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Tea drinking is associated with positive effects on bone health and may protect against osteoporosis, especially in elderly women. Pu-erh tea has many beneficial effects on human health; however, whether Pu-erh tea has anti-osteoporotic potential remains unclear. Thus, we investigated the effects of Pu-erh tea extract (PTE) on ovariectomy-induced osteoporosis in rats and on osteoclastogenesis . Female Wistar rats were divided into six groups: the sham, model, and Xian-Ling-Gu-Bao capsule (XLGB) groups, and the low-, medium-, and high-dose PTE groups. Ovariectomized (OVX) rats were used as an animal model of osteoporosis. The animals were intragastrically administered distilled water, XLGB, or different concentrations of PTE for 13 weeks. Body weight, blood biochemical indicators, relative organ coefficients, femoral bone mineral density (BMD), bone biomechanical properties, and bone microarchitecture were examined and analyzed. Additionally, the effects of PTE on osteoclastic activities were investigated using the RAW 264.7 cell line as an osteoclast differentiation model. The effects of PTE on osteoclast differentiation and the expression of osteoclast-specific genes and proteins were determined. PTE reduced OVX-induced body weight gain after 6 weeks of treatment, and the high-dose exerted a significant effect. High-dose PTE significantly ameliorated OVX-induced estradiol (E ) deficiency. PTE treatment maintained calcium and phosphorus homeostasis and improved other blood biochemical parameters to various degrees. In addition, PTE treatment improved organ coefficients of the femur, uterus, and vagina and improved femoral BMD and bone biomechanical properties. PTE treatment strikingly ameliorated bone microarchitecture. Moreover, in the studies, osteoclast differentiation using the differentiation cell model was significantly inhibited by PTE without cytotoxic effects. Additionally, PTE efficaciously suppressed the expression of key osteoclast-specific genes and proteins. PTE can ameliorate ovariectomy-induced osteoporosis in rats and suppress osteoclastogenesis .

Tumor necrosis factor (TNF)-stimulated nuclear factor-kappa B (NF-κB) signaling plays very crucial roles in cancer development and progression, and represents a potential target for drug discovery. Roburic acid is a newly discovered tetracyclic triterpene acid isolated from oak galls and exhibits anti-inflammatory activity. However, whether roburic acid exerts antitumor effects through inhibition of TNF-induced NF-κB signaling remains unknown. Here, we demonstrated that roburic acid bound directly to TNF with high affinity ( K D = 7.066 μM), blocked the interaction between TNF and its receptor (TNF-R1), and significantly inhibited TNF-induced NF-κB activation. Roburic acid exhibited antitumor activity in numerous cancer cells and could effectively induce G0/G1 cell cycle arrest and apoptosis in colorectal cancer cells. Importantly, roburic acid inhibited the TNF-induced phosphorylation of IKKα/β, IκBα, and p65, degradation of IκBα, nuclear translocation of p65, and NF-κB-target gene expression, including that of XIAP, Mcl-1, and Survivin, in colorectal cancer cells. Moreover, roburic acid suppressed tumor growth by blocking NF-κB signaling in a xenograft nude mouse model of colorectal cancer. Taken together, our findings showed that roburic acid directly binds to TNF with high affinity, thereby disrupting its interaction with TNF-R1 and leading to the inhibition of the NF-κB signaling pathway, both in vitro and in vivo . The results indicated that roburic acid is a novel TNF-targeting therapeutics agent in colorectal cancer as well as other cancer types.

In spectrum sharing cognitive radio networks, unauthorized users (secondary users) are allowed to use the spectrum of authorized users (primary users) to improve spectrum utilization. Due to limited spectrum resources, how to formulate a reasonable spectrum allocation scheme is very important. As a mathematical analysis tool, game theory can solve the problem of resource allocation well. In recent years, it has been applied to the research of resource allocation in spectrum sharing networks by some literatures. In a cellular network consisting of multiple cellular users and full-duplex end-to-end communication users D2D (device-to-device), the self-interference caused by full-duplex communication and the interference caused by the D2D users to the cellular users will significantly reduce system throughput. In order to reduce the interference in the network, this paper introduces a power control algorithm based on Stackelberg game, which sets the cellular users and D2D users as the leaders and followers, respectively. The cellular users and the D2D users compete with each other to minimize the cost, and we propose new utility functions. We build an optimization problem under the outage probability constraint and power constraint and the transmission power of the users is obtained by using the Lagrangian dual decomposition method. The simulation results show that the proposed game algorithm improves network performance compared with other existing schemes.

