This paper presents an efficient pathway to achieve the dielectric constant as low as 2.48 @ 25 °C, 1 MHz for nonporous poly(imide siloxane) films with mechanical and thermal robustness. A symmetric disiloxane-linked alkyl diamine, bis(aminopropyl)tetramethyldisiloxane (BATMS) with a well-defined molecular formula NH2CH2CH2CH2Si(CH3)2OSi(CH3)2CH2CH2CH2NH2, has been used to controllably reduce the dielectric constant of the polymer films by adjusting the loading of BATMS. The thermal stability of all the polymer films remains robust with T5 and T10 no less than 458 and 472 °C, respectively, while the glass-transition temperature decreases with increasing incorporation of flexible disiloxane-alkyl segments into a polymer backbone. There exists a consistent regularity between the thermal, optical, and dielectric properties with the loading amount of BATMS in the polymer films, inferring that the disiloxane-alkyl segments are homogeneously distributed in the polymer backbone. Charge-transfer complex inhibition of polymer films by disiloxane segments has been revealed by an enlarged d-spacing in wide-angle X-ray diffraction spectra and a blue shift in film fluorescence emission spectra. The combined low dielectric constant, robust mechanical and thermal stability, and improved hydrophobicity make the series of BATMS-resulting poly(imide siloxane) films promising candidates for sophisticated flexible microelectronic application.

Cardiovascular disease is one of the main human health risks, and the incidence is increasing. Salidroside is an important bioactive component of Rhodiola rosea L., which is used to treat Alzheimer’s disease, tumor, depression, and other diseases. Recent studies have shown that salidroside has therapeutic effects, to some degree, in cardiovascular diseases via an antioxidative mechanism. However, evidence-based clinical data supporting the effectiveness of salidroside in the treatment of cardiovascular diseases are limited. In this review, we discuss the effects of salidroside on cardiovascular risk factors and cardiovascular diseases and highlight potential antioxidant therapeutic strategies.

Background. With the development of biological technology, biomarkers for the prevention and diagnosis of acute coronary syndrome (ACS) have become increasingly evident. However, the study of novel circular RNAs (circRNAs) in ACS is still in progress. This study aimed to investigate whether the regulation of circRNA-miRNA networks is involved in ACS pathogenesis. Methods. We used microarray analysis to detect significantly expressed circRNAs and miRNAs in the peripheral blood of patients in the control group (CG) and ACS groups, including an unstable angina pectoris (UAP) group and an acute myocardial infarction (AMI) group. A circRNA-miRNA interaction network analysis was carried out with open-source bioinformatics. The gene ontology (GO), pathway, and disease enrichment analyses for differentially expressed circRNAs were further analysed with hierarchical clustering. Results. A total of 266 circRNAs (121 upregulated and 145 downregulated, P<0.05, fold change FC ≥2) and 3 miRNAs (1 upregulated and 2 downregulated, P<0.05, FC ≥ 1.2) were differentially expressed in the ACS groups compared with those in the CG. In addition, among these expressed circRNAs and miRNAs, a single circRNA could bind to more than 1–100 miRNAs, and vice versa. Next, an AMI-UAP network, an AMI-CG network, a UAP-CG network, and an AMI-CG-UAP network were constructed. The top 30 enriched GO terms among the three groups were emphasized as differentially expressed. Disease enrichment analysis showed that these differentially expressed circRNAs are involved in the pathogenesis of cardiovascular diseases. KEGG pathway analysis was performed to identify pathways associated with circRNAs targeting mRNAs. Conclusion. CircRNAs are closely related to the pathological process of ACS via a mechanism that may be related to the up- or down-regulation of circRNAs and miRNAs and circRNA-miRNA coexpression. The metabolic pathways, signalling pathways, and diseases affected by these circRNAs can be predicted by enrichment analysis.

Mitophagy is involved in the development of various cardiovascular diseases, such as atherosclerosis, heart failure, myocardial ischemia/reperfusion injury, and hypertension. Mitophagy is essential for maintaining intracellular homeostasis and physiological function in most cardiovascular origin cells, such as cardiomyocytes, endothelial cells, and vascular smooth muscle cells. Mitophagy is crucial to ensuring energy supply by selectively removing dysfunctional mitochondria, maintaining a balance in the number of mitochondria in cells, ensuring the integrity of mitochondrial structure and function, maintaining homeostasis, and promoting cell survival. Substantial research has indicated a "dual" effect of mitophagy on cardiac function, with inadequate and increased mitochondrial degradation both likely to influence the progression of cardiovascular disease. This review summarizes the main regulatory pathways of mitophagy and emphasizes that an appropriate amount of mitophagy can prevent endothelial cell injury, vascular smooth muscle cell proliferation, macrophage polarization, and cardiomyocyte apoptosis, avoiding further progression of cardiovascular diseases.