[Analysis of mortality relative factors in patients with ventricular septal rupture complicating myocardial infarction].

Objective: To examine the mortality rate and relative factors associate with ventricular septal rupture in myocardial infarction patients. Methods: A total of 51 patients who suffered from myocardial infarction complicating with ventricular septal rupture received operative procedures between January 2005 and December 2018 in Department of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, were retrospectively analyzed. There were 34 males and 17 females, with an age of (63±8) years (range: 44 to 82 years). The time between ventricular septal rupture and surgical procedure was (44±39) days (range: 3 to 187 days). The t test and χ(2) test were used for univariate analysis, Logistics regression model was used for multivariate analysis of in-hospital mortality relative factors. Results: There were 8 patients dead in hospital, 43 patients survived, the overall mortality rate was 15.7% in hospital. The post-operation mortality rate was 2/3 of who suffered ventricular septal rupture and underwent operation within 1 week, but it's markedly decreased to 6.5% if the time over 4 weeks. Univariate analysis showed that renal failure before operation, creatinine before operation, left ventricular ejection fraction, cardiac function (New York Heart Association) grade Ⅳ, severe tricuspid regurgitation, dialysis post-operation, creatinine of the first day of post-operation, the time between and operation more than 4 weeks were in-hospital mortality relative factors. Multivariate analysis reflected that advanced age (OR=1.32, 95%CI: 1.05 to 1.75, P=0.033), cardiac function grade Ⅳ (OR=2.25, 95%CI: 1.62 to 2.82, P=0.003), severe tricuspid regurgitation (OR= 1.82, 95%CI: 1.31 to 2.43, P=0.001), renal failure before operation (OR=1.78, 95%CI: 1.26 to 2.32, P=0.015), the time between ventricular septal rupture and operation less than 1 week (OR=2.50, 95%CI: 1.52 to 2.98, P=0.012), were independent in-hospital mortality relative factors. Conclusions: The surgery operation is an effective way to deal with ventricular septal rupture combined with myocardial infarction. The independent relative factors of in-hospital mortality are advanced age, cardiac function grade Ⅳ, renal failure before operation, severe tricuspid regurgitation, the time between ventricular septal rupture and operation less than 1 week.

MiR-100 regulates cell differentiation and survival by targeting RBSP3, a phosphatase-like tumor suppressor in acute myeloid leukemia.

Acute myeloblastic leukemia (AML) is characterized by the accumulation of abnormal myeloblasts (mainly granulocyte or monocyte precursors) in the bone marrow and blood. Though great progress has been made for improvement in clinical treatment during the past decades, only minority with AML achieve long-term survival. Therefore, further understanding mechanisms of leukemogenesis and exploring novel therapeutic strategies are still crucial for improving disease outcome. MicroRNA-100 (miR-100), a small non-coding RNA molecule, has been reported as a frequent event aberrantly expressed in patients with AML; however, the molecular basis for this phenotype and the statuses of its downstream targets have not yet been elucidated. In the present study, we found that the expression level of miR-100 in vivo was related to the stage of the maturation block underlying the subtypes of myeloid leukemia. In vitro experiments further demonstrated that miR-100 was required to promote the cell proliferation of promyelocytic blasts and arrest them differentiated to granulocyte/monocyte lineages. Significantly, we identified RBSP3, a phosphatase-like tumor suppressor, as a bona fide target of miR-100 and validated that RBSP3 was involved in cell differentiation and survival in AML. Moreover, we revealed a new pathway that miR-100 regulates G1/S transition and S-phase entry and blocks the terminal differentiation by targeting RBSP3, which partly in turn modulates the cell cycle effectors pRB/E2F1 in AML. These events promoted cell proliferation and blocked granulocyte/monocyte differentiation. Our data highlight an important role of miR-100 in the molecular etiology of AML, and implicate the potential application of miR-100 in cancer therapy.