<|begin_of_text|><|start_header_id|>system<|end_header_id|>You are an expert on climate change, human mobility and migration. Answer the question truthfully.<|eot_id|><|start_header_id|>user<|end_header_id|>Here are the title and abstract of a scientific paper probably related to climate change, human mobility and migration..
Title:"Diet-induced obesity alters myeloid cell populations in naive and injured lung."
Abstract:"Background: There are pulmonary consequences to obesity, including increased prevalence of asthma, greater susceptibility to influenza, and possibly reduced susceptibility to lung injury. Although it is well established that obesity is associated with alterations to the immune system, little is known about obesity-associated changes to pulmonary immune cells. Objectives: We hypothesized that obesity would alter the inflammatory milieu in the unchallenged lung and circulation; thereby contributing to altered susceptibility to lung injury. Methods: We used a murine model of diet-induced obesity and evaluated bone marrow and blood leukocytes at 3 months, and pulmonary leukocytes at 3 and 6 months for changes in their adhesion and chemokine receptors, markers of activation states, and cell numbers. We also evaluated the inflammatory response to LPS in obese mice. Results: In the lung, diet-induced obesity was associated with increased leukocyte numbers over-time. Adhesion receptors were increased in a cell-and site-specific fashion, and there was an evolution of macrophage and neutrophil polarization toward M1 and N1, respectively. After LPS-challenge, obesity was associated with increased neutrophil recruitment to the lung with impaired migration into the alveolar space. Associated with these changes, obesity increased LFA-1 and ICAM-1 neutrophil expression and altered CXCL1 gradients. Conclusion: Our results highlight the effects of diet-induced obesity on the murine blood and lung leukocyte populations, including increases in adhesion receptor expression that may contribute to altered recruitment or retention within the lung. Translation of these findings to people with obesity will be critical for determining the basic inflammatory underpinnings of pulmonary disease susceptibility.."
I have six questions you need to answer.
Q1: Is this article is about 'human migration mobility': 1 = yes; 0 = no. Answer with a number. Do not give a textual explanation.

Q2: What drivers of migration and mobility does the article study? 0 = 'other', 1 = 'climate', 2 = 'environment', 3 = 'economic', 4 = 'conflict', 5 = 'political', 6 = 'social', 7 = 'family'. Answer with a number or a sequence of numbers separated by commas. Do not give a textual explanation. 

Q3: What is the overall sentiment of the article?:0 = 'neutral', 1 = 'negative', 2 = 'positive'. Answer with a number. Do not give a textual explanation.

Q4: What type of climate or environmental keywords are explicitly mentioned?:  0 = 'none', 1 = 'algal blooms', 2 = 'infestation', 3 = 'infectious diseases', 4 = 'ocean acidification', 5 = 'sea ice', 6 = 'acid rain', 7 = 'drought', 8 = 'cold wave', 9 = 'heat wave', 10 = 'glacial', 11 = 'wildfire', 12 = 'air pollution', 13 = 'biodiversity loss', 14 = 'coastal erosion', 15 = 'land degradation', 16 = 'deforestation', 17 = 'desertification', 18 = 'water pollution', 19 = 'diebacks', 20 = 'permafrost loss', 21 = 'sand mining', 22 = 'sea level rise', 23 = 'earthquake', 24 = 'tsunami', 25 = 'volcanic', 26 = 'flood', 27 = 'avalanche', 28 = 'landslide', 29 = 'downburst', 30 = 'thunderstorm', 31 = 'sandstorm', 32 = 'haze', 33 = 'storm', 34 = 'cyclone', 35 = 'blizzard', 36 = 'hail', 37 = 'snow', 38 = 'tornado', 39 = 'wind', 40 = 'hurricane', 41 = 'typhoon', 42 = 'other'. Answer with a number or a sequence of numbers separated by commas. Do not give a textual explanation. 

Q5: What discipline does the article belong to?: 0 = 'other', 1 = 'social science', 2 = 'natural science', 3 = 'arts and humanities', 4 = 'multidiscipline and interdiscipline'. Answer with a number. Do not give a textual explanation.

Q6: Does the article apply quantitative and/or statistical analysis?: 0 = 'no', 1 = 'yes'. Answer with a number. Do not give a textual explanation.

Use the following template: 

Q1 = [];
Q2 = [];
Q3 = [];
Q4 = [];
Q5 = [];
Q6 = [].<|eot_id|><|start_header_id|>assistant<|end_header_id|>Answer:
Q1 = [0];
Q2 = [];
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Q4 = [];
Q5 = [];
Q6 = [1].
Diet-induced obesity alters myeloid cell populations in naive and injured lung
Background: There are pulmonary consequences to obesity, including increased prevalence of asthma, greater susceptibility to influenza, and possibly reduced susceptibility to lung injury. Although it is well established that obesity is associated with alterations to the immune system, little is known about obesity-associated changes to pulmonary immune cells. Objectives: We hypothesized that obesity would alter the inflammatory milieu in the unchallenged lung and circulation; thereby contributing to altered susceptibility to lung injury. Methods: We used a murine model of diet-induced obesity and evaluated bone marrow and blood leukocytes at 3 months, and pulmonary leukocytes at 3 and 6 months for changes in their adhesion and chemokine receptors, markers of activation states, and cell numbers. We also evaluated the inflammatory response to LPS in obese mice. Results: In the lung, diet-induced obesity was associated with increased leukocyte numbers over-time. Adhesion receptors were increased in a cell-and site-specific fashion, and there was an evolution of macrophage and neutrophil polarization toward M1 and N1, respectively. After LPS-challenge, obesity was associated with increased neutrophil recruitment to the lung with impaired migration into the alveolar space. Associated with these changes, obesity increased LFA-1 and ICAM-1 neutrophil expression and altered CXCL1 gradients. Conclusion: Our results highlight the effects of diet-induced obesity on the murine blood and lung leukocyte populations, including increases in adhesion receptor expression that may contribute to altered recruitment or retention within the lung. Translation of these findings to people with obesity will be critical for determining the basic inflammatory underpinnings of pulmonary disease susceptibility.