TASK DEFINITION: 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.
PROBLEM: We summarize herein the results of various virologic studies of acute otitis media (AOM) conducted at our site over a ten -year period. Among 566 children with AOM, respiratory syncytial virus (RSV) was the most common virus identified in either middle ear fluid or nasal wash; it was found in 16% of all children and 38% of virus-positive children. Seventy-one percent of the children with RSV were one year of age or older, which was significantly older than all other viruses combined (P = 0.045). RSV infection was associated with the common bacterial pathogens causing AOM. Past efforts to develop vaccines for RSV have emphasized prevention of lower respiratory tract infection in infants, which is a more serious problem but less common than AOM. Our results suggest that RSV vaccines that work only against infection in older children may have value in preventing AOM, the most common pediatric disease.

SOLUTION: ROLE OF RESPIRATORY SYNCYTIAL VIRUS IN ACUTE OTITIS MEDIA: IMPLICATIONS FOR VACCINE DEVELOPMENT

PROBLEM: Background: Complement proteins and activation products have been found associated with neuropathology in Alzheimer's disease (AD). Recently, a C5a receptor antagonist was shown to suppress neuropathology in two murine models of AD, Tg2576 and 3xTg. Previously, a genetic deficiency of C1q in the Tg2576 mouse model showed an accumulation of fibrillar plaques similar to the complement sufficient Tg2576, but reactive glia were significantly decreased and neuronal integrity was improved suggesting detrimental consequences for complement activation in AD. The goal of this study was to define the role of the classical complement activation pathway in the progression of pathology in the 3xTg mouse that develops tangles in addition to fibrillar plaques (more closely reflecting human AD pathology) and to assess the influence of complement in a model of AD with a higher level of complement hemolytic activity. Methods: 3xTg mice deficient in C1q (3xTgQ-/-) were generated, and both 3xTg and 3xTgQ-/-were backcrossed to the BUB mouse strain which has higher in vitro hemolytic complement activity. Mice were aged and perfused, and brain sections stained for pathological markers or analyzed for proinflammatory marker expression. Results: 3xTgQ-/-mice showed similar amounts of fibrillar amyloid, reactive glia and hyperphosphorylated tau as the C1q-sufficient 3xTg at the ages analyzed. However, 3xTg and 3xTgQ-/-on the BUB background developed pathology earlier than on the original 3xTg background, although the presence of C1q had no effect on neuropathological and pro-inflammatory markers. In contrast to that seen in other transgenic models of AD, C1q, C4 and C3 immunoreactivity was undetectable on the plaques of 3xTg in any background, although C3 was associated with reactive astrocytes surrounding the plaques. Importantly, properdin a component of the alternative complement pathway was associated with plaques in all models. Conclusions: In contrast to previously investigated transgenic models of AD, development of neuropathology in 3xTg mice, which progresses much slower than other murine models, may not be influenced by fibrillar amyloid mediated activation of the classical complement pathway, suggesting that the alternative complement pathway activation or a C3-independent cleavage of C5 could account for the detrimental effects in these mice that are prevented by the C5a receptor antagonist. Furthermore, the paucity of complement activation may be a factor in the slower kinetics of progression of pathology in the 3xTg model of this disease.

SOLUTION: Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease

PROBLEM: The indoor transmission of airborne particles can spread disease and have health-related and even life-threatening effects on occupants, thus necessitating effective ways to locate indoor particle sources. The identification of particle sources from concentration distributions is a difficult task because particles are often released at a time-varying rate, and particle transport mechanisms are more complex than those of gas. This study proposes an improved multi-robot olfactory search method for locating two types of time-varying indoor particle sources: 1) periodic sources such as occupants' respiratory activities and 2) decaying sources such as laboratory leaky containers with hazardous chemicals. The method considers both particle concentrations and indoor air velocities by including an upwind term in the standard particle swarm optimization (PSO) algorithm, preventing robots from becoming trapped into a local optimum, which occurs when using other algorithms. We also considered two ventilation types (mixing ventilation and displacement ventilation) when particles are emitted from different source types, comprising four scenarios. For each scenario, particle concentration and air velocity were simulated using computational fluid dynamics (CFD) and then fed to the PSO algorithm for source localization. In addition, we validated the CFD approach for one scenario by comparing experimental data (e.g., velocities and particle concentrations) under laboratory settings. The results showed that the proposed method can locate the two types of particle sources within approximately 55 s, and the success rates of source localization exceeding 96%, which is a much higher level than levels achieved from the standard PSO and wind utilization II algorithms.

SOLUTION:
An improved particle swarm optimization method for locating time-varying indoor particle sources