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Treatment with steroid tape is the standard of care for keloid and hypertrophic scars in Japan. In this article, we present a woman with an aggressive and progressive keloid of the anterior chest wall. At the time of presentation, the keloid had been present for 40 years, and was continuing to worsen and expand. Initially, it was believed that a multidisciplinary approach, including surgery and radiation, would be necessary to achieve an acceptable scar outcome. However, we successfully treated her keloid using only steroid tape (deprodone propionate plaster), and no other treatment modality. The case therefore supports the effectiveness of deprodone propionate plaster, and emphasizes its potential for wider future use. With the paucity of experience reported in the literature on steroid tape for scars, more reports are useful to inform plastic surgeons and dermatologists worldwide about this therapeutic option., Competing Interests: The authors have no financial interest to declare in relation to the content of this article., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons.)

North American residency programs are transitioning to competency-based medical education (CBME) to standardize training programs, and to ensure competency of residents upon graduation. At the centre of assessment in CBME are specific surgical procedures, or procedural competencies, that trainees must be able to perform. A study previously defined 31 procedural competencies for aesthetic surgery. In this transition period, understanding current educational trends in resident exposure to these aesthetic procedures is necessary. The aim of this study was to characterize aesthetic procedures performed by Canadian plastic surgery residents during training, as well as to describe resident performance confidence levels and degree of resident involvement during those procedures. Case logs were retrieved from all 10 English-language plastic surgery programs. All aesthetic procedures were identified, and coded according to previously defined core procedural competencies (CPCs) in the aesthetic domain of plastic surgery. Data extracted from each log included the procedure, training program, resident academic year, resident procedural role, and personal competence. From July 2004 to June 2014, 6113 aesthetic procedures were logged by 55 graduating residents. Breast augmentation, mastopexy, and abdominoplasty were the most commonly performed CPCs, and residents report high levels of competence and surgical role in these procedures. Facial procedures, in particular rhinoplasty, as well as nonsurgical CPCs are associated with low exposure and personal competence levels. Canadian plastic surgery residents are exposed to most of the core aesthetic procedural competencies, but the range of procedures performed is variable. With the implementation of CBME, consideration should be given to supplementation where gaps may exist in aesthetic case exposure., (© 2021 The Aesthetic Society. Reprints and permission: journals.permissions@oup.com.)

Leptin signaling in the central nervous system, and particularly the arcuate hypothalamic nucleus, is important for regulating energy and glucose homeostasis. However, the roles of extra-arcuate leptin responsive neurons are less defined. In the current study, we generated mice with widespread inactivation of the long leptin receptor isoform in the central nervous system via Synapsin promoter-driven Cre (Lepr(flox/flox) Syn-cre mice). Within the hypothalamus, leptin signaling was disrupted in the lateral hypothalamic area (LHA) and ventral premammillary nucleus (PMV) but remained intact in the arcuate hypothalamic nucleus and ventromedial hypothalamic nucleus, dorsomedial hypothalamic nucleus, and nucleus of the tractus solitarius. To investigate the role of LHA/PMV neuronal leptin signaling, we examined glucose and energy homeostasis in Lepr(flox/flox) Syn-cre mice and Lepr(flox/flox) littermates under basal and diet-induced obese conditions and tested the role of LHA/PMV neurons in leptin-mediated glucose lowering in streptozotocin-induced diabetes. Lepr(flox/flox) Syn-cre mice did not have altered body weight or blood glucose levels but were hyperinsulinemic and had enhanced glucagon secretion in response to experimental hypoglycemia. Surprisingly, when placed on a high-fat diet, Lepr(flox/flox) Syn-cre mice were protected from weight gain, glucose intolerance, and diet-induced hyperinsulinemia. Peripheral leptin administration lowered blood glucose in streptozotocin-induced diabetic Lepr(flox/flox) Syn-cre mice as effectively as in Lepr(flox/flox) littermate controls. Collectively these findings suggest that leptin signaling in LHA/PMV neurons is not critical for regulating glucose levels but has an indispensable role in the regulation of insulin and glucagon levels and, may promote the development of diet-induced hyperinsulinemia and weight gain.

