Chylous ascites may result from a variety of pathological conditions, most of them from nontraumatic causes, such as congenital defects of the lymphatic system, infections, liver cirrhosis, and malignancy. Rarely, chylous ascites occurs as an iatrogenic complication after left-sided laparoscopic donor nephrectomy (LDN). Injury to the cisterna chyli and its main lymphatic tributaries around the para-aortic region intraoperatively can cause the lymphatic fluid to accumulate. There is currently no standardized treatment for chylous ascites as there have only been 54 cases documented to date. Most patients can be managed with conservative therapy. Recommended guidelines include high-protein and low-fat diet with medium-chain triglycerides. Paracentesis is often used as a diagnostic and therapeutic first-line measure with total parenteral nutrition (TPN), bowel rest, and somatostatin analogue as adjunct therapies. We present a case of massive chylous ascites refractory to conservative therapy. The patient had progressive abdominal distention and unintentional weight gain 2 weeks postoperatively warranting multiple paracenteses of >7 L of chylous fluid. Ultimately, the patient was successfully treated with lymphatic embolization using N-butyl cyanoacrylate glue.

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Homologous recombination (HR) is a DNA repair process critical for maintaining genomic integrity. HR is generally beneficial, but over‐ or under‐utilization of HR can lead to can lead to deleterious rearrangements and cancer. To study HR, our laboratory previously developed the Fluorescent Yellow Direct Repeat (FYDR) mouse in which HR yields a fluorescent signal.We have utilized this mouse to study the interplay between HR and non‐homologous end‐joining (NHEJ) by knocking out the Ku86 protein. Both pathways are known to repair double strand breaks (DSB); preventing NHEJ in Ku86−/− mice resulted in an increase in HR. The newly proposed alternative end‐joining pathway was explored by knocking down the repair protein Ercc1. The Ercc1−/Δ mice showed an increase in HR in the pancreas, confirming in vivo an alternative DSB repair pathway and implicating ERCC1 in this pathway.While an excellent tool, the FYDR mouse is limited to study of HR in the pancreas and skin. We created the RADR (Recombination at a Direct Repeat) mouse, an improved model that has enabled our study of HR in a wide range of tissues including gut and liver. We can now study DNA damage and HR in multiple tissues in response to a treatment or exposure.Grant Funding Source : NIEHS Grant T32‐ES07020, NSF GRF, NIH Grant# P01‐CA026731‐31, R33‐CA112151‐01A2

Homologous recombination (HR) is a DNA repair process that is critical for maintaining genomic integrity. HR is necessary for survival of vertebrate cells, but over‐ or under‐utilization of HR can lead to deleterious rearrangements and cancer. To study HR in vivo, we created the RADR (Rosa26 Direct Repeat) mouse that has enabled study of HR in a variety of tissues. The RADR mouse harbors two truncated EGFP genes integrated in the Rosa26 locus. Repair via HR at the substrate can yield a full‐length EGFP gene, resulting in a fluorescent cell. The frequency of HR can be estimated by flow cytometry or visualized in situ. The RADR mouse enables studies of DNA damage and repair in response to endogenous and exogenous factors in multiple tissues, which has never before been possible. We observed the accumulation of recombinant cells in the colon, liver and pancreas with age; this correlates with our understanding of age as a risk factor for cancer. We have also crossed the RADR mice with GPT‐Δ mice, enabling quantification of point mutations and small deletions. We crossed these mice with Rag2−/− mice allowing the study of sequence changes with enhanced innate immune response. In ongoing studies, we are investigating the impact of environmentally induced inflammation on susceptibility to large‐scale sequence rearrangements, point mutations and small deletions in multiple tissues. This work is supported by the NCI, NIEHS, NSF GRF.Grant Funding Source: NSF GRF, NCI, NIEHS