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941.
Ai Ping Zhang Xin Kang Li Hai Lan Lin Zhao Xin Zhang Shang Ke Yang Xun Tao Zhang Liu Xin Xiao Jun Bian Dai Qiang Chen 《Polymer Engineering and Science》2023,63(2):562-573
Polyimide (PI) dielectric nanocomposites containing functional nanofillers based on layered structure (single-layer: BT@Al2O3@PI, double-layer: PI/BT@Al2O3@PI, three-layer: PI/BT@Al2O3@PI/PI) were designed and prepared by using PI as matrix, barium titanate (BT)@alumina (Al2O3) as nanofillers through in-situ polymerization compounding technology. FTIR tests indicated that PI and PI dielectric nanocomposites have been synthesized successfully. The molecular mass of BaTiO3@Al2O3@PAA oligomer was higher than that of pure PAA when BT and Al2O3 nanofillers were incorporated simultaneously, as verified by GPC and intrinsic viscosity tests. XRD analysis showed that the addition of nanofillers destroyed the order of PI molecular structure and reduced the arrangement density of PI molecular chains. Both FESEM and HRTEM observations showed that the nanofillers were homogeneously dispersed in the PI matrix, contributing to the property improvements of PI dielectric nanocomposites. TGA results indicated that adding nanofillers improved the thermal stability and heat resistance of PI dielectric nanocomposites. The dielectric constant of PI/BT@Al2O3@PI double-layer nanocomposites was between the single-layer nanocomposites and pure PI. Due to the effective medium theory, the dielectric constant of three-layer PI/BT@Al2O3@PI/PI nanocomposites containing 5 wt% BT@Al2O3 reached 5.43. This work can be expected to provide an effective strategy to fabricate PI dielectric nanocomposite films for energy storage applications. 相似文献
942.
943.
针对直驱永磁同步风力发电系统存在非线性、参数不确定性以及转矩扰动等问题,研究了一种基于自耦PI控制理论的最大功率跟踪控制方法.该方法以转速跟踪为目标,将发电机内部动态与外部输入转矩的不确定性定义为一个总和扰动,从而将非线性不确定系统映射为未知线性系统,并构建了一个在总和扰动反相激励下的受控误差系统.据此设计了基于误差速... 相似文献
944.
María Montes-Casado Gloria Ojeda Gabriel Criado Jos M. Rojo Pilar Portols 《International journal of molecular sciences》2021,22(12)
The phosphatidylinositol 3-kinase (PI3K) family of enzymes plays a determinant role in inflammation and autoimmune responses. However, the implication of the different isoforms of catalytic subunits in these processes is not clear. Rheumatoid arthritis (RA) is a chronic, systemic autoimmune inflammatory disease that entails innate and adaptive immune response elements in which PI3K is a potential hub for immune modulation. In a mouse transgenic model with T-cell-specific deletion of p110α catalytic chain (p110α−/−ΔT), we show the modulation of collagen-induced arthritis (CIA) by this isoform of PI3K. In established arthritis, p110α−/−ΔT mice show decreased prevalence of illness than their control siblings, higher IgG1 titers and lower levels of IL-6 in serum, together with decreased ex vivo Collagen II (CII)-induced proliferation, IL-17A secretion and proportion of naive T cells in the lymph nodes. In a pre-arthritis phase, at 13 days post-Ag, T-cell-specific deletion of p110α chain induced an increased, less pathogenic IgG1/IgG2a antibodies ratio; changes in the fraction of naive and effector CD4+ subpopulations; and an increased number of CXCR5+ T cells in the draining lymph nodes of the p110α−/−ΔT mice. Strikingly, T-cell blasts in vitro obtained from non-immunized p110α−/−ΔT mice showed an increased expression of CXCR5, CD44 and ICOS surface markers and defective ICOS-induced signaling towards Akt phosphorylation. These results, plus the accumulation of cells in the lymph nodes in the early phase of the process, could explain the diminished illness incidence and prevalence in the p110α−/−ΔT mice and suggests a modulation of CIA by the p110α catalytic chain of PI3K, opening new avenues of intervention in T-cell-directed therapies to autoimmune diseases. 相似文献
945.
Abdelrahman M. Elsayed Emine Bayraktar Paola Amero Salama A. Salama Abdelaziz H. Abdelaziz Raed S. Ismail Xinna Zhang Cristina Ivan Anil K. Sood Gabriel Lopez-Berestein Cristian Rodriguez-Aguayo 《International journal of molecular sciences》2021,22(4)
Many long noncoding RNAs have been implicated in tumorigenesis and chemoresistance; however, the underlying mechanisms are not well understood. We investigated the role of PRKAR1B-AS2 long noncoding RNA in ovarian cancer (OC) and chemoresistance and identified potential downstream molecular circuitry underlying its action. Analysis of The Cancer Genome Atlas OC dataset, in vitro experiments, proteomic analysis, and a xenograft OC mouse model were implemented. Our findings indicated that overexpression of PRKAR1B-AS2 is negatively correlated with overall survival in OC patients. Furthermore, PRKAR1B-AS2 knockdown-attenuated proliferation, migration, and invasion of OC cells and ameliorated cisplatin and alpelisib resistance in vitro. In proteomic analysis, silencing PRKAR1B-AS2 markedly inhibited protein expression of PI3K-110α and abrogated the phosphorylation of PDK1, AKT, and mTOR, with no significant effect on PTEN. The RNA immunoprecipitation detected a physical interaction between PRKAR1B-AS2 and PI3K-110α. Moreover, PRKAR1B-AS2 knockdown by systemic administration of 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine nanoparticles loaded with PRKAR1B-AS2–specific small interfering RNA enhanced cisplatin sensitivity in a xenograft OC mouse model. In conclusion, PRKAR1B-AS2 promotes tumor growth and confers chemoresistance by modulating the PI3K/AKT/mTOR pathway. Thus, targeting PRKAR1B-AS2 may represent a novel therapeutic approach for the treatment of OC patients. 相似文献
946.
