BackgroundObesity is associated with low-grade chronic inflammation, and serum markers of inflammation are independent risk factors for cardiovascular disease (CVD). However, the molecular and cellular mechanisms that link obesity to chronic inflammation and CVD are poorly understood.Methods and FindingsAcute-phase serum amyloid A (A-SAA) mRNA levels, and A-SAA adipose secretion and serum levels were measured in obese and nonobese individuals, obese participants who underwent weight-loss, and persons treated with the insulin sensitizer rosiglitazone. Inflammation-eliciting activity of A-SAA was investigated in human adipose stromal vascular cells, coronary vascular endothelial cells and a murine monocyte cell line. We demonstrate that A-SAA was highly and selectively expressed in human adipocytes. Moreover, A-SAA mRNA levels and A-SAA secretion from adipose tissue were significantly correlated with body mass index ( r = 0.47; p = 0.028 and r = 0.80; p = 0.0002, respectively). Serum A-SAA levels decreased significantly after weight loss in obese participants ( p = 0.006), as well as in those treated with rosiglitazone ( p = 0.033). The magnitude of the improvement in insulin sensitivity after weight loss was significantly correlated with decreases in serum A-SAA ( r = −0.74; p = 0.034). SAA treatment of vascular endothelial cells and monocytes markedly increased the production of inflammatory cytokines, e.g., interleukin (IL)-6, IL-8, tumor necrosis factor alpha, and monocyte chemoattractant protein-1. In addition, SAA increased basal lipolysis in adipose tissue culture by 47%. ConclusionsA-SAA is a proinflammatory and lipolytic adipokine in humans. The increased expression of A-SAA by adipocytes in obesity suggests that it may play a critical role in local and systemic inflammation and free fatty acid production and could be a direct link between obesity and its comorbidities, such as insulin resistance and atherosclerosis. Accordingly, improvements in systemic inflammation and insulin resistance with weight loss and rosiglitazone therapy may in part be mediated by decreases in adipocyte A-SAA production.

A 3-mm surgical margin can be safely used for nonmorpheaform basal cell carcinoma to attain 95 percent cure rates for lesions 2 cm or smaller. A positive pathologic margin has an average recurrence rate of 27 percent.

This study investigates whether human acellular dermis (Alloderm; LifeCell, Branchburg, NJ) revascularizes when used to reconstruct abdominal wall defects in rabbits. This could prove useful in infected situations in which prosthetic mesh is suboptimal. Twenty-five rabbits were randomly assigned to one of three groups: primary closure (n = 5), expanded polytetrafluoroethylene (GoreTex; W.L. Gore, Flagstaff, AZ) repair (n = 10), or AlloDerm (LifeCell) repair (n = 10). The rabbits in the primary closure group received a 7 cm x 0.5 cm full-thickness abdominal wall defect that was closed primarily. A 7 cm x 3 cm full-thickness abdominal wall defect was created in the other two groups. The defects were repaired with a GoreTex Mycromesh (W.L. Gore), or AlloDerm (LifeCell) patch. At 30 days, the following endpoints were evaluated: (1) incidence of herniation; (2) presence of intra-abdominal adhesions; (3) the breaking strength of the patch-fascial interface; and (4) evaluation of graft vascularization by fluorescein dye infusion and histological analysis. There was no incidence of herniation in any of the rabbits. Visceral adhesions to the patch were found in all animals in the Gore-Tex (W.L. Gore) group but in none in the AlloDerm (LifeCell) group. The size of the patch was unchanged in all the rabbits except for two rabbits in the AlloDerm (LifeCell) group that stretched 1 cm in the transverse dimension. The change in size was not statistically significant (p = 0.17) when compared with the change in size in the Gore-Tex (W.L. Gore) group. The mean breaking strength of the primary closure group was significantly higher (521.2 N/mm2 +/- 223.0) than that of the two patch-repair groups (p < 0.05). But there was no significant difference between the mean breaking strength of the AlloDerm (LifeCell) fascial interface (288.6 N/mm2 +/- 97.1 SD) and that of the Gore-Tex (W.L. Gore) fascial interface (337.0 N/mm2 +/- 141.2). Fluorescein dye infusion and histological analysis confirmed vascularization of the AlloDerm (LifeCell) graft. This study demonstrates that AlloDerm (LifeCell) does become vascularized when used as a fascial interposition graft for abdominal wall reconstruction. AlloDerm (LifeCell) also performs mechanically as effectively as Gore-Tex (W.L. Gore) in ventral hernia repair at 1 month after operation in the rabbit model.

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In this study, we were unable to demonstrate a difference between ADM and ePTFE in their ability to repair ventral hernias at 9 months in a swine model. The ADM additionally supports vascular ingrowth and exhibits increased breaking strength at the fascia-implant interface.