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Front Hum Neurosci ; 15: 707816, 2021.
Article de Anglais | MEDLINE | ID: mdl-34512294

RÉSUMÉ

BACKGROUND: Hardware-related infection in deep brain stimulation (DBS) is one of the most commonly reported complications frequently resulting in the removal of implantable pulse generator (IPG). OBJECTIVE: The aim of this study was to establish a useful strategy to better prevent and treat those infections and to improve the preservation rates of IPG. METHODS: We conducted a retrospective and historical controlled study of all adult patients (≥18 years old) who had undergone initial DBS implantation at a single center. All participants were enrolled in the control group (between June 2005 and June 2014) or intervention group (between July 2014 and May 2019) based on their surgery dates. We used the intraoperative irrigation with hydrogen dioxide solution in the intervention group. Based on the dates of diagnosis, patients with hardware-related infection after DBS were enrolled in group A (between June 2005 and June 2014) or group B (between July 2014 and May 2019). IPG-sparing algorithm (Isa) was applied for group B. The early-onset IPG infections of the control and intervention groups were evaluated. The IPG preservation rates in both groups A and B were statistically analyzed. RESULTS: Six cases of early IPG infection and subsequent IPG removal occurred in the control group, while none occurred after intraoperative usage of the hydrogen dioxide in the intervention group. IPG preservation rate of infected cases in group B was significantly higher than that in group A (70% vs.16%, p = 0.004). CONCLUSION: The combined application of hydrogen dioxide solution and Isa seems to be an effective strategy to prevent IPG infection.

2.
Expert Opin Ther Targets ; 22(9): 783-797, 2018 09.
Article de Anglais | MEDLINE | ID: mdl-30107134

RÉSUMÉ

INTRODUCTION: Triggering of the glucocorticoid-induced TNFR-related gene (GITR) increases the activation of T lymphocytes and other immune system cells; furthermore, its ligand, GITRL, delivers signals in the cells where it is expressed. Areas covered: This review describes the effects of GITR/GITRL triggering/inhibition in conventional T cells, regulatory T cells (Tregs), monocytes/macrophages, endothelial cells and other cells of the immune system. GITR triggering appears to be an approach for promoting tumor rejection, treating infection and boosting vaccinations in several murine models. GITR inhibition may be useful for inhibiting inflammation and autoimmune disease development. Expert opinion: The exciting antitumor activity of anti-GITR mAbs depends on CD8+ effector T cell activation and inhibition/deletion of tumor-infiltrating Tregs. Whether one of these effects is more relevant is still under debate. Inhibition of GITR triggering plays an interesting anti-inflammatory role, but the potential effect of long-term treatment is to be investigated. The use of adjuvants able to trigger GITR is promising regarding new vaccines. Finally, caution is recommended when translating the findings of experimental murine models to human diseases; biologicals modulating human GITR/GITRL system can behave differently from those modulating the murine GITR/GITRL system.


Sujet(s)
Protéine associée au récepteur du TNF induit par les corticoïdes/antagonistes et inhibiteurs , Immunothérapie/méthodes , Thérapie moléculaire ciblée , Animaux , Maladies auto-immunes/immunologie , Maladies auto-immunes/thérapie , Modèles animaux de maladie humaine , Protéine associée au récepteur du TNF induit par les corticoïdes/génétique , Protéine associée au récepteur du TNF induit par les corticoïdes/immunologie , Humains , Inflammation/immunologie , Inflammation/thérapie , Souris , Tumeurs/immunologie , Tumeurs/thérapie , Spécificité d'espèce
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