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The residual direct current (RDC) almost always brings serious image sticking (IS) problems in LCDs and is mainly related to the liquid crystal (LC) and photoaligned polyimide. In this paper, we propose a novel method, to the best of our knowledge, to evaluate the RDC of the FFS-LCDs through an optical measurement system. By this means, the accumulation and release of the ions can be seen distinctly through the transmittance-time curves with the voltage regulation. Hence, it is helpful to compare and analyze the RDC problem of different displays. Moreover, this method possesses the advantage of high efficiency and simplicity in order to benefit the material design in photoaligned polyimide or the LC.
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This study aims to improve the slow-release performance of a film material for a controlled-release fertilizer (CRF) while enhancing its biodegradability. A water-based biodegradable polymer material doped with biochar (BC) was prepared from modified polyvinyl alcohol (PVA) with polyvinylpyrrolidone (PVP) and chitosan (CTS), hereinafter referred to as PVA/PVP-CTSaBCb. An environmentally friendly novel controlled-release phosphate fertilizer (CRPF) was developed using PVA/PVP-CTS8%BC7% as the film. The effect of the PVA/PVP-CTS8%BC7% coating on the service life of the CRPF was investigated. The film was characterized via stress-strain testing, SEM, FTIR, XRD, and TGA analyses. The addition of the CTS modifier increased the stress of PVA/PVP-CTS8% by 7.6% compared with that of PVA/PVP owing to the decrease in the crystallinity of PVP/PVP-CTS8%. The hydrophilic -OH groups were reduced due to the mixing of CTS and PVA/PVP. Meanwhile, the water resistance of the PVA/PVP-CTS8%BC7% was improved. And the controlled-release service life of the CRPF was prolonged. Moreover, the addition of BC increased the crystallinity of the PVA/PVP-CTS8% by 10%, reduced the fracture elongation of the material, and further improved the biodegradability of the PVA/PVP-CTS8%BC7%. When the amount of BC added was 7%, the phosphorus release rate of the CRPF was 30% on the 28th day. Moreover, the degradation rate of the PVA/PVP-CTS8%BC7% polymer film was 35% after 120 days. This study provides basic data for applying water-based degradable polymer materials in CRFs.
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The process of bone regeneration is intricately regulated by various cytokines at distinct stages. The establishment of early and efficient vascularization, along with the maintenance of a sustained osteoinductive microenvironment, plays a crucial role in the successful utilization of bone repair materials. This study aimed to develop a composite hydrogel that would facilitate the creation of an osteogenic microenvironment for bone repair. This was achieved by incorporating an early rapid release of VEGF and a sustained slow release of BMP-2. Herein, the Schiff base was formed between VEGF and the composite hydrogel, and VEGF could be rapidly released to promote vascularization in response to the early acidic bone injury microenvironment. Furthermore, the encapsulation of BMP-2 within mesoporous silica nanoparticles enabled a controlled and sustained release, thereby facilitating the process of bone repair. Our developed composite hydrogel released more than 80% of VEGF and BMP-2 in the acidic medium, which was significantly higher than that in the neutral medium (about 60%). Moreover, the composite hydrogel demonstrated a significant improvement in the migratory capacity and tube formation ability of human umbilical vein endothelial cells (HUVECs). Furthermore, the composite hydrogel exhibited an augmented ability for osteogenesis, as confirmed by the utilization of ALP staining, alizarin red staining, and the upregulation of osteogenesis-related genes. Notably, the composite hydrogel displayed substantial osteoinductive properties, compared with other groups, the skull defect in the composite hydrogels combined with BMP-2 and VEGF was full of new bone, basically completely repaired, and the BV/TV value was greater than 80%. The outcomes of animal experiments demonstrated that the composite hydrogel effectively promoted bone regeneration in cranial defects of rats by leveraging the synergistic effect of an early rapid release of VEGF and a sustained slow release of BMP-2, thereby facilitating vascularized bone regeneration. In conclusion, our composite hydrogel has demonstrated promising potential for vascularized bone repair through the enhancement of angiogenesis and osteogenic microenvironment.
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BACKGROUND: Arachidonic acid (AA), one of the most ubiquitous polyunsaturated fatty acids (PUFAs), provides fluidity to mammalian cell membranes. It is derived from linoleic acid (LA) and can be transformed into various bioactive metabolites, including prostaglandins (PGs), thromboxanes (TXs), lipoxins (LXs), hydroxy-eicosatetraenoic acids (HETEs), leukotrienes (LTs), and epoxyeicosatrienoic acids (EETs), by different pathways. All these processes are involved in AA metabolism. Currently, in the context of an increasingly visible aging world population, several scholars have revealed the essential role of AA metabolism in osteoporosis, chronic obstructive pulmonary disease, and many other aging diseases. AIM OF REVIEW: Although there are some reviews describing the role of AA in some specific diseases, there seems to be no or little information on the role of AA metabolism in aging tissues or organs. This review scrutinizes and highlights the role of AA metabolism in aging and provides a new idea for strategies for treating aging-related diseases. KEY SCIENTIFIC CONCEPTS OF REVIEW: As a member of lipid metabolism, AA metabolism regulates the important lipids that interfere with the aging in several ways. We present a comprehensivereviewofthe role ofAA metabolism in aging, with the aim of relieving the extreme suffering of families and the heavy economic burden on society caused by age-related diseases. We also collected and summarized data on anti-aging therapies associated with AA metabolism, with the expectation of identifying a novel and efficient way to protect against aging.
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Bone is a dynamic tissue reshaped by constant bone formation and bone resorption to maintain its function. The skeletal system accounts for approximately 70% of the total volume of the body, and continuous bone remodeling requires quantities of energy and material consumption. Adipose tissue is the main energy storehouse of the body and has a strong adaptive capacity to participate in the regulation of various physiological processes. Considering that obesity and metabolic syndrome have become major public health challenges, while osteoporosis and osteoporotic fractures have become other major health problems in the aging population, it would be interesting to explore these 2 diseases together. Currently, an increasing number of researchers are focusing on the interactions between multiple tissue systems, i.e., multiple organs and tissues that are functionally coordinated together and pathologically pathologically interact with each other in the body. However, there is lack of detailed reviews summarizing the effects of lipid metabolism on bone homeostasis and the interactions between adipose tissue and bone tissue. This review provides a detailed summary of recent advances in understanding how lipid molecules and adipose-derived hormones affect bone homeostasis, how bone tissue, as a metabolic organ, affects lipid metabolism, and how lipid metabolism is regulated by bone-derived cytokines.
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As a highly dynamic tissue, bone is continuously rebuilt throughout life. Both bone formation by osteoblasts and bone resorption by osteoclasts constitute bone reconstruction homeostasis. The equilibrium of bone homeostasis is governed by many complicated signaling pathways that weave together to form an intricate network. These pathways coordinate the meticulous processes of bone formation and resorption, ensuring the structural integrity and dynamic vitality of the skeletal system. Dysregulation of the bone homeostatic regulatory signaling network contributes to the development and progression of many skeletal diseases. Significantly, imbalanced bone homeostasis further disrupts the signaling network and triggers a cascade reaction that exacerbates disease progression and engenders a deleterious cycle. Here, we summarize the influence of signaling pathways on bone homeostasis, elucidating the interplay and crosstalk among them. Additionally, we review the mechanisms underpinning bone homeostatic imbalances across diverse disease landscapes, highlighting current and prospective therapeutic targets and clinical drugs. We hope that this review will contribute to a holistic understanding of the signaling pathways and molecular mechanisms sustaining bone homeostasis, which are promising to contribute to further research on bone homeostasis and shed light on the development of targeted drugs.