No abstract

ObjectiveTo investigate the therapeutic effects of repetitive electrical stimulation of the suprahyoid muscles in brain-injured patients with dysphagia.MethodTwenty-eight brain-injured patients who showed reduced laryngeal elevation and supraglottic penetration or subglottic aspiration during a videofluoroscopic swallowing study (VFSS) were selected. The patients received either conventional dysphagia management (CDM) or CDM with repetitive electrical stimulation of the suprahyoid muscles (ESSM) for 4 weeks. The videofluoroscopic dysphagia scale (VDS) using the VFSS and American Speech-Language-Hearing Association National Outcome Measurement System (ASHA NOMS) swallowing scale (ASHA level) was used to determine swallowing function before and after treatment.ResultsVDS scores decreased from 29.8 to 17.9 in the ESSM group, and from 29.2 to 16.6 in the CDM group. However, there was no significant difference between the groups (p=0.796). Six patients (85.7%) in the ESSM group and 14 patients (66.7%) in the CDM group showed improvement according to the ASHA level with no significant difference between the ESSM and CDM groups (p=0.633).ConclusionAlthough repetitive neuromuscular electrical stimulation of the suprahyoid muscles did not further improve the swallowing function of dysphagia patients with reduced laryngeal elevation, more patients in the ESSM group showed improvement in the ASHA level than those in the CDM group. Further studies with concurrent controls and a larger sample group are required to fully establish the effects of repetitive neuromuscular electrical stimulation of the suprahyoid muscles in dysphagia patients.

The purpose of this study was to assess the effect of repeated sessions of electrical stimulation therapy (EST) on the neck muscles with respect to the stimulation site by using quantitative kinematic analysis of videofluoroscopic swallowing studies (VFSS) in dysphagia patients with acquired brain injury. We analyzed 50 patients in a tertiary hospital who were randomly assigned into two different treatment groups. One group received EST on the suprahyoid muscle only (SM), and the other group received stimulation with one pair of electrodes on the suprahyoid muscle and the other pair on the infrahyoid muscle (SI). All patients received 10-15 sessions of EST over 2-3 weeks. The VFSS was carried out before and after the treatment. Temporal and spatial parameters of the hyoid excursion and laryngeal elevation during swallowing were analyzed by two-dimensional motion analysis. The SM group (n = 25) revealed a significant increase in maximal anterior hyoid excursion distance (mean ± SEM = 1.56 ± 0.52 mm, p = 0.008) and velocity (8.76 ± 3.42 mm/s, p = 0.017), but there was no significant increase laryngeal elevation. The SI group (n = 25), however, showed a significant increase in maximal superior excursion distance (2.09 ± 0.78 mm, p = 0.013) and maximal absolute excursion distance (2.20 ± 0.82 mm, p = 0.013) of laryngeal elevation, but no significant increase in hyoid excursion. There were no significant differences between the two groups with respect to changes in maximal anterior hyoid excursion distance (p = 0.130) and velocity (p = 0.254), and maximal distance of superior laryngeal elevation (p = 0.525). EST on the suprahyoid muscle induced an increase in anterior hyoid excursion, and infrahyoid stimulation caused an increase in superior laryngeal elevation. Hyolaryngeal structural movements were increased in different aspects according to the stimulation sites. Targeted electrical stimulation based on pathophysiology is necessary.

The purpose of this study is to determine whether neuromuscular electrical stimulation of the suprahyoid muscle is effective compared to that of the infrahyoid muscle in brain-injured patients with dysphagia. A total of 132 patients with stroke, traumatic brain injury, or brain tumor in 2 university hospitals were allocated to 2 groups: those who received electrical stimulation therapy (EST) on the suprahyoid muscles (SM group, n = 66) and those who received EST with one pair of electrodes on the suprahyoid muscle and the other pair on the infrahyoid muscle (SI group, n = 66). Patients received 11.2 ± 3.4 sessions of electrical stimulation in the SM group and 11.9 ± 3.4 sessions in the SI group. The functional dysphagia scale (FDS), swallow function score (SFS), supraglottic penetration, and subglottic aspiration were measured using videofluoroscopic swallowing study. FDS scores decreased from 42.0 ± 19.1 to 32.3 ± 17.8 in the SM group and from 44.8 ± 17.4 to 32.9 ± 18.8 in the SI group by per-protocol (PP) analysis, and those decreased from 41.2 ± 20.9 to 34.5 ± 20.3 in the SM group and from 44.3 ± 19.1 to 35.7 ± 20.5 in the SI group by intention-to-treat (ITT) analysis, after electrical stimulation (p < 0.001 for each). SFSs increased from 3.3 ± 1.8 to 4.2 ± 1.6 in the SM group and from 2.8 ± 1.8 to 4.0 ± 1.8 in the SI group by PP analysis, and those increased from 3.3 ± 1.6 to 3.9 ± 1.6 in the SM group and from 2.8 ± 1.9 to 3.6 ± 2.0 in the SI group by ITT analysis, after electrical stimulation (p < 0.001, respectively). However, changes in FDS scores, SFSs, penetration, and aspiration were comparable between the SM and the SI groups. The results suggest that both SM and SI therapies induced similar improvements in swallowing function in brain-injured patients.

Cartilage loss is a central event in the pathogenesis of osteoarthritis (OA), though other than mechanical loading, the biochemical mechanisms underlying OA pathology remain poorly elucidated. We investigated the role of Pink1-mediated mitophagy in mitochondrial fission, a crucial process in OA pathogenesis. We used a monosodium iodoacetate (MIA)-induced rodent model of OA, which inhibits the activity of articular chondrocytes, leading to disruption of glycolytic energy metabolism and eventual cell death. The OA rat cartilage exhibits significant induction of autophagy-related proteins LC3B and p62, similar to human osteoarthritic cartilage. Moreover, expression of Pink1 and Parkin proteins were also increased in OA. Here, we confirm that Pink1-mediated mitophagy leads to cell death in chondrocytes following MIA treatment, while deficiency in Pink1 expression was associated with decreased cartilage damage and pain behaviors in MIA-induced OA. Finally, we found that autophagy and mitophagy-related genes are highly expressed in human osteoarthritic cartilage. These results indicate that OA is a degenerative condition associated with mitophagy, and suggest that targeting the Pink1 pathway may provide a therapeutic avenue for OA treatment.

No abstract

No abstract

Osteoarthritis (OA) is the most common joint disorder that has had an increasing prevalence due to the aging of the population. Recent studies have concluded that OA progression is related to oxidative stress and reactive oxygen species (ROS). ROS are produced at low levels in articular chondrocytes, mainly by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and ROS production and oxidative stress have been found to be elevated in patients with OA. The cartilage of OA-affected rat exhibits a significant induction of p47phox, a cytosolic subunit of the NADPH oxidase, similarly to human osteoarthritis cartilage. Therefore, this study tested whether siRNA p47phox that is introduced with poly (D,L-lactic-co-glycolic acid) (PLGA) nanoparticles (p47phox si_NPs) can alleviate chondrocyte cell death by reducing ROS production. Here, we confirm that p47phox si_NPs significantly attenuated oxidative stress and decreased cartilage damage in mono-iodoacetate (MIA)-induced OA. In conclusion, these data suggest that p47phox si_NPs may be of therapeutic value in the treatment of osteoarthritis.