Objective: Leptin reverses hyperglycemia in rodent models of type 1 diabetes (T1D). Direct application of leptin to the brain can lower blood glucose in diabetic rodents, and can activate autonomic efferents and non-shivering thermogenesis in brown adipose tissue (BAT). We investigated whether leptin reverses hyperglycemia through a mechanism that requires autonomic innervation, or uncoupling protein 1 (UCP1)-mediated thermogenesis., Methods: To examine the role of parasympathetic and sympathetic efferents in the glucose-lowering action of leptin, mice with a subdiaphragmatic vagotomy or 6-hydroxydopamine induced chemical sympathectomy were injected with streptozotocin (STZ) to induce hyperglycemia, and subsequently leptin treated. To test whether the glucose-lowering action of leptin requires activation of UCP1-mediated thermogenesis in BAT, we administered leptin in STZ-diabetic Ucp1 knockout (Ucp1 (-/-)) mice and wildtype controls., Results: Leptin ameliorated STZ-induced hyperglycemia in both intact and vagotomised mice. Similarly, mice with a partial chemical sympathectomy did not have an attenuated response to leptin-mediated glucose lowering relative to sham controls, and showed intact leptin-induced Ucp1 expression in BAT. Although leptin activated BAT thermogenesis in STZ-diabetic mice, the anti-diabetic effect of leptin was not blunted in Ucp1 (-/-) mice., Conclusions: These results suggest that leptin lowers blood glucose in insulin-deficient diabetes through a manner that does not require parasympathetic or sympathetic innervation, and thus imply that leptin lowers blood glucose through an alternative CNS-mediated mechanism or redundant target tissues. Furthermore, we conclude that the glucose lowering action of leptin is independent of UCP1-dependent thermogenesis.

Objective: The purpose of this study was to measure the toe-brachial index (TBI) in healthy young adults and to compare it with the accepted reference range., Methods: Medical students from the undergraduate classes at the University of British Columbia were prospectively recruited. Participants were surveyed on physical parameters (height, weight), lifestyle factors (physical activity and type, smoking status, alcohol consumption), and medical history (current medications, medical conditions, family history). Bilateral brachial, ankle (using both dorsalis pedis and posterior tibial arteries), and toe blood pressures were measured by stethoscope, Doppler device, and photoplethysmograph, respectively. Ankle-brachial index (ABI) and TBI were calculated and assessed against published reference ranges. TBI was calculated as the mean great toe blood pressure divided by the average of the higher arm systolic blood pressures., Results: Seventy-three medical students with a mean age of 24.3 ± 2.0 years without any comorbidity were studied. Participants maintained relatively healthy lifestyles (hours of activity per week, 4.6 ± 2.7; body mass index, 21.9 ± 2.4). Caffeine and alcohol consumption was modest (8.2 ± 8.0 and 1.7 ± 2.6 servings/week, respectively). There were no current or past smokers. No significant differences in lifestyle factors were observed between men and women. Mean brachial blood pressure was 116 ± 10 mm Hg (left) and 120 ± 11 mm Hg (right). Mean TBI was 0.98 ± 0.12 (left) and 0.97 ± 0.12 (right) for men and 0.95 ± 0.21 (left) and 0.94 ± 0.21 (right) for women. The overall ABI was 1.10 ± 0.07 when averaged by gender and side. Whereas men had significantly higher blood pressures in the arm, toe, and ankle compared with women, these differences disappeared when the indices were determined. There were no significant differences in TBI or ABI between men and women., Conclusions: In comparison to published reference values, the TBI in young, healthy individuals is significantly higher. Whereas no gender difference existed, greater variability of the TBI was observed in women. Further studies are recommended to determine if the threshold for diagnosis of peripheral arterial disease based on TBI should be raised., (Copyright © 2016. Published by Elsevier Inc.)

The "stinger" or "burner" is a form of transient brachial plexopathy termed for its characteristic knife-like pain extending from the neck to the fingertips. Muscle weakness and paresthesia are oftentimes associated symptoms and are similarly temporary. Commonly observed in athletes of contact sports, the stinger results from high force trauma causing either traction/direct compression to the brachial plexus or extension/compression of the cervical nerve roots. We describe a pediatric case of a stinger in a 14-year-old boy, which was caused by a relatively low force trauma accident. Our management strategy and recommendations are discussed.

