Based on the grey theory,the grey relational analysis is used to realize the fault analysis by the data of the temperature humidity and leakage current from on-line monitoring of 220 kV insulators.The result of the analysis shows that the leakage current of insulators on HV lines is affected by all of the meteorological conditions.And the humidity is decisive factor among them.The degree of relation between the leakage current and the humidity is above 0.9.In the subsequent working,this conclusion provides foundation to set the weight of each element in the prediction to the contamination of the isolators on HV lines.
The first synthesis of dolastatin 11, a potent antineoplastic agent from the sea hare Dolabella auricularia, confirmed the proposed structure and established the last configuration in this natural product and in dolastatin 12, majusculamide C, and 57-normajusculamide C.
Carboxymethyl hyaluronic acid (CMHA) is a semisynthetic derivative of HA that is recognized by HA binding proteins but contains an additional carboxylic acid on some of the 6-hydroxyl groups of the N-acetyl glucosamine sugar units. These studies tested the ability of CMHA to stabilize the formation of calcium phosphate nanoparticles and evaluated their potential to target therapy resistant, CD44 + /CD24 −/low human breast cancer cells (BT-474 EMT ). CMHA stabilized particles (nCaP CMHA ) were loaded with the chemotherapy drug cis -diamminedichloroplatinum(II) (CDDP) to form nCaP CMHA CDDP. nCaP CMHA CDDP was determined to be poorly crystalline hydroxyapatite, 200 nm in diameter with a −43 mV zeta potential. nCaP CMHA CDDP exhibited a two-day burst release of CDDP that tapered resulting in 86% release by 7 days. Surface plasmon resonance showed that nCaP CMHA CDDP binds to CD44, but less effectively than CMHA or hyaluronan. nCaPCMHA-AF488was taken up by CD44 + /CD24 − BT-474 EMT breast cancer cells within 18 hours. nCaP CMHA CDDP was as cytotoxic as free CDDP against the BT-474 EMT cells. Subcutaneous BT-474 EMT tumors were more reproducibly inhibited by a near tumor dose of 2.8 mg/kg CDDP than a 7 mg/kg dose nCaP CMHA CDDP. This was likely due to a lack of distribution of nCaP CMHA CDDP throughout the dense tumor tissue that limited drug diffusion.
We demonstrated exciton electroluminescence by impact excitation in a monolayer WSe2 based field effect transistor on SiO2/Si substrate at room temperature. Hot electrons or holes can be controlled as impact sources through the back gate.
Two-dimensional (2D) semiconductors have emerged as promising candidates for various optoelectronic devices especially electroluminescent (EL) devices. However, progress has been hampered by many challenges including metal contacts and injection, transport, and confinement of carriers due to small sizes of materials and the lack of proper double heterostructures. Here, we propose and demonstrate an alternative approach to conventional current injection devices. We take advantage of large exciton binding energies in 2D materials using impact generation of excitons through an alternating electric field, without requiring metal contacts to 2D materials. The conversion efficiency, defined as the ratio of the emitted photons to the preexisting carriers, can reach 16% at room temperature. In addition, we demonstrate the first multiwavelength 2D EL device, simultaneously operating at three wavelengths from red to near-infrared. Our approach provides an alternative to conventional current-based devices and could unleash the great potential of 2D materials for EL devices.
Long-term use of opioids such as morphine has negative side effects, such as morphine analgesic tolerance and morphine-induced hyperalgesia (MIH). These side effects limit the clinical use and analgesic efficacy of morphine. Elucidation of the mechanisms and identification of feasible and effective methods or treatment targets to solve this clinical phenomenon are important. Here, we discovered that YTHDF1 and TNF receptor-associated factor 6 (TRAF6) are crucial for morphine analgesic tolerance and MIH. The m6A reader YTHDF1 positively regulated the translation of TRAF6 mRNA, and chronic morphine treatments enhanced the m6A modification of TRAF6 mRNA. TRAF6 protein expression was drastically reduced by YTHDF1 knockdown, although TRAF6 mRNA levels were unaffected. By reducing inflammatory markers such as IL-1β, IL-6, TNF-α and NF-κB, targeted reduction of YTHDF1 or suppression of TRAF6 activity in ventrolateral periaqueductal gray (vlPAG) slows the development of morphine analgesic tolerance and MIH. Our findings provide new insights into the mechanism of morphine analgesic tolerance and MIH indicating that YTHDF1 regulates inflammatory factors such as IL-1β, IL-6, TNF-α and NF-κB by enhancing TRAF6 protein expression.
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