Recently, cardiac telocytes were found in the myocardium. However, the functional role of cardiac telocytes and possible changes in the cardiac telocyte population during myocardial infarction in the myocardium are not known. In this study, the role of the recently identified cardiac telocytes in myocardial infarction (MI) was investigated. Cardiac telocytes were distributed longitudinally and within the cross network of the myocardium, which was impaired during MI. Cardiac telocytes in the infarction zone were undetectable from approximately 4 days to 4 weeks after an experimental coronary occlusion was used to induce MI. Although cardiac telocytes in the non-ischaemic area of the ischaemic heart experienced cell death, the cell density increased approximately 2 weeks after experimental coronary occlusion. The cell density was then maintained at a level similar to that observed 1–4 days after left anterior descending coronary artery (LAD)-ligation, but was still lower than normal after 2 weeks. We also found that simultaneous transplantation of cardiac telocytes in the infarcted and border zones of the heart decreased the infarction size and improved myocardial function. These data indicate that cardiac telocytes, their secreted factors and microvesicles, and the microenvironment may be structurally and functionally important for maintenance of the physiological integrity of the myocardium. Rebuilding the cardiac telocyte network in the infarcted zone following MI may be beneficial for functional regeneration of the infarcted myocardium.

The midterm effects of cardiac telocytes (CTs) transplantation on myocardial infarction (MI) and the cellular mechanisms involved in the beneficial effects of CTs transplantation are not understood. In the present study, we have revealed that transplantation of CTs was able to significantly decrease the infarct size and improved cardiac function 14 weeks after MI. It has established that CT transplantation exerted a protective effect on the myocardium and this was maintained for at least 14 weeks. The cellular mechanism behind this beneficial effect on MI was partially attributed to increased cardiac angiogenesis, improved reconstruction of the CT network and decreased myocardial fibrosis. These combined effects decreased the infarct size, improved the reconstruction of the LV and enhanced myocardial function in MI. Our findings suggest that CTs could be considered as a potential cell source for therapeutic use to improve cardiac repair and function following MI, used either alone or in tandem with stem cells.

BackgroundImprovements in vitrification and frozen embryo transfer (FET) technologies have rapidly increased, and some evidence suggests that FET may increase pregnancy rates and lead to more favourable perinatal outcomes. However, the outcome of interest should be offspring safety. Therefore, the primary objective of our study was to investigate whether FET was preferable to fresh embryo transfer (ET) in terms of full-term neonatal birthweight and congenital malformations.MethodsThis was a retrospective cohort study of patients with no pregnancy-related complications who underwent first fresh ETs (n = 2059) or FETs (n = 2053), resulting in full-term singletons births. Outcome measures were neonatal birthweight, low birthweight (LBW), small-for-gestational age (SGA), large-for-gestational age (LGA), macrosomia and congenital malformations. Additionally, we used logistic regression to adjust for baseline characteristics (age, BMI, No. of embryos transferred and embryo stage) between the two groups.ResultsThe mean neonatal birthweight was higher for singletons born after FET than for singletons born after fresh ET (3468.7 ± 475.3 vs. 3386.7 ± 448.1; p < 0.001). The frequencies of full-term singleton LBW and SGA after FET were significantly lower than those after fresh ET (1.7% vs. 3.0 and 4.4% vs. 6.7%, respectively), with adjusted rate ratios of 0.59 (95% CI, 0.37 to 0.98; p = 0.026) and 0.73 (95% CI, 0.55 to 0.99; p = 0.041), respectively. FET resulted in higher frequencies of macrosomia and LGA (15.1% vs 10.2 and 22.8% vs. 17.5%, respectively) than fresh ET, with adjusted rate ratios of 1.43 (95% CI, 1.16 to 1.75; p = 0.001) and 1.26 (95% CI, 1.07 to 1.49; p = 0.007), respectively. Furthermore, the incidence of congenital malformations was not different between the two groups (1.2% vs. 0.9%), with a rate ratio of 0.288.ConclusionsAfter the cycles with pregnancy-related complications were excluded and after adjustments for baseline characteristics, women undergoing FET were associated with a higher neonatal birthweight than women undergoing fresh ET cycles. Additionally, the FET protocol was associated with lower rates of LBW and SGA and higher rates of macrosomia and LGA than the fresh ET protocol. Meanwhile, no difference in the congenital malformation rate was evident between the two groups.

A limited number of studies have explored whether the role of circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) in the pathogenesis of acute myocardial infarction (AMI) is sex specific. The purpose of the present study was to examine sex differences in plasma PCSK9 in Chinese patients with AMI. In this study, a total of 281 records from patients presenting with AMI were analyzed.We compared hospital data and plasma PCSK9 levels by sex difference for inpatients presenting with AMI. After 1 year of follow-up, major adverse cardiac events(MACE) were recorded. A Cox proportional hazards model was used to calculate hazard ratios with 95% confidence intervals. We found that, compared with male groups, PCSK9 levels were higher in female patients not only for overall patients with AMI but also for patients with ST-elevation myocardial infarction (STEMI) (median: 273.6 [215.6–366.8] vs. 325.1 [247.5–445.3] ng/ml, P = 0.0136; 273.4 [215.6–369.7] vs. 317.1 [249.6–450.1], P = 0.0275, respectively). The cumulative incidence of cardiac death and 1-year MACE were significantly higher in the female group compared with male group (10% vs. 2.74%, P = 0.025; 15% vs. 4.11%, P = 0.0054, respectively). On multivariate Cox regression analysis, female sex, total triglyceride, glycosylated hemoglobin A, and homocysteic acid were independent risk factors of 1-year MACE. There was no significant correlation between PCSK9 and 1-year MACE in total AMI patients. In conclusion, PCSK9 levels and 1-year MACE were higher in women with AMI than in men with AMI, however, female sex but not PCSK9 were significant correlated with the 1-year MACE. The clinical implications of this finding are worthy of further investigations and must be confirmed in larger cohorts.

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