Herniation of the Right Colon, From the Cecum to the Hepatic Flexure, Through the Foramen of Winslow: A Case Report.

Herniation of bowel contents between the peritoneal cavity proper and the omental bursa, through the foramen of Winslow, can present diagnostic challenges that can potentially delay necessary surgical intervention. This case describes a 49-year-old female with a past medical history of hiatal hernia and biliary dyskinesia who presented to the emergency department with severe epigastric and right lower quadrant abdominal pain one day after a reported gastrointestinal illness of unknown etiology. Initial emergency department workup demonstrated an elevated white blood cell count without lactic acidosis. Computed tomography imaging was interpreted as gastric distension with volvulus around the mesentery and second portion of the duodenum. Intraoperatively, the entirety of the right colon was noted to have passed through the foramen of Winslow into the lesser sac. This led to twisting of the mesocolon causing compression of the duodenum and a gastric outlet obstruction. After surgical reduction of the herniation, the patient noted great improvement in pain and other symptoms.

Multifaceted Effects of Kinase Inhibitors on Pancreatic Cancer Cells Reveals Pivotal Entities with Therapeutic Implications.

Pancreatic cancer is one of the most aggressive forms of cancer and is the seventh leading cause of cancer deaths worldwide. Pancreatic ductal adenocarcinoma (PDAC) accounts for over 90% of pancreatic cancers. Most pancreatic cancers are recalcitrant to radiation, chemotherapy, and immunotherapy, highlighting the urgent need for novel treatment options for this deadly disease. To this end, we screened a library of kinase inhibitors in the PDAC cell lines PANC-1 and BxPC-3 and identified two highly potent molecules: Aurora kinase inhibitor AT 9283 (AT) and EGFR kinase inhibitor WZ 3146 (WZ). Both AT and WZ exhibited a dose-dependent inhibition of viability in both cell lines. Thus, we conducted an in-depth multilevel (cellular, molecular, and proteomic) analysis with AT and WZ in PANC-1 cells, which harbor KRAS mutation and exhibit quasimesenchymal properties representing pancreatic cancer cells as having intrinsic chemoresistance and the potential for differential response to therapy. Elucidation of the molecular mechanism of action of AT and WZ revealed an impact on the programmed cell death pathway with an increase in apoptotic, multicaspase, and caspase 3/7 positive cells. Additionally, the key survival molecule Bcl-2 was impacted. Moreover, cell cycle arrest was observed with both kinase inhibitors. Additionally, an increase in superoxide radicals was observed in the AT-treated group. Importantly, proteomic profiling revealed differentially regulated key entities with multifaceted effects, which could have a deleterious impact on PDAC. These findings suggest potential targets for efficacious treatment, including a possible increase in the efficacy of immunotherapy using PD-L1 antibody due to the upregulation of lactoferrin and radixin. Furthermore, combination therapy outcomes with gemcitabine/platinum drugs may also be more effective due to an increase in the NADH dehydrogenase complex. Notably, protein-protein interaction analysis (STRING) revealed possible enrichment of reactome pathway entities. Additionally, novel therapy options, such as vimentin-antibody--drug conjugates, could be explored. Therefore, future studies with the two kinases as monotherapy/combination therapy are warranted.