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.

Ex Input:
Animal antimicrobial use and husbandry practices increase risk of emerging zoonotic disease and antibiotic resistance. We surveyed 700 households to elicit information on human and animal medicine use and husbandry practices. Households that owned livestock (n=265/459, 57.7%) reported using animal treatments 630 times during the previous 6 months; 57.6% obtained medicines, including antibiotics, from drug-sellers. Government animal health care providers were rarely visited (9.7 %), respondents more often sought animal health care from pharmacies and village doctors (70.6% and 11.9% respectively), citing the latter two as less costly and more successful based on past performance. Animal husbandry practices that could promote the transmission of microbes from animals to humans included: the proximity of chickens to humans (50.1% of households reported that the chickens slept in the bedroom); the shared use of natural bodies of water for human and animal bathing (78.3%); the use of livestock waste as fertilizer (60.9%); and gender roles that dictate that females are the primary care takers of poultry and children (62.8%). In the absence of an effective animal health care system, villagers must depend on local animal health care practitioners for treatment of their animals. Suboptimal use of antimicrobials coupled with unhygienic animal husbandry practices are important risk factors for emerging zoonotic disease and resistant pathogens.

Ex Output:
Household animal and human medicine use and animal husbandry practices in rural Bangladesh: risk factors for emerging zoonotic disease and antibiotic resistance HHS Public Access

Ex Input:
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious 24 disease localized to China, Japan, and Korea that is characterized by severe hemorrhage and a 25 high fatality rate. Currently, no specific vaccine or treatment has been approved for this 26 disease. To develop a therapeutic agent for SFTS, we isolated antibodies from a phage-27 displayed antibody library that was constructed from a patient who recovered from SFTS 28 virus (SFTSV) infection. One antibody, designated as Ab10, was reactive to the Gn envelope 29 glycoprotein of SFTSV and protected host cells and A129 mice from infection in both in 30 vitro and in vivo experiments. Notably, Ab10 protected 80% of mice, even when injected 5 31 days after inoculation with a lethal dose of SFTSV. Using cross-linker assisted mass 32 spectrometry and alanine scanning, we located the non-linear epitope of Ab10 on the Gn 33 glycoprotein domain II and an unstructured stem region, suggesting that Ab10 may inhibit a 34 conformational alteration that is critical for cell membrane fusion between the virus and host 35 cell. Ab10 reacted to recombinant Gn glycoprotein in Gangwon/Korea/2012, HB28, and SD4 36 strains. Additionally, based on its epitope, we predict that Ab10 binds the Gn glycoprotein in 37 247 of 272 reported SFTSV isolates previously reported. Together, these data suggest that 38 Ab10 has potential to be developed into a therapeutic agent that could protect against more 39 than 90% of reported SFTSV isolates. 40 41

Ex Output:
An anti-Gn glycoprotein antibody from a convalescent patient potently 2 inhibits the infection of severe fever with thrombocytopenia syndrome virus

Ex Input:
CD8 + cytotoxic T cell (CTL) responses are necessary for the lysis of virally infected cells and control of infection. CTLs are activated when their TCRs bind a major histocompatibility complex (MHC)-I/peptide complex on the surface of antigen presenting cells such as macrophages (M). It is now apparent that M display remarkable plasticity in response to environmental signals to polarize into classically activated M(LPS + IFN-) or alternatively activated M(IL-4). However, little is known about how M activation status influences their antigen presentation function to CD8 + T cell in models of virus infection. Consequently, we tested how polarization of spleen-derived (Sp)-M impacts direct presentation of viral antigens to influence effector and proliferative CD8 + T-cell responses. We show that M(IL-4) Sp-M retain MHC-I surface expression and the ability to stimulate IFN- production by CTL following peptide stimulation and lymphocytic choriomeningitis virus infection to levels similar to M0 and M(LPS + IFN-) M. However, memory CD8 + T cells cultured in the presence of M(IL-4) M underwent significantly reduced proliferation and produced similar IFN- levels as coculturing with M0 or M(LPS + IFN-) cells. Thus, these results show a novel ability of polarized M to regulate CD8 + T-cell proliferation and effector functions during virus infection.

Ex Output:
M(il-4) Tissue Macrophages support efficient interferon-gamma Production in antigen-specific cD8 + T cells with reduced Proliferative capacity