Di-μ-cyanido-1:2κ2 C:N,2:3κ2 N:C-hexa­cyanido-1κ3 C,3κ3 C-tetra­kis(1,10-phenanthroline)-1κ2 N,N′;2κ4 N,N′;3κ2 N,N′-1,3-dicobalt(III)-2-iron(II) tetra­hydrate

The hydro­thermal reaction of CoCl2·6H2O, 1,10-phenanthroline (phen) and K3[Fe(CN)6] in deionized water yielded the title cyanide-bridged trinuclear cluster, [Co2Fe(CN)8(C12H8N2)4]·4H2O or [{CoIII(phen)(CN)4}2{FeII(phen)2}]·4H2O, which contains two CoIII centers and one FeII center linked by cyanide bridges. The combination of coordinative bonds, O—H⋯N and O—H⋯O hydrogen bonds and π–π stacking inter­actions [centroid–centroid distance = 3.630 (2) Å] results in the stabilization of a supra­molecular structure. All uncoordinated water molecules are disordered. Thermogravimetric analysis reveals that the title complex loses the four crystal water mol­ecules at about 333 K, then the anhydrous phase loses no further mass up to about 573 K, above which decomposition occurs

(E)-5-(3,5-Dimethyl­phen­yl)-N-[4-(methyl­sulfan­yl)benzyl­idene]-1,3,4-thia­diazol-2-amine

The title compound, C18H17N3S2, was synthesized by the reaction of 5-(3,5-dimethyl­phen­yl)-1,3,4-thia­diazol-2-amine and 4-(methyl­sulfan­yl)benzaldehyde. An intra­molecular C—H⋯S hydrogen bond results in the formation of a planar (r.m.s. deviation = 0.003 Å) five-membered ring. In the crystal structure, inter­molecular C—H⋯N hydrogen bonds link the mol­ecules to form layers parallel to (011)

The “Groundwater Benefit Zone”, Proposals, Contributions and New Scientific Issues

The groundwater has great potential for water resource utilization, accounting for about a quarter of vegetation transpiration globally and contributing up to 84% in shallow groundwater areas. However, in irrigated agricultural regions or coastal areas with shallow groundwater levels, due to the high groundwater salinity, the contribution of groundwater to transpiration is small and even harmful. This paper proposes a new conception of groundwater benefit zone in the groundwater-soil–plant-atmosphere continuum (GSPAC) system. Firstly, it analyzes the mutual feedback processes of the underground hydrological process and aboveground farmland ecosystem. Secondly, it elaborates on the regional water and salt movement model proposed vital technologies based on the optimal regulation of the groundwater benefit zone and is committed to building a synergy that considers soil salt control and groundwater yield subsidies. Finally, based on the GSPAC system water-salt coupling transport mechanism, quantitative model of groundwater benefit zone, and technical parameters of regional water-salt regulation and control, the scientific problems and development opportunities related to the conception of groundwater benefit zone have been prospected

Advances of digital twins for predictive maintenance

Digital twins (DT), aiming to improve the performance of physical entities by leveraging the virtual replica, have gained significant growth in recent years. Meanwhile, DT technology has been explored in different industrial sectors and on a variety of topics, e.g., predictive maintenance (PdM). In order to understand the state-of-the-art of DT in PdM, this paper focuses on the recent advances of how DT has been deployed in PdM, especially on the challenges faced and the opportunities identified. Based on the relevant research efforts recognised, we classify them into three main branches: 1) the frameworks reported for application, 2) modelling methods, and 3) interaction between the physical entity and virtual replica. We intend to analyse the techniques and applications regarding each category, and the perceived benefits of PdM from the DT paradigm are summarized. Finally, challenges of current research and opportunities for future research are discussed especially concerning the issue of framework standardisation for DT-driven PdM, needs for high-fidelity models, holistic evaluation methods, and the multi-component, multi-level model issue

Liraglutide-induced reduction of myocardial ischemiareperfusion injury in rats via ERK1/2 signaling pathway

Purpose: To investigate the protective effect of liraglutide on myocardial ischemia reperfusion (I/R) injury and its molecular mechanism.Methods: Ischemia reperfusion model male Sprague-Dawley (SD) rats were randomly divided into negative control group, I/R group (saline), liraglutide group (liraglutide) and PD group (liraglutide + PD98059). The weight of myocardium in ischemic and infarction areas of the heart, myocardial injury biomarker, oxidative stress, as well as expressions of mRNA molecules of apoptosis were determined.Results: The myocardial mass of ischemic and infarcted areas of the heart (relative to left ventricular mass) of I/R group were significantly higher (p ˂ 0.05) than those of negative control group, but significantly lower in liraglutide group than in I/R group (p > 0.05). However, the parameters were significantly higher in PD group than in liraglutide group (p ˂ 0.05). CK, CK-MB and LDH activities, as well as levels of cTnI and cTnT in I/R group were significantly higher (p ˂ 0.05) than those of negative control group. However, the parameters were significantly lower (p ˂ 0.05) in liraglutide group than in I/R group, but higher in PD group (p ˂ 0.05) than in liraglutide group. Serum SOD, GSH-Px, CAT activities and tBcl-2 mRNA expression were significantly lower in I/R group than those of negative control group (p ˂ 0.001), while those PD group were significantly lower than those of liraglutide group (p ˂ 0.001).Conclusion: Liraglutide alleviates myocardial ischemia-reperfusion injury and inhibits oxidative stress and apoptosis via ERK1/2 signaling pathway in rats, but further studies are required to ascertain the clinical efficacy and safety of the compound.Keywords: Ischemia-reperfusion injury, Liraglutide, ERK1/2 signal pathway, Oxidative stress, Apoptosi

Sequence-dependent abnormal aggregation of human Tau fragment in an inducible cell model

AbstractA pathological hallmark of Alzheimer disease (AD) is the accumulation of misfolded hyperphosphorylated microtubule-associated protein Tau within neurons, forming neurofibrillary tangles and leading to synaptic dysfunction and neuronal death. Here we study sequence-dependent abnormal aggregation of human fragment Tau244–372 in an inducible cell model. As evidenced by confocal laser scanning microscopy, Western blot, and immunogold electron microscopy, fibril-forming motifs are essential and sufficient for abnormal aggregation of Tau244–372 in SH-SY5Y neuroblastoma cells induced by Congo red: when its two fibril-forming segments PHF6 and PHF6* are deleted, Tau244–372 does lose its ability to form fibrils in SH-SY5Y cells, and the replacement of PHF6 and PHF6* with an unrelated amyloidogenic sequence IFQINS from human lysozyme does rescue the fibril-forming ability of Tau244–372 in SH-SY5Y cells. By contrast, insertion of a non-fibril forming peptide GGGGGG does not drive the disabled Tau244–372 to misfold in SH-SY5Y cells. Furthermore, as revealed by quantum dots based probes combined with annexin V staining, annexin V-FITC apoptosis detection assay, and immunofluorescence, fibril-forming motifs are essential and sufficient for early apoptosis of living SH-SY5Y cells induced by abnormal aggregation of Tau244–372. Our results suggest that fibril-forming motifs could be the determinants of Tau protein tending to misfold in living cells, thereby inducing neuronal apoptosis and causing the initiation and development of AD