Glucose-6-phosphate dehydrogenase (G6PDH) is the rate-limiting enzyme in the pentose phosphate pathway (PPP) and plays a crucial role in the maintenance of redox homeostasis by producing nicotinamide adenine dinucleotide phosphate (NADPH), the major intracellular reductant. G6PDH has been shown to be a biomarker and potential therapeutic target for renal cell carcinoma (RCC). Here, we report a previously unknown biochemical mechanism through which caffeine, a well-known natural small molecule, regulates G6PDH activity to disrupt cellular redox homeostasis and suppress RCC development and progression. We found that caffeine can inhibit G6PDH enzymatic activity. Mechanistically, caffeine directly binds to G6PDH with high affinity ( K D = 0.1923 μM) and competes with the coenzyme NADP+ for G6PDH binding, as demonstrated by the decreased binding affinities of G6PDH for its coenzyme and substrate. Molecular docking studies revealed that caffeine binds to G6PDH at the structural NADP+ binding site, and chemical cross-linking analysis demonstrated that caffeine inhibits the formation of dimeric G6PDH. G6PDH inhibition abrogated the inhibitory effects of caffeine on RCC cell growth. Moreover, inhibition of G6PDH activity by caffeine led to a reduction in the intracellular levels of NADPH and reactive oxygen species (ROS), and altered the expression of redox-related proteins in RCC cells. Accordingly, caffeine could inhibit tumor growth through inhibition of G6PDH activity in vivo . Taken together, these results demonstrated that caffeine can target G6PDH to disrupt redox homeostasis and inhibit RCC tumor growth, and has potential as a therapeutic agent for the treatment of RCC.

Abstract Photovoltaic (PV) modules convert solar energy into electricity; however, in actual applications, the conversion efficiency of PV modules is low. This is because the temperature of PV modules increases, most of the incoming solar radiation absorbed is discarded to the PV modules as wasted heat; this wasted heat generated can be utilized and transferred to a heat exchanger in contact to the rear PV modules. A proposed model is considered with a variation of solar cell temperature due to solar radiation and its effects on output power are modeled and evaluated, seeing PV modules as a thermal absorber, a part of the heat dissipated in the PV modules can be recovered by means of a heat transfer fluid running behind the PV modules, this method improves the PV efficiency, as well as produces thermal and electrical energy simultaneously, thus, the PV modules provide a multifunctional performance cited above, this plays the role of a hybrid solar collector system. The aim of this study is to improve the efficiency of the PV module, through the analysis of a detailed Photovoltaic-Thermal (PVT) collector model performance. The study also estimates the electrical power and thermal energy produced; using MATLAB as an application-oriented design method, the method proposed in this paper can better improve the efficiency of PV power generation and has a wide range of application prospects.

The interaction between the receptor activator of nuclear factor‐κB ligand (RANKL) and its receptor RANK is known to regulate osteoclastogenesis in bone remodelling and has become an important therapeutic target for the treatment of osteoporosis. Stephanine (SA), an isoquinoline aporphine‐type alkaloid isolated from Stephania plants, possesses excellent anti‐inflammatory effects and can be used for rheumatoid arthritis treatment. However, its specific role in osteoclastogenesis and osteoporosis remains unknown. In this study, we investigated the influence of SA on osteoclastogenesis in RANKL‐stimulated RAW 264.7 cells and osteoporosis in an ovariectomised (OVX) mouse model and elucidated the underlying molecular mechanism. In vitro, SA can bind to RANK and RANKL with the KD values of 3.7 and 76.47 μM, respectively, and disrupt the RANKL–RANK interaction, which inhibits RANKL‐stimulated RANK–tumour necrosis factor receptor associated factor 6 (TRAF6) binding and RANK signalling pathways activation, downregulates the expression of key osteoclastogenesis‐related regulatory factors in osteoclast precursors, ultimately suppresses osteoclast differentiation and activation. In vivo, SA significantly ameliorated bone loss through inhibiting osteoclastogenesis in OVX mice because of the decreased number of osteoclasts and the increased trabecular bone area. SA markedly inhibited the serum levels of tartrate‐resistant acid phosphatase 5b (TRACP‐5b), c‐telopeptide of type I collagen (CTX‐I), and RANKL, whereas it increased that of osteoprotegerin (OPG) in OVX mice. Additionally, SA strikingly downregulated the OVX‐induced expression of osteoclast‐specific genes and proteins. Taken together, this study elucidated that SA can effectively protect against osteoporosis by suppressing osteoclastogenesis via inhibition of the RANKL–RANK interaction, which supports the potential application of SA as a natural therapeutic agent for osteoporosis.

