In order to better constrain the paleogeographic evolution of south China we measured Sm‐Nd and Rb‐Sr isotopic compositions for 23 Mesozoic granites that crop out throughout the area. Tightly grouped neodymium depleted mantle model ages (1.4 ± 0.3 Ga) suggest the region is underlain by relatively homogeneous Proterozoic crust and fail to define crustal provinces. Neither the isotopic nor geologic data suggest that a Mesozoic suture exists. However, granites possessing anomalously high Sm (>8 ppm) and Nd (>45 ppm) concentrations, relatively high initial epsilon neodymium (−4 to −8), and high but variable initial 87Sr/86Sr (0.759 to 0.713) form a northeast trending zone that coincides with two prominent Mesozoic basins. Southeast of the zone lie the majority of Mesozoic intrusives and Upper Triassic to Lower Cretaceous extensional basins found in south China. Mesozoic paleomagnetic poles are well clustered northwest of the zone. Pre‐Cretaceous poles southeast of it are discordant with respect to those from the northwest. The only recognized tectonostratigraphic terrane in south China lies southeast of the zone. The terrane is bordered by a northeast trending sinistral fault that was active in the Mesozoic. Other faults in south China have similar attitudes, ages, and sense of shear. Together, the observations suggest that the Mesozoic tectonic regime in south China consisted of strike‐slip activity plus concomitant rifting as terranes or fragments of similar crust were transported north along sinistral faults. The zone, defined by the granites enriched in Nd and Sm, demarcates displaced terranes to the southeast from relatively stable land to the northwest.

Three noncovalently fused-ring electron acceptors with good solubility, near-infrared absorption, and high electron mobility are precisely designed for high-efficiency OSCs.

Vascular smooth muscle (VSM) plays an important role in the regulation of vascular function. Identifying the mechanisms of VSM contraction has been a major research goal in order to determine the causes of vascular dysfunction and exaggerated vasoconstriction in vascular disease. Major discoveries over several decades have helped to better understand the mechanisms of VSM contraction. Ca has been established as a major regulator of VSM contraction, and its sources, cytosolic levels, homeostatic mechanisms and subcellular distribution have been defined. Biochemical studies have also suggested that stimulation of Gq protein-coupled membrane receptors activates phospholipase C and promotes the hydrolysis of membrane phospholipids into inositol 1,4,5-trisphosphate (IP) and diacylglycerol (DAG). IP stimulates initial Ca release from the sarcoplasmic reticulum, and is buttressed by Ca influx through voltage-dependent, receptor-operated, transient receptor potential and store-operated channels. In order to prevent large increases in cytosolic Ca concentration ([Ca]), Ca removal mechanisms promote Ca extrusion via the plasmalemmal Ca pump and Na/Ca exchanger, and Ca uptake by the sarcoplasmic reticulum and mitochondria, and the coordinated activities of these Ca handling mechanisms help to create subplasmalemmal Ca domains. Threshold increases in [Ca] form a Ca-calmodulin complex, which activates myosin light chain (MLC) kinase, and causes MLC phosphorylation, actin-myosin interaction, and VSM contraction. Dissociations in the relationships between [Ca], MLC phosphorylation, and force have suggested additional Ca sensitization mechanisms. DAG activates protein kinase C (PKC) isoforms, which directly or indirectly via mitogen-activated protein kinase phosphorylate the actin-binding proteins calponin and caldesmon and thereby enhance the myofilaments force sensitivity to Ca. PKC-mediated phosphorylation of PKC-potentiated phosphatase inhibitor protein-17 (CPI-17), and RhoA-mediated activation of Rho-kinase (ROCK) inhibit MLC phosphatase and in turn increase MLC phosphorylation and VSM contraction. Abnormalities in the Ca handling mechanisms and PKC and ROCK activity have been associated with vascular dysfunction in multiple vascular disorders. Modulators of [Ca], PKC and ROCK activity could be useful in mitigating the increased vasoconstriction associated with vascular disease.

We report a new ALD process for Ni3C and explore its applications for supercapacitors and electrocatalytic H2 evolution.

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Agglomeration is a critical issue for depositing copper (Cu) thin films, and therefore the deposition should be preferably performed below 100 °C. This work explores an atomic layer deposition (ALD) process for copper thin films deposited at temperature as low as 50 °C. The process employs copper(I)-N,N'-di-iso-propylacetamidinate precursor and H 2 plasma, which are both highly reactive at low temperature. The deposition process below 100 °C follows an ideal self-limiting ALD fashion with a saturated growth rate of 0.071 nm/cycle. Benefited from the low process temperature, the agglomeration of Cu thin films is largely suppressed, and the Cu films deposited at 50 °C are pure, continuous, smooth, and highly conformal, with the resistivity comparable to PVD Cu films. In-situ reaction mechanism studies by using quartz crystal microbalance and optical emission spectroscopy are followed, and the results confirm the high reactivity of the Cu amidinate precursor at low temperature. To the best of our knowledge, this is the first successful implementation of metal amidinate precursors for low-temperature (~50 °C) ALD process. The strategy of using metal amidinate precursors in combination with highly reactive H 2 plasma is believed to be extendable for the depositions of other pure metals at low temperature.

Aim: Matrine is an alkaloid from Sophora alopecuroides L, which has shown a variety of pharmacological activities and potential therapeutic value in cardiovascular diseases. In this study we examined the protective effects of matrine against diabetic cardiomyopathy (DCM) in rats. Methods: Male SD rats were injected with streptozotocin (STZ) to induce DCM. One group of DCM rats was pretreated with matrine (200 mg·kg -1 ·d -1, po) for 10 consecutive days before STZ injection. Left ventricular function was evaluated using invasive hemodynamic examination, and myocardiac apoptosis was assessed. Primary rat myocytes were used for in vitro experiments. Intracellular ROS generation, MDA content and GPx activity were determined. Real-time PCR and Western blotting were performed to detect the expression of relevant mRNAs and proteins. Results: DCM rats exhibited abnormally elevated non-fasting blood glucose levels at 4 weeks after STZ injection, and LV function impairment at 16 weeks. The cardiac tissues of DCM rats showed markedly increased apoptosis, excessive ROS production, and activation of TLR-4/MyD-88/caspase-8/caspase-3 signaling. Pretreatment with matrine significantly decreased non-fasting blood glucose levels and improved LV function in DCM rats, which were associated with reducing apoptosis and ROS production, and suppressing TLR-4/MyD-88/caspase-8/caspase-3 signaling in cardiac tissues. Incubation in a high-glucose medium induced oxidative stress and activation of TLR-4/MyD-88 signaling in cultured myocytes in vitro, which were significantly attenuated by pretreatment with N-acetylcysteine. Conclusion: Excessive ROS production in DCM activates the TLR-4/MyD-88 signaling, resulting in cardiomyocyte apoptosis, whereas pretreatment with matrine improves cardiac function via suppressing ROS/TLR-4 signaling pathway.

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