Hunter syndrome is a multisystem genetic disease in which a significant proportion of morbidity and mortality arise from respiratory dysfunction. Notably, tracheal abnormalities in Hunter syndrome can compromise clinical stability, and management is primarily supportive. We describe here the first successful implementation of aorto-tracheopexy in a 19-year-old patient as a surgical strategy to resolve progressive respiratory deterioration., (Copyright © 2015 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Aims/hypothesis: Leptin has profound glucose-lowering effects in rodent models of type 1 diabetes, and is currently being tested clinically to treat this disease. In addition to reversing hyperglycaemia, leptin therapy corrects multiple lipid, energy and neuroendocrine imbalances in rodent models of type 1 diabetes, yet the precise mechanism has not been fully defined. Thus, we performed metabolic analyses to delineate the downstream metabolic pathway mediating leptin-induced glucose lowering in diabetic mice., Methods: Mice were injected with streptozotocin (STZ) to induce insulin-deficient diabetes, and were subsequently treated with 20 μg/day recombinant murine leptin or vehicle for 5 to 14 days. Energy-yielding substrates were measured in the liver and plasma, and endogenous glucose production was assessed by tolerance to extended fasting., Results: STZ-leptin-treated mice developed severe hypoketotic hypoglycaemia during prolonged fasting, indicative of suppressed endogenous ketone and glucose production. STZ-leptin mice displayed normal gluconeogenic and glycogenolytic capacity, but had depleted circulating glycerol and NEFA. The depletion of glycerol and NEFA correlated tightly with the kinetics of glucose lowering in response to chronic leptin administration, and was not mimicked by single leptin injection. Administration of glycerol acutely reversed fasting-induced hypoglycaemia in leptin-treated mice., Conclusions/interpretation: The findings of this study suggest that the diminution of circulating glycerol reduces endogenous glucose production, contributing to severe fasting-induced hypoglycaemia in leptin-treated rodent models of type 1 diabetes, and support that depletion of glycerol contributes to the glucose-lowering action of leptin.

Islet transplantation is an effective method to obtain long-term glycemic control for patients with type 1 diabetes, yet its widespread use is limited by an inadequate supply of donor islets. The hormone leptin has profound glucose-lowering and insulin-sensitizing action in type 1 diabetic rodent models. We hypothesized that leptin administration could reduce the dose of transplanted islets required to achieve metabolic control in a mouse model of type 1 diabetes. We first performed a leptin dose-response study in C57Bl/6 mice with streptozotocin (STZ)-induced diabetes to determine a leptin dose insufficient to reverse hyperglycemia. Subsequently, we compared the ability of suboptimal islet transplants of 50 or 125 syngeneic islets to achieve glycemic control in STZ-induced diabetic C57Bl/6 mice treated with or without this dose of leptin. The dose-response study revealed that leptin reverses STZ-induced diabetes in a dose-dependent manner. Supraphysiological leptin levels were necessary to restore euglycemia but simultaneously increased risk of hypoglycemia, and also lost efficacy after 12 days of administration. In contrast, 1 µg/day leptin only modestly reduced blood glucose but maintained efficacy throughout the study duration. We then administered 1 µg/day leptin to diabetic mice that underwent transplantation of 50 or 125 islets. Although these islet doses were insufficient to ameliorate hyperglycemia alone, coadministration of leptin with islet transplantation robustly improved control of glucose and lipid metabolism, without increasing circulating insulin levels. This study reveals that low-dose leptin administration can reduce the number of transplanted islets required to achieve metabolic control in STZ-induced diabetic mice.

The low-density lipoprotein receptor (Ldlr) is a key molecule involved with lipid clearance. The Ldlr(-/-) mouse has been used extensively as a model for studying atherosclerosis. This study sought to characterize the energy balance phenotype of Ldlr(-/-) mice with respect to weight gain, body composition, energy expenditure (EE), glucose homeostasis, and leptin sensitivity. Adult Ldlr(-/-) mice and Ldlr(+/+) controls on a C57Bl/6J background were fed either a chow or a high-fat, high-sucrose Western-type diet (WTD) for eight wk. Physiological studies of food intake, EE, activity, insulin sensitivity, and leptin responsiveness were performed. The effect of these diet interventions on circulating leptin and on leptin gene expression was also examined. On the chow diet, Ldlr(-/-) mice had lower EE and higher activity levels relative to controls. On the WTD, Ldlr(-/-) mice gained less weight relative to Ldlr(+/+) mice, specifically gaining less fat mass. Increased thermogenesis in Ldlr(-/-) mice fed the WTD was detected. Additionally, leptin responsiveness was blunted in chow-fed Ldlr(-/-) mice, suggesting a novel role for the Ldlr pathway that extends to leptin's regulation of energy balance. In addition to its known role in lipid transport, these results demonstrate the importance of the Ldlr in energy homeostasis and suggest a direct physiological link between altered lipid transport and energy balance.