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Modified-release dosage is a mechanism that (in contrast to immediate-release dosage) delivers a drug with a delay after its administration (delayed-release dosage) or for a prolonged period of time (extended-release [ER, XR, XL] dosage) or to a specific target in the body (targeted-release dosage). [1]
Beginning in the sympathetic nervous system, an external stimulus affects the adrenal medulla and causes a release of catecholamines. The sympathoadrenal system is a physiological connection between the sympathetic nervous system and the adrenal medulla and is crucial in an organism's physiological response to outside stimuli. [ 1 ]
They are modified postganglionic sympathetic neurons of the autonomic nervous system that have lost their axons and dendrites, receiving innervation from corresponding preganglionic fibers. The cells form clusters around fenestrated capillaries where they release norepinephrine and epinephrine into the blood.
The definition and use of the term myokine first occurred in 2003. [5] In 2008, the first myokine, myostatin, was identified. [4] [6] The gp130 receptor cytokine IL-6 (Interleukin 6) was the first myokine found to be secreted into the blood stream in response to muscle contractions.
Biological response modifiers (BRMs) are substances that modify immune responses. They can be endogenous (produced naturally within the body) or exogenous (as pharmaceutical drugs ), and they can either enhance an immune response or suppress it .
Ambient temperature is an example of exogenous vasoconstriction. Cutaneous vasoconstriction will occur because of the body's exposure to the severe cold. Examples of endogenous factors include the autonomic nervous system, circulating hormones, and intrinsic mechanisms inherent to the vasculature itself (also referred to as the myogenic response).
In immunology, cytokine release syndrome (CRS) is a form of systemic inflammatory response syndrome (SIRS) that can be triggered by a variety of factors such as infections and certain drugs. [3] It refers to cytokine storm syndromes (CSS) [ 4 ] and occurs when large numbers of white blood cells are activated and release inflammatory cytokines ...
Two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca 2+ concentration and this has been linked to long-term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely ...