A new microporous MIL-100­(Fe)/Ti3C2 MXene composite was constructed as a non-noble metal-based Schottky junction photocatalyst with improved nitrogen fixation ability. Ti3C2 MXene nanosheets exhibited excellent metal conductivity and were employed as two-dimensional support to optimize the composite’s energy band structure. MIL-100­(Fe) with a large specific surface area was used as an adsorbent and a photocatalytic oxidation center. The MIL-100­(Fe)/Ti3C2 MXene composite not only exhibited higher thermal stability but also showed significantly increased nitrogen fixation activity under visible light. The NO conversion rate of the composite catalyst was about four and three times higher than that of the pure Ti3C2 MXene and the pure MIL-100­(Fe) samples, respectively. Although adsorption plays an important role in the nitrogen fixation process, the synergistic effects of the Schottky junctions are the main cause of the enhanced photocatalytic activity. The built-in electric field can be generated to form charge-transfer channels, which help to achieve a desirable photocatalytic activity.

In this work, a novel heterojunction catalyst was constructed by introducing Ti3C2 MXene quantum dots (QDs) into SiC. The Ti3C2 MXene QDs/SiC composite showed 74.6% efficiency in NO pollutant removal under visible light irradiation, which is 3.1 and 3.7 times higher than those of the bare Ti3C2 MXene quantum dots and SiC, respectively. The Ti3C2 MXene quantum dots existing in SiC can function as a channel for electron and hole transfer. The enhanced visible light absorption, increased superoxide radical, and strong oxidization ability endow the Ti3C2 MXene QDs/SiC composite with a superior photocatalytic performance for NOx removal. The increased superoxide radical formation and enhanced oxidization ability of Ti3C2 MXene QDs/SiC were demonstrated by theoretical calculations. The robust stability in both photocatalytic performance and crystal structures was revealed in the Ti3C2 MXene QDs/SiC composite using the cycling test, transient photocurrent response, XRD, and TG.

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Patients with advanced IAB were at an increased risk of AF recurrence after catheter ablation.

Cassava (Manihot esculenta) is valued mainly for high content starch in its roots. Our understanding of mechanisms promoting high starch accumulation in the roots is, however, still very limited. Two field-grown cassava cultivars, Huanan 124(H124) with low root starch and Fuxuan 01(F01) with high root starch, were characterised comparatively at four main growth stages. Changes in key sugars in the leaves, stems and roots seemed not to be strongly associated with the final amount of starch accumulated in the roots. However, when compared with H124, F01 exhibited a more compact arrangement of xylem vascular bundles in the leaf axils, much less callose around the phloem sieve plates in the stems, higher starch synthesis-related enzymatic activity but lower amylase activity in the roots, more significantly up-regulated expression of related genes, and a much higher stem flow rate (SFR). In conclusion, higher starch accumulation in the roots results from the concurrent effects of powerful stem transport capacity highlighted by higher SFR, high starch synthesis but low starch degradation in the roots, and high expression of sugar transporter genes in the stems. A model of high starch accumulation in cassava roots was therefore proposed and discussed.

Aim: To evaluate the role of CHADS2 and CHA2DS2-VASc scores in predicting the risk of ischemic stroke or transient ischemic attack (TIA) outcomes in patients with interatrial block (IAB) without a history of atrial fibrillation (AF).Methods: A retrospective study was conducted, including 1,046 non-anticoagulated inpatients (612 males, 434 females; mean age: 63 ± 10 years) with IAB and without AF. IAB was defined as P-wave duration > 120 ms using a 12-lead electrocardiogram. CHADS2 and CHA2DS2-VASc scores were retrospectively calculated. The primary outcomes evaluated were ischemic stroke or TIA.Results: During the mean follow-up period of 4.9 ± 0.7 years, 55 (5.3%) patients had an ischemic stroke or TIA. Receiver operating characteristic (ROC) curve analysis showed that the CHADS2 score [area under the curve (AUC), 0.638; 95% confidence interval (CI), 0.562–0.715; P = 0.001] and the CHA2DS2-VASc score (AUC, 0.671; 95% CI, 0.599–0.744; P <0.001) were predictive of ischemic strokes or TIA. Cut-off point analysis showed that a CHADS2 score ≥ 3 (sensitivity = 0.455 and specificity = 0.747) and a CHA2DS2-VASc score ≥ 4 (sensitivity = 0.564 and specificity = 0.700) provided the highest predictive value for ischemic stroke or TIA. The multivariate Cox regression analysis showed that CHADS2 [hazard ratio (HR), 1.442; 95% CI, 1.171–1.774; P = 0.001] and CHA2DS2-VASc (HR, 1.420; 95% CI, 1.203–1.677; P <0.001) scores were independently associated with ischemic stroke or TIA following adjustment for smoking, left atrial diameter, antiplatelet agents, angiotensin inhibitors, and statins.Conclusions: CHADS2 and CHA2DS2-VASc scores may be predictors of risk of ischemic stroke or TIA in patients with IAB without AF.

Oxidative stress and apoptosis serve an essential role in cisplatin-induced cardiotoxicity, which limits its clinical use, and increases the risk of cardiovascular disease. As a natural drug, the antioxidant and antitumor effects of cyanidin have been recognized, but its protective effect on cisplatin-induced cardiomyocyte cytotoxicity remains unclear. H9c2 cells were treated with cisplatin (1–40 µM) in the presence or absence of cyanidin (40–80 µM), subsequently; oxidative stress, apoptosis and mitochondrial function were assessed using several techniques. The results demonstrated that cyanidin was able to dose-dependently reverse cisplatin-induced cell damage and apoptosis, attenuate the accumulation of reactive oxygen species (ROS), and mitochondrial membrane potential depolarization, downregulate the expression of Bcl-2 homologous antagonist/killer, upregulate the expression of apoptosis regulator Bcl-2, and reduce the activation of caspase 3, caspase 9, but not caspase 8. Furthermore, the results revealed that the translocation of apoptosis regulator Bax (Bax) from the cytoplasm to the mitochondrial membrane serves an essential role in cisplatin-induced apoptosis. Cyanidin was able to block the translocation of Bax and reduce the release of cytochrome c from cytoplasm. These data indicate that cyanidin attenuates cisplatin-induced cardiotoxicity by inhibiting ROS-mediated apoptosis, while the mitochondrial and extracellular regulated kinase signaling pathways may also serve important roles.

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