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This study demonstrated that both copper oxide nanoparticles (CuO‐NPs) and copper nanoparticles (Cu‐NPs) can cause swelling, inflammation, and cause damage to the mitochondria of alveolar type II epithelial cells in mice. Cellular examinations indicated that both CuO‐NPs and Cu‐NPs can reduce cell viability and harm the mitochondria of human bronchial epithelial cells, particularly Beas‐2B cells. However, it is clear that CuO‐NPs exhibit a more pronounced detrimental effect compared with Cu‐NPs. Using bafilomycin A1 (Bafi A1), an inhibitor of lysosomal acidification, was found to enhance cell viability and alleviate mitochondrial damage caused by CuO‐NPs. Additionally, Bafi A1 also reduces the accumulation of dihydrolipoamide S‐acetyltransferase (DLAT), a marker for mitochondrial protein toxicity, induced by CuO‐NPs. This observation suggests that the toxicity of CuO‐NPs depends on the distribution of copper particles within cells, a process facilitated by the acidic environment of lysosomes. The release of copper ions is thought to be triggered by the acidic conditions within lysosomes, which aligns with the lysosomal Trojan horse mechanism. However, this association does not seem to be evident with Cu‐NPs. In mice, CuO‐NPs caused more extensive lung tissue damage than Cu‐NPs. In Beas‐2B cells, inhibition of lysosomal acidification with Bafi A1 markedly decreased CuO‐NPs‐induced mitochondrial damage. The lysosomal Trojan horse mechanism of aggravates CuO‐NPs‐induced cuproptosis in Beas‐2B cells, which can be reversed by Bafi A1. [ABSTRACT FROM AUTHOR]

The severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is continuously producing new variants, necessitating effective therapeutics. Patients are not only confronted by the immediate symptoms of infection but also by the long‐term health issues linked to long COVID‐19. Activation of epidermal growth factor receptor (EGFR) signalling during SARS‐CoV‐2 infection promotes virus propagation, mucus hyperproduction, and pulmonary fibrosis, and suppresses the host's antiviral response. Over the long term, EGFR activation in COVID‐19, particularly in COVID‐19‐induced pulmonary fibrosis, may be linked to the development of lung cancer. In this review, we have summarised the significance of EGFR signalling in the context of SARS‐CoV‐2 infection. We also discussed the targeting of EGFR signalling as a promising strategy for COVID‐19 treatment and highlighted erlotinib as a superior option among EGFR inhibitors. Erlotinib effectively blocks EGFR and AAK1, thereby preventing SARS‐CoV‐2 replication, reducing mucus hyperproduction, TNF‐α expression, and enhancing the host's antiviral response. Nevertheless, to evaluate the antiviral efficacy of erlotinib, relevant clinical trials involving an appropriate patient population should be designed. [ABSTRACT FROM AUTHOR]

The upstream role of sensory innervation during bone homeostasis is widely underestimated in bone repairing strategies. Herein, a neuromodulation approach is proposed to orchestrate bone defect healing by constructing engineered sensory nerves (eSN) in situ to leverage the adaptation feature of SN during tissue formation. NGF liberated from ECM‐constructed eSN effectively promotes sensory neuron differentiation and enhances CGRP secretion, which lead to improved RAOECs mobility and osteogenic differentiation of BMSC. In turn, such eSN effectively drives ossification in vivo via NGF‐TrkA signaling pathway, which substantially accelerates critical size bone defect healing. More importantly, eSN also adaptively suppresses excessive bone formation and promotes bone remodeling by activating osteoclasts via CGRP‐dependent mechanism when combined with BMP‐2 delivery, which ingeniously alleviates side effects of BMP‐2. In sum, this eSN approach offers a valuable avenue to harness the adaptive role of neural system to optimize bone homeostasis under various clinical scenario. [ABSTRACT FROM AUTHOR]

