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.

Input: Consider Input: Bio-aerosols originate from different sources and their potentially pathogenic nature may form a hazard to healthcare workers and patients. So far no extensive review on existing evidence regarding bio-aerosols is available. This study aimed to review evidence on bio-aerosols in healthcare and the dental setting. The objectives were 1) What are the sources that generate bio-aerosols?; 2) What is the microbial load and composition of bio-aerosols and how were they measured?; and 3) What is the hazard posed by pathogenic micro-organisms transported via the aerosol route of transmission? Systematic scoping review design. Searched in PubMed and EMBASE from inception to 09-03-2016. References were screened and selected based on abstract and full text according to eligibility criteria. Full text articles were assessed for inclusion and summarized. The results are presented in three separate objectives and summarized for an overview of evidence. The search yielded 5,823 studies, of which 62 were included. Dental hand pieces were found to generate aerosols in the dental settings. Another 30 sources from human activities, interventions and daily cleaning performances in the hospital also generate aerosols. Fiftyfive bacterial species, 45 fungi genera and ten viruses were identified in a hospital setting and 16 bacterial and 23 fungal species in the dental environment. Patients with certain risk factors had a higher chance to acquire Legionella in hospitals. Such infections can lead to irreversible septic shock and death. Only a few studies found that bio-aerosol generating procedures resulted in transmission of infectious diseases or allergic reactions.

Output: A scoping review on bio-aerosols in healthcare and the dental environment

Input: Consider Input: medRxiv preprint Interpretation Parameters that successfully reproduce the observed number of cases indicate that both R 0 and the prevalence of the virus might be underestimated. This is in concordance with the newest research on undocumented COVID-19 cases. Consequently, the actual mortality rate is putatively lower than estimated. Confirmation of the pandemic characteristic by further refinement of the model and screening tests is crucial for developing an effective strategy for the global epidemiological crisis. 1 Balcan D, Goncalves B, Hu H, Ramasco JJ, Colizza V, Vespignani A. Modeling the spatial spread of infectious diseases: the GLobal Epidemic and Mobility computational model. J Comput Sci 2010; 1 : 132-45. 2 Van den Broeck W, Gioannini C, Goncalves B, Quaggiotto M, Colizza V, Vespignani A. The GLEaMviz computational tool, a publicly available software to explore realistic epidemic spreading scenarios at the global scale. BMC Infect Dis 2011; 11 : 37. 3 Tizzoni M, Bajardi P, Poletto C, et al. Real-time numerical forecast of global epidemic spreading: case study of 2009 A/H1N1pdm. BMC Med 2012;

Output: From a single host to global spread. The global mobility based modelling of the COVID-19 pandemic implies higher infection and lower detection rates than current estimates

Input: Consider Input: Multiple sclerosis (MS) is an inflammatory, demyelinating, central nervous system disease mediated by myelin-specific T cells. Environmental triggers that cause a breakdown of myelinspecific T cell tolerance are unknown. We found that CD8 + myelin basic protein (MBP)-specific T cell tolerance can be broken and autoimmunity induced by infection with a virus that does not express MBP cross-reactive epitopes and does not depend on bystander activation. Instead, the virus activated dual T cell receptor (TCR)-expressing T cells capable of recognizing both MBP and viral antigens. These results demonstrate the importance of dual TCR T cells in autoimmunity and suggest a mechanism by which a ubiquitous viral infection could trigger autoimmunity in a subset of infected individuals, as hypothesized in the etiology of MS. Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS) that affects more than one million people worldwide. It is believed to be an autoimmune disease in which exposure of genetically predisposed individuals to environmental factors triggers a breakdown in T cell tolerance to myelin antigens. The specific types of myelin-specific T cells that contribute to the pathogenesis of MS are not known. Most studies have focused on the pathogenic role of myelin-specific CD4 + T cells because of the relatively strong association of MS susceptibility with major histocompatibility complex (MHC) class II alleles. In addition, CD4 + T cells are the primary effector T cells in experimental autoimmune encephalomyelitis (EAE), a widely used animal model of MS. However, there has been increasing recognition of the potential importance of CD8 + T cells in the pathogenesis of MS. CD8 + T cells typically outnumber CD4 + T cells in acute and chronic lesions in MS patients, and the CD8 + T cell subset exhibits more evidence of antigen-driven activation compared to CD4 + T cells in the CNS and blood of MS patients1, 2. The frequency of CNS antigen-specific CD8 + , but not CD4 + , using Power SYBR Green PCR Master Mix (Applied Biosystems). Tcra V gene primers and a C primer have been previously described50. Reactions were run in duplicate, and samples were normalized to the internal actin control. All P values were calculated with a two-tailed Student's t-test.
Output: Viral Infection Triggers Central Nervous System Autoimmunity Via Activation of Dual TCR-Expressing CD8 + T Cells HHS Public Access Author manuscript