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This "indirect" pathway has an opposite effect. The striatal projection neurons express a set of ion channels that give them a high threshold for activation, whereas neurons in all other parts of the basal ganglia have a resting discharge that allows for modulation in both an increased and decreased direction. © 2020 American Physiological Society. Compr Physiol 101241-1275, 2020.In the past decades, there has been growing evidence for a functional interaction between the thyroid hormone and the immune system. Selleck KRIBB11 This article provides an overview of the mechanisms by which thyroid hormones affect the innate and adaptive immune response during infection. The influence of thyroid hormone on the most important players of the innate [neutrophils, macrophages, natural killer (NK) cells, and dendritic cells (DCs)] and adaptive immune system (B- and T-lymphocytes) is reviewed here based on both clinical and preclinical studies. The effects of modulation of the immune system by drugs, such as monoclonal antibodies, tyrosine kinase inhibitors, and interferons on thyroid function, are beyond the scope of this article. Thyroid hormones regulate the activity of neutrophils which is reflected by higher numbers of neutrophils outside the bloodstream and enhanced activity of the respiratory burst following stimulation with thyroid hormone. Hyperthyroidism affects neutrophil function to a larger extent than hypothyroidism. In addition to neutrophil function, macrophage function is strongly affected by thyroid hormones, with triiodothyronine having a pro-inflammatory effect in these cells. NK cell proliferation and cytotoxic activity are also dependent on thyroid hormone levels. Finally, thyroid hormones enhance DC proliferation and maturation. In the adaptive immune system, a hyperthyroid state leads to increased activation of lymphocytes. This effect of thyroid hormone is mediated by various factors including NF-κB and protein kinase C signaling pathways and the β-adrenergic receptor. In general, a hyperthyroid state leads to a more activated immune system whereas hypothyroidism leads to a less activated immune system. © 2020 American Physiological Society. Compr Physiol 101277-1287, 2020.
Intestinal bacteria produce metabolites and by-products necessary for homeostasis. Imbalance in this equilibrium is linked to multiple pathologies including inflammatory bowel disease (IBD). The role of the gut microbiota in determining treatment response is becoming apparent, and may act as biomarker for efficacy.
To describe knowledge about the intestinal microbiota on disease severity and treatment outcomes in IBD METHODS Descriptive review using PubMed to identify literature on the intestinal microbiota in IBD RESULTS Severe IBD has a less diverse microbiota with fewer commensal microbiota communities and more opportunistic pathogenic bacteria originating from the oral cavity or respiratory tract. IBD treatments can alter gut microbiota composition, but in vitro/in vivo studies are needed to prove causation. A diversification of the microbiota is observed during remission. Patients with a more diverse baseline microbiome and higher microbial diversity show better response to anti-tumour necrosis factor-α, vedolizumab and ustekinumab therapy. Higher abundance of short chain fatty acid-producing bacteria, fewer mucus-colonising bacteria and lower abundance of pro-inflammatory bacteria have also been associated with a favourable outcome. Predictive models, based on a combination of microbiota, clinical data and serological markers, have good accuracy for treatment outcome and disease severity.
The intestinal microbiota in IBD carries a set of promising biomarkers of disease activity and prediction of therapeutic outcome. Current insights may also help in designing microbiota modulation strategies to improve outcomes in IBD.
The intestinal microbiota in IBD carries a set of promising biomarkers of disease activity and prediction of therapeutic outcome. Current insights may also help in designing microbiota modulation strategies to improve outcomes in IBD.There is an array of youth participatory approaches relevant to health equity efforts in community psychology, adolescent health, youth development, and education. While they share some commonalities, they also reflect important distinctions regarding key processes and intended level of impact. Here, we consider the following (a) youth-led participatory action research (YPAR), (b) youth organizing (YO), (c) youth-led planning, (d) human-centered design, (e) participatory arts, and (f) youth advisory boards. Informed by community psychology theories on empowerment and levels of change and social epidemiology frameworks that focus on the social determinants of health inequities, we aim to promote greater clarity in the conceptualization, implementation, and evaluation of youth participatory approaches; frame the "landscape" of youth participatory approaches and their similarities and differences; present an integrative review of the evidence regarding the impact of youth participatory approaches; and describe several illustrative cases so as to consider more deeply how some youth participatory approaches aim to influence the social determinants of health that lead to the physical embodiment of health inequities. We conclude by identifying areas of future policy- and practice-relevant research for advancing youth participation and health equity.
Achieving a favorable pacing threshold with a Micra transcatheter pacing system (Micra-TPS) is needed to reduce battery depletion. In some cases, the threshold increases shortly after the device is implanted, and a higher pacing threshold may be required. This study aims to identify the causes and predictors of the increase in pacing threshold observed shortly after Micra-TPS implantation.
The study included 64 consecutive patients who underwent Micra-TPS implantation between 2017 and 2020. The patients were divided into two groups depending on their pacing threshold the increased pacing threshold (IPT) group (threshold increased by ≥0.5 V/0.24 ms within 1 month of implantation) and the stable pacing threshold (SPT) group.
Excluding four patients who could not be followed up, of the 60 remaining patients, nine (15%) were in the IPT group and 51 (85%) were in the SPT group. The IPT group had significantly lower implant impedance values and higher implant thresholds than the SPT group (582 ± 59vs 755 ± 167 Ω [P<.
Read More: https://www.selleckchem.com/products/kribb11.html
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