We herein report a facile two‐pot method to prepare a series of the two‐dimensional Ni(OH)2 nanocrystals with varied surface structures via the in‐situ surface transformation derived from Nickel metal‐organic framework (Ni‐MOF) in KOH solution at room temperature. The Ni(OH)2 obtained at the KOH concentration of 0.25 M displayed superior performance among the samples in terms of activities and stability. Further investigation proves that the enhanced urea oxidation reaction (UOR) activities can be ascribed to the cooperation of the larger electrochemical surface area, a faster electronic transfer speed, and a lower transfer resistance on the surface. These findings provide a new route for the rational design and synthesis of advanced electrocatalysts with relatively lower energy consumption that aims to be large‐scale synthesized and utilized in clean energy conversion and applications. [ABSTRACT FROM AUTHOR]

Background: This study aimed to overexpress or silence connexin 43 (Cx43) and A‐kinase anchoring protein 95 (AKAP95) in human A549 cells to explore their effects on cyclins and on G1/S conversion when the interrelationship of Cx43, AKAP95, and cyclin E1/E2 changes. Methods: The study mainly used Western blot analysis and Co‐immuno precipitation to detect the target protein in Cx43/AKAP95 over expressed human A549 cells, and the relationship of proteins Cx43, AKAP95 and Cyclin E during G1‐S phase was explored with qualitative and quantitative analysis. Results: The overexpression of Cx43 inhibited the expression of cyclin D1 and E1 by accelerating their degradation and reduced the Cdk2 activity that blocked the DNA transcription activity. However, the overexpression of AKAP95 increased the expression of cyclin D1 and E1 and inhibited their degradation, and enhanced the Cdk2 activity that promoted the DNA transcription activity. Cx43 and AKAP95 competitively bound to cyclin E1/E2, and the competitive binding affected the Cdk2 activity, Rb phosphorylation, DNA transcription activity, and G1/S conversion. Conclusions: This study showed that the expression of ERK1/2, PKA, and PKB increased when BEAS‐2B cells were treated with PDGF‐BB, suggesting that ERK1/2, PKA, and PKB might be involved in the binding of AKAP95 with cyclin E, or the separation of AKAP95 from Cx43 from cyclin E1/E2. The specific mechanism underlying this process still needs further exploration. [ABSTRACT FROM AUTHOR]

This paper presents an experimental investigation into the shrinkage behavior of strain‐hardening cementitious composite (SHCC), which focuses on the influences of varied ingredients in mix proportions and curing condition. The experimental results confirm that the shrinkage strains of SHCC are obviously influenced by the investigated ingredients of SHCC, in which expansion agent can induce expansion strain for nominally reducing the shrinkage strains of SHCC, the shrinkage strains of SHCC's matrix are decreased with increasing fiber volume content and water‐to‐binder ratio, whereas those are increased with increasing silica‐fume‐to‐binder ratio. Moreover, the curing condition has significant influence for the shrinkage behavior of SHCC, and water curing can significantly reduce the shrinkage strains. This work provides experimental foundations for shrinkage behavior of SHCC. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to investigate the correlation between the expression of A‐kinase anchor protein95 (AKAP95), p‐retinoblastoma (phosphorylated Rb, p‐Rb), cyclin D2, cyclin D3 and cyclin E2 in esophageal cancer tissues and clinicopathological indexes. Method: The protein expression levels of AKAP95, p‐Rb, cyclin D2/3 and cyclin E2 in 40 esophageal cancer tissues were detected using immunohistochemistry, and the correlation between them was analyzed. Result: The percentage of p‐Rb (Ser780)‐, cyclin D2‐, cyclin D3‐ and cyclin E2‐positive samples was 62.50%, 70.00%, 67.50% and 60.00%, respectively. Also, the positive expression did not correlate with the histological type, histological differentiation or lymph node metastasis. The expression of AKAP95 and p‐Rb (Ser780), p‐Rb (Ser780) and cyclin D2 and p‐Rb (Ser780) and cyclin D3 in esophageal cancer tissues was found to be correlated (P < 0.05). Conclusions: The expression of AKAP95 and p‐Rb (Ser780), p‐Rb(Ser780) and cyclin D2, and p‐Rb (Ser780) and cyclin D3 in esophageal cancer tissue was correlated, suggesting that these proteins might play a synergistic role in cell‐cycle progression. Cyclin D2/D3 and p‐Rb (Ser780) were correlated whereas cyclin E2 and p‐Rb (Ser780) were not, suggesting that p‐Rb (Ser780) might be highly expressed and the Ser780 site of Rb protein might be phosphorylated in the early stage of the G1 phase. Ser780 was the site in the primary phosphorylation stage of several phosphorylation sites during stepwise phosphorylation (from primary to high phosphorylation). [ABSTRACT FROM AUTHOR]

