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The zebrafish (Danio rerio) is an emerging genetic model for regenerative medicine. In humans, myocardial infarction results in the irreversible loss of cardiomyocytes. However, zebrafish hearts fully regenerate after a 20% ventricular resection, without either scarring or arrhythmias. To study this cardiac regeneration, we developed implantable flexible multi-microelectrode membrane arrays that measure the epicardial electrocardiogram signals of zebrafish in real-time. The microelectrode electrical signals allowed for a high level of both temporal and spatial resolution (~20 μm), and the signal to noise ratio of the epicardial ECG was comparable to that of surface electrode ECG (7.1 dB vs. 7.4 dB, respectively). Processing and analysis of the signals from the microelectrode array demonstrated distinct ECG signals: namely, atrial conduction (P waves), ventricular contraction (QRS), and ventricular repolarization (QT interval). The electrical signals were in synchrony with optically measured Calcium concentration gradients in terms of d[Ca2+]/dt at both whole heart and tissue levels. These microelectrodes therefore provide a real-time analytical tool for monitoring conduction phenotypes of small vertebral animals with a high temporal and spatial resolution.

It appears that nonsense, frameshift, and mutations on Arg466 can cause lower level of C1 inhibitor antigen than missense and in-frame mutations; however, it does not affect severity of symptoms.

The development of early B cells, which are generated from hematopoietic stem cells (HSCs) in a series of well-characterized stages in bone marrow (BM), represents a paradigm for terminal differentiation processes. Akt is primarily regulated by phosphorylation at Thr308 by PDK1 and at Ser473 by mTORC2, and Akt signaling plays a key role in hematopoiesis. However, the role of mTORC2 in the development of early B cells remains poorly understood. In this study, we investigated the functional role of mTORC2 by specifically deleting an integral component, Rictor, in a hematopoietic system. We demonstrated that the deletion of Rictor induced an aberrant increase in the FoxO1 and Rag-1 proteins in BM B cells and that this increase was accompanied by a significant decrease in the abundance of B cells in the peripheral blood (PB) and the spleen, suggesting impaired development of early B cells in adult mouse BM. A BM transplantation assay revealed that the B cell differentiation defect induced by Rictor deletion was not affected by the BM microenvironment, thus indicating a cell-intrinsic mechanism. Furthermore, the knockdown of FoxO1 in Rictor-deleted HSCs and hematopoietic progenitor cells (HPCs) promoted the maturation of B cells in the BM of recipient mice. In addition, we revealed that treatment with rapamycin (an mTORC1 inhibitor) aggravated the deficiency in B cell development in the PB and BM. Taken together, our results provide further evidence that Rictor regulates the development of early B cells in a cell-intrinsic manner by modifying the expression of FoxO1 and Rag-1.

Purpose This study aimed to assess the effects of transitional health management on adherence and prognosis in elderly patients with acute myocardial infarction undergoing percutaneous coronary intervention. Methods We conducted the trial from June 2016 to December 2016. A total of one hundred and fifty patients with acute myocardial infarction after PCI who met the inclusion criteria were randomly divided into an experimental (n = 75) group and a control (n = 75) group. The participants in the experimental group received transitional health management for three months. The two groups of patients were evaluated for treatment adherence, quality of life, clinical indicators, adverse cardiovascular events and statistics regarding readmission rates at baseline and 6 months after discharge. Results Compared with the controls, patients in the intervention group demonstrated better medication adherence, reexamination adherence, healthy lifestyle and clinical indicators (all P<0.05) and lower rates of adverse cardiovascular events and readmission (all P<0.05). Conclusion Transitional health management effectively improved adherence in elderly patients with acute myocardial infarction after PCI, ameliorated clinical indicators, and effectively reduced the incidence of adverse cardiovascular events and readmission rates. Transitional health management was an effective intervention for PCI patients after discharge.

Long non-coding RNAs (lncRNAs) play an important role in epigenetic regulation, and abnormalities may lead to male infertility. To investigate whether lncRNAs are involved in intergenerational inheritance of obesity and obesity-induced decline in fertility, we divided mice into obesity (F0 mice fed a high-fat diet, F0-HFD) and non-obese (F0 mice fed normal chow, F0-NC) model groups and their male offspring (F1-HFD and F1-NC, respectively). We examined the differences in the expression levels of lncRNAs and mRNAs in the F0-HFD/F0-NC and F1-HFD/F1-NC groups. The results revealed similar expression patterns in the F1-HFD/F0-HFD groups at both the lncRNA and mRNA levels. The maximum difference in the lncRNA expression was observed between the F0-HFD and F0-NC groups. The differentially expressed lncRNA targets and mRNAs identified in our study are mainly involved in GnRH signalling pathway, metabolic process, and Hippo signalling pathway; similarly expressed lncRNAs and mRNAs in F1-HFD/F0-HFD are closely linked with G-protein coupled receptor signalling pathway, pancreatic polypeptide receptor activity, and lysine biosynthesis, which may play an important role in the molecular mechanism of intergenerational inheritance of obesity. Furthermore, potential genes that might play important roles in the pathogenesis of obesity-related low fertility were revealed by lncRNA-and mRNA-interaction studies based on the microarray expression profiles. In conclusion, we found that lncRNA could be involved in obesity-induced infertility by expressing abnormalities, which could act as genetic vectors of paternal inheritance of obesity.

Coronary atherosclerosis is a long‐term, sustained, and evolving inflammatory disease manifested with the remodeling of the coronary arteries. The purpose of this study is to explore the potential role of microRNA‐107 (miR‐107) in vascular endothelial cells (VECs) in coronary atherosclerosis by regulating the KRT1 gene and the Notch signaling pathway. A mouse model of coronary atherosclerosis was established. The relationship between miR‐107 and KRT1 was analyzed and verified by dual‐luciferase reporter assay. The functional role of miR‐107 in coronary atherosclerosis was determined using ectopic expression and depletion. Blood lipid levels and atherosclerotic index (AI) were measured in atherosclerotic mice. Expression pattern of miR‐107, KRT1, Notch signaling pathway, inflammatory/anti‐inflammatory factors, and endoplasmic reticulum (ER) stress‐related genes was evaluated by means of reverse transcription quantitative polymerase chain reaction, western blot analysis, and enzyme‐linked immunosorbent assay. Meanwhile, cell‐cycle distribution and cell apoptosis in VECs were assessed by flow cytometry. Atherosclerotic mice exhibited higher blood lipid levels, AI, apoptotic index, and KRT1‐positive expression as well as inhibited Notch signaling pathway when compared with normal mice. The miR‐107 was revealed to bind to KRT1; miR‐107 upregulation or KRT1 silencing resulted in reductions in blood lipid levels and AI, inhibition in cell apoptosis, inflammation, and ER stress. Restored miR‐107 or downregulated KRT1 activated the Notch signaling pathway. These results supported the notion that miR‐107‐targeted KRT1 inhibition activated the Notch pathway, thereby, protecting against the coronary atherosclerosis. Findings in this study might provide a novel biomarker for the coronary atherosclerosis treatment.