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 Q]: Acute cough is a major symptom of viral respiratory tract infection and causes excessive morbidity in human populations across the world. A wide variety of viruses play a role in the development of cough after acute infection and all of these manifest a similar clinical picture across different age groups. Despite the large disease burden surprisingly little is known about the mechanism of acute cough following viral infection. Both in vitro and in vivo experiments show that increased production of neuropeptides and leukotrienes mediate cough after viral infection, along with altered expression of neural receptors. Increased airway mucus production is also likely to play a significant role. This work is reviewed in this article. Following the recent development of a mouse model for rhinovirus infection and the establishment of experimental models of rhinovirus challenge in human subjects with both asthma and COPD the field is expanding to translate in vitro research into clinical studies and hopefully eventually into clinical practice. Developing a clearer understanding of the mechanisms underlying virus induced cough may lead to more specific and effective therapies.
[EX A]: Cough and viruses in airways disease: Mechanisms

[EX Q]: Background: The novel corona virus SARS-CoV-2 (COVID-19) can infect healthcare workers. We developed an institutional algorithm to protect operating room team members during the COVID-19 pandemic and rationally conserve personal protective equipment (PPE). Study Design: An interventional platform (operating room, interventional suites, and endoscopy) PPE taskforce was convened by the hospital and medical school leadership and tasked with developing a common algorithm for PPE use, to be used throughout the interventional platform. In conjunction with our infection disease experts, we developed our guidelines based upon potential patterns of spread, risk of exposure and conservation of PPE. A decision tree algorithm describing our institutional guidelines for precautions for operating room team members was created. This algorithm is based on urgency of operation, anticipated viral burden at the surgical site, opportunity for a procedure to aerosolize virus, and likelihood a patient could be infected based on symptoms and testing. Conclusion: Despite COVID-19 being a new threat, we have shown that by developing an easyto-follow decision tree algorithm for the interventional platform teams, we can ensure optimal healthcare worker safety.
[EX A]: Journal Pre-proof Precautions for Operating Room Team Members during the COVID-19 Pandemic Precautions for Operating Room Team Members during the COVID-19 Pandemic

[EX Q]: Acoustic trauma was recently shown to induce an inflammatory response in the ear characterized by rapid entry of macrophages in the spiral ligament. The current study seeks to elucidate the mechanisms involved in summoning macrophages to the cochlear lateral wall and the role macrophages play in noiseinduced injury or repair. CCL2 and its primary receptor, CCR2, are the most widely validated effectors of monocyte chemotaxis in vivo. CCL2 -/and CCR2 -/mice have been used extensively in studies of monocyte activation in neuronal injury. However, the function of CCL2 and CCR2 in the cochlea has not been studied. The present study examines the role of CCL2 and CCR2 in acoustic injury. CCL2 -/and CCR2 -/mice on a CX3CR1 +/GFP background were exposed to octave band noise (8-16 kHz) for 2 h to determine the effect of CCL2 and CCR2 on monocyte migration into the cochlea, threshold shift, and cell survival. We found that threshold shift was unchanged in the two knockout mouse strains when compared to the background strain (CX3CR1 +/GFP ). Surprisingly, we found that monocyte migration was also unchanged, despite the absence of CCL2 or CCR2. However, there was a dramatic increase in noise-induced hair cell death in the CCR2 -/strain. This observation suggests that CCR2, independent of CCL2, plays a protective role in the cochlea after noise, and neither ligand nor receptor is necessary for monocyte migration. Possible mechanisms of neuroprotection by CCR2 are discussed.
[EX A]:
CC Chemokine Receptor 2 is Protective Against Noise-Induced Hair Cell Death: Studies in CX3CR1 +/GFP Mice