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Harbi Khalayleh,Ashraf Imam,Oded Cohen-Arazi,Pikkel Yoav,Brigitte Helou,Bala Miklosh,Alon J. Pikarsky,Abed Khalaileh 한국간담췌외과학회 2022 Annals of hepato-biliary-pancreatic surgery Vol.26 No.2
Backgrounds/Aims: Traumatic pancreatic injury (TPI) is rare as an isolated injury. There is a trend to perform conservative treatment even in patients with complete duct dissection and successful treatment. This study reviewed our 20 years of experience in the management of TPI and assessed patient outcomes according to age group and treatment strategy. Methods: A retrospective analysis of patients diagnosed and treated with TPI at a level-I trauma center from 2000–2019. Patients were divided into two groups: adults and pediatrics. Conservative treatment cases were subjected to subgroup analysis. Level of evidence: IV. Results: Of a total of 77 patients, the mean age was 24.89 ± 15.88 years. Fifty-six (72.7%) patients had blunt trauma with motor vehicle accident. Blunt trauma was the predominant mechanism in 42 (54.5%) patients. Overall, 38 (49.4%) cases had grade I or II injury, 24 (31.2%) had grade III injury, and 15 (19.5%) had grade IV injury. A total of 30 cases had non-operative management (NOM). Successful NOM was observed in 16 (20.8%) cases, including eight (32.0%) pediatric cases and eight (15.4%) adult cases. Higher American association for the surgery of trauma (AAST) grade of injury was associated with NOM failure (16.7% for grade I/II, 100% for grade III, and 66.7% for grade IV injury; p = 0.001). An independent factor for NOM failure was female sex (69.2% in females vs. 29.4% in males; p = 0.03). Conclusions: High AAST grade TPI is associated with a high rate of NOM failure in both pediatric and adults.
KPC1-Mediated Ubiquitination and Proteasomal Processing of NF-κB1 p105 to p50 Restricts Tumor Growth
Kravtsova-Ivantsiv, Y.,Shomer, I.,Cohen-Kaplan, V.,Snijder, B.,Superti-Furga, G.,Gonen, H.,Sommer, T.,Ziv, T.,Admon, A.,Naroditsky, I.,Jbara, M.,Brik, A.,Pikarsky, E.,Kwon, Y.,Doweck, I.,Ciechanover, Cell Press ; MIT Press 2015 Cell Vol.161 No.2
NF-κB is a key transcriptional regulator involved in inflammation and cell proliferation, survival, and transformation. Several key steps in its activation are mediated by the ubiquitin (Ub) system. One uncharacterized step is limited proteasomal processing of the NF-κB1 precursor p105 to the p50 active subunit. Here, we identify KPC1 as the Ub ligase (E3) that binds to the ankyrin repeats domain of p105, ubiquitinates it, and mediates its processing both under basal conditions and following signaling. Overexpression of KPC1 inhibits tumor growth likely mediated via excessive generation of p50. Also, overabundance of p50 downregulates p65, suggesting that a p50-p50 homodimer may modulate transcription in place of the tumorigenic p50-p65. Transcript analysis reveals increased expression of genes associated with tumor-suppressive signals. Overall, KPC1 regulation of NF-κB1 processing appears to constitute an important balancing step among the stimulatory and inhibitory activities of the transcription factor in cell growth control.