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.
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Question: Previous studies have suggested that mass media's reports of new suicide methods will increase suicides using the same method. The same pattern seems not to apply to a conventional suicide method, unless it was used by a celebrity. Objective 1) to examine media effects on both new and non-new suicide methods during 1998 and 2005 in Hong Kong (HK), when a new method by burning charcoal (CB suicide) was spreading in the region. 2) to examine how CB competed with non-CB methods in terms of media coverage and "recruiting" suicidal persons in the socio-economic context. A self-and mutual-exciting process model was fitted to the data, adjusting for divorce rate, unemployment rate, and property price index. Breaking the whole period into onset, peak, and post-peak stages, the model was fitted again to examine the differences. Comparable copycat effects were found on both CB and non-CB suicide news. The only cross-method media effects were found in the onset stage when non-CB suicide news showed suppressing effect on CB suicides. CB suicides reported a significant self-excitation effect. A higher divorce rate and lower property price index were associated with significantly more suicides incidences and more suicide news. The emerging of CB suicide method did not substitute media coverage of non-CB suicide in HK. Media effects in this case were not limited to new suicide method or celebrity suicide. The effects were further fueled by adverse socio-economic conditions.

Answer: Media effects on suicide methods: A case study on Hong Kong 1998-2005


Question: A potent immunosuppressive drug cyclosporin A (CsA) is known to inhibit human cell infection by the pathogenic protozoan parasite Leishmania major both in vitro and in vivo. The proposed mechanism of action involves CsA binding to Leishmania major-expressed cyclophilin and subsequent down-regulation of signaling events necessary for establishing productive infection. Recently, we identified a ubiquitously expressed membrane protein, CD147, as a signaling receptor for extracellular cyclophilins in mammalian cells. Here we demonstrate that, while being enzymatically active, the Leishmania cyclophilin, unlike its human homologue, does not interact with CD147 on the cell surface of target cells. CD147 facilitates neither Leishmania binding nor infection. Primary structure and biochemical analyses revealed that the parasite's cyclophilin is defective in heparan binding, an event required for signaling interaction between CD147 and human cyclophilin. When the heparan-binding motif was reconstituted in Leishmania cyclophilin, it regained the CD147-dependent signaling activity. These results underscore a critical role of cyclophilinheparan interactions in CD147-mediated signaling events and argue against the role of Leishmania cyclophilin in parasite binding to target cells.

Answer: Functional analysis of Leishmania major cyclophilin


Question: 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-κB 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-κB 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.

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