TASK DEFINITION: In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
PROBLEM: This paper discusses actions aimed at sustainable management of healthcare wastes (HCW) in China, taking into account the current national situation in this field, as well as the requirements deriving from the Stockholm Convention on Persistent Organic Pollutants and the WHO recommendations. By the end of 2005, there were 149 low-standard HCW disposal facilities in operation in China, distributed throughout different areas. According to the National Hazardous Waste and Healthcare Waste Disposal Facility Construction Plan, 331 modern, high-standard, centralized facilities will be built up in China in municipal level cities. Although incineration is still the main technical option for HCW disposal in China, it is expected that, especially for medium and small size facilities, non-incineration technologies will develop quickly and will soon become the main technical option. The basic management needs -both from the point of view of pollution control and final disposal -have been defined, and a system of technical and environmental standards has been formulated and implemented; however, there are still some shortages. This is particularly true when considering the best available techniques and best environmental practices developed under the Stockholm Convention, with which the present technological and managing situations are not completely compliant. In this framework, the lifecycle (from generation to final disposal of wastes) of HCW and holistic approaches (technology verification, facilities operation, environmental supervision, environmental monitoring, training system, financial mechanism, etc.) towards HCW management are the most important criteria for the sustainable and reliable management of HCW in China.

SOLUTION: Sustainable management measures for healthcare waste in China

PROBLEM: Duck plague virus (DPV) is a representative pathogen transmitted among aquatic animals that causes gross lesions and immune inhibition in geese and ducks. The mechanism of organ tropism and innate immune evasion of DPV has not been completely deciphered due to a lack of cell models to study the innate immune manipulation and pathogenicity of aquatic viruses. In the present study, we isolated five types of duck primary cells [duck embryo fibroblasts (DEFs), neurons, astrocytes, peripheral blood mononuclear cells (PBMCs), and monocytes/macrophages] to identify appropriate cell models for DPV, using tropism infection and innate immunologic assays. Cells responded differently to stimulation with DNA viruses or RNA virus analogs. DPV infection exhibited broad tropism, as the recombinant virulent strain (CHv-GFP) infected DEFs, neurons, astrocytes, and monocytes/macrophages, but not the PBMCs, as the expression of EGFP was negligible. The basal levels of innate immunity molecules were highest in monocytes/macrophages and lower in DEFs and astrocytes. Conversely, the titer and genomic copy number of the attenuated virus strain was higher in DEFs and astrocytes than in neurons and monocytes/macrophages. The titer and genomic copy number of the attenuated virus strain were higher compared with the virulent strain in DEFs, neurons, and astrocytes. The innate immune response was not significantly induced by either DPV strain in DEFs, neurons, or astrocytes. The virulent strain persistently infected monocytes/macrophages, but the attenuated strain did so abortively, and this was accompanied by the phenomenon of innate immune inhibition and activation by the virulent and attenuated strains, respectively. Blockage of IFNAR signaling promoted replication of the attenuated strain. Pre-activation of IFNAR signaling inhibited infection by the virulent strain. The selection assay results indicated that induction of innate immunity plays an essential role in controlling DPV infection, and monocytes/macrophages are an Tian et al. Duck Primary Cells Infection Models important cell model for further investigations. Our study provided practical methods for isolating and culturing duck primary cells, and our results will facilitate further investigations of organ tropism, innate immune responses, latent infection, and the effectiveness of antiviral drugs for treating DPV and potentially other aerial bird pathogens.

SOLUTION: Isolation and Selection of Duck Primary Cells as Pathogenic and Innate Immunologic Cell Models for Duck Plague Virus

PROBLEM: The new porcine epidemic diarrhea (PED) has caused devastating economic losses to the swine industry worldwide. Despite extensive research on the relationship between autophagy and virus infection, the concrete role of autophagy in porcine epidemic diarrhea virus (PEDV) infection has not been reported. In this study, autophagy was demonstrated to be triggered by the effective replication of PEDV through transmission electron microscopy, confocal microscopy, and Western blot analysis. Moreover, autophagy was confirmed to benefit PEDV replication by using autophagy regulators and RNA interference. Furthermore, autophagy might be associated with the expression of inflammatory cytokines and have a positive feedback loop with the NF-B signaling pathway during PEDV infection. This work is the first attempt to explore the complex interplay between autophagy and PEDV infection. Our findings might accelerate our understanding of the pathogenesis of PEDV infection and provide new insights into the development of effective therapeutic strategies. Viruses 2017, 9, 53 2 of 16 damaged organelles are delivered to lysosomes for degradation and recycling [8, 9] . Autophagy can be induced by diverse intracellular and extracellular stimuli, such as nutrient starvation, endoplasmic reticulum (ER) stress, pathogen-associated molecular patterns (PAMPs), and virus infection [10] . Increasing evidence indicates that autophagy plays both anti-viral and pro-viral roles in the life cycles and pathogenesis of a broad range of viruses [11] . Specifically, autophagy is an intrinsic host defense mechanism that inhibits viral replication or eliminates viruses by delivering them to the lysosomal compartment for degradation. Meanwhile, viruses develop many mechanisms to block autophagy or even hijack it for their own benefit, such as human cytomegalovirus (HCMV) and herpes simplex virus type 1 (HSV-1) [9, [12] [13] [14] . However, autophagy is also believed to serve as a platform for viral replication, especially for RNA viruses, such as classical swine fever virus (CSFV), porcine reproductive and respiratory syndrome virus (PRRSV), and rotavirus (RV), utilizing the membranes of the autophagosome-like vesicles for their replication [15] [16] [17] . These polar characteristics reveal the complicated relationship between autophagy and viral infection. A previous proteomic study indicated that more differentially expressed proteins were mapped to the autophagy pathway, and the microtubule-associated protein 1B, a useful biomarker protein for autophagy was up-regulated in PEDV-infected Vero cells [18] . In addition, our previous study demonstrated that mTOR (the mammalian target of rapamycin) pathway, which was closely associated with cellular autophagy, was down-regulated, and that the autophagy associated protein ATG5 was up-regulated during PEDV infection [19] . These studies indicated that autophagy might participate in PEDV infection, but the specific function of autophagy in the process of PEDV infection has not been elucidated. In the present study, we demonstrated for the first time that autophagy was triggered in Vero cells during PEDV infection to promote its replication. Moreover, autophagy might mediate the inflammatory responses induced by PEDV infection and have a positive correlation with the NF-B signaling pathway. Program of China (2016YFD0500702) and the China Agricultural Research System (CARS-36). We thank prof. Xiang Mao from the Shanghai Veterinary Research Institute, for providing the GFP-mRFP-LC3 tandem reporter construct.

SOLUTION:
Porcine Epidemic Diarrhea Virus Induces Autophagy to Benefit Its Replication