A rare case of incarcerated appendix in a port site hernia: A case report.

INTRODUCTION AND IMPORTANCE: Hernias containing the vermiform appendix are very rare. The more common of these have eponyms, such as Amyand's hernia (incidence of 0.5-1 %) and de Garengeot's hernia (incidence of 0.8-1 %). Laparoscopic port site hernias containing the vermiform appendix are even more obscure with only seven previously reported cases. PRESENTATION OF CASE: A 71-year-old male presented with a palpable, non-reducible right lateral periumbilical mass, diagnosed preoperatively as an irreducible hernia at a port site from prior laparoscopic surgery. He had previously undergone laparoscopic bilateral inguinal hernia repairs with the 10 mm right lateral periumbilical port site defect within the musculoaponeurotic abdominal wall. DISCUSSION: There are recommendations regarding the closure of most 10-12 mm port sites, and all 15 mm port sites, given most port site hernias are associated with larger trocars. It is reasonable to conclude that if our patient's 10 mm right lateral periumbilical port site received fascial closure, the resultant hernia may have been prevented. CONCLUSION: Fascial closure of port sites >5 mm poses an easy and effective way to reduce risk of port site hernias as well as other potential complications, therein reducing readmission, need for additional surgery, and improving patient quality of life.

Hepatic neddylation deficiency triggers fatal liver injury via inducing NF-κB-inducing kinase in mice.

The conjugation of neural precursor cell expressed, developmentally downregulated 8 (NEDD8) to target proteins, termed neddylation, participates in many cellular processes and is aberrant in various pathological diseases. Its relevance to liver function and failure remains poorly understood. Herein, we show dysregulated expression of NAE1, a regulatory subunit of the only NEDD8 E1 enzyme, in human acute liver failure. Embryonic- and adult-onset deletion of NAE1 in hepatocytes causes hepatocyte death, inflammation, and fibrosis, culminating in fatal liver injury in mice. Hepatic neddylation deficiency triggers oxidative stress, mitochondrial dysfunction, and hepatocyte reprogramming, potentiating liver injury. Importantly, NF-κB-inducing kinase (NIK), a serine/Thr kinase, is a neddylation substrate. Neddylation of NIK promotes its ubiquitination and degradation. Inhibition of neddylation conversely causes aberrant NIK activation, accentuating hepatocyte damage and inflammation. Administration of N-acetylcysteine, a glutathione surrogate and antioxidant, mitigates liver failure caused by hepatic NAE1 deletion in adult male mice. Therefore, hepatic neddylation is important in maintaining postnatal and adult liver homeostasis, and the identified neddylation targets/pathways provide insights into therapeutically intervening acute liver failure.