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Abstracts: As the ‘Green Revolution’ gene, SD1 (encoding GA20ox2), has been widely applied to improve yield in rice breeding. However, research on its transcriptional regulation is limited. Here, we identified a transcription factor OsbZIP01, which can suppress the expression of SD1 and regulate gibberellin (GA) biosynthesis in rice. Knockout mutants of OsbZIP01 exhibited increased plant height, while the over- expression lines showed a semi-dwarf phenotype and diminished germination rate. Furthermore, the semi-dwarf phenotype of OE-bZIP01, was caused by the reduced internode length, which was accompanied by a thin stem width. The predominant expression of OsbZIP01 was observed in leaves and sheaths. OsbZIP01 protein was localized in the nucleus and showed transcriptional repression activity. In addition, OsbZIP01 could directly bind to the promoter of the OsSD1 gene, and inhibit its transcription. The semi-dwarf phenotype of OE-bZIP01 could be rescued by exogenous GA3. Meanwhile, the bzip01 sd1 double mutant showed a shorter shoot length compared with the wild type, indicating that OsbZIP01 regulated plant growth mainly through the GA biosynthesis pathway. Collectively, OsbZIP01 negatively regulates GA biosynthesis by restraining SD1 transcription, thereby affecting plant growth and development.

In this paper, the performance of 60GHz wireless communication system with SC and OFDM is studied, the models of OFDM 60GHz system and SC 60GHz frequency domain equalization (SC-FDE) system are established, and the bit error rate (BER) performance of OFDM 60GHz system and SC-FDE 60GHz system in 802.15.3c channels is compared. The simulation results show that SC-FDE 60GHz system has a slight advantage over OFDM system in line-of-sight (LOS) channels, while OFDM 60GHz system has a slight advantage over SC-FDE system in non-line-of-sight (NLOS) channels. For 60GHz system, OFDM 60GHz system has a slight advantage over SC-FDE system in overcoming multipath fading, but the performance of both is close whether in the LOS or NLOS case.

A mechanized direct seeding of rice with less labor and water usage, has been widely adopted. However, this approach requires varieties that exhibit uniform seedling emergence. Mesocotyl elongation (ME) offers the main drive of fast emergence of rice seedlings from soils; nevertheless, its genetic basis remains unknown. Here, we identify a major rice quantitative trait locus Mesocotyl Elongation1 (qME1), an allele of the Green Revolution gene Semi‐Dwarf1 (SD1), encoding GA20‐oxidase for gibberellin (GA) biosynthesis. ME1 expression is strongly induced by soil depth and ethylene. When rice grains are direct‐seeded in soils, the ethylene core signaling factor OsEIL1 directly promotes ME1 transcription, accelerating bioactive GA biosynthesis. The GAs further degrade the DELLA protein SLENDER RICE 1 (SLR1), alleviating its inhibition of rice PHYTOCHROME‐INTERACTING FACTOR‐LIKE13 (OsPIL13) to activate the downstream expansion gene OsEXPA4 and ultimately promote rice seedling ME and emergence. The ancient traits of long mesocotyl and strong emergence ability in wild rice and landrace were gradually lost in company with the Green Revolution dwarf breeding process, and an elite ME1‐R allele (D349H) is found in some modern Geng varieties (long mesocotyl lengths) in northern China, which can be used in the direct seeding and dwarf breeding of Geng varieties. Furthermore, the ectopic and high expression of ME1 driven by mesocotyl‐specific promoters resulted in rice plants that could be direct‐seeded without obvious plant architecture or yield penalties. Collectively, we reveal the molecular mechanism of rice ME, and provide useful information for breeding new Green Revolution varieties with long mesocotyl suitable for direct‐seeding practice. [ABSTRACT FROM AUTHOR]

