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- Matsuzaki, Satoshi, et al.
(författare)
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Effect of mandibular advancement device on plasticity in corticomotor control of tongue and jaw muscles
- 2021
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Ingår i: Journal of Clinical Sleep Medicine (JCSM). - : American Academy of Sleep Medicine. - 1550-9389 .- 1550-9397. ; 17:9, s. 1805-1813
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Tidskriftsartikel (refereegranskat)abstract
- STUDY OBJECTIVES: This study aims to investigate if the use of a mandibular advancement device (MAD) is associated with neuroplasticity in corticomotor control of tongue and jaw muscles.METHODS: Eighteen healthy individuals participated in a randomized crossover study with 3 conditions for 2 weeks each: baseline, wearing an oral appliance (OA: sham MAD) or MAD during sleep. The custom-made MAD was constructed by positioning the mandible to 50% of its maximal protrusion limit. Transcranial magnetic stimulation (TMS) was applied to elicit motor evoked potentials (MEPs). The MEPs were assessed by constructing stimulus-response curves at four stimulus intensities: 90%, 100%, 120%, and 160% of the motor threshold (MT) from the right tongue and right masseter, and the first dorsal interosseous muscles (FDI, control) at baseline, after the first and the second intervention.RESULTS: There was a significant effect of condition and stimulus intensity both on the tongue and as well as on masseter MEPs (P < 0.01). Tongue and masseter MEPs were significantly higher at 120% and 160% following the MAD compared to the OA (P < 0.05). There were no effects of condition on FDI MEPs (P = 0.855).CONCLUSIONS: The finding suggests that MAD induces neuroplasticity in the corticomotor pathway of the tongue and jaw muscles associated with the new jaw position. Further investigations are required in patients with obstructive sleep apnea (OSA) to see if this cortical neuroplasticity may contribute or perhaps predict treatment effects with MADs in OSA.
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| 2. |
- Singel, Kelly L., et al.
(författare)
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Mature neutrophils suppress T cell immunity in ovarian cancer microenvironment
- 2019
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Ingår i: JCI Insight. - : American Society for Clinical Investigation. - 2379-3708. ; 4:5
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Tidskriftsartikel (refereegranskat)abstract
- Epithelial ovarian cancer (EOC) often presents with metastases and ascites. Granulocytic myeloid-derived suppressor cells are an immature population that impairs antitumor immunity. Since suppressive granulocytes in the ascites of patients with newly diagnosed EOC were morphologically mature, we hypothesized that PMN were rendered suppressive in the tumor microenvironment (TME). Circulating PMN from patients were not suppressive but acquired a suppressor phenotype (defined as ≥1 log10 reduction of anti-CD3/CD28-stimulated T cell proliferation) after ascites supernatant exposure. Ascites supernatants (20 of 31 supernatants) recapitulated the suppressor phenotype in PMN from healthy donors. T cell proliferation was restored with ascites removal and restimulation. PMN suppressors also inhibited T cell activation and cytokine production. PMN suppressors completely suppressed proliferation in naive, central memory, and effector memory T cells and in engineered tumor antigen-specific cytotoxic T lymphocytes, while antigen-specific cell lysis was unaffected. Inhibition of complement C3 activation and PMN effector functions, including CR3 signaling, protein synthesis, and vesicular trafficking, abrogated the PMN suppressor phenotype. Moreover, malignant effusions from patients with various metastatic cancers also induced the C3-dependent PMN suppressor phenotype. These results point to PMN impairing T cell expansion and activation in the TME and the potential for complement inhibition to abrogate this barrier to antitumor immunity.
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