Glutamate excitotoxicity, oxidative stress, and mitochondrial dysfunctions are common
features leading to neuronal death in cerebral ischemia, traumatic brain injury, Parkinson's …

To determine whether exposure to chronic hypoxia and subsequent development of pulmonary
hypertension induces alterations of endothelium-dependent relaxation in rat pulmonary …

… endothelium intact rings of rat aorta precontracted with PE, indicating a lack of interaction
of … , the loss of tonicity of the contractile response to PE that reflects activation of iNOS (11-14) …

In addition to inhibition of acetylcholine release in the neuromuscular junction botulinum
toxin type A (BoNT-A) also inhibits the release of mediators involved in pain perception. We …

Nitric oxide (NO) and reactive oxygen species (ROS) act independently as well as cooperatively
to induce neuronal death in acute neurological disorders. Inhibition of neuronal nitric …

Botulinum neurotoxin B is a Food and Drug Administration-approved therapeutic toxin.
However, it has lower binding affinity toward the human version of its major receptor, …

Novel phenolic thiazoles compounds were prepared which demonstrated potent antioxidant
activity and potent in vivo neuroprotection in mitochondrial toxin models and also possess …

Histology is the gold standard to unveil microscopic brain structures and pathological alterations
in humans and animal models of disease. However, due to tedious manual interventions…

There is substantial evidence that excitotoxicity and oxidative damage may contribute to
Huntington's disease (HD) pathogenesis. We examined whether the novel anti‐oxidant …

In recent years, two key concepts having numerous interrelationships were advanced for the
understanding of various cardiovascular diseases: the “endothelial dysfunction” and the “…