Sentences with phrase «agent model of disease»

This human - agent model of disease dynamics can then be used to provide reproducible empirical analyses, yielding greater insights into the behavioural reactions and individual responses of people threatened by outbreaks of disease.

Not exact matches

But epidemiologists are increasingly turning to agent - based models to include factors that the equations ignore, such as geography, transportation networks, family structure, and behavior change — all of which can strongly affect how disease spreads.

«The study results elucidate the molecular mechanisms underlying disease progression in multiple sclerosis models, providing a basis for future clinical trials to determine safety and efficacy of these chemical agents in humans with demyelinating disorders,» says Patrizia Casaccia, MD, PhD, Professor of Neuroscience, Genetics and Genomic Sciences at Mount Sinai and senior author of the study.

Specifically, the Mount Sinai study was designed to test whether pharmacological compounds designed to block the function of XPO1 / CRM1 could stop disease progression in mouse models that exhibit some of the characteristics of MS. Researchers found that two chemical agents (called KPT - 276 and KPT - 350) prevented XPO1 / CRM1 from shuttling cargo out of the nucleus of nerve cells, which protected them from free radicals and structural damage.

«Our interest in the body's own (innate) immune system as the culprit began when we discovered that immune system agents become activated in a laboratory model of Huntington's Disease,» he says.

«Our work and that of our colleagues on stress and CRF have been mechanistically implicated in Alzheimer's disease, but agents that impact CRF signaling have not been carefully tested for therapeutic efficacy or long - term safety in animal models,» said the study's principal investigator and corresponding author Robert Rissman, PhD, assistant professor in the Department of Neurosciences and Biomarker Core Director for the Alzheimer's Disease Cooperative Study disease, but agents that impact CRF signaling have not been carefully tested for therapeutic efficacy or long - term safety in animal models,» said the study's principal investigator and corresponding author Robert Rissman, PhD, assistant professor in the Department of Neurosciences and Biomarker Core Director for the Alzheimer's Disease Cooperative Study Disease Cooperative Study (ADCS).

To investigate whether person - to - person spread of an infectious agent could fit the observed data, a simple susceptible — exposed — infected — recovered (SEIR) population disease model was built (SI Data and Methods).

However, mouse models are not always exact replicas of the human condition, and they are inadequate to study the onset and evolution of diseases that are caused by human - tropic infectious agents, such as HIV - 1.

Using agent - based modelling and simulation approaches, we contribute to a better understanding of disease development and / or treatment effects (e.g. the context of leukaemia treatment or gene therapy approaches).

Both recent experience with immunotherapy for clearance of Aβ in AD, and their own (and Prothena's) experience with AS - clearing immunotherapies in animal models, indicate that in order to be effective as disease - modifying agents when administered alone, therapies that remove proteinaceous aggregates from the brain must be initiated in the early clinical or even preclinical stages of the disease, before the burden of other forms of aging damage becomes entrenched.

The profiling methods used in this research to identify molecular changes may be a general approach for differentiating the molecular pathology of disease models resulting from agent - specific effects, such as the effects of the two neurotoxins used in this research.

Two new NSG mouse models allow immunological dissection of graft - versus - host disease (GVHD) responses and in vivo testing of therapeutic agents targeting human CD4 T cells.

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.

Diuk - Wasser, M. A., G. Vourc» h, P. Cislo, A. G. Hoen, F. Melton, S. A. Hamer, M. Rowland, R. Cortinas, G. J. Hickling, J. I. Tsao, A. G. Barbour, U. Kitron, J. Piesman, and D. Fish, 2010: Field and climate - based model for predicting the density of host - seeking nymphal Ixodes scapularis, an important vector of tick - borne disease agents in the eastern United States.