ABSTRACT
Ischemic stroke is a leading cause of death and disability. Tissue plasminogen activator is the only U.S. Food and Drug Administration approved thrombolytic therapy for ischemic stroke patients till date. However, its use is limited due to increased risk of bleeding and narrow therapeutic window. Most of the preclinically tested pharmacological agents failed to be translated to the clinic. This drives the need for alternative therapeutic approaches that not only provide enhanced neuroprotection, but also reduce the risk of stroke. Physical exercise is a sort of preconditioning that provides the body with brief ischemic episodes that can protect the body from subsequent severe ischemic attacks like stroke. Physical exercise is known to improve cardiovascular health. However, its role in providing neuroprotection in stroke is not clear. Clinical observational studies showed a correlation between regular physical exercise and reduced risk and severity of ischemic stroke and better outcomes after stroke. However, the underlying mechanisms through which prestroke exercise can reduce the stroke injury and improve the outcomes are not completely understood. The purpose of this review is to: demonstrate the impact of exercise on stroke outcomes and show the potential role of exercise in stroke prevention and recovery; uncover the underlying mechanisms through which exercise reduces the neurovascular injury and improves stroke outcomes aiming to develop novel therapeutic approaches.
ABSTRACT
Ischemic stroke is a leading cause of death and disability. Tissue plasminogen activator is the only U.S. Food and Drug Administration approved thrombolytic therapy for ischemic stroke patients till date. However, its use is limited due to increased risk of bleeding and narrow therapeutic window. Most of the preclinically tested pharmacological agents failed to be translated to the clinic. This drives the need for alternative therapeutic approaches that not only provide enhanced neuroprotection, but also reduce the risk of stroke. Physical exercise is a sort of preconditioning that provides the body with brief ischemic episodes that can protect the body from subsequent severe ischemic attacks like stroke. Physical exercise is known to improve cardiovascular health. However, its role in providing neuroprotection in stroke is not clear. Clinical observational studies showed a correlation between regular physical exercise and reduced risk and severity of ischemic stroke and better outcomes after stroke. However, the underlying mechanisms through which prestroke exercise can reduce the stroke injury and improve the outcomes are not completely understood. The purpose of this review is to: demonstrate the impact of exercise on stroke outcomes and show the potential role of exercise in stroke prevention and recovery; uncover the underlying mechanisms through which exercise reduces the neurovascular injury and improves stroke outcomes aiming to develop novel therapeutic approaches.
ABSTRACT
<p><b>OBJECTIVE</b>To test Candonocypris novaezelandiae (Baird) (C. novaezelandiae), sub-class Ostracoda, obtained from the Nile, Egypt for its predatory activity on snail, Biomphalaria alexandrina (B. alexandrina), intermediate host of Schistosoma mansoni (S. mansoni) and on the free-living larval stages of this parasite (miracidia and cercariae).</p><p><b>METHODS</b>The predatory activity of C. novaezelandiae was determined on B. alexandrina snail (several densities of eggs, newly hatched and juveniles). This activity was also determined on S. mansoni miracidia and cercariae using different volumes of water and different numbers of larvae. C. novaezelandiae was also tested for its effect on infection of snails and on the cercarial production.</p><p><b>RESULTS</b>C. novaezelandiae was found to feed on the eggs, newly hatched and juvenile snails, but with significant reduction in the consumption in the presence of other diet like the blue green algae (Nostoc muscorum). This ostracod also showed considerable predatory activity on the free-living larval stages of S. mansoni which was affected by certain environmental factors such as volume of water, density of C. novaezelandiae and number of larvae of the parasite.</p><p><b>CONCLUSIONS</b>The presence of this ostracod in the aquatic habitat led to significant reduction of snail population, infection rate of snails with schistosme miracidia as well as of cercarial production from the infected snails. This may suggest that introducing C. novaezelandiae into the habitat at schistosome risky sites could suppress the transmission of the disease.</p>
