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.
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Question: Objectives: We compared the expelled air dispersion distances during coughing from a human patient simulator (HPS) lying at 45u with and without wearing a surgical mask or N95 mask in a negative pressure isolation room. Methods: Airflow was marked with intrapulmonary smoke. Coughing bouts were generated by short bursts of oxygen flow at 650, 320, and 220L/min to simulate normal, mild and poor coughing efforts, respectively. The coughing jet was revealed by laser light-sheet and images were captured by high definition video. Smoke concentration in the plume was estimated from the light scattered by smoke particles. Significant exposure was arbitrarily defined where there was $ 20% of normalized smoke concentration. Results: During normal cough, expelled air dispersion distances were 68, 30 and 15 cm along the median sagittal plane when the HPS wore no mask, a surgical mask and a N95 mask, respectively. In moderate lung injury, the corresponding air dispersion distances for mild coughing efforts were reduced to 55, 27 and 14 cm, respectively, p , 0.001. The distances were reduced to 30, 24 and 12 cm, respectively during poor coughing effort as in severe lung injury. Lateral dispersion distances during normal cough were 0, 28 and 15 cm when the HPS wore no mask, a surgical mask and a N95 mask, respectively. Conclusions: Normal cough produced a turbulent jet about 0.7 m towards the end of the bed from the recumbent subject. N95 mask was more effective than surgical mask in preventing expelled air leakage during coughing but there was still significant sideway leakage.

Answer: Exhaled Air Dispersion during Coughing with and without Wearing a Surgical or N95 Mask


Question: The Tasmanian devil (Sarcophilus harrisii), so named for its blood-curdling, nocturnal shrieks and snarls, is the largest of the carnivorous marsupials. Although once widely persecuted, concerted efforts are now being made to save the devil from extinction following the emergence of a fatal transmissible malignancy known as devil facial tumour disease (DFTD). DFTD is unusual in that the infectious agent is the cancer cell itself. This chapter discusses the aetiology and pathogenesis of DFTD as well as the profound impact the spread of DFTD has had on the devil's conservation status. Strategies for managing DFTD and conserving the devil will be explored and the contribution of new sequencing technology to the field of conservation genetics and genomics will be examined with regard to the Tasmanian devil and DFTD.

Answer: Devil Facial Tumour Disease (DFTD): Using Genetics and Genomics to Investigate Infectious Disease in an Endangered Marsupial


Question: This experiment was conducted to evaluate whether pretreatment with fenofibrate could mitigate acute lung injury (ALI) in a mice model of intestinal ischemia/reperfusion (I/R). Male C57BL/6 mice were randomly assigned into three groups (n = 6): sham, intestinal I/R + vehicle, and intestinal I/R + fenofibrate. Intestinal I/R was achieved by clamping the superior mesenteric artery. Fenofibrate (100 mg/kg) or equal volume of vehicle was injected intraperitoneally 60 minutes before the ischemia. At the end of experiment, measurement of pathohistological score, inflammatory mediators and other markers were performed. In addition, a 24-hour survival experiment was conducted in intestinal I/R mice treated with fenofibrate or vehicle. The chief results were as anticipated. Pathohistological evaluation indicated that fenofibrate ameliorated the local intestine damage and distant lung injury. Pretreatment with fenofibrate significantly decreased inflammatory factors in both the intestine and the lung. Consistently, renal creatine levels and hepatic ALT levels were significantly decreased in the fenofibrate group. Moreover, serum systemic inflammatory response indicators were significantly alleviated in the fenofibrate group. In addition, fenofibrate administration significantly improved the survival rate. Collectively, our data indicated that pretreatment with fenofibrate prior to ischemia attenuated intestinal I/R injury and ALI. Acute lung injury (ALI) is a critically severe, life-threatening condition in ICU, characterized by high mortality of approximately 40% 1 . ALI, along with its more severe form, acute respiratory distress syndrome, often results from a massive insult to the lung, whether be the direct alveolar infiltration or the indirect effects of systemic inflammatory response syndrome or multiple organ dysfunction syndromes 2 . An effective treatment of this life-threatening disorder calls for a better understanding of the molecular pathophysiology of ALI. The intestine is recognized to be one of the largest immune barrier systems and to be the source of bacteria and endotoxins in the body 3 . Previous reports indicate that the intestinal organ plays a crucial role in the development of ALI 4 . Mesenteric artery ischemia, a commonly seen critical state during small bowel transplantation or trauma, may lead to intestinal ischemia/reperfusion (I/R) injury. During the process of intestinal I/R injury, local bacteria overgrow and translocate, gastrointestinal mobility decreases, and mucosal permeability increases, all of which subsequently lead to the local intestine damage or distant lung injuries through the activation of systemic inflammatory response syndrome or multiple organ dysfunction syndromes 5,6 . Intestinal I/R is, therefore, a useful model for the investigation of pathophysiological mechanism of indirect ALI. Fenofibrate is known as an agonist of the peroxisome proliferator-activated receptor -α (PPARα ), the nuclear receptor superfamily member 7 . As a nuclear receptor activator, fenofibrate up-regulates or down-regulates genes that are involved in many pathophysiological processes, such as oxidative stress, inflammation, and leukocyte endothelium interactions 8, 9 . Recent studies have demonstrated an anti-oxidant, anti-inflammatory, and anti-ischemic role of fenofibrate to attenuate I/R injury in kidney 10,11 , liver 12 , brain 13,14 and heart 15 . But to date there are no literatures reporting the protective effects of fenofibrate in I/R injury in the organ of intestine. Moreover, the functional significance of fenofibrate in the intestinal I/R-induced ALI remains unclear. Therefore, this experiment is aimed to investigate whether fenofibrate administration would ameliorate the lung injury and inflammation in the model of intestinal I/R injury. Animals. The male C57BL/6 mice (8-10-wk-old; 20 ± 2 g) were purchased from Charles River (Beijing, China). Mice were kept in a temperature (21 ± 2 °C) and humidity (60 ± 5%) controlled room on a 12-hour light/dark cycle. They were fed a standard mice chow and water ad liblitum. All experiments were performed in accordance with the Declaration of Helsinki and were approved by the Institutional Animal Ethical Committee of the Peking Union Medical College Hospital.

Answer:
Protective effects of fenofibrate against acute lung injury induced by intestinal ischemia/reperfusion in mice OPEN