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Plasma aldosterone escape is found during long-term ACE inhibitor therapy of chronic heart failure. Evidence for aldosterone production in cardiovascular tissues raised the question of whether aldosterone escape occurs or not in these tissues. Rats with infarction-induced chronic heart failure were treated with enalapril (20 mg/kg/d) and losartan (15 mg/kg/d) for 20 weeks. Untreated chronic heart failure and sham-operated rats were used as positive and normal controls, respectively. Ex vivo mesenteric artery and heart perfusion, high performance liquid chromatography, and RIA for aldosterone were performed. Chronic heart failure due to myocardial infarction was associated with tissue-specific activation of cardiovascular aldosterone synthesis. In the mesenteric artery, enalapril significantly inhibited aldosterone production compared to untreated, chronic heart failure rats, and losartan lowered aldosterone production to that of sham rats. In myocardium, enalapril failed to significantly inhibit aldosterone production, and losartan significantly inhibited aldosterone production compared to untreated, chronic heart failure rats. These results provide the first evidence that long-term ACE inhibition therapy induces aldosterone escape in myocardium but not in mesenteric artery of chronic heart failure. The angiotensin II subtype 1 receptor blocker losartan tranquilized aldosterone levels in the cardiovascular tissues of chronic heart failure rats.

Background and Objective Previous research has indicated that altered expression of microRNAs (miRNAs) is in connection with osteogenesis of human periodontal ligament‐derived stem cells (hPDLSCs). We investigated the mechanisms by which miR‐543 promotes osteogenic differentiation of hPDLSCs. Material and Methods First, the expression of miR‐543 in hPDLSCs cultured with or without an osteogenic inductive cocktail was explored. Then, the function of miR‐543 during osteogenesis of hPDLSCs was investigated by overexpressing and inhibiting miR‐543. Next, 3 databases were used to predict target genes of miR‐543 and a luciferase report was used to validate the direct regulation of miR‐543 on the target gene. Further, a rescue experiment using co‐transfection of miR‐543 mimic and target mimic was performed to evaluate whether overexpressing the target gene could partly rescue the efficiency of overexpressing miR‐543 on osteogenesis in hPDLSCs. Results miR‐543 was upregulated during osteogenic differentiation of hPDLSCs. Functional experiments showed that overexpressing miR‐543 could enhance osteogenesis, while inhibiting miR‐543 resulted in reduced formation of mineralized nodules. The transducer of ERBB2, 2 (TOB2) was identified as a target gene of miR‐543 and luciferase report revealed that miR‐543 interacts directly with the 3′‐untranslated repeat sequence of TOB2 mRNA. Overexpression of miR‐543 inhibited the expression of TOB2 in both mRNA and protein levels while inhibiting miR‐543 increased. Furthermore, the rescue experiment confirmed the promotional role of miR‐543 TOB2 expression could be abrogated by overexpressing TOB2, which also had the effect of reducing osteogenic differentiation. Conclusion Our research confirmed that miR‐543 is a promoter of osteogenesis in hPDLSCs, acting by inhibiting its target gene TOB2, which suggests that miR‐543 may be a potential therapy for bone loss in periodontitis.

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Objective: To determine if qualitative and quantitative measures of prefemoral fat pad (PFP) and quadriceps fat pad (QFP) are associated with incident radiographic osteoarthritis (iROA) over 4 years in the Osteoarthritis Initiative (OAI) study. Design: Participants in this nested caseecontrol study were selected from the OAI study with knees that had Kellgren Lawrence grades (KLG) of 0 or 1 at baseline. Case knees were defined by iROA (KLG 2) over 4 years. Control knees without iROA were matched 1:1 with case knees. Magnetic resonance images (MRIs) were read at P0 (time of onset of iROA), P-1 (1 year prior to P0) and baseline, and used to assess PFP (i.e., prefemoral hyperintensity alteration, patellofemoral hyperintensity alteration, maximum axial area) and QFP (i.e., hyperintensity alteration, mass effect, maximum axial area). Conditional logistic regression analyses were performed to study the associations between PFP/QFP measures and iROA, after adjustment for covariates. Results: 354 case knees with iROA were matched to 354 control knees. 66.9% of the participants were female, with an average age of 60.1 years. PFP prefemoral hyperintensity alteration measured at three time points (OR [95%CI]: 1.46 [1.18e1.82], 1.50 [1.20e1.88], 1.52 [1.22e1.89] respectively), PFP maximum axial area (OR [

Asthenozoospermia (AZS) is a major cause of male infertility, aetiology of which is reported to be related with gene mutation or deletion. However, studies on candidate genes for AZS are very scarce. In this study, we examined the gene expression profiles of asthenozoosperm. Gene expression profile analyses with microarray on spermatozoa specimens from 12 asthenozoosperm patients and 12 age-matched volunteers were performed; data analysis was performed with bioinformatics tools. Data analysis revealed that 1265 and 262 genes were significantly (P < 0.05) and differently expressed (≥2-fold) between groups performed with GeneSpring and BRB-ArrayTools respectively. Of these differently expressed genes, 71 were identified as molecular signatures of asthenozoosperm, of which most involved in primary metabolic process and cellular metabolic process. Molecular signatures were filtered performed with NextBio, 21 genes were identified to be specially expressed in asthenozoosperm. We used Finding Associated Concepts with Text Analysis to match the specially expressed genes against the MEDLINE database and found SEMG1 and PGAP1 were related to male fertility. Validation of the microarray data of SEMG1 was carried out using real-time PCR. Our study demonstrated that SEMG1 was significantly changed in asthenozoosperm, which could be the candidate gene for the development of diagnostic marker and provided the opportunity to further illustrate the biological mechanisms of asthenozoosperm.

In the Machine Learning (ML) era, faced with challenges, including exponential multi-sensor data, an increasing number of actuators, and data-intensive algorithms, the development of Unmanned Aerial Vehicles (UAVs) is standing on a new footing. In particular, the Flight Management System (FMS) plays an essential role in UAV design. However, the trade-offs between performance and SWaP-C (Size, Weight, Power, and Cost) and reliability–efficiency are challenging to determine for such a complex system. To address these issues, the identification of a successful approach to managing heterogeneity emerges as the critical question to be answered. This paper investigates Heterogeneous Computing (HC) integration in FMS in the UAV domain from academia to industry. The overview of cross-layer FMS design is firstly described from top–down in the abstraction layer to left–right in the figurative layer. In addition, the HC advantages from Light-ML, accelerated Federated Learning (FL), and hardware accelerators are highlighted. Accordingly, three distinct research focuses detailed with visual-guided landing, intelligent Fault Diagnosis and Detection (FDD), and controller-embeddable Power Electronics (PE) to distinctly illustrate advancements of the next-generation FMS design from sensing, and computing, to driving. Finally, recommendations for future research and opportunities are discussed. In summary, this article draws a road map that considers the heterogeneous advantages to conducting the Flight-Management-as-a-Service (FMaaS) platform for UAVs.

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