The excessive release of wastewater into the environment is a major concern worldwide.
Global cerebral ischemia (GCI) causes energy deficiency results in excessive release of glutamate from neurons.
High levels of LPS cause excessive release of inflammatory mediators and are responsible for the septic shock syndrome.
Its hyperactivation is associated with excessive release of stress hormones (e.g. glucocorticoid, cortisol) and subsequently results in various health problems25,47.
Loss of coolant or enduring loss of cooling conditions would ultimately result in loss of cladding integrity at elevated temperatures with excessive release of fission products and hydrogen.
We speculate that this locally produced angiotensin, acts in a paracrine mode, and stimulates AT1 receptors on the cardiac sympathetic nerves, leading to excessive release of norepinephrine during ischemia.
Our recent findings demonstrate that angiotensin is capable of stimulating the Na+/H+ exchanger in the cardiac sympathetic nerve endings and may play a pivotal role in promoting excessive release of norepinephrine as seen with myocardial ischemia.
These findings demonstrate that activation of the H3-receptor in cardiac sympathetic nerve endings diminishes excessive release of neurotransmitter as occurs with ischemia, by inhibiting the actions of two distinct norepinephrine releasing mechanisms and may serve a cardioprotective role.
This negative feedback loop might be beneficial to the host since excessive release of type I IFNs is associated with increased pathology in both acute and chronic infection16,44.
The injured cellular components of neuronal cells induce immune cell infiltration and excessive release of pro-inflammatory cytokines through binding with their receptors advanced glycation end products (RAGE 4.
Necrosis can be caused by inflammatory factors produced in the brain, by free radicals entering into the brain, or by the excessive release of excitatory neurotransmitters, such as glutamate.
