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The short-term residential electricity demand forecast tasks are essential for designing the portfolio of the decision-making process of aggregators for the selection of control targets and derivation of specific control target values for demand response. The implementation of edge computing on the forecast functionality, which provides forecasting and minimal communication functions based on the data accumulated at the end-user-side using an inexpensive computational resource deployed locally, is an attractive framework for practical implementation. To achieve good accuracy while forecasting the demands of individual households during practical long-term operation, it is necessary to follow the changes in demand characteristics quickly by updating the prediction models frequently. This study focused on the concept of deep reservoir computing, which has a high affinity for implementation in edge computing frameworks from the viewpoint of hardware implementability, while utilizing the deep architecture and avoiding high computational cost. In particular, this study proposed an online learning scheme for the implementation of edge computing, which does not require large-scale computation for updating the prediction models. The effectiveness of the proposed approach was evaluated considering the calculation cost and accuracy through numerical experiments using real-world residential load data.

Agonists of peroxisome proliferator-activated receptor gamma (PPARγ) have been examined as chemopreventive and chemotherapeutic agents. The aim was to investigate the cytotoxicity of troglitazone (TGZ) and its mechanisms in terms of PPARγ dependency and the p38 mitogen-activated protein kinase (MAPK) pathway in three human renal cell carcinoma (RCC) cell lines, 786-O, Caki-2 and ACHN cells. TGZ induced apoptosis and exerted cytotoxicity in a PPARγ-independent manner. We demonstrated that TGZ activated the p38 MAPK pathway and was involved in the cytotoxicity of TGZ. It was also revealed that TGZ induced G(2)/M cell cycle arrest through activation of p38 MAPK.

The concentration of calcium in the cerebrospinal fluid (CSF) affects systemic blood pressure; an increase in calcium concentration lowers blood pressure, whereas a decrease raises it. Although this phenomenon has been known for more than 50 years, the precise mechanism is not completely understood. We examined whether the extracellular calcium-sensing receptor (CaSR), which was originally cloned from the parathyroid cells and later found in the brain, contributes to blood pressure regulation by calcium in the CSF. In urethane-anesthetized and artificially ventilated Wistar–Kyoto rats, an intracisternal injection of NPS R-467, an allosteric CaSR activator, decreased blood pressure associated with sympathoinhibition in a dose-dependent manner. Treatment with an inactivator of the CaSR elicited an increase in blood pressure. Similar results were observed in awake and freely moving animals. In contrast, when the CaSR activator/inactivator was administered into the lateral ventricle, the cardiovascular changes were minimal. These results indicate that the CaSR in the brain contributes, at least in part, to the hypotensive effect of centrally administered calcium and suggests that the CaSR in the lower brainstem participates in tonic regulation of blood pressure by sensing a change in the CSF Ca 2+ concentration.

A new ion-pair receptor bis(3-bromoindol-2-ylmethyl)(2-pyridylmethyl)amine ( 1 ) was synthesized and studied for its anion and cation binding behavior using ESI-MS and 1 H NMR spectroscopy. Among halides, 1 exhibits the strongest binding with Cl − to form a 1:1 adduct ( K a = 1042 ± 21 in CD 3 CN). Among alkali metal ions, Li + and Na + showed the strongest binding in the formation of a 1 ·M + complex. The simultaneous binding of Cl − and Li + to 1 was confirmed by 1 H NMR titration of a 1:1 mixture of 1 and Cl − with LiPF 6 in 83:17 v/v mixture of CDCl 3 and DMSO- d 6 . DFT-optimized structures of 1 ·Cl − , 1 ·Li + , and 1 ·Li + ·Cl − are consistent with the chemical shift changes observed in 1 H NMR studies.

A landscape of mechanistic possibilities for the oxidation of olefins by bio-inspired non-heme iron catalysts has been explored in this work. The complexes studied consist of iron centers coordinated to the tetradentate N4 ligands tpa and bpmen, which provide two cis -labile sites to the iron center. These complexes catalyze conversion of olefin substrates into epoxide and/or cis -diol products. The diol-to-epoxide ratio is very sensitive to the nature of the tetradentate ligand and reaction conditions. With the aim of understanding how these systems can be modulated, the effects of additives such as water, acetone or acetic acid have been explored. These additives significantly alter the catalytic activity of Fe(bpmen) and Fe(tpa) complexes. Accordingly, the initial mechanistic proposals where the HO–Fe V O intermediate appeared as the unique active oxidizing species have been expanded and other key catalytic intermediates such as Fe III (OOH) or Fe IV O are implicated as a consequence of the results reported in this work.