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Previously we showed that neuropeptide Y (NPY), a sympathetic vasoconstrictor neurotransmitter, stimulates endothelial cell migration, proliferation, and differentiation in vitro. Here, we report on NPY’s actions, receptors, and mediators in ischemic angiogenesis. In rats, hindlimb ischemia stimulates sympathetic NPY release (attenuated by lumbar sympathectomy) and upregulates NPY-Y2 (Y2) receptor and a peptidase forming Y2/Y5-selective agonist. Exogenous NPY at physiological concentrations also induces Y5 receptor, stimulates neovascularization, and restores ischemic muscle blood flow and performance. NPY-mediated ischemic angiogenesis is not prevented by a selective Y1 receptor antagonist but is reduced in Y2–/– mice. Nonischemic muscle vascularity is also lower in Y2–/– mice, whereas it is increased in NPY-overexpressing rats compared with their WT controls. Ex vivo, NPY-induced aortic sprouting is markedly reduced in Y2–/– aortas and spontaneous sprouting is severely impaired in NPY–/– mice. NPY-mediated aortic sprouting, but not cell migration/proliferation, is blocked by an antifetal liver kinase 1 antibody and abolished in mice null for eNOS. Thus, NPY mediates neurogenic ischemic angiogenesis at physiological concentrations by activating Y2/Y5 receptors and eNOS, in part due to release of VEGF. NPY’s effectiveness in revascularization and restoring function of ischemic tissue suggests its therapeutic potential in ischemic conditions

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Objective: To investigate the occurrence, nature, and reporting of sexual harassment in surgical training and to understand why surgical trainees who experience harassment might not report it. This information will inform ways to overcome barriers to reporting sexual harassment. Summary/ Background Data: Sexual harassment in the workplace is a known phenomenon with reports of high frequency in the medical field. Aspects of surgical training leave trainees especially vulnerable to harassing behavior. The characteristics of sexual harassment and reasons for its underreporting have yet to be studied on the national level in this population. Methods: An electronic anonymous survey was distributed to general surgery trainees in participating program; all general surgery training programs nationally were invited to participate. Results: Sixteen general surgery training programs participated, yielding 270 completed surveys (response rate of 30%). Overall, 48.9% of all respondents and 70.8% of female respondents experienced at least 1 form of sexual harassment during their training. Of the respondents who experienced sexual harassment, 7.6% reported the incident. The most common cited reasons for nonreporting were believing that the action was harmless (62.1%) and believing reporting would be a waste of time (47.7%). Conclusion: Sexual harassment occurs in surgical training and is rarely reported. Many residents who are harassed question if the behavior they experienced was harassment or feel that reporting would be ineffectual—leading to frequent nonreporting. Surgical training programs should provide all-level education on sexual harassment and delineate the best mechanism for resident reporting of sexual harassment.

Recently, there has been an increased recognition of neoplasms of the pancreas other than ductal adenocarcinoma. Although not as well studied or characterized as pancreatic adenocarcinoma there are many distinct lesions which exhibit diverse biological behaviors and varying degrees of malignancy. These lesions include: endocrine neoplasms, cystic tumors, solid pseudopapillary tumors, acinar cell carcinoma, squamous cell carcinoma, primary lymphoma of the pancreas, and metastatic lesions to the pancreas. These less common neoplasms are being diagnosed more frequently as the number and sensitivity of diagnostic imaging studies increase. This review article discusses the clinical course, diagnosis, and treatment of these less common, but quite relevant, neoplasms of the pancreas.

To examine the role of intramyocellular lipid (IMCL) accumulation as well as circulating cytokines, branched-chain amino acids and acylcarnitines in the pathogenesis of muscle insulin resistance in healthy, young, lean insulin-resistant offspring of parents with type 2 diabetes (IR offspring), we measured these factors in plasma and used 1 H magnetic resonance spectroscopy to assess IMCL content and hyperinsulinemic-euglycemic clamps using [6,6-2 H 2 ] glucose to assess rates of insulin-stimulated peripheral glucose metabolism before and after weight reduction. Seven lean (body mass index < 25 kg/m 2 ), young, sedentary IR offspring were studied before and after weight stabilization following a hypocaloric (1,200 Kcal) diet for ∼9 wks. This diet resulted in an average weight loss of 4.1 ± 0.6 kg (P < 0.0005), which was associated with an ∼30% reduction of IMCL from 1.1 ± 0.2% to 0.8 ± 0.1% (P = 0.045) and an ∼30% improvement in insulin-stimulated muscle glucose uptake [3.7 ± 0.3 vs. 4.8 ± 0.1 mg/ (kg-min), P = 0.01]. This marked improvement in insulin-stimulated peripheral insulin responsiveness occurred independently of changes in plasma concentrations of TNF-α, IL-6, total adiponectin, C-reactive protein, acylcarnitines, and branched-chain amino acids. In conclusion, these data support the hypothesis that IMCL accumulation plays an important role in causing muscle insulin resistance in young, lean IR offspring, and that both are reversible with modest weight loss.I nsulin resistance is the best predictor for an increased risk of developing type 2 diabetes (T2D) yet the cellular mechanism responsible for the insulin resistance remains unknown (1-4). Previous studies have demonstrated that skeletal muscle insulin resistance, due to defects in insulin-stimulated glucose transport activity resulting in decreased muscle glycogen synthesis, is the earliest defect detectable in healthy, young, lean insulin-resistant offspring of parents with T2D (IR offspring) (5-8). Furthermore, previous studies have found a strong relationship between intramyocellular lipid (IMCL) content assessed by 1 H magnetic resonance spectroscopy (MRS) and muscle insulin resistance (9-13), suggesting that intracellular lipid metabolites (e.g., diacylglycerols, ceramides) might be a causal factor in its pathogenesis (14-16).To directly examine this hypothesis, we studied whether modest weight reduction would result in a reduction in IMCL content in lean IR offspring, and if so whether this reduction in IMCL would be associated with improvements in insulin-stimulated skeletal muscle glucose uptake, assessed by a hyperinsulinemic-euglycemic clamp. Furthermore, because changes in inflammatory adipocytokines (17-20), branched-chain amino acids (21,22), and acylcarnitines (23) have also been implicated in the pathogenesis of insulin resistance, we also measured plasma levels of these factors before and after this modest weight-loss intervention. ResultsThe IR offspring were markedly insulin-resistant, as reflected by their insulin sensitivity index...