Other Mediators (other + mediator)

Distribution by Scientific Domains


Selected Abstracts


Modulation and metamodulation of synapses by adenosine

ACTA PHYSIOLOGICA, Issue 2 2010
J. A. Ribeiro
Abstract The presence of adenosine in all nervous system cells (neurones and glia) together with its intensive release following insults makes adenosine as a sort of ,regulator' of synaptic communication, leading to the homeostatic coordination of brain function. Besides the direct actions of adenosine on the neurosecretory mechanisms, to tune neurotransmitter release, adenosine receptors interact with other receptors as well as with transporters as part of its attempt to fine-tune synaptic transmission. This review will focus on examples of the different ways adenosine can use to modulate or metamodulate synapses, in other words, to trigger or brake the action of some neurotransmitters and neuromodulators, to cross-talk with other G protein-coupled receptors, with ionotropic receptors and with receptor kinases as well as with transporters. Most of these interactions occur through A2A receptors, which in spite of their low density in some brain areas, such as the hippocampus, may function as amplifiers of the signalling of other mediators at synapses. [source]


Neuroanatomy and neurophysiology of itch

DERMATOLOGIC THERAPY, Issue 4 2005
Joanna Wallengren
ABSTRACT:, The specific pathway of "pure," histaminergic itch is traced from the mechano-insensitive nerve fibers in the skin to their central cortical projections. Neuropathic itch created at different levels of this anatomical pathway is reviewed. In this review the present author discusses damage to pruritoceptors in the skin, entrapment syndromes, damage to spinal ganglia, nerve root impingement, injury of the spinal cord, and cerebral damage in the distribution of the middle cerebral artery, capsula interna, or thalamus. Itch in inflamed skin resulting from interactions between nerve transmitters and other mediators of inflammation is described. [source]


Mutation rate of MAP2K4/MKK4 in breast carcinoma ,,

HUMAN MUTATION, Issue 1 2002
Gloria H. Su
Abstract The stress-activated protein kinase (SAPK) pathways represent phosphorylation cascades that convey pro-apoptotic signals. The relevant inputs include Ras proteins as well as exposure of cells to ultraviolet light, tumor-necrosis factor, and other stress-related inputs. The mitogen-activated protein kinase kinase (MAPKK) homolog MAP2K4 (MKK4, SEK, JNKK1) is a centrally-placed mediator of the SAPK pathways. MAP2K4 mutations or homozygous deletions are reported in about 5% of a wide variety of tumor types. The exception is breast cancer, where genetic inactivation in 3 of 22 (15%) cell lines had suggested that the mutational involvement of MAP2K4 might be accentuated in this tumor type. This finding might have represented an important difference, or solely a chance numerical variation. To address this question, we studied an independent panel of 20 breast cancer cell lines and xenografts for MAP2K4 alterations. We found a splice acceptor mutation accompanied by loss of the other allele in the cell line MPE600. This was the sole alteration in this panel (5% of tumors). These data seem to re-establish a rather consistent rate of genetic inactivation of MAP2K4 among most tumor types, including breast cancer. The genetic evaluation of other mediators of the SAPK pathways might offer insight into a promising, but as yet poorly defined, tumor-suppressive system. © 2001 Wiley-Liss, Inc. [source]


The neurophysiology of dyspnea

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 6 2008
Matthew Scott Mellema DVM
Abstract Objective , To review the human and veterinary literature regarding the neurophysiology of dyspnea and to provide evidence for the beneficial effects of several novel therapies aimed at the alleviation of dyspneic sensations. Data Sources , Data sources included scientific reviews, case reports, original research publications, and recent research conference proceedings. Human Data Synthesis , The use of blood oxygenation level-dependent functional magnetic resonance imaging technology has revealed that the brain regions activated by air hunger in humans are also those activated by fear, pain, and thirst perception. In human subjects, it has been found that agents known to enhance the firing of pulmonary slowly adapting receptors (SARs) can alleviate the sensation of dyspnea without altering central respiratory drive. Several small studies have also shown that nebulized opioids can reduce the sensation of dyspnea apparently via activation of peripheral opioid receptors in the lung. Veterinary Data Synthesis , There are several animal models relevant to both small and large animal clinical patient populations. Treatment of rats with a nebulized SAR sensitizing agent (furosemide) enhances SAR firing in response to lung inflation. Behavioral escape responses to airway occlusion are reduced in lightly anesthetized cats when treated with nebulized furosemide. Opioid agonists have been shown to inhibit the release of acetylcholine and other mediators from the airways of dogs and guinea pigs. Studies using a goat model with bilateral destruction of the pre-Bötzinger Complex do not support current paradigms of air hunger origination. Conclusions , Veterinary patients may benefit from an approach to dyspnea that incorporates an understanding of the origins of the unpleasant sensations associated with the condition. Several novel therapies have shown promise in alleviating dyspneic sensations without altering respiratory drive. Further study is needed to determine the safety and efficacy of these therapies in veterinary patients. [source]


The cells and mediators of allergic inflammation

CLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 1 2002
A. B. Kay
Summary In sensitized atopic subjects allergen administration results in an immediate-type reaction and, depending on the dose of the allergen, an additional late-phase reaction. The early reaction results largely from the release of histamine, leukotrienes and other mediators from mast cells. The cutaneous late-phase reaction is probably also predominantly mast-cell-dependent. The late asthmatic reaction, however, also involves T-cell activation. T cells release a cascade of factors which evoke the migration of many cell types, including eosinophils, neutrophils and macrophages into the site of inflammation, under the influence of a complex combination of cytokines and chemokines. Neural inflammation (i.e. neuropeptides and neurotrophins) may also be involved. The identification of the processes underlying the inflammatory response to allergens, and their control mechanisms, provides specific targets for therapeutic measures (such as the use of monoclonal antibodies and soluble receptor molecules) which are designed to impede or abolish the allergic inflammatory cascade. [source]