Human-disease interactions involve the transmission of infectious diseases among individuals and the practice of preventive behavior by individuals. Both infectious diseases and preventive behavior diffuse simultaneously through human networks and interact with one another, but few existing models have coupled them together. This article proposes a conceptual framework to fill this knowledge gap and illustrates the model establishment. The conceptual model consists of two networks and two diffusion processes. The two networks include: an infection network that transmits diseases and a communication network that channels inter-personal influence regarding preventive behavior. Both networks are composed of same individuals but different types of interactions. This article further introduces modeling approaches to formulize such a framework, including the individual-based modeling approach, network theory, disease transmission models and behavioral models. An illustrative model was implemented to simulate a coupled-diffusion process during an influenza epidemic. The simulation outcomes suggest that the transmission probability of a disease and the structure of infection network have profound effects on the dynamics of coupled-diffusion. The results imply that current models may underestimate disease transmissibility parameters, because human preventive behavior has not been considered. This issue calls for a new interdisciplinary study that incorporates theories from epidemiology, social science, behavioral science, and health psychology.
Economic impacts of seasonal influenza vary across US counties, but little estimation has been conducted at the county level. This research computed annual economic costs of seasonal influenza for 3143 US counties based on Census 2010, identified inherent spatial patterns, and investigated cost-benefits of vaccination strategies. The computing model modified existing methods for national level estimation, and further emphasized spatial variations between counties, in terms of population size, age structure, influenza activity, and income level. Upon such a model, four vaccination strategies that prioritize different types of counties were simulated and their net returns were examined. The results indicate that the annual economic costs of influenza varied from $13.9 thousand to $957.5 million across US counties, with a median of $2.47 million. Prioritizing vaccines to counties with high influenza attack rates produces the lowest influenza cases and highest net returns. This research fills the current knowledge gap by downscaling the estimation to a county level, and adds spatial variability into studies of influenza economics and interventions. Compared to the national estimates, the presented statistics and maps will offer detailed guidance for local health agencies to fight against influenza.
Based on accumulating evidence, cholesterol metabolism dysfunction has been suggested to contribute to the pathophysiological process of traumatic brain injury (TBI) and lead to neurological deficits. As a key transporter of cholesterol that efflux from cells, the ATP‐binding cassette (ABC) transporter family exerts many beneficial effects on central nervous system (CNS) diseases. However, there is no study regarding the effects and mechanisms of ABCG1 on TBI. As expected, TBI resulted in the different time‐course changes of cholesterol metabolism‐related molecules in the injured cortex. Considering ABCG1 is expressed in neuron and glia post‐TBI, we generated nestin‐specific
Abcg1
knockout (
Abcg1
‐KO) mice using the Cre/loxP recombination system. These
Abcg1
‐KO mice showed reduced plasma high‐density lipoprotein cholesterol levels and increased plasma lower‐density lipoprotein cholesterol levels under the base condition. After TBI, these
Abcg1
‐KO mice were susceptible to cholesterol metabolism turbulence. Moreover,
Abcg1
‐KO exacerbated TBI‐induced pyroptosis, apoptosis, neuronal cell insult, brain edema, neurological deficits, and brain lesion volume. Importantly, we found that treating with retinoid X receptor (RXR, the upstream molecule of ABCG1) agonist, bexarotene, in
Abcg1
‐KO mice partly rescued TBI‐induced neuronal damages mentioned above and improved functional deficits versus vehicle‐treated group. These data show that, in addition to regulating brain cholesterol metabolism,
Abcg1
improves neurological deficits through inhibiting pyroptosis, apoptosis, neuronal cell insult, and brain edema. Moreover, our findings demonstrate that the cerebroprotection of
Abcg1
on TBI partly relies on the activation of the RXRalpha/PPARgamma pathway, which provides a potential therapeutic target for treating TBI.
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