Sentences with phrase «for cytokine production»

Not exact matches

Previous studies have shown that such vulnerability can lead to more frequent anxiety, and anxiety is known to activate a metabolic pathway responsible for the production of pro-inflammatory cytokines, signaling proteins that include interleukin - 6 (IL - 6).

«Knowing that immune cytokines can change pigment production in melanocytes, while also knowing that chronic inflammation has the potential to increase the number of melanocytes, has clear implications for the design of future therapies to address a set of common skin disorders,» says Dr. Krueger, director of Milstein Research Program and D. Martin Carter Professor in Clinical Investigation.

Severity of AP has been predicted by the magnitude of local and systemic inflammatory cytokine production [33] and several reports have well documented for over activation of leukocytes being the major contributor of inflammation leading to multiple organ dysfunction syndrome [34].

iTeos Therapeutics has developed a novel and potent best - in - class A2A blocker that has been specifically optimized for immuno - oncology indications to retain a high potency in the adenosine - rich environment found in tumors and to restore cytokine production even in the presence of high concentrations of adenosine.

The Raf ‐ 1 kinase inhibitor protein participates in the pathogenesis of IL ‐ 17 ‐ mediated autoimmune diseases and inflammation by promoting the formation of the IL ‐ 17RA ‐ Act1 complex, required for downstream signaling and cytokine production.

Remarkably, recent studies from several laboratories including Dr. Kim's lab identified Nurr1 as a key modulator of (neuro) inflammation functioning as a transcriptional repressor for neurotoxic cytokine production.

During sleep, cortisol levels are low, allowing for increased activity of pro-inflammatory hormone and cytokine production.

The detrimental effects of omega - 6s are articulated by Fernandes and Venkatraman (1993), with, «The increased consumption of many vegetable oils particularly of the n - 6 series is... viewed as pro-inflammatory and is suspected as one of the possible causes for the rise in certain malignant tumors, rheumatoid arthritis and autoimmune diseases primarily due to the increased production of pro-inflammatory cytokines» (p. S19).

«a major active polyphenol of green tea, has been shown to down - regulate inflammatory responses in dendritic cells (DCs)... In addition, EGCG - treated DCs inhibited lipopolysaccharide (LPS)- induced production of pro-inflammatory cytokines» Also apropos: «Autoimmunity, dendritic cells and relevance for Parkinson's disease» http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535404/

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasFor example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasfor example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.

Another is local inflammation which is an increased production of what are called cytokines, like tumour necrosis factor for example.

Although greater early local production of proinflammatory cytokines at wound sites is beneficial because it is associated with enhanced healing, greater systemic production of proinflammatory cytokines can represent a maladaptive response.24 Both physical and psychological stressors can provoke transient increases in plasma levels of proinflammatory cytokines, particularly IL - 6,25 as can negative emotions like depression and anxiety.26 - 28 More frequent or persistent stress - related changes have broad implications for physical and mental health; sustained elevated levels of proinflammatory cytokines have been linked to a variety of age - related diseases, including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes mellitus, certain cancers, and frailty and functional decline.29 - 31

However, consistent with the differences between visits in wound healing, production of IL - 6, IL - 1β, and TNF - α increased more steeply between 4 and 22 hours following the social support interaction than after the conflict interaction, ending up higher at 22 hours at the first visit for all 3 cytokines (IL - 6, F2, 81 = 3.55; P =.03; IL - 1β, F2, 81 = 9.12; P <.001; TNF - α, F2, 81 = 3.56; P =.03).

To separate the effects of the short - term stress of a marital conflict from the long - term strains of marital discord on local and systemic proinflammatory cytokine production as well as wound healing, couples were recruited for two 24 - hour admissions to our General Clinical Research Center (GCRC).

Psychological well - being ratings have also been positively associated with cytokine production after vaccination for influenza and hepatitis (21).

The substantial increases in local cytokine production over time (Figure 2) have been assumed to be primarily a function of their local synthesis at the site by the cells that are migrating to the chamber.22, 58 In our data, correlations between cell numbers and cytokine levels at 22 hours after the social support interaction were r = 0.29 and P <.01 for IL - 6; r = 0.08 and P =.45 for TNF - α; and r = 0.13 for IL - 1β and after the conflict interaction, r = 0.52 and P <.001 for IL - 6 and r = 0.38 and P <.001 for both TNF - α and IL - 1β.