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: Madin Darby canine kidney (MDCK) cells were adapted to serum-free RPMI 1640 medium and used for cultivation of canine viruses. RPMI 1640 medium was supplemented with a soybean peptone, l-glutamine and antibiotics, so that the protein concentration was less than 5 g/ml (RPMI/SP medium). The resulting adapted MDCK-SP cells showed steady growth after the twenty-eighth passage in RPMI/SP medium (MDCK-SP cell culture). Canine distemper virus, canine parvovirus, canine adenoviruses and canine parainfluenza virus, which are the principal components of canine combined virus vaccines, grew in the MDCK-SP cell culture as efficiently as the parental MDCK cells cultured in the conventional Eagle's MEM containing fetal bovine serum. Consequently, the use of MDCK-SP cell culture can make current canine vaccine products much safer, of higher quality and at lower cost.

A: Growth characteristics of canine pathogenic viruses in MDCK cells cultured in RPMI 1640 medium without animal protein
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Q: Background: In the healthy central nervous system (CNS), microglia are found in a homeostatic state and peripheral macrophages are absent from the brain. Microglia play key roles in maintaining CNS homeostasis and acting as first responders to infection and inflammation, and peripheral macrophages infiltrate the CNS during neuroinflammation. Due to their distinct origins and functions, discrimination between these cell populations is essential to the comprehension of neuroinflammatory disorders. Studies comparing the gene profiles of microglia and peripheral macrophages, or macrophages in vitro-derived from bone marrow, under non-infectious conditions of the CNS, have revealed valuable microglial-specific genes. However, studies comparing gene profiles between CNS-infiltrating macrophages and microglia, when both are isolated from the CNS during viral-induced neuroinflammation, are lacking. Methods: We isolated, via flow cytometry, microglia and infiltrating macrophages from the brains of Theiler's murine encephalomyelitis virus-infected C57BL/6 J mice and used RNA-Seq, followed by validation with qPCR, to examine the differential transcriptional profiles of these cells. We utilized primary literature defining subcellular localization to determine whether or not particular proteins extracted from the transcriptional profiles were expressed at the cell surface. The surface expression and cellular specificity of triggering receptor expressed on myeloid cells 1 (TREM-1) protein were examined via flow cytometry. We also examined the immune response gene profile within the transcriptional profiles of these isolated microglia and infiltrating macrophages. We have identified and validated new microglial-and macrophage-specific genes, encoding cell surface proteins, expressed at the peak of neuroinflammation. TREM-1 protein was confirmed to be expressed by infiltrating macrophages, not microglia, at the peak of neuroinflammation. We also identified both unique and redundant immune functions, through examination of the immune response gene profiles, of microglia and infiltrating macrophages during neurotropic viral infection. The differential expression of cell surface-specific genes during neuroinflammation can potentially be used to discriminate between microglia and macrophages as well as provide a resource that can be further utilized to target and manipulate specific cell responses during neuroinflammation.

A:
Differential transcriptional profiles identify microglial-and macrophage-specific gene markers expressed during virus-induced neuroinflammation
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