Background and Aims Macrophage-derived foam cells play a causal role during the pathogenesis of atherosclerosis. P2Y6 receptor (P2Y6R) highly expressed has been considered as a disease-causing factor in atherogenesis, but the detailed mechanism remains unknown. This study aims to explore P2Y6R in regulation of macrophage foaming, atherogenesis, and its downstream pathways. Furthermore, the present study sought to find a potent P2Y6R antagonist and investigate the feasibility of P2Y6R-targeting therapy for atherosclerosis. Methods The P2Y6R expression was examined in human atherosclerotic plaques and mouse artery. Atherosclerosis animal models were established in whole-body P2Y6R or macrophage-specific P2Y6R knockout mice to evaluate the role of P2Y6R. RNA sequencing, DNA pull-down experiments, and proteomic approaches were performed to investigate the downstream mechanisms. High-throughput Glide docking pipeline from repurposing drug library was performed to find potent P2Y6R antagonists. Results The P2Y6R deficiency alleviated atherogenesis characterized by decreasing plaque formation and lipid deposition of the aorta. Mechanically, deletion of macrophage P2Y6R significantly inhibited uptake of oxidized low-density lipoprotein through decreasing scavenger receptor A expression mediated by phospholipase Cβ/store-operated calcium entry pathways. More importantly, P2Y6R deficiency reduced the binding of scavenger receptor A to CALR, accompanied by dissociation of calreticulin and STIM1. Interestingly, thiamine pyrophosphate was found as a potent P2Y6R antagonist with excellent P2Y6R antagonistic activity and binding affinity, of which the pharmacodynamic effect and mechanism on atherosclerosis were verified. Conclusions Macrophage P2Y6R regulates phospholipase Cβ/store-operated calcium entry/calreticulin signalling pathway to increase scavenger receptor A protein level, thereby improving foam cell formation and atherosclerosis, indicating that the P2Y6R may be a potential therapeutic target for intervention of atherosclerotic diseases using P2Y6R antagonists including thiamine pyrophosphate. [ABSTRACT FROM AUTHOR]

Cardiovascular disease is a kind of heart, brain, and blood vessel injury disease by the interaction of various pathological factors. The pathogenesis of cardiovascular disease is complex with various risk factors, including abnormally elevated blood pressure, glucose, and lipid metabolism disorders, atherosclerosis, thrombosis, etc. Plant polysaccharides are a special class of natural products derived from plant resources, which have the characteristics of wide sources, diverse biological activities, and low toxicity or side effects. Many studies have shown that plant polysaccharides improve cardiovascular diseases through various mechanisms such as anti-oxidative stress, restoring the metabolism of biological macromolecules, regulating the apoptosis cascade to reduce cell apoptosis, and inhibiting inflammatory signal pathways to alleviate inflammation. This article reviews the pharmacological effects and protective mechanisms of some plant polysaccharides in modulating the cardiovascular system, which is beneficial for developing more effective drugs with low side effects for management of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

In order to study the mixing effect of natural gas calorific value control process, this study establishes the pipeline models for the mixing of the natural gas with different calorific value, meshing for the pipeline models, and caries out the numerical simulation on the natural gas mixing for one branch pipe and one manifold by using ANSYS Fluent 16.0 software. Based on the distribution characteristics of the velocity Held and the components Held in pipeline after natural gas mixing, the effect of natural gas mixing is compared and analyzed. In addition, the effect of natural gas mixing is evaluated by analyzing the percentage of the gas components at different pipe diameter positions after natural gas mixing. The numerical results show that for the branch pipe nixing flow, the mixing effect is not as good as that of the manifold because of the low-speed stagnation area at the mixing corner. For the branch pipe mixing flow, the mixing is relatively sufficient and the gas components are relatively inform at the distance of 15D=3 000 mm from the mixing center. However, with the development of flow in the downstream, the mixing is still in progress. For the mixing flow of the manifold, the direction of fluid flow is changed due to the existence of the manifold, which aggravates the mixing of natural gas flow. Therefore, the mixing effect is better. At the outlet of the manifold, that is, the inlet of the branch pipe, the gas components have reached a relatively uniform state. [ABSTRACT FROM AUTHOR]

