The phrase "augmented sensitization" is correct and usable in written English.
It can be used in contexts related to psychology, neuroscience, or any field discussing heightened sensitivity or awareness due to external factors or enhancements.
Example: "The study focused on the effects of augmented sensitization in patients undergoing therapy, leading to improved emotional responses."
Alternatives: "enhanced sensitivity" or "increased awareness".
It is further known that pain originating in the muscle, including latent or active myofascial trigger points, can induce or augment central sensitization in both healthy controls and persons with fibromyalgia [ 7, 8].
Using an asthmatic phenotype modeled by allergic sensitization of the respiratory tract, effects of O3 on pulmonary function have been found to be augmented by allergic sensitization in infant rhesus monkeys (Fanucchi et al. 2006; Joad et al. 2006; Schelegle et al. 2003), mice (Funabashi et al. 2004), and rats (Wagner et al. 2007).
Using a murine model of ovalbumin (OVA -induced asthma, we revealed that GOVA -inducedthe sensitizasthmastage, augmented airwey hyperevealediveness and airway remodeling in thatform of GOblet cell hyperplasia and smooth muscle hypertrophy.
Of note, as a functional consequence of FcεRI upregulation, TNF-α pre-sensitization of B/TSM potentially augmented the CC (eotaxin-1/CCL11 and RANTES/CCL5, but not TARC/CCL17) and CXC (IL-8/CXCL8, IP-10/CXCL10) chemokines release following IgE stimulation (p<0.05, n = 3).
Locomotor enhancing effects of a low dose of apomorphine were augmented upon repeated administration suggesting drug-induced sensitization.
This indicates that the combination of s.c. sensitization and intravesical treatment indeed augmented the systemic immune response at least in some animals.
Behavioral sensitization is characterized by a progressively augmented response following repetitive administration of a drug.
More specifically, the responsiveness of central neurons to input from unimodal and polymodal receptors is augmented, resulting in a pathophysiological state corresponding to central sensitization, characterized by generalized or widespread hypersensitivity.
This leads inevitably to the conclusion that protein synthesis inhibition leading to loss of cFLIP, potentially augmented by loss of MCL-1 and increased cell surface DR5, result in sensitization of TRAIL-resistant RCC cells to TRAIL-induced apoptosis.
Interestingly, TNF-α pre-sensitization (and thus FcεRI upregulation) followed by IgE stimulation augmented the selective eotaxin-1/CCL11, IL-8/CXCL8, IP-10/CXCL10, and RANTES/CCL5 chemokines release, compared to IgE non-stimulated control.
