10 research outputs found
Survey on Flight Control Technology for Large-Scale Helicopter
A literature review of flight control technology is presented for large-scale helicopter. Challenges of large-scale helicopter flight control system (FCS) design are illustrated. Following this, various flight control methodologies are described with respect to their engineering implementation and theoretical developments, whose advantages and disadvantages are also analyzed. Then, the challenging research issues on flight control technology are identified, and future directions are highlighted
Avian Metapneumovirus Subgroup C Induces Mitochondrial Antiviral Signaling Protein Degradation through the Ubiquitin-Proteasome Pathway
The mitochondrial antiviral signaling (MAVS) protein, a critical adapter, links the upstream recognition of viral RNA to downstream antiviral signal transduction. However, the interaction mechanism between avian metapneumovirus subgroup C (aMPV/C) infection and MAVS remains unclear. Here, we confirmed that aMPV/C infection induced a reduction in MAVS expression in Vero cells in a dose-dependent manner, and active aMPV/C replication was required for MAVS decrease. We also found that the reduction in MAVS occurred at the post-translational level rather than at the transcriptional level. Different inhibitors were used to examine the effect of proteasome or autophagy on the regulation of MAVS. Treatment with a proteasome inhibitor MG132 effectively blocked MAVS degradation. Moreover, we demonstrated that MAVS mainly underwent K48-linked ubiquitination in the presence of MG132 in aMPV/C-infected cells, with amino acids 363, 462, and 501 of MAVS being pivotal sites in the formation of polyubiquitin chains. Finally, E3 ubiquitin ligases for MAVS degradation were screened and identified and RNF5 targeting MAVS at Lysine 363 and 462 was shown to involve in MAVS degradation in aMPV/C-infected Vero cells. Overall, these results reveal the molecular mechanism underlying aMPV/C infection-induced MAVS degradation by the ubiquitin-proteasome pathway
The Role of Interleukin-17 in Lung Cancer
Tumour-associated inflammation is a hallmark of malignant carcinomas, and lung cancer is a typical inflammation-associated carcinoma. Interleukin-17 (IL-17) is an important inflammatory cytokine that plays an important role in chronic inflammatory and autoimmune diseases and in inflammation-associated tumours. Numerous studies have shown that IL-17 directly or indirectly promotes tumour angiogenesis and cell proliferation and that it inhibits apoptosis via the activation of inflammatory signalling pathways. Therefore, IL-17 contributes to the metastasis and progression of lung cancer. Research advances with respect to the role of IL-17 in lung cancer will be presented as a review in this paper
Enhancing the reaction kinetics and structural stability of high-voltage LiCoO2via polyanionic species anchoring
Increasing the charging voltage to 4.6 V directly enhances battery capacity and energy density of LiCoO2 cathodes for lithium-ion batteries. However, issues of the activated harmful phase evolution and surface instability in high-voltage LiCoO2 lead to dramatic battery capacity decay. Herein, polyanionic PO43− species have been successfully anchored at the surface of LiCoO2 materials, achieving superior battery performance. The polyanionic species acting as micro funnels at the material surface, could expand LiCoO2 surface lattice spacing by 10%, contributing to enhanced Li diffusion kinetics and consequent excellent rate performance of 164 mA h g−1 at 20C (1C = 274 mA g−1). Crucially, polyanionic species with high electronegativity could stabilize surface oxygen at high voltage by reducing O 2p and Co 3d orbital hybridization, thus suppressing surface Co migration and harmful H1-3 phase formation and leading to superior cycling stability with 84% capacity retention at 1C after 300 cycles. Furthermore, pouch cells containing modified LiCoO2 and Li metal electrodes deliver an ultra-high energy density of 513 W h kg−1 under high loadings of 32 mg cm−2. This work provides insightful directions for modifying the material surface structure to obtain high-energy-density cathodes with high-rate performance and long service life
Retinoic Acid Receptor-Related Orphan Receptors: Critical Roles in Tumorigenesis
Retinoic acid receptor-related orphan receptors (RORs) include RORα (NR1F1), RORβ (NR1F2), and RORγ (NR1F3). These receptors are reported to activate transcription through ligand-dependent interactions with co-regulators and are involved in the development of secondary lymphoid tissues, autoimmune diseases, inflammatory diseases, the circadian rhythm, and metabolism homeostasis. Researches on RORs contributing to cancer-related processes have been growing, and they provide evidence that RORs are likely to be considered as potential therapeutic targets in many cancers. RORα has been identified as a potential therapeutic target for breast cancer and has been investigated in melanoma, colorectal colon cancer, and gastric cancer. RORβ is mainly expressed in the central nervous system, but it has also been studied in pharyngeal cancer, uterine leiomyosarcoma, and colorectal cancer, in addition to neuroblastoma, and recent studies suggest that RORγ is involved in various cancers, including lymphoma, melanoma, and lung cancer. Some studies found RORγ to be upregulated in cancer tissues compared with normal tissues, while others indicated the opposite results. With respect to the mechanisms of RORs in cancer, previous studies on the regulatory mechanisms of RORs in cancer were mostly focused on immune cells and cytokines, but lately there have been investigations concentrating on RORs themselves. Thus, this review summarizes reports on the regulation of RORs in cancer and highlights potential therapeutic targets in cancer
The ACE2/Angiotensin-(1–7)/Mas Receptor Axis: Pleiotropic Roles in Cancer
Cancer remains one of the most common causes of death and disability and represents a major economic burden in industrialized nations. The renin-angiotensin system (RAS) has been well-recognized as one of the most important regulators of both normal and pathological physiological processes in the brain, kidney, heart, and blood vessels. The activation of the angiotensin-converting enzyme 2/angiotensin-(1–7)/mitochondrial assembly receptor [ACE2/Ang-(1–7)/MasR] axis, which is one component of the RAS, has recently been identified as a critical component of pulmonary systems, gastric mucosa, and cancer. However, the ability of the ACE2/Ang-(1–7)/MasR axis to suppress or promote cancer has not been fully elucidated. In this review, we focus on recent experimental and clinical studies investigating the basic properties, roles, and mechanisms of ACE2, Ang-(1–7), and the MasR, as well as the axis pathway, to provide insights into possible therapeutic strategies for treating cancer that target the ACE2/Ang-(1–7)/MasR axis
The Role of Interleukin-17 in Lung Cancer
Tumour-associated inflammation is a hallmark of malignant carcinomas, and lung cancer is a typical inflammation-associated carcinoma. Interleukin-17 (IL-17) is an important inflammatory cytokine that plays an important role in chronic inflammatory and autoimmune diseases and in inflammation-associated tumours. Numerous studies have shown that IL-17 directly or indirectly promotes tumour angiogenesis and cell proliferation and that it inhibits apoptosis via the activation of inflammatory signalling pathways. Therefore, IL-17 contributes to the metastasis and progression of lung cancer. Research advances with respect to the role of IL-17 in lung cancer will be presented as a review in this paper