Combination of myocardial perfusion imaging, left ventricle function parameters and coronary artery calcium score in risk evaluation in patients with diabetes mellitus.

OBJECTIVE: Myocardial perfusion imaging (MPI) can be challenging in some cases of multi vessel involvement. Our aim was to examine specific group of patients with diabetes mellitus (DM), who did not have significant reversible ischaemia diagnosed on perfusion study itself, and asses additional value of functional parameters obtained from gated acquisition and added information from coronary artery calcium score (CACS). SUBJECTS AND METHODS: One hundred and seventy eight patients with a history of DM, with summed difference score (SDS)≤1, were included in the study. All patients underwent gated acquisition with recording of functional parameters and CACS evaluation. During the follow-up, cardiac events (CE) were recorded. RESULTS: During the median follow-up of 20.3 months there were 23 CE encountered. Optimal cut-off value for CACS to predict CE was found at 1427, higher values were significantly related to CE (P<0.001). Low stress left ventricular ejection fraction (LVEF) <45% and induced stress LVEF drop for 5% were also more frequent in CE group (P=0.001, P=0.008). Multivariable Cox analysis revealed low stress LVEF (P=0.001, HR=4.48, 95%CI 1.79-11.22), stress induced LVEF drop (P=0.017, HR 3.13, 95%CI 1.22-8.01) and high CACS (P<0.001, HR 10.52, 95%CI 4.32-25.63) as significant predictors of CE. CONCLUSION: Low stress LVEF under 45%, post-stress LVEF drop for more than 5% and CACS more than or equal to 1427 are significant predictors of CE in patients with DM, who did not have reversible ischemia detected on MPI single photon emission computed tomography (SPECT).

Aurora kinase A drives MTOC biogenesis but does not trigger resumption of meiosis in mouse oocytes matured in vivo.

Aurora kinase A (AURKA) is an important mitotic kinase involved in the G2/M transition, centrosome maturation and separation, and spindle formation in somatic cells. We used transgenic models that specifically overexpress in mouse oocytes either wild-type (WT-AURKA) or a catalytically inactive (kinase-dead) (KD-AURKA) AURKA to gain new insights regarding the role of AURKA during oocyte maturation. AURKA activation occurs shortly after hCG administration that initiates maturation in vivo. Although AURKA activity is increased in WT-AURKA oocytes, resumption of meiosis is not observed in the absence of hCG administration. Control oocytes contain one to three microtubule organizing centers (MTOCs; centrosome equivalent) at prophase I. At the time of germinal vesicle breakdown (GVBD), the first visible marker of resumption of meiosis, the MTOC number increases. In WT-AURKA oocytes, the increase in MTOC number occurs prematurely but transiently without GVBD, whereas the increase in MTOC number does not occur in control and KD-AURKA oocytes. AURKA activation is biphasic with the initial activation not requiring CDC25B-CDK1 activity, whereas full activation, which is essential for the increase in MTOCs number, depends on CDK1 activity. AURKA activity also influences spindle length and regulates, independent of its protein kinase activity, the amount of MTOC associated with gamma-tubulin. Both WT-AURKA and KD-AURKA transgenic mice have normal fertility during first 6 mo of life. These results suggest that although AURKA is not a trigger kinase for G2/M transition in mouse oocytes, it regulates MTOC number and spindle length, and, independent of its protein kinase activity, gamma-tubulin recruitment to MTOCs.