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.

Q: lord mayor and aldermen of the city of London put into place a set of orders "concerning the infection of the plague," which was then sweeping through the population. He intended that these actions would be "very expedient for preventing and avoiding of infection of sickness" (1). At that time, London faced a public health crisis, with an inadequate scientific base in that the role of rats and their fleas in disease transmission was unknown. Nonetheless, this crisis was faced with good intentions by the top medical and political figures of the community. Daniel Defoe made an observation that could apply to many public health interventions then and today, "This shutting up of houses was at first counted a very cruel and unchristian method… but it was a public good that justified a private mischief" (1). Then, just as today, a complex relationship existed between the science of public health and the practice of public health and politics. We address the relationship between science, public health, and politics, with a particular emphasis on infectious diseases. Science, public health, and politics are not only compatible, but all three are necessary to improve the public's health. The progress of each area of public health is related to the strength of the other areas. The effect of politics in public health becomes dangerous when policy is dictated by ideology. Policy is also threatened when it is solely determined by science, devoid of considerations of social condition, culture, economics, and public will. When using the word "politics," we refer not simply to partisan politics but to the broader set of policies and sys-tems. Although ideology is used in many different ways, in this case, it refers to individual systems of belief that may color a person's attitudes and actions and that are not necessarily based on scientific evidence (2).

A: Plagues, Public Health, and Politics 1
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Q: Npl4 is likely to be the most upstream factor recognizing Lys48-linked polyubiquitylated substrates in the proteasomal degradation pathway in yeast. Along with Ufd1, Npl4 forms a heterodimer (UN), and functions as a cofactor for the Cdc48 ATPase. Here, we report the crystal structures of yeast Npl4 in complex with Lys48-linked diubiquitin and with the Npl4binding motif of Ufd1. The distal and proximal ubiquitin moieties of Lys48-linked diubiquitin primarily interact with the C-terminal helix and N-terminal loop of the Npl4 C-terminal domain (CTD), respectively. Mutational analysis suggests that the CTD contributes to linkage selectivity and initial binding of ubiquitin chains. Ufd1 occupies a hydrophobic groove of the Mpr1/Pad1 N-terminal (MPN) domain of Npl4, which corresponds to the catalytic groove of the MPN domain of JAB1/MPN/Mov34 metalloenzyme (JAMM)-family deubiquitylating enzyme. This study provides important structural insights into the polyubiquitin chain recognition by the Cdc48-UN complex and its assembly.

A: Structural insights into ubiquitin recognition and Ufd1 interaction of Npl4
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Q: The evolution of influenza viruses is remarkably dynamic. Influenza viruses evolve rapidly in sequence and undergo frequent reassortment of different gene segments. Homologous recombination, although commonly seen as an important component of dynamic genome evolution in many other organisms, is believed to be rare in influenza. In this study, 256 gene segments from 32 influenza A genomes were examined for homologous recombination, three recombinant H1N1 strains were detected and they most likely resulted from one recombination event between two closely rated parental sequences. These findings suggest that homologous recombination in influenza viruses tends to take place between strains sharing high sequence similarity. The three recombinant strains were isolated at different time periods and they form a clade, indicating that recombinant strains could circulate. In addition, the simulation results showed that many recombinant sequences might not be detectable by currently existing recombinant detection programs when the parental sequences are of high sequence similarity. Finally, possible ways were discussed to improve the accuracy of the detection for recombinant sequences in influenza.

A:
Evidence of intra-segmental homologous recombination in influenza A virus
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