[Gastric adenocarcinoma of the fundic gland type: clinicopathological analysis of six cases].

Objective: To investigate the clinicopathological characteristics of gastric adenocarcinoma of the fundic gland(GA-FG). Methods: A total of 6 patients with GA-FG admitted from January 2014 to May 2019 were identified at Shanghai Songjiang District Central Hospital.Analyzed endoscopic findings, pathological characteristics and immunohistochemical staining of the lesions and reviewed relevant literatures. Results: Among the 6 patients, 3 were male, 3 were female, and the mean age was 66 years. The most common clinical presentation was epigastric discomfort. Gastroscopic examination revealed an elevated or flat lesion in the body of the stomach, with a diameter of 0.4 to 1.0 cm. Histopathologically, they mainly composed of main cells, but there were also scattered parietal cells, arranged in an irregular tubular or cord-like structure, and formed anastomosis branches. The tumor cells were immunohistochemically positive for MUC6 and pepsinogen 1. Conclusions: GA-FG is a rare variant of well-differentiated adenocarcinoma. It is important to understand its clinical features and histological morphology for more accurate diagnosis.

[Tumor necrosis factor-α inhibitor protects against myocardial ischemia/reperfusion injury via Notch1 mediated inhibition of oxidative/nitrative stress in traumatic mice].

OBJECTIVE: To test the effects of TNF-α inhibitor Etanercept on myocardial ischemia/reperfusion (MI/R) injury in posttraumatic mice, and explore related mechanisms. METHODS: Traumatic mouse model was established with Noble-Collip drum. Five days after trauma, Notch1 was knocked down by intramyocardial injection of Notch1 small interfering RNAs (siRNA) or scrambled siRNA (20 µg). Seven days after trauma, mice were subjected to MI/R (30 minutes ischemia followed by reperfusion). Sham operation was similarly performed without coronary artery ligation. Ten minutes before reperfusion, mice received Etanercept (8 mg/kg, i. p.). ELISA was used to detect plasma levels of TNF-α and troponin I (cTnI) and myocardial nitrotyrosine content. Twenty-four hours after reperfusion, left ventricular ejection fraction (LVEF) was measured by echocardiography. Infarct size was determined by Evans blue/2, 3, 5-triphenyl tetrazolium chloride (TTC) double staining. Cardiac caspase-3 activity was detected using a caspase-3 kit. Myocardial TNF-α and Notch1 intracellular domains (Notch1 ICD) expressions were determined by Western blot. Chemiluminescence was used to assess myocardial superoxide anion content. RESULTS: (1) Compared to vehicle group, Etanercept treatment significantly reduced cTnI content, infarct size and caspase-3 activity (all P<0.01), while obviously increased LVEF (P<0.01). (2) Etanercept treatment also significantly reduced plasma and myocardial TNF-α contents (P<0.01), whereas markedly increased myocardial Notch1 ICD content (P<0.05). (3) Compared to scrambled siRNA group, Notch1 deficiency significantly increased cTnI content, infarct size and caspase-3 activity (P<0.05), whereas obviously reduced LVEF (P<0.05). (4) Etanercept significantly reduced myocardial superoxide anion and nitrotyrosine content (P<0.01), which was reversed by downregulation of Notch1 (P<0.05). CONCLUSIONS: TNF-α inhibitor Etanercept can alleviate MI/R injury after trauma by reducing myocardial oxidative/nitrative stress via activating Notch1 signaling pathway.