ABSTRACT
As a new means of rehabilitation, blood flow restriction training (BFRT) is widely used in the field of musculoskeletal rehabilitation. To observe whether BFRT can improve the efficacy of routine rehabilitation intervention in patients with chronic ankle instability (CAI). Twenty-three patients with CAI were randomly divided into a routine rehabilitation group (RR Group) and a routine rehabilitation â+ âblood flow restriction training group (RR â+ âBFRT Group) according to the Cumberland Ankle Instability Tool (CAIT) score. The RR Group was treated with routine rehabilitation means for intervention, and the RR â+ âBFRT Group was treated with a tourniquet to restrict lower limb blood flow for rehabilitation training based on routine training. Before and after the intervention, the CAIT score on the affected side, standing time on one leg with eyes closed, comprehensive scores of the Y-balance test, and surface electromyography data of tibialis anterior (TA) and peroneus longus (PL) were collected to evaluate the recovery of the subjects. Patients were followed up 1 year after the intervention. After 4 weeks of intervention, the RR â+ âBFRT Group CAIT score was significantly higher than the RR Group (19.33 VS 16.73, p â< â0.05), the time of standing on one leg with eyes closed and the comprehensive score of Y-balance were improved, but there was no statistical difference between groups (p â> â0.05). RR â+ âBFRT Group increased the muscle activation of the TA with maximum exertion of the ankle dorsal extensor (p â< â0.05) and had no significant change in the muscle activation of the PL with maximum exertion of the ankle valgus (p â> â0.05). There was no significant difference in the incidence of resprains within 1 year between the groups (36.36% VS 16.67%, p â> â0.05). The incidence of ankle pain in the RR â+ âBFRT Group was lower than that in the RR Group (63.64% VS 9.09%, p â< â0.01). Therefore, four-weeks BFRT improves the effect of the routine intervention, and BFRT-related interventions are recommended for CAI patients with severe ankle muscle mass impairment or severe pain.
ABSTRACT
Background: Although neuroregulation plays an important role in tissue healing, the key neuroregulatory pathways and related neurotransmitters involved in bone-tendon interface (BTI) healing are still unknown. It is reported that sympathetic nerves can regulate cartilage and bone metabolism, which are the basic aspects of BTI repair after injury, through the release of norepinephrine (NE). Thus, the purpose of this study was to explore the effect of local sympatholysis (LS) on BTI healing in a murine rotator cuff repair model. Methods: Specifically, C57BL/6 mice underwent unilateral supraspinatus tendon (SST) detachment and repair was established on a total of 174 mature C57BL/6 mice (12 weeks old): 54 mice were used to examine the sympathetic fibers and its neurotransmitter NE for the representation of sympathetic innervation of BTI, while the rest of them were randomly allocated into (LS) group and control group to verify the effect of sympathetic denervation during BTI healing. The LS group were intervened with fibrin sealant containing 10 âng/ml guanethidine, while the control group received fibrin sealant only. Mice were euthanized at postoperative 2, 4 and 8 weeks for immunofluorescent, qRT-PCR, ELISA, Micro-computed tomography (CT), histology and biomechanical evaluations. Results: Immunofluorescence, qRT-PCR and ELISA evaluations indicated that there were the expression of tyrosine hydroxylase (TH), NE and ß2-adrenergic receptor (ß2-AR) at the BTI site. All the above showed a trend of increasing at the early postoperative stage and they started to decrease with the healing time after a significant peak. Meanwhile, local sympathetic denervation of BTI was achieved after the use of guanethidine as shown in the NE ELISA outcomes in two groups. QRT-PCR analysis revealed that the healing interface in the LS group expressed more transcription factors, such as Runx2, Bmp2, Sox9, and Aggrecan, than the control group. Further, radiographic data showed that the LS group significantly possessed higher bone volume fraction (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), and lower trabecular spacing (Tb.Sp) than the control group. Also, histological test results showed that there was more fibrocartilage regenerated at the healing interface in the LS group compared with the control group. Mechanical testing results demonstrated that the failure load, ultimate strength and stiffness in the LS group were significantly higher at postoperative week 4 (P â< â0.05), but not at postoperative week 8 (P â> â0.05), compared to the control group. Conclusion: The regulation of sympathetic innervation was involved in the healing process of injured BTI, and local sympathetic denervation by using guanethidine was beneficial for BTI healing outcomes.The translational potential of this article: This is the first study to evaluate the expression and specific role of sympathetic innervation during BTI healing. The findings of this study also imply that the antagonists of ß2-AR could serve as a potential therapeutic strategy for BTI healing. Also, we firstly successfully constructed a local sympathetic denervation mouse model by using guanethidine loaded fibrin sealant, which provided a new effective methodology for future neuroskeletal biology study.
ABSTRACT
Alzheimer's disease (AD) is a chronic neurodegenerative disease. Better imaging and early diagnosis of biomarkers of AD is extremely important for therapeutic interventions. The amyloid cascade hypothesis and its revised version identify insoluble ß-amyloid deposition as a good diagnostic biomarker for AD. Moreover, lipid droplets may also act as an auxiliary biomarker related to AD pathology based on recent studies. Herein, two quinoline-based AIE probes were designed and synthesized for the imaging of Aß plaques and lipid droplets. The probes exhibited remarkable turn-on fluorescence enhancements with the Aß aggregates. The lipid droplets-targeting probe FB exhibited high selectivity and binding affinity towards the Aß aggregates with a detection limit as low as 26.9 nM. Furthermore, FB was capable of readily imaging Aß plaques and lipid droplets at the cellular level and in brain sections of transgenic AD mice. The probe FB can serve as a promising tool for developing early diagnosis and innovative therapeutics of AD.