Background Skin photoaging is the damage caused by excessive exposure to ultraviolet (UV) irradiation. We investigated the effect of adenosine triphosphate (ATP) supplementation on UVB‐induced photoaging in HaCaT cells and its potential molecular mechanism. Materials and methods The toxicity of ATP on HaCaT cells was examined by the MTT assay. The effects of ATP supplementation on the viability and apoptosis of HaCaT cells were determined by crystal‐violet staining and flow cytometry, respectively. Cellular and mitochondrial ROS were stained using fluorescent dyes. Expression of Bax, B‐cell lymphoma (Bcl)‐2, sirtuin (SIRT)3, and superoxide dismutase (SOD)2 was measured via western blotting. Results ATP (1, 2 mM) exerted no toxic effect on the normal growth of HaCaT cells. UVB irradiation caused the apoptosis of HaCaT cells, and ATP supplementation inhibited the apoptosis induced by UVB significantly, as verified by expression of Bax and Bcl‐2. UVB exposure resulted in accumulation of cellular and mitochondrial reactive oxygen species (ROS), but ATP supplementation suppressed these increases. Expression of SIRT3 and SOD2 was decreased upon exposure to UVB irradiation but, under ATP supplementation, expression of SIRT3 and SOD2 was reversed, which was consistent with the reduction in ROS level observed in ATP‐treated HaCaT cells after exposure to UVB irradiation. Conclusions ATP supplementation can suppress UVB irradiation‐induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2.

This article seeks to examine the distinct way in which China has developed its public interest law, particularly as China can be differentiated from many other countries examined in the symposium as a one-party authoritarian state. While foreign models have played a role in developing China's public interest law, a larger part of the public interest law movement has developed from within. It will examine this in four parts: 1) China's evolving relationship with foreign concepts, models, and resources; 2) the development of various forms of public interest lawyering in China; 3) public interest litigation and its response to domestic obstacles; 4) litigation as a mobilization resource even in a country with a highly constrained judiciary and authoritarian political structure.

Organic room-temperature phosphorescence, a spin-forbidden radiative process, has emerged as an interesting but rare phenomenon with multiple potential applications in optoelectronic devices, biosensing and anticounterfeiting. Covalent organic frameworks (COFs) with accessible nanoscale porosity and precisely engineered topology can offer unique benefits in the design of phosphorescent materials, but these are presently unexplored. Here, we report an approach of covalent doping, whereby a COF is synthesized by copolymerization of halogenated and unsubstituted phenyldiboronic acids, allowing for random distribution of functionalized units at varying ratios, yielding highly phosphorescent COFs. Such controlled halogen doping enhances the intersystem crossing while minimizing triplet–triplet annihilation by diluting the phosphors. The rigidity of the COF suppresses vibrational relaxation and allows a high phosphorescence quantum yield (ΦPhos ≤ 29%) at room temperature. The permanent porosity of the COFs and the combination of the singlet and triplet emitting channels enable a highly efficient COF-based oxygen sensor, with an ultra-wide dynamic detection range (~103–10−5 torr of partial oxygen pressure).Room-temperature phosphorescence in organic solids is attractive for practical applications but remains rare. Now, highly phosphorescent boroxine-linked covalent organic frameworks have been prepared by covalent doping with halogen atoms through the use of halogenated precursors. The resulting porous COFs exhibited oxygen-sensing capabilities with millisecond response time over a wide range of partial oxygen pressures.

This work is devoted to establishing the local-in-time well-posedness of strong solutions to the three-dimensional compressible primitive equations of atmospheric dynamics. It is shown that strong solutions exist, are unique, and depend continuously on the initial data, for a short time in two cases: with gravity but without vacuum, and with vacuum but without gravity.