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Recently, additional roles of TRPV1 receptors or its variants have been proposed in the off taste of artificial sweeteners and metallic taste of Cu2+, Zn2+, and Fe2+ (Riera et al. 2007) and in the sensitization of changes in osmolarity to CAP in trigeminal sensory neurons (Liu et al. 2007).
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Looking further into the OVA adjuvant-free model, we also tested whether varying the site of sensitization induced changes in allergic sensitization; the differences between i.p. and s.c. routes of delivery were examined using Protocol 1B and 1C (Fig. 1).
The neural changes accompanying sensitization of the gill-withdrawal reflex in Aplysia are associated with presynaptic facilitation at monosynaptic connections between sensory neurons and motor cells.
These phenotypic changes may lead to activation of central nociceptive pathways explaining the contralateral sensitization, but are also associated to ipsilateral changes involving sensitization of nociceptors through activation of their glutamatergic receptors.
Central sensitization is the result of a complex series of changes in neuronal excitability driven by descending pathways from the brainstem, local interneurons, and glial activity (Kuner, 2010).
These changes lead to sensitization of the first order trigeminal neurons, explaining pulsating pain, pain aggravated by movements of the head, bending down, and physical exercise [20].
This peripheral process may induce secondary central changes resulting in sensitization of nociceptive neurons at the trigeminal nucleus and/or higher brain structures [3, 4].
The hypersensitivity is mediated by local sensitization of nociceptors and involves immune response and changes in the central nervous system [ 35].
Changes in joint pathology often result in an increased sensitization of primary sensory neurons and central sensitization, due to the changes in ascending or descending modulatory pathways [ 52].
Mitochondrial changes may be involved in DCA sensitization of cancer cells toward apoptosis.
Although we have yet to establish a clear role for eosinophils or other inflammatory cells in parathion-induced hyperreactivity, our data show that sensitization changes the mechanism of parathion-induced hyperreactivity from IL-5 independent to IL-5 dependent.
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