“
“Objective: Nonfunctional popliteal entrapment is due to selleck chemicals llc embryologic maldevelopment within the popliteal fossa. Functional entrapment occurs in the apparent absence of an anatomic abnormality. Gastrocnemius hypertrophy has been associated with the latter. Both forms of entrapment may cause arterial injury and lower limb ischemia. This study

assessed the attachment of the medial head of the gastrocnemius muscle in healthy occluders and healthy nonoccluders.

Methods: provocative tests were used to identify, 58 nonoccluders and 16 occluders. Ten subjects from each group underwent magnetic resonance imaging evaluation of the popliteal fossa. The medial head of the gastrocnemius muscle attachment was assessed in the supracondylar, pericondylar, and intercondylar areas.

Results: In the occluder group, significantly more muscle was attached towards the femoral midline (supracondylar), around the lateral border of the medial condyle (pericondylar), and within the intercondylar fossa.

Conclusion: The more extensive midline position of the medial

head of the gastrocnemius in occluders is likely to be a normal embryological variation. Forceful contraction results in compression and occlusion of the adjacent popliteal artery. The clinical significance of these anatomic variations remains unclear. However, these new observations may provide insight for future analysis of the causes and natural history of functional compression and the potential progression to clinical entrapment. (J Vasc Surg 2008;48:1189-96.)”
“Pituitary adenylate cyclase-activating Selleckchem LY2835219 polypeptide ( PACAP) and the proopiomelanocortin (POMC)-derived

peptide, alpha-melanocyte-stimulating hormone (alpha-MSH), exert anorexigenic activities. While a-MSH is known to inhibit food intake and stimulate catabolism via activation of the central melanocortin-receptor MC4-R, little is known regarding the mechanism by which PACAP inhibits food consumption. We have recently found that, in the arcuate nucleus of the hypothalamus, a high proportion of POMC neurons express PACAP receptors. This observation led us to investigate whether PACAP may inhibit food intake through a POMC-dependent mechanism. In mice deprived of food for 18 h, intracerebroventricular administration Nintedanib (BIBF 1120) of PACAP significantly reduced food intake after 30 min, and this effect was reversed by the PACAP antagonist PACAP6-38. In contrast, vasoactive intestinal polypeptide did not affect feeding behavior. Pretreatment with the MC3-R/MC4-R antagonist SHU9119 significantly reduced the effect of PACAP on food consumption. Central administration of PACAP induced c-Fos mRNA expression and increased the proportion of POMC neuron-expressing c-Fos mRNA in the arcuate nucleus. Furthermore, PACAP provoked an increase in POMC and MC4-R mRNA expression in the hypothalamus, while MC3-R mRNA level was not affected.