain as a model. In many studies, results obtained in one WAT depot are often extrapolated to all WAT. However, functional differences among WAT depots are now becoming apparent. Thus, to identify the molecular mechanisms responsible for WAT depot-specific differences under "normal" conditions, four C57BL/6J mouse WAT depots (inguinal, mesenteric, epididymal, and retroperitoneal) were analyzed. Depot proteomic profiles, along with weights, protein contents, adipocyte sizes and oxidative stress were determined. Mesenteric WAT had almost twice the protein content of the other depots analyzed. Mean adipocyte size was highest in epididymal and lowest in mesenteric and inguinal depots. The proteome of inguinal WAT displayed low levels of enzymes involved in ATP generation, glucose and lipid metabolism, and antioxidant proteins. Higher levels of these proteins were observed in mesenteric and epididymal WAT, with variable levels in the retroperitoneal depot. Some of these proteins showed depot-specific correlations with plasma levels of insulin, leptin, and adiponectin. In agreement with the proteomic data, levels of the antioxidant protein heat shock protein ß1 (HSPß1) also were lower in inguinal WAT when analyzed by western blotting and immunohistochemistry. Also, lipid peroxidation products showed similar trends. Our results are consistent with lower triglyceride turnover and lower oxidative stress in inguinal than mesenteric and epididymal WAT. The observed WAT depot-specific differences provide clues as to the mechanisms leading to these depots' respective diverse functions.

Growth hormone and adipose tissue: beyond the adipocyte.

The last two decades have seen resurgence in research focused on adipose tissue. In part, the enhanced interest stems from an alarming increase in obesity rates worldwide. However, an understanding that this once simple tissue is significantly more intricate and interactive than previously realized has fostered additional attention. While few would argue that growth hormone (GH) radically alters fat mass, newer findings revealing the complexity of adipose tissue requires that GH's influence on this tissue be reexamined. Therefore, the objective of this review is to describe the more recent understanding of adipose tissue and to summarize our current knowledge of how GH may influence and contribute to these newer complexities of this tissue with special focus on the available data from mice with altered GH action.