Squamous cell carcinomas of the lung, head and neck, esophagus, and cervix account for more than two million cases of cancer per year worldwide with very few targetable therapies available and minimal clinical improvement in the past three decades. Although these carcinomas are differentiated anatomically, their genetic landscape shares numerous common genetic alterations. Amplification of the third chromosome’s distal portion (3q) is a distinguishing genetic alteration in most of these carcinomas and leads to copy-number gain and amplification of numerous oncogenic proteins. This area of the chromosome harbors known oncogenes involved in squamous cell fate decisions and differentiation, including TP63, SOX2, ECT2, and PIK3CA. Furthermore, novel targetable oncogenic kinases within this amplicon include PRKCI, PAK2, MAP3K13, and TNIK. TCGA analysis of these genes identified amplification in more than 20% of clinical squamous cell carcinoma samples, correlating with a significant decrease in overall patient survival. Alteration of these genes frequently co-occurs and is dependent on 3q-chromosome amplification. The dependency of cancer cells on these amplified kinases provides a route toward personalized medicine in squamous cell carcinoma patients through development of small-molecules targeting these kinases. 相似文献
947.
María N. Barrachina Irene Izquierdo Lidia Hermida-Nogueira Luis A. Morn Amparo Prez Ana B. Arroyo Nuria García-Barber Rocío Gonzlez-Conejero Sara Troitio Johannes A. Eble Jos Rivera Constantino Martínez María I. Loza Eduardo Domínguez ngel García 《International journal of molecular sciences》2021,22(7)
Background: Clinical management of ischemic events and prevention of vascular disease is based on antiplatelet drugs. Given the relevance of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) as a candidate target in thrombosis, the main goal of the present study was to identify novel antiplatelet agents within the existing inhibitors blocking PI3K isoforms. Methods: We performed a biological evaluation of the pharmacological activity of PI3K inhibitors in platelets. The effect of the inhibitors was evaluated in intracellular calcium release and platelet functional assays, the latter including aggregation, adhesion, and viability assays. The in vivo drug antithrombotic potential was assessed in mice undergoing chemically induced arterial occlusion, and the associated hemorrhagic risk evaluated by measuring the tail bleeding time. Results: We show that PI3K Class IA inhibitors potently block calcium mobilization in human platelets. The PI3K p110δ inhibitor Idelalisib inhibits platelet aggregation mediated by ITAM receptors GPVI and CLEC-2, preferentially by the former. Moreover, Idelalisib also inhibits platelet adhesion and aggregation under shear and adhesion to collagen. Interestingly, an antithrombotic effect was observed in mice treated with Idelalisib, with mild bleeding effects at high doses of the drug. Conclusion: Idelalisib may have antiplatelet effects with minor bleeding effects, which provides a rationale to evaluate its antithrombotic efficacy in humans. 相似文献
948.
Suzanne Gascon Jessica Jann Chlo Langlois-Blais Mlanie Plourde Christine Lavoie Nathalie Faucheux 《International journal of molecular sciences》2021,22(11)
Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by progressive neuron losses in memory-related brain structures. The classical features of AD are a dysregulation of the cholinergic system, the accumulation of amyloid plaques, and neurofibrillary tangles. Unfortunately, current treatments are unable to cure or even delay the progression of the disease. Therefore, new therapeutic strategies have emerged, such as the exogenous administration of neurotrophic factors (e.g., NGF and BDNF) that are deficient or dysregulated in AD. However, their low capacity to cross the blood–brain barrier and their exorbitant cost currently limit their use. To overcome these limitations, short peptides mimicking the binding receptor sites of these growth factors have been developed. Such peptides can target selective signaling pathways involved in neuron survival, differentiation, and/or maintenance. This review focuses on growth factors and their derived peptides as potential treatment for AD. It describes (1) the physiological functions of growth factors in the brain, their neuronal signaling pathways, and alteration in AD; (2) the strategies to develop peptides derived from growth factor and their capacity to mimic the role of native proteins; and (3) new advancements and potential in using these molecules as therapeutic treatments for AD, as well as their limitations. 相似文献
949.
Mayra Colardo Marco Segatto Sabrina Di Bartolomeo 《International journal of molecular sciences》2021,22(9)
Gliomas are the most common and challenging malignancies of the central nervous system (CNS), due to their infiltrative nature, tendency to recurrence, and poor response to treatments. Indeed, despite the advances in neurosurgical techniques and in radiation therapy, the modest effects of therapy are still challenging. Moreover, tumor recurrence is associated with the onset of therapy resistance; it is therefore critical to identify effective and well-tolerated pharmacological approaches capable of inducing durable responses in the appropriate patient groups. Molecular alterations of the RTK/PI3K/Akt/mTOR signaling pathway are typical hallmarks of glioma, and several clinical trials targeting one or more players of this axis have been launched, showing disappointing results so far, due to the scarce BBB permeability of certain compounds or to the occurrence of resistance/tolerance mechanisms. However, as RTK/PI3K/mTOR is one of the pivotal pathways regulating cell growth and survival in cancer biology, targeting still remains a strong rationale for developing strategies against gliomas. Future rigorous clinical studies, aimed at addressing the tumor heterogeneity, the interaction with the microenvironment, as well as diverse posology adjustments, are needed—which might unravel the therapeutic efficacy and response prediction of an RTK/PI3K/mTOR-based approach. 相似文献
950.