The activation of P2Y 14 receptor (P2Y 14 R) promotes osteoclast formation and causes neuropathic pain, exhibiting possible link to osteoarthritis (OA). Given lack of P2Y 14 R antagonist, the present study aims to search a novel P2Y 14 R antagonist with low toxicity and high activity from natural products as a possible drug candidate in treatment of OA. The role of P2Y 14 R on OA was verified using P2Y 14 R knockout (KO) rats. Molecular docking virtual screening strategy and activity test in P2Y 14 R stably-expressed HEK293 cells were used to screen target compound from natural product library. The MM/GBSA free energy calculation/decomposition technique was used to determine the principal interaction mechanism. Next, the binding of target compound to P2Y 14 R was examined using cellular thermal shift assay and drug affinity responsive target stability test. Finally, the therapeutic effect of target compound was performed in monosodium iodoacetate (MIA)-induced OA mouse model. To verify whether the effect of target compound was attributed to P2Y 14 R, we establish the osteoarthritis model in P2Y 14 R KO mice to perform pharmacodynamic evaluation. Importantly, to investigate the potential mechanism by which target compound attenuate OA, expressions of the major transcription factors involved in osteoclast differentiation were detected by western blot, while markers of nerve damage in dorsal root ganglion (DRG) were evaluated by RT-qPCR and immunofluorescence techniques. Deficiency of P2Y 14 R alleviated pain behavior and cartilage destruction in MIA-induced OA rats. 14 natural compounds were screened by Glide docking-based virtual screening, among which paederosidic acid exhibited the highest antagonistic activity to P2Y 14 R with IC 50 of 8.287 μM. As a bioactive component extracted from Paederia scandens, paederosidic acid directly interacted with P2Y 14 R to enhance the thermostability and decrease the protease sensitivity of target protein, which significantly inhibited receptor activator for nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis. More importantly, paederosidic acid suppressed osteoclast formation by downregulating expressions of NFAT2 and ATP6V0D2, as well as relieved neuropathic pain by decreasing expressions of CGRP, CSF1 and galanin in DRG. Paederosidic acid targeted P2Y 14 R to improve OA through alleviating osteoclast formation and neuropathic pain, which provided an available strategy for developing novel drug leads for treatment of OA. [Display omitted] [ABSTRACT FROM AUTHOR]

Hydroxygenkwanin (HGK) has an anticancer effect in a variety of tumors, but its role in osteosarcoma has not been explored. The purpose of the present study was to investigate the therapeutic effect of HGK on osteosarcoma and its specific molecular mechanism. Osteosarcoma cells (MG-63 and U2OS) treated with various concentrations of HGK were assigned to the treatment group. MTT, clone formation, wound healing and Transwell assays were performed to assess the viability, proliferation, migration, and invasion of MG-63 and U2OS cells. RT-qPCR was conducted to quantify the expression levels of of microRNA (miR)-320a and SRY-box transcription factor 9 (SOX9) in MG-63 and U2OS cells. The binding sites of miR-320a and SOX9 were predicted by starBase database, and verified using the dual-luciferase reporter assay. The expression levels of SOX9 and EMT-related proteins (N-cadherin, E-cadherin and vimentin) were detected by western blot analysis. HGK inhibited cell proliferation, migration, invasion, but promoted the expression of miR-320a in MG-63 and U2OS cells. Downregulation of miR-320a reversed the effects of HGK on proliferation, migration and invasion of MG-63 and U2OS cells, while upregulation of miR-320a had the opposite effect. HGK inhibited the expression of SOX9 by promoting the expression of miR-320a. Upregulation of SOX9 could partially reverse miR-320a-induced migration and invasion of MG-63 and U2OS cells. In addition, upregulation of miR-320a promoted E-cadherin expression and inhibited the expression of N-cadherin and vimentin, and the effect of miR-320a was also reversed by SOX9. In conclusion, HGK inhibited proliferation, migration and invasion of MG-63 and U2OS cells through the miR-320a/SOX9 axis. [ABSTRACT FROM AUTHOR]

The average symbol error probability (ASEP) and outage probability (OP) performance of mobile-to-mobile (M2M) senor networks employing transmit antenna selection (TAS) and selection combining (SC) over N-Nakagami fading channels are investigated in this paper. Based on the moment generating function (MGF) approach, the exact ASEP expressions are derived for several modulation schemes. The exact closed-form OP expressions are also presented. Then, the ASEP and OP performance under different conditions are evaluated through numerical simulations to confirm the accuracy of the analysis. The simulation results show that the number of antennas, the fading coefficient, and the number of cascaded components have an important influence on the ASEP and OP performance. [ABSTRACT FROM AUTHOR]

Being applied widely, electromagnetic wave is closely related with our life. But this material has brought pollutions to the environment as well as influences on functions of organisms. In order to explore the influence of electromagnetic radiation on nervous system, this paper takes adult mice on 35th day as research objects, designs a water maze experiment and explores features of escaping latency of mice in the control group and in the group with radiation. In this research, methods of building a GHz TEM cell and a simulation model of mouse head with AutoCAD 2010 and XFDTD are provided, verifying that the simulation model meets the needs of the experiment. It concludes that the electromagnetic radiation causes memory deterioration of mice, and exerts its certain influence on nervous system.

