experimental animals were adoptively transferred with 107 CD4+ cells. Control animals (n¼8) received injections of PBS. Tail vol- umes, lymphatic function (uptake of Tc99) and histology were per- formed 6-weeks postoperatively. RESULTS: Adoptive transfer resulted in significant CD4+ popula- tions in spleen and lymph nodes of recipient mice. These mice had significantly greater tail volume and decreased lymphatic transport (Tc99) as compared with controls (both p<0.001). Furthermore, these mice developed significant subcutaneous adipose deposition in the regions of the tail distal to the zone of injury (p<0.05). Us- ing flow cytometry and histology we found that there was signifi- cant accumulation of CD4+ cells in the dermis/subcutaneous fat (p<0.001) and that this response was associated with a significant fibrotic response (type I collagen deposition; p<0.03 compared with controls). CONCLUSIONS: We demonstrate that the adoptive transfer of naı ¨ve CD4+ cells into CD4KO mice recapitulates the lymphedema observed in wild type mice. These findings therefore suggest that CD4+ cells are instrumental in the pathology seen in lymphedema. Future studies will determine how CD4+ cell subtypes contribute to this process. Prophylactic administration of amifostine protects vessel thickness and luminal diameter in the setting of irradiation Erin E Page, BS, Sagar S Deshpande, BS, Noah S Nelson, Peter A Felice, MD, Alexis Donneys, MD, MS, Jose J Rodriguez, Samir S Deshpande, Steven R Buchman, MD University of Michigan, Ann Arbor, MI INTRODUCTION: Although often beneficial in the treatment of head and neck cancer (HNC), radiation therapy (XRT) leads to the depletion of vessel volume fraction (VVF) and vessel thickness (VT). Amifostine (AMF) provides protection from the detrimental effects of radiation damage, allowing for reliable post-irradiation fracture healing in the murine mandible. The purpose of this study is to investigate the prophylactic ability of AMF to protect the vascular network in an irradiated field. METHODS: Sprague-Dawley rats (n¼17) were divided into 3 groups: control (C, n¼5), radiated (XRT, n¼7), and radiated man- dibles treated with Amifostine (AMF XRT, n¼5). Both groups receiving radiation underwent a human equivalent dose of XRT totaling 35 Gray, equally fractionated over 5 days. The AMF XRT group received a weight dependent (0.5mg AMF/5g body weight) subcutaneous injection of AMF 45 minutes prior to XRT. Following a 56-day recovery period, mandibles were perfused, dissected, and imaged with mCT. Analysis of variance (ANOVA)was used for comparisons between groups and p < 0.05 was considered statistically significant. RESULTS: Stereologic analysis demonstrated a significant and quantifiable restoration of VT in AMF treated mandibles as compared to those treated with radiation alone (0.061.011mm vs 0.0420.004mm, p¼0.027). Further analysis demonstrated no signif- icant difference in VT between control mandibles and those treated with AMF (0.0670.016mm vs 0.0610.011mm, p¼0.633). CONCLUSIONS: Our findings support the contention that AMF therapy acts prophylactically to protect the vascular network from damage imparted by radiation, thus we support the continued investigation of this treatment paradigm in its potential translation for the prevention of vascular depletion after radiotherapy. Obesity worsens lymphedema via an exaggerated inflammatory response Ira L Savetsky, MD, Jeremy Torrisi, BA, Daniel Cuzzone, MD, Swapna Ghanta, MD, Nicholas Albano, BS, Jason C Gardenier, MD, Walter J Joseph, BS, Babak J Mehrara, MD, FACS Memorial Sloan-Kettering Cancer Center, New York, NY INTRODUCTION: Although obesity is a significant risk factor for the development of post-surgical lymphedema, the cellular mecha- nisms underlying this effect remain unclear. Therefore, the purpose of this study was to delineate the pathophysiologic effects of obesity on lymphatic physiology in a mouse model of lymphedema. METHODS: Adult male C57BL/6J mice were fed either a normal chow diet (lean) or a high fat diet (60% fat) for eight weeks to cause diet induced obesity (DIO). At this point, animals underwent superficial and deep lymphatic ligation in the tail to induce lym- phedema followed by analysis of inflammation, lymphatic func- tion, and fibrosis six weeks after surgery. RESULTS: DIO mice were significantly heavier (p<0.0001) and had markedly decreased lymphatic transport capacity after lymphatic injury as compared with controls (p<0.0001). In addi- tion, DIO mice had significantly increased tissue inflammation (CD45+ cells, p<0.0001; CD4+ cells, p¼0.0023) and increased collagen deposition (p¼0.0006). Interestingly, using a topical irritant model, we found that DIO mice had a significantly increased propensity to tissue inflammation as compared to lean mice with markedly increased infiltration of macrophages and neutrophils. CONCLUSIONS: We have shown for the first time that DIO worsens lymphedema and that this response is associated with an exaggerated chronic inflammatory response. In addition, we have found that DIO results in an exaggerated acute inflammatory response in subcutaneous tissues in response to irritation or injury. This is important since acute and chronic inflammatory responses may be a key mechanism by which obesity increases the risk of wound healing problems and lymphedema. Pharmacologic rescue of motor and sensory function following neonatal peripheral nerve injury Gregory H Borschel, MD, FACS, Stephen Kemp, PhD, Mark Szynkaruk, Joseph Ready, PhD, Simon Beggs, PhD, Vol. 219, No. 4S, October 2014 Scientific Poster Presentations: 2014 Clinical Congress e135