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Diabetes mellitus has become a serious and growing public health concern. It has high morbidity and mortality because of its complications, such as diabetic nephropathy, diabetic cardiovascular complication, diabetic neuropathy, diabetic retinopathy, and diabetic hepatopathy. Epidemiological studies revealed that the consumption of tea was inversely associated with the risk of diabetes mellitus and its complications. Experimental studies demonstrated that tea had protective effects against diabetes mellitus and its complications via several possible mechanisms, including enhancing insulin action, ameliorating insulin resistance, activating insulin signaling pathway, protecting islet β-cells, scavenging free radicals, and decreasing inflammation. Moreover, clinical trials also confirmed that tea intervention is effective in patients with diabetes mellitus and its complications. Therefore, in order to highlight the importance of tea in the prevention and management of diabetes mellitus and its complications, this article summarizes and discusses the effects of tea against diabetes mellitus and its complications based on the findings from epidemiological, experimental, and clinical studies, with the special attention paid to the mechanisms of action. [ABSTRACT FROM AUTHOR]

An immobilization-free electrochemical impedance biosensor for microRNA detection was developed in this work, which was based on both the duplex-specific nuclease assisted target recycling (DSNATR) and capture probes (Cps) enriched from the solution to electrode surface via magnetic beads (MBs). In the absence of miR-21, Cps cannot be hydrolyzed due to the low activity of duplex-specific nuclease (DSN) against ssDNA. Therefore, the intact Cps could be attached to the surface of magnetic glass carbon electrode (MGCE), resulting in a compact negatively charged layer as well as a large charge-transfer resistance. While in the presence of miR-21, it hybridized with Cp to form a DNA–RNA heteroduplex. Due to the considerable cleavage preference for DNA in DNA–RNA hybrids, DSN hydrolyzed the target-binding part of the Cp while liberating the intact miR-21 to hybridize with a new Cp and initiate the second cycle of hydrolysis. In this way, a single miR-21 was able to trigger the permanent hydrolysis of multiple Cps. Finally, all Cps were digested. Thus, the negatively charged layer could not be formed, resulting in a small charge-transfer resistance. By employing the above strategy, the proposed biosensor achieved ultrahigh sensitivity toward miR-21 with a detection limit of 60 aM. Meanwhile, the method showed little cross-hybridization among the closely related miRNA family members even at the single-base-mismatched level. Successful attempts were made in applying the approach to detect miR-21 in human serum samples of breast cancer patients. [ABSTRACT FROM AUTHOR]

The simultaneous detection of various mycotoxins is indispensable for food safety since the agricultural products are often contaminated by multiple mycotoxins. Herein, we report a signal-enhancement fluorescent aptasensor based on DNA-scaffolded silver nanoculsters (DNA/AgNCs) for simultaneous detection of Ochratoxin A (OTA) and Aflatoxin B 1 (AFB 1 ). The OTA aptamer (Ap1) and the AFB 1 aptamer (Ap2) immobilized on magnetic beads surface hybridize with signal probe1 (Sp1) and signal probe2 (Sp2), respectively. In the presence of these two mycotoxins, the single-strand Sps are released after Aps binding with mycotoxins due to the higher stability of mycotoxin-Ap. Through the magnetic separation, the Sps in the supernatant liquid are acted as the corresponding scaffolds to synthesize AgNCs with different photoluminescence emission bands. Intriguingly, we find that the fluorescence intensity is obviously increased after adding Zn(II)-ion into the system, leading to a linear range from 0.001 ng/mL to 0.05 ng/mL both for OTA and AFB 1 with the detection limit of 0.2 pg/mL for OTA and 0.3 pg/mL for AFB 1 . The proposed fluorescent aptasensor shows excellent performance towards the analytical application in real samples, providing a new model for the simultaneous detection for other mycotoxins by simple change of the aptamer. [ABSTRACT FROM AUTHOR]

A high-salt diet (HSD) is a major cause of many chronic and age-related defects such as myocardial hypertrophy, locomotor impairment and mortality. Exercise training can efficiently prevent and treat many chronic and age-related diseases. However, it remains unclear whether endurance exercise can resist HSD-induced impairment of climbing capacity and longevity in aging individuals. In our study, flies were given exercise training and fed a HSD from 1-week old to 5-weeks old. Overexpression or knockdown of salt and dFOXO were built by UAS/Gal4 system. The results showed that a HSD, salt gene overexpression and dFOXO knockdown significantly reduced climbing endurance, climbing index, survival, dFOXO expression and SOD activity level, and increased malondialdehyde level in aging flies. Inversely, in a HSD aging flies, endurance exercise and dFOXO overexpression significantly increased their climbing ability, lifespan and antioxidant capacity, but they did not significantly change the salt gene expression. Overall, current results indicated that a HSD accelerated the age-related decline of climbing capacity and mortality via upregulating salt expression and inhibiting the dFOXO /SOD pathway. Increased dFOXO /SOD pathway activity played a key role in mediating endurance exercise resistance to the low salt tolerance-induced impairment of climbing capacity and longevity in aging Drosophila This article has an associated First Person interview with the first author of the paper., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)