Hospitals are important sources of pollutants resulted from diagnostic, laboratory and research activities as well as medicine excretion by patients, which include active component of drugs and metabolite, chemicals, residues of pharmaceuticals, radioactive markers, iodinated contrast media, etc. The discharge of hospital wastes and wastewater, especially those without appropriate treatment would expose the public in danger of infection. In particular, under the Coronavirus Disease 2019 (COVID-19) pandemic context in China, it is of great significance to reduce the health risks to the public and environment. In this study, technologies of different types of hospital wastes and wastewater disinfection have been summarized. Liquid chlorine, sodium hypochlorite, chlorine dioxide, ozone, and ultraviolet irradiation disinfection are commonly used for hospital wastewater disinfection. While incineration, chemical disinfection, and physical disinfection are commonly used for hospital wastes disinfection. In addition, considering the characteristics of various hospital wastes, the classification and selection of corresponding disinfection technologies are discussed. On this basis, this study provides scientific suggestions for management, technology selection, and operation of hospital wastes and wastewater disinfection in China, which is of great significance for development of national disinfection strategy for hospital wastes and wastewater during COVID-19 pandemic.
Mechanistic target of rapamycin (mTOR) is a protein kinase regulating cell growth, survival, metabolism, and immunity. mTOR is usually assembled into several complexes such as mTOR complex 1/2 (mTORC1/2). In cooperation with raptor, rictor, LST8, and mSin1, key components in mTORC1 or mTORC2, mTOR catalyzes the phosphorylation of multiple targets such as ribosomal protein S6 kinase β-1 (S6K1), eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), Akt, protein kinase C (PKC), and type-I insulin-like growth factor receptor (IGF-IR), thereby regulating protein synthesis, nutrients metabolism, growth factor signaling, cell growth, and migration. Activation of mTOR promotes tumor growth and metastasis. Many mTOR inhibitors have been developed to treat cancer. While some of the mTOR inhibitors have been approved to treat human cancer, more mTOR inhibitors are being evaluated in clinical trials. Here, we update recent advances in exploring mTOR signaling and the development of mTOR inhibitors for cancer therapy. In addition, we discuss the mechanisms underlying the resistance to mTOR inhibitors in cancer cells.
We establish a connection between anomalous heat conduction and anomalous diffusion in one-dimensional systems. It is shown that if the mean square of the displacement of the particle is =2Dt(alpha)(01) implies anomalous heat conduction with a divergent thermal conductivity (beta>0). More interestingly, subdiffusion (alpha<1) implies anomalous heat conduction with a convergent thermal conductivity (beta<0), and, consequently, the system is a thermal insulator in the thermodynamic limit. Existing numerical data support our results.
CCR4, an evolutionarily conserved member of the CCR4-NOT complex, is the main cytoplasmic deadenylase. It contains a C-terminal nuclease domain with homology to the endonuclease-exonuclease-phosphatase (EEP) family of enzymes. We have determined the high-resolution three-dimensional structure of the nuclease domain of CNOT6L, a human homologue of CCR4, by X-ray crystallography using the single-wavelength anomalous dispersion method. This first structure of a deadenylase belonging to the EEP family adopts a complete alpha/beta sandwich fold typical of hydrolases with highly conserved active site residues similar to APE1. The active site of CNOT6L should recognize the RNA substrate through its negatively charged surface. In vitro deadenylase assays confirm the critical active site residues and show that the nuclease domain of CNOT6L exhibits full Mg(2+)-dependent deadenylase activity with strict poly(A) RNA substrate specificity. To understand the structural basis for poly(A) RNA substrate binding, crystal structures of the CNOT6L nuclease domain have also been determined in complex with AMP and poly(A) DNA. The resulting structures suggest a molecular deadenylase mechanism involving a pentacovalent phosphate transition.
P4-ATPases translocate aminophospholipids, such as phosphatidylserine (PS), to the cytosolic leaflet of membranes. PS is highly enriched in recycling endosomes (REs) and is essential for endosomal membrane traffic. Here, we show that PS flipping by an RE-localized P4-ATPase is required for the recruitment of the membrane fission protein EHD1. Depletion of ATP8A1 impaired the asymmetric transbilayer distribution of PS in REs, dissociated EHD1 from REs, and generated aberrant endosomal tubules that appear resistant to fission. EHD1 did not show membrane localization in cells defective in PS synthesis. ATP8A2, a tissue-specific ATP8A1 paralogue, is associated with a neurodegenerative disease (CAMRQ). ATP8A2, but not the disease-causative ATP8A2 mutant, rescued the endosomal defects in ATP8A1-depleted cells. Primary neurons from Atp8a2−/− mice showed a reduced level of transferrin receptors at the cell surface compared to Atp8a2+/+ mice. These findings demonstrate the role of P4-ATPase in membrane fission and give insight into the molecular basis of CAMRQ.
These results demonstrate that miR-34a acts as a tumor suppressor in uveal melanoma cell proliferation and migration through the downregulation of c-Met.
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