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Abstract Grape is a globally significant fruit-bearing crop, and the grape flower bud differentiation essential to fruit production is closely related to light quality. To investigate the regulatory mechanism of grape flower bud differentiation under red‒blue light, the transcriptome and hormone content were determined at four stages of flower bud differentiation. The levels of indole-3-acetic acid (IAA) and abscisic acid (ABA) in grape flower buds at all stages of differentiation under red‒blue light were higher than those in the control. However, the levels of cytokinins (CKs) and gibberellic acid (giberellins, GAs) fluctuated continuously over the course of flower bud differentiation. Moreover, many differentially expressed genes were involved in auxin, CK, GA, and the ABA signal transduction pathways. There were significant differences in the AUX/IAA, SAUR, A-RR, and ABF gene expression levels between the red‒blue light treatment and the control buds, especially in regard to the ABF genes, the expression levels of which were completely different between the two groups. The expression of GBF4 and AI5L2 in the control was always low, while the expression under red‒blue light increased. AI5L7 and AI5L5 expression levels showed an upwards trend in the control plant buds and gradually decreased in red‒blue light treatment plant buds. Through weighted gene coexpression network analysis, we determined that the transcription factors WRK48 (WRKY family), EF110 (ERF family), ABR1, CAMTA3 (CAMTA family), and HSFA3 (HSF family) may be involved in the regulation of the GBF4 gene. This study lays a foundation for further analysis of grape flower bud differentiation regulation under red‒blue light.

Abstract Cardiovascular disease is one of the main causes of death in diabetes mellitus (DM) patients. The aim of the current study was to explore the value of peak strain dispersion (PSD) for discovering early-stage left ventricular (LV) dysfunction in type 2 diabetes mellitus (T2DM) patients. One hundred and one T2DM patients and sixty healthy subjects were selected for this study. T2DM patients were further divided into controlled blood glucose (HbA1c

Abstract Obesity causes low-grade inflammation that is involved in male infertility. Interleukin 1 beta (IL1β) plays an important role in this process. A high-fat diet (HFD) is the most common cause of obesity. However, the effect of a HFD on IL1β and its consequence in reproduction remain unclear. We established a HFD model in mice treated at immature stage (mice-TIS) and mice treated at mature stage (mice-TMS). Surprisingly, we found that a HFD decreased IL1β levels and was accompanied by an increase in testosterone in mice-TIS, while the reverse results were observed in mice-TMS. In addition, a HFD caused a reduction in testis macrophages and in the expression of inflammasome-related genes and proteins in mice-TIS. Furthermore, we found that IL1β inhibited testosterone secretion through down-regulating the gene expression of P450SCC and P450c17. However, the influence on mice-TIS that were induced by a HFD was recovered by stopping the HFD. In this study, we are the first to report that a HFD impairs the reproductive system by decreasing IL1β and enhancing testosterone levels in mice-TIS, which are different from the effects in mice-TMS. This provides new ideas for the treatment of obesity-induced infertility.