Background This study was conducted to investigate the exchange protein directly activated by c AMP ( Epac1), PDE4, and PKC expression in breast cancer tissues, and the correlation between these proteins and AKAP95, Cx43, cyclin D2, and cyclin E1. Methods PV-9000 two-step immunohistochemistry was used to analyze protein expression. Results The positive rate of Epac1 protein expression in breast cancer tissues (58%) was higher than in para-carcinoma tissues (10%) ( P < 0.05). There were no significant differences in the positive rates of PDE4 and PKC expression between breast cancer and para-carcinoma tissues ( P > 0.05). The positive expression rate of PDE4 was higher in the P53 protein positive group compared to the P53 negative group ( P < 0.05). Correlations between Epac1 and cyclin D2, PDE4 and cyclin D2, AKAP95 and PKC, Cx43 and PKC, and cyclin D2 and PKC proteins were observed ( P < 0.05). Conclusion Epac1 expression in breast cancer tissues was increased, suggesting that the protein may be involved in the development of breast cancer. Correlations between Epac1 and cyclin D2, PDE4 and cyclin D2, AKAP95 and PKC, Cx43 and PKC, and cyclin D2 and PKC proteins suggested synergistic effects among these proteins in the development of breast cancer. [ABSTRACT FROM AUTHOR]

Broadband absorption enhancement in metal nanomaterials for high‐performance organic solar cells (OSCs) is highly desirable in the plasmonic‐enhanced OSCs. Here, a new dual plasmonic device is proposed by strategically designing device structures and managing two types of plasmonic structures (e.g., metal grating and metal nanoparticles (NPs)) in one device to achieve the broadband enhancement with better reproducibility, including (a) selecting Ag grating with 600 nm period as an anode, (b) introducing metal NPs into the electron transport layer (not active layer), and (c) adopting ZnO as the electron transport layer (not TiO2). The device shows broadband absorption enhancement in the range of 350–800 nm due to multiple plasmonic effects. As a result, the maximum power conversion efficiency (PCE) of 9.62% has been achieved from the device, which is one of the highest efficiencies in plasmonic OSCs reported for a single junction OSC. Importantly, the as‐proposed dual device in this work shows an excellent reproducibility of high PCE in experiment, which is much more applicable for practical applications. This work demonstrates the significance of rational design of the device structure and plasmonic nanostructures in achieving high‐performance plasmonic OSCs with broadband plasmonic absorption enhancement and reliable reproducibility. [ABSTRACT FROM AUTHOR]

Background This study examined the expression of exchange protein directly activated by c AMP1 ( Epac1), PDE4, and PKC in esophageal cancer tissues, and analyzed the association of each protein with the pathological parameters of the samples. Methods Epac1, PDE4, and PKC protein expression was evaluated by PV-9000 two-step immunohistochemical techniques in 51 esophageal cancer specimens and 10 para-carcinoma tissues. Results The positive expression rates of Epac1 and PKC in esophageal cancer tissues (62.7% and 68.6%, respectively) were higher compared to those in para-carcinoma tissues (20% and 20%, respectively) ( P < 0.05). The positive expression rate of PDE4 in esophageal cancer tissues (54.1%) was higher than in para-carcinoma tissues (30%), ( P > 0.05). Epac1, PDE4, and PKC protein expression levels were not associated with the extent of tumor differentiation and/or lymph node metastasis ( P > 0.05). Epac1 protein expression levels correlated with PDE4, PKC, and AKAP95 protein expression levels. In addition, there was a correlation between PKC and Cx43 protein levels ( P < 0.05). Conclusion The expression rates of Epac1, PDE4, and PKC protein in esophageal cancer tissues were significantly higher compared to the rates in para-carcinoma tissues, suggesting an association between these proteins and the development and progression of esophageal cancer. The correlations between these proteins also revealed that they may exert a synergistic effect during the development of esophageal cancer. [ABSTRACT FROM AUTHOR]