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Background: The spinal cord expresses brain-derived neurotrophic factor precursor (proBDNF) and its receptor pan neurotrophin receptor 75 (p75NTR). However, the role of spinal proBDNF signaling in the pathogenesis of inflammatory pain remains unknown. Methods: Rats were locally injected with complete Freund's adjuvant (CFA) to induce inflammatory pain. The proBDNF signal expression was detected by double-labeled immunofluorescence. ProBDNF protein, p75NTR extracellular domain (p75NTR-ECD), or monoclonal anti-proBDNF (McAb-proB) were administrated by intrathecal injection to investigate their effects on pain behavior. Paw withdrawal thermal latency (PWL) and paw withdrawal mechanical threshold (PWT) were performed to evaluate pain behavior. Immunoblotting, immunohistochemistry, and immunofluorescence were used to assess inflammation-induced biochemical changes. Results: CFA induced a rapid increase in proBDNF in the ipsilateral spinal cord, and immunofluorescence revealed that CFA-enhanced proBDNF was expressed in NeuN positive neurons and GFAP positive astrocytes. The administration of furin cleavage-resistant proBDNF via intrathecal injection (I.t.) significantly decreased the PWT and PWL, whereas McAb-proB by I.t. alleviated CFA-induced pain-like hypersensitivity in rats. Meanwhile, CFA administration triggered the activation of p75NTR and its downstream signaling extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor (NF)-kappaB p65 in the spinal cord. I.t. administration of p75NTR-ECD suppressed CFA-induced pain and neuroinflammation, including the expression of p-ERK1/2, p-p65, and the gene expression of tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6). Conclusion: Our study reveals that the activated proBDNF/p75NTRsignaling in the spinal cord contributes to the development of CFA-induced inflammatory pain. McAb-proB and p75NTR-ECD appear to be promising therapeutic agents for inflammatory pain. [ABSTRACT FROM AUTHOR]

Background: The spinal cord expresses brain-derived neurotrophic factor precursor (proBDNF) and its receptor pan neurotrophin receptor 75 (p75 NTR ). However, the role of spinal proBDNF signaling in the pathogenesis of inflammatory pain remains unknown., Methods: Rats were locally injected with complete Freund's adjuvant (CFA) to induce inflammatory pain. The proBDNF signal expression was detected by double-labeled immunofluorescence. ProBDNF protein, p75 NTR extracellular domain (p75 NTR -ECD), or monoclonal anti-proBDNF (McAb-proB) were administrated by intrathecal injection to investigate their effects on pain behavior. Paw withdrawal thermal latency (PWL) and paw withdrawal mechanical threshold (PWT) were performed to evaluate pain behavior. Immunoblotting, immunohistochemistry, and immunofluorescence were used to assess inflammation-induced biochemical changes., Results: CFA induced a rapid increase in proBDNF in the ipsilateral spinal cord, and immunofluorescence revealed that CFA-enhanced proBDNF was expressed in NeuN positive neurons and GFAP positive astrocytes. The administration of furin cleavage-resistant proBDNF via intrathecal injection ( I.t .) significantly decreased the PWT and PWL, whereas McAb-proB by I.t . alleviated CFA-induced pain-like hypersensitivity in rats. Meanwhile, CFA administration triggered the activation of p75 NTR and its downstream signaling extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor (NF)-kappaB p65 in the spinal cord. I.t . administration of p75 NTR -ECD suppressed CFA-induced pain and neuroinflammation, including the expression of p-ERK1/2, p-p65, and the gene expression of tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6)., Conclusion: Our study reveals that the activated proBDNF/p75 NTR signaling in the spinal cord contributes to the development of CFA-induced inflammatory pain. McAb-proB and p75 NTR -ECD appear to be promising therapeutic agents for inflammatory pain., Competing Interests: The authors report no conflicts of interest in this work., (© 2023 Li et al.)

Objective: To explore the perioperative and long-term oxygenation status after uvulopalatopharyngealplasty (UPPP) in patients with obstructive sleep apnea syndrome (OSAS) and evaluate the predictive performance of STOP-BANG questionnaire and modified Epworth sleepiness scale (mESS) scales., Methods: Oxygen saturation was continuously monitored with pulse oximeter wristwatch for up to 72 h postoperatively in 46 patients undergoing UPPP. They were followed up after 3 years with polysomnography, STOP-BANG questionnaire and mESS scales., Results: Oxygen saturation significantly improved postoperatively. The mean SPO₂ was 96.6% during 1 to 4 hour after extubation, 94.9% on POD1, 95.3% on POD2 and 91.1% on pre-operation respectively. The differences were statistically significant (Z = 1.000, P < 0.01). However, there were still episodes of hypoxemia, especially during 1st postoperative night (Z = -3.601 4, P < 0.01). There was no difference (t = 1.029, P > 0.05) in mean SPO2 between pre-operation (89.72 ± 4.88)% and 3 years (88.84 ± 6.16)% after UPPP., Conclusions: Although UPPP significantly improves oxygen saturation in OSA patients, hypoxemic episodes still occur in the first 24 hours after surgery, especially during the first postoperative night. UPPP does not improve long-term hypoxemia.

The goal of our research is try to explain the electrophysiological mechanisms of alternation in T-wave of ECG in ultrahigh static magnetic field (SMF). The magneto-hydrodynamics model study shows that ultrahigh SMF can induce reduction in the volume flow rate of the blood in human arota more than 10%, thus may lead to anoxia condition of acute ischemia. Using an ionic-based theoretical model of the cardiac ventricular cell, we simulate transmural heterogeneous suppression of the action potential plateau and action potential duration shortening in case of different anoxia degree. The results demonstrated that anoxia may produce a significant increase in the T-wave amplitude, which may be another mechanism for the influence of ultrahigh SMF to T-wave. This finding is consistent with experimental observation. This study suggests that one should strengthen the safety inspection of ECG in MRI scan and in other application of ultrahigh SMF.