Effects of position-triggered electrical stimulation on poststroke hemiparetic shoulder subluxation.

BACKGROUND: Shoulder subluxation is a frequent complication after stroke causing joint instability, shoulder pain, decreased activities of daily living, and impedance to rehabilitation progress. Electrical stimulation (ES) is considered an effective modality to reduce shoulder subluxation in acute stroke. However, few studies have investigated the effect of position-triggered ES, which induces active muscle contraction though accurate motion detection. AIM: The aim of this study was to investigate whether position-triggered ES was more effective in reducing acute hemiplegic shoulder subluxation after stroke than passive ES. DESIGN: Single-blind, randomized controlled trial. SETTING: The study setting was the university hospital rehabilitation center. POPULATION: Fifty poststroke subacute hemiparetic patients with shoulder subluxation. METHODS: Patients were randomly assigned into two groups. The position-triggered ES group received 30-minute ES sessions, 5 days per week for 3 weeks with specially modified Novastim® CU-FS1 (CU Medical Systems, Inc., Gangwon-do, South Korea) for motion triggering. The passive ES group received the same protocol without motion triggering. The vertical distance (VD) and the joint distance (JD), relative VD and JD (rVD, rJD), upper extremity component of Fugl-Meyer Motor Assessment (FMAupper), Motricity Index (MI), Manual Function Test (MFT), and peak torque of affected shoulder abductor (PT) were assessed at baseline (T0), end of electrical stimulation session (T1), and 3 weeks (T2) after treatment. RESULTS: Repeated-measures analysis of variance revealed significant interaction between time and intervention on JD and rJD, indicating that shoulder subluxation was significantly more reduced in position-triggered ES than in passive ES (P<0.05). However, FMAupper, MI, MFT, and PT did not show this significance. The change of (∆)JD, ∆rVD, and ∆rJD in the motion-triggered ES group improved significantly more at T1 than in the passive ES group (P<0.05). This significant improvement was not seen at T2. CONCLUSIONS: Position-triggered ES may be more effective than passive ES in improving poststroke shoulder subluxation; however, this effect was not maintained after the withdrawal of stimulation. CLINICAL REHABILITATION IMPACT: Position-triggered ES may be useful to reducing poststroke shoulder subluxation.

Expression and functional roles of the chemokine receptor CXCR7 in acute myeloid leukemia cells.

BACKGROUND: The C-X-C chemokine receptor 7 (CXCR7) has been shown to be a decoy receptor for CXCR4 in certain cell types. We investigated the expression status and functional roles of CXCR7 in acute myeloid leukemia (AML) cells in vitro. METHODS: CXCR7 mRNA was knocked down in AML cells by using small interfering RNA (siRNA) technology, and subsequent biological alterations in the cells were evaluated in vitro. RESULTS: All AML cell lines examined in this study (U937, K562, KG1a, HL-60, and MO7e) and primary CD34(+) cells obtained from patients with AML expressed CXCR7 mRNA at various levels. Western blotting showed that all AML cells produced CXCR7. Furthermore, all AML cells expressed CXCR7 in both the cytoplasm and on the cell surface at various levels. Stromal cell-derived factor-1 (SDF-1; C-X-C motif ligand 12 (CXCL12)) induced internalization of cell surface CXCR7. However, neither hypoxia nor the examined hematopoietic growth factors (interleukin-1ß (IL-1ß), IL-3, IL-6, granulocyte-colony-stimulating factor, granulocyte, macrophage-colony-stimulating factor, and stem cell factor) and proinflammatory cytokines (interferon-γ, transforming growth factor-ß, and tumor necrosis factor-α) were found to alter cell surface CXCR7 expression. The transfection of AML cells with CXCR4 siRNA, but not CXCR7 siRNA, significantly impaired the CXCL12-induced transmigration of the cells. The transfection of AML cells with CXCR7 siRNA did not affect the survival or proliferation of these cells. Knockdown of CXCR7, but not CXCR4, induced the upregulation of CXCL12 mRNA expression and CXCL12 production in AML cells. CONCLUSION: CXCR7 is involved in the regulation of autocrine CXCL12 in AML cells.