Effectiveness of a home-based exercise program among patients with lower limb spasticity post-stroke: A randomized controlled trial.

PURPOSE: To evaluate the effectiveness of advanced practice nurse-guided home-based rehabilitation exercise program (HREPro) among patients with lower limb spasticity post-stroke. METHODS: This randomized controlled study recruited 121 patients with lower limb spasticity post-stroke. Intervention (n = 59) and control (n = 62) groups underwent 12-month HREPro and conventional rehabilitation, respectively, after discharge. The Fugl-Meyer assessment of spasticity measurement, modified Ashworth scale of motor function, 10-Meter Walk Test of walking ability, and Barthel index of activities of daily living (ADL) were evaluated at 0, 3, 6, and 12 months after discharge. RESULTS: Significant differences were found in spasticity degree, motor function, walking ability, and ADL at 6 and 12 months after discharge between the control and intervention groups. Lower limb spasticity and ADL in the intervention group were significantly improved. CONCLUSION: HREPro is effective for rehabilitation of patients with lower limb spasticity post-stroke and has favorable home application.

Knockdown of lncRNA NEAT1 inhibits Th17/CD4+ T cell differentiation through reducing the STAT3 protein level.

CD4+ T cells differentiated into Th17 cells are a main cause for occurrence and development of rheumatoid arthritis (RA). This study aims to define the role of long noncoding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) and its downstream molecule in Th17 cell differentiation. Determination of lncRNA NEAT1 expression in the peripheral blood mononuclear cells (PBMCs) of patients with RA and in Th17 cells induced differentiation in vitro used quantitative real-time polymerase chain reaction. Lentivirus-constructed short hairpin RNA interference for NEAT1 (Lenti-siRNA-NEAT1) was pretransfected into CD4+ T cells before inducing treatment of Th17 cell differentiation. NEAT1 targets STAT3 protein was proved by RNA pull down. Lenti-siRNA-NEAT1 was injected into the joint of the mice arthritis model to verify the function of NEAT1 knockdown. Our results showed that NEAT1 is significantly upregulated in the PBMCs of RA patients, as well as in Th17 cells in vitro induced from CD4+ T cells. The knockdown of NEAT1 restrains CD4+ T cells differentiate into Th17 cells. STAT3 protein, a critical molecule for Th17 cell differentiation, is a downstream molecule for NEAT and its cellular level can be positively targeted and regulated by NEAT via reducing the ubiquitination level. Moreover, the cotreatment of NEAT1 knockdown and STAT3 overexpression promotes Th17 cell differentiation compared with NEAT1 knockdown alone. Knockdown of Th17 by in vivo injection of lenti-siRNA-NEAT1 relieves arthritis degree in II type collagen induced mice arthritis model. These data concluded that NEAT1 is auxo-active molecule for CD4+ T cells differentiating into Th17 cells and knockdown of NEAT1 positively inhibits Th17/CD4+ T cell differentiation through reducing the STAT3 protein level.