In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

Q: Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus. Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage. We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue. To test this hypothesis of monocyte conversion from a normal quiescent phenotype to an inflammatory phenotype, we used Affymetrix Microarray to acquire a transcriptional profile of infected monocytes at a time point our data emphasized is a key temporal regulatory point following infection. We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection. Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection. We found that 65% of genes strictly associated with M1 polarization were up-regulated, while only 4% of genes solely associated with M2 polarization were up-regulated. Analysis of the monocyte chemokinome at the transcriptional level showed that 44% of M1 and 33% of M2 macrophage chemokines were up-regulated. Proteomic analysis using chemokine Ab arrays confirmed the secretion of these chemotactic proteins from HCMV-infected monocytes. Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype.

A: Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.
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Q: The debate around the frequency and importance of genetic exchange in parasitic protozoa is now several decades old. Recently, fresh assertions have been made that predominant clonal evolution explains the population structures of several key protozoan pathogens. Here, we present an alternative perspective. On the assumption that much apparent clonality may be an artefact of inadequate sampling and study design, we review current research to define why sex might be so difficult to detect in protozoan parasite populations. In doing so, we contrast laboratory models of genetic exchange in parasitic protozoa with natural patterns of genetic diversity and consider the fitness advantage of sex at different evolutionary scales. We discuss approaches to improve the accuracy of efforts to characterize genetic exchange in the field. We also examine the implications of the first population genomic studies for the debate around sex and clonality in parasitic protozoa and discuss caveats for the future.

A: Reproductive clonality in protozoan pathogens--truth or artefact?
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Q: Both to address unmet medical needs and to improve industry competitiveness, regulators in both the United States and the European Union have taken bold steps to translate academic research from the university lab to the patient. A pharmaceutical public-private partnership (PPPP), which is a legally binding contract between a private pharmaceutical enterprise and a public research university (or a private university doing research funded with public funds), can be a significant tool to ensure a more efficient payoff in the highly regulated world of pharmaceuticals. In particular, a properly framed binding contract, coupled with respect for positive social norms, can move the parties away from an inefficient prisoners' dilemma Nash Equilibrium to the Pareto Optimal Frontier. When coupled with appropriate attention to the difficult task of coordinating the actions of interdependent actors, a PPPP arrangement can enhance the likelihood of successful commercialization by flipping the parties' incentives as compared with more traditional contracts. Because PPPPs are less common in Europe than in the United States, a key purpose of this article is to provide an annotated roadmap that universities, private firms, and EU policy makers can use to create efficient PPPPs to enhance for-profit innovation in the pharmaceutical industry in Europe. A secondary purpose is to suggest amendments to the U.S. laws governing the patenting of government-funded technology to prevent undue burdens on the sharing of certain upstream medical discoveries and research tools. Our analysis is not only comparative; it also combines, we believe for the first time, a game theory and law and management approach to for-profit PPPPs.

A:
Pharmaceutical Public-Private Partnerships in the United States and Europe: Moving from the Bench to the Bedside
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