ABSTRACT
In this paper, the required models and methods to analyze and quantify the potential demand for urban air mobility (UAM) complementing public transport and possible impacts were defined and applied to the Munich Metropolitan region. An existing agent-based transport model of the study area were used and extended to cover socio-demographic changes up to the year 2030 and intermodal UAM services. An incremental logit model for UAM was derived to simulate demand for this new mode. An airport access model was developed as well. Three different UAM networks with different numbers of vertiports were defined. Sensitivity studies of ticket fare and structure, flying vehicle cruise speed, passenger process times at vertiports and different Urban Air Mobility networks sizes were performed. For the reference case, UAM accounts for a modal share of 0.5%. The absolute UAM demand is concentrated on very short routes; hence, UAM vehicle flight speed variation shows low UAM demand impacts. Kilometer-based fare, number of UAM vehicles per vertiport and passenger process times at vertiports show a significant impact on UAM demand.
ABSTRACT
The differences between the immune response elicited during a self-limiting and a life-threatening lung infection with Streptococcus pneumoniae was analyzed in a mouse model of intranasal challenge using two different pneumococcal strains. M10, a serotype 11A strain, induced an early response within the first 12 h after the challenge, which was characterized by the early local secretion of TNF-á and IL-6, followed by a sharp and rapid neutrophil influx. Bacterial loads in the lungs already started to fall at 12 h after the challenge and no pneumococci could be recovered after 36 h, at the time point when the animals started to show improvement in disease symptoms. ATCC6303, a serotype 3 strain, on the other hand, showed only a late increase in local TNF-á and IL-6 levels, when bacterial growth already seems to be out of control. Although cell influx was also observed, neutrophil rise was not as marked as with M10 (type 11A). Pneumococcal loads increased constantly and bacteria started to be recovered from the blood at 30 h after the challenge. After this time point, animals showed worsening of symptoms and became lethargic. The resolution of the acute infection could be thus correlated with the early induction of proinflammatory cytokines, which could be due to the presence of a thinner polysaccharide capsule in M10 (type 11A), rendering bacterial components capable of activating the innate immune response more accessible.