Background and Aims: Macrophage-derived foam cells play a causal role during the pathogenesis of atherosclerosis. P2Y6 receptor (P2Y6R) highly expressed has been considered as a disease-causing factor in atherogenesis, but the detailed mechanism remains unknown. This study aims to explore P2Y6R in regulation of macrophage foaming, atherogenesis, and its downstream pathways. Furthermore, the present study sought to find a potent P2Y6R antagonist and investigate the feasibility of P2Y6R-targeting therapy for atherosclerosis., Methods: The P2Y6R expression was examined in human atherosclerotic plaques and mouse artery. Atherosclerosis animal models were established in whole-body P2Y6R or macrophage-specific P2Y6R knockout mice to evaluate the role of P2Y6R. RNA sequencing, DNA pull-down experiments, and proteomic approaches were performed to investigate the downstream mechanisms. High-throughput Glide docking pipeline from repurposing drug library was performed to find potent P2Y6R antagonists., Results: The P2Y6R deficiency alleviated atherogenesis characterized by decreasing plaque formation and lipid deposition of the aorta. Mechanically, deletion of macrophage P2Y6R significantly inhibited uptake of oxidized low-density lipoprotein through decreasing scavenger receptor A expression mediated by phospholipase Cβ/store-operated calcium entry pathways. More importantly, P2Y6R deficiency reduced the binding of scavenger receptor A to CALR, accompanied by dissociation of calreticulin and STIM1. Interestingly, thiamine pyrophosphate was found as a potent P2Y6R antagonist with excellent P2Y6R antagonistic activity and binding affinity, of which the pharmacodynamic effect and mechanism on atherosclerosis were verified., Conclusions: Macrophage P2Y6R regulates phospholipase Cβ/store-operated calcium entry/calreticulin signalling pathway to increase scavenger receptor A protein level, thereby improving foam cell formation and atherosclerosis, indicating that the P2Y6R may be a potential therapeutic target for intervention of atherosclerotic diseases using P2Y6R antagonists including thiamine pyrophosphate., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: The activation of P2Y 14 receptor (P2Y 14 R) promotes osteoclast formation and causes neuropathic pain, exhibiting possible link to osteoarthritis (OA). Given lack of P2Y 14 R antagonist, the present study aims to search a novel P2Y 14 R antagonist with low toxicity and high activity from natural products as a possible drug candidate in treatment of OA., Methods: The role of P2Y 14 R on OA was verified using P2Y 14 R knockout (KO) rats. Molecular docking virtual screening strategy and activity test in P2Y 14 R stably-expressed HEK293 cells were used to screen target compound from natural product library. The MM/GBSA free energy calculation/decomposition technique was used to determine the principal interaction mechanism. Next, the binding of target compound to P2Y 14 R was examined using cellular thermal shift assay and drug affinity responsive target stability test. Finally, the therapeutic effect of target compound was performed in monosodium iodoacetate (MIA)-induced OA mouse model. To verify whether the effect of target compound was attributed to P2Y 14 R, we establish the osteoarthritis model in P2Y 14 R KO mice to perform pharmacodynamic evaluation. Importantly, to investigate the potential mechanism by which target compound attenuate OA, expressions of the major transcription factors involved in osteoclast differentiation were detected by western blot, while markers of nerve damage in dorsal root ganglion (DRG) were evaluated by RT-qPCR and immunofluorescence techniques., Results: Deficiency of P2Y 14 R alleviated pain behavior and cartilage destruction in MIA-induced OA rats. 14 natural compounds were screened by Glide docking-based virtual screening, among which paederosidic acid exhibited the highest antagonistic activity to P2Y 14 R with IC 50 of 8.287 μM. As a bioactive component extracted from Paederia scandens, paederosidic acid directly interacted with P2Y 14 R to enhance the thermostability and decrease the protease sensitivity of target protein, which significantly inhibited receptor activator for nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis. More importantly, paederosidic acid suppressed osteoclast formation by downregulating expressions of NFAT2 and ATP6V0D2, as well as relieved neuropathic pain by decreasing expressions of CGRP, CSF1 and galanin in DRG., Conclusions: Paederosidic acid targeted P2Y 14 R to improve OA through alleviating osteoclast formation and neuropathic pain, which provided an available strategy for developing novel drug leads for treatment of OA., Competing Interests: Declaration of Competing Interest All the authors state that they have no interest conflicts for this work., (Copyright © 2023 Elsevier GmbH. All rights reserved.)