Artesunate possesses the potential of intervening with glioma, however, its pharmacological mechanisms remain unclarified. Firstly, the effects of artesunate on cell activity, proliferation and apoptosis of U87 and U251 human glioma cells were explored. It was found that artesunate exerted stronger inhibitory effects on the activity and proliferation of U87 cells than U251 cells. It could significantly promote apoptosis in U87 cells (P < 0.05), while only high dose of artesunate can promote that of U251 cells (P < 0.01), detected by Hoechst and TUNEL cell apoptosis staining. Further, the differential expression gene sets between artesunate-sensitive and non-sensitive cell line, as well the therapeutic effects-related genes of artesunate were obtained through transcriptome sequencing and differential data analysis by using the lysates of U87 and U251 cells before and after artesunate treatment, aiming to explore the molecular mechanism of distinct artesunate sensitivity to two types of cells. Then, key putative targets that related to therapeutic effects were screened by constructing the interaction network of differential genes of three above comparison groups, and calculating their topological characteristics. Pathway enrichment analysis showed that those key putative targets were significantly enriched in several signaling pathways that were closely associated with the main pathological changes of glioma, among which apoptosis-related activating transcription factor 4 (ATF4)-DNA damage induced transcript 3 (DDIT3)- polyadenosine diphosphate ribose polymerase 1 (PARP1) signaling axis was the most enriched in. Molecular docking indicated that artesunate had fine binding affinities with ATF4 and DDIT3. Above all, this study preliminarily revealed that ATF4-DDIT3-PARP1 signaling axis is the target pathway of artesunate intervening with U87 glioma cells, and PARP1 may be an important gene for U251 cells to develop resistance to artesunate. Our results not only provide fundamental experimental evidence for artesunate as a potential therapeutic drug in glioma treatment, but shed light into overcoming drug resistance in its clinical therapy.

Gerbode defect is a communication between the left ventricle and right atrium. It is usually congenital rather than acquired, but can occur as a complication of endocarditis, myocardial infarction, trauma, or cardiac surgery. We report a case of surgical repair of acquired Gerbode defect resulting from infective endocarditis. A 69-year-old woman with aortic regurgitation due to infective endocarditis was referred to our hospital with a diagnosis of congestive heart failure. She was hospitalized and underwent medical treatment (intensive antibiotic therapy). Preoperative transthoracic and transesophageal echocardiography were performed and revealed a mobile mass (vegetation) on the aortic valve. The patient also had severe aortic regurgitation and a communication between the left ventricle and right atrium. The communication was visualized in the atrioventricular membranous septum. Due to the mobility of the mass (vegetation) and uncontrollable congestive heart failure caused by severe aortic regurgitation, surgical treatment was advised. Surgery was performed through a median sternotomy with the patient on cardiopulmonary bypass. After aortic cross-clamping, the vegetation was approached through a horizontal incision in the ascending aorta and a right atriotomy. The communication site from the left view was below the commissure between the right coronary and non-coronary cusps ; from the right view, it was just above the tricuspid annulus of the septal leaflet. The defect was closed with two 0.4-mm thick Gore-Tex cardiovascular patches : one was placed on the LV side and the other on the RA side. The aortic valve was replaced with a bioprosthetic valve (SJM Epic 21 mm). The operation was finished and her clinical course was almost uneventful.

Calcified amorphous tumor (CAT) is a non-neoplastic cardiac mass composed of nodules of calcium with a background of amorphous fibrous material and was first described in 1997. This report describes a 61-year-old man, who had been on hemodialysis for 10 years and was referred to our hospital with a diagnosis of acute myocardial infarction. He had percutaneous coronary intervention (PCI) for stenosis of the left anterior descending artery (LAD). He was hospitalized and under medical treatment. A follow-up echocardiogram was performed and revealed a normal ejection fraction of 0.60. Moderate mitral annular calcification with mild-to-moderate mitral stenosis was seen. An ultrasound-mobile mass was visualized in the left ventricular outflow tract (LVOT). There was no hemodynamic evidence of LVOT obstruction on Doppler echocardiography. Transesophageal echocardiography showed a mobile mass attached to the LVOT in the mitral valve annulus that extended almost to the membranous septum. Due to the mobility of the mass and potential for embolism, surgical removal was advised. Concomitant procedures (coronary artery bypass grafting (CABG) and a full maze operation) were proposed because he still had symptoms of chest pain with myocardial ischemia and palpitations due to chronic atrial fibrillation. Surgery was performed through a median sternotomy on cardiopulmonary bypass. After aortic cross-clamping, the mass was approached through a horizontal incision in the ascending aorta. The white tumor was resected easily from the membranous septum. The operation was finished after CABG and a full maze procedure, and his clinical course was uneventful. Histological examination showed that the tumor contained many calcified nodules and fibrino-sanguineous deposits ; these findings are compatible with CAT.