To explore the active constituents of Sedum aizoon L in the treatment of coronary heart disease based on network pharmacology and molecular docking methodology.

Background: There is a lack of effective drugs for the treatment of coronary heart disease (CHD). Sedum aizoon L (SL) has multiple effects, and there is no report on CHD in SL at present. The aim of this study is to explore the mechanisms of action of SL in the treatment of CHD based on network pharmacology and molecular docking technology. Methods: The targets and active ingredients of SL were screened using the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database, and CHD-related targets were obtained by searching GeneCards and DisGeNet databases. The intersection of LS active ingredient targets and CHD targets was used to construct a "drug-ingredient-disease-target" network using the Cytoscape software. The STRING database was used to construct a protein-protein interaction (PPI) network, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed. Key targets and core active ingredients were selected and molecular docking was performed using the AutoDock software. Results: According to the predicted results, a total of 134 corresponding target genes for LS, 12 active components, 1,704 CHD-related targets, and 52 intersecting targets were obtained. GO function and KEGG pathway analysis showed that the key targets were involved with signal transducer and activator of transcription 3 (STAT3), tumor protein p53 (TP53), and vascular endothelial growth factor A (VEGFA). The molecular docking results showed that the key targets bound to the important active ingredients in a stable conformation. The core active ingredients of LS in the treatment of CHD were determined to be ursolic acid, myricetin, and beta-sitosterol. Conclusions: SL may act on targets such as STAT3, TP53, and VEGFA through tumor necrosis factor (TNF) signaling pathway, interleukin 17A (IL-17A) signaling pathway, AGE-RAGE signaling pathway in diabetic complications, and other related pathways, thereby playing a role in preventing and treating CHD.

Fatal pulmonary embolism complicating a postoperative chylothorax despite adequate thromboprophylaxis.

Chylothorax is a recognized complication of intrathoracic surgery, but its occurrence after coronary artery bypass grafting (CABG) is very rare. We report a case of a fatal pulmonary embolism as a complication of chylothorax following CABG. The patient was an 82-year-old woman who presented with increasing chest pain 2 weeks after discharge after an uncomplicated CABG. A computerized tomography (CT) scan with contrast angiogram showed a left-sided pleural effusion and no concurrent pulmonary embolus. Analysis of the pleural effusion revealed a chylothorax, which was treated with chest tube drainage and total parenteral nutrition followed by an oral medium-chain fatty acid diet. The patient improved steadily but, on day 6, she developed acute hypoxemic respiratory failure and shock. A CT angiogram revealed a massive pulmonary embolus and, despite thrombolysis, the patient died. Autopsy confirmed an acute saddle embolus in the pulmonary trunk. The patient had received appropriate venous thromboembolism prophylaxis with subcutaneous unfractionated heparin during her hospital course. This is the first reported case of a fatal pulmonary embolism that occurred in the setting of a post-CABG chylothorax in adults. The occurrence of this complication despite unfractionated heparin thromboprophylaxis may suggest a role for other, more effective medications, such as low molecular weight heparin or fondaparinux in patients with chylothorax.

Mixed adenoneuroendocrine carcinoma (MANEC) of the gallbladder: a possible stem cell tumor?

A 48 year-old African American woman presented to her physician complaining of a rapidly evolving epigastric and right upper quadrant abdominal pain. A PET-CT of the abdomen and pelvis demonstrated hypermetabolic, polypoid masses within the gallbladder and several tumors in the left lobe of the liver for which she underwent diagnostic laparoscopy. The gallbladder revealed a 3.5 × 3.3 × 2.4 tan-brown exophytic mass located at the fundus and growing into the lumen with multiple contiguous papillary projections arising from the mucosal surface. A concurrent large cell neuroendocrine carcinoma and papillary adenocarcinoma of the gallbladder was revealed histologically. There was shared reactivity to antibodies directed against the distinct antigens for each morphological component with transitional tumor cells (of both histological components) located at the areas where the two tumor types merged, revealing common immunoreactivity for carcinoembryonic antigen, cancer antigen 19-9, keratin 19, c-kit (cluster of differentiation protein 117 (CD117)) and epithelial cell adhesion molecule. Ultrastructurally, individual cells were demonstrated to have overlapping features of neuroendocrine and glandular differentiation. The aforementioned histological, ultrastructural and immunohistochemical profile is strongly suggestive of a biphenotypic stem/progenitor cell tumor of the gallbladder.