Table1_Effects of compression running pants and treadmill running stages on knee proprioception and fatigue-related physiological responses in half-marathon runners.XLSX

Background: Knee injury is common in half-marathon runners, however, the effect of compression running pants on fatigue and knee proprioception remains unclear.Objectives: The study aims to investigate whether wearing compression running pants (CRP) and treadmill running stages affect knee proprioception and fatigue-related physiological responses during half-marathon running.Methods: Eighteen half-marathon runners completed two self-paced 21 km treadmill running trials, once wearing CRP and once wearing loose running shorts (LRS). For each 21 km run, RPE, heart rate, blood lactic acid, and knee flexion proprioception were assessed before starting, and after each 7 km stage.Results: Data analysis revealed no difference between CRP and LRS conditions in heart rate, RPE, or blood lactic acid. Repeated measures ANOVA showed a significant garment condition main effect whereby wearing CRP was associated with higher knee proprioceptive acuity (p = 0.006). Polynomial trend analysis showed a significant linear downwards trend in proprioceptive acuity across the four measurement occasions (p = 0.048). Stage analysis showed that wearing CRP was associated with better knee proprioception at running distances of 14 km (p = 0.007, 95%CI = -0.054, -0.010) and 21 km (p = 0.016, 95%CI = -0.051, -0.006).Conclusion: Compression running pants provide an overall positive effect on knee proprioception, particularly after 14 km and 21km, which may reduce the probability of knee injury. CRP had no significant effect on physiological measures in half-marathon running.</p

Additional file 2: of Improving physical activity, pain and function in patients waiting for hip and knee arthroplasty by combining targeted exercise training with behaviour change counselling: study protocol for a randomised controlled trial

SPIRIT 2013 Checklist. (DOC 138 kb

Additional file 1: of Improving physical activity, pain and function in patients waiting for hip and knee arthroplasty by combining targeted exercise training with behaviour change counselling: study protocol for a randomised controlled trial

Participant booklet. (PDF 705 kb

RelA-Mediated BECN1 Expression Is Required for Reactive Oxygen Species-Induced Autophagy in Oral Cancer Cells Exposed to Low-Power Laser Irradiation

<div><p>Low-power laser irradiation (LPLI) is a non-invasive and safe method for cancer treatment that alters a variety of physiological processes in the cells. Autophagy can play either a cytoprotective role or a detrimental role in cancer cells exposed to stress. The detailed mechanisms of autophagy and its role on cytotoxicity in oral cancer cells exposed to LPLI remain unclear. In this study, we showed that LPLI at 810 nm with energy density 60 J/cm² increased the number of microtubule associated protein 1 light chain 3 (MAP1LC3) puncta and increased autophagic flux in oral cancer cells. Moreover, reactive oxygen species (ROS) production was induced, which increased RelA transcriptional activity and beclin 1 (BECN1) expression in oral cancer cells irradiated with LPLI. Furthermore, ROS scavenger or knockdown of RelA diminished LPLI-induced BECN1 expression and MAP1LC3-II conversion. In addition, pharmacological and genetic ablation of autophagy significantly enhanced the effects of LPLI-induced apoptosis in oral cancer cells. These results suggest that autophagy may be a resistant mechanism for LPLI-induced apoptosis in oral cancer cells.</p></div

LPLI induces ROS-mediated RelA activation and BECN1 expression in human oral cancer cells.

<p>(A) OECM-1 (white) and Ca9-22 (black) cells were pretreated with (+) or without (-) 10 mM NAC prior to irradiation with LPLI (810 nm, 60 J/cm²). The ROS production in LPLI-treated cells was determined using an ROS assay kit and 100 μM H₂O₂ as a positive control. (B) OECM-1 (white) and Ca9-22 (black) cells transfected with the NF-κB-responsive luciferase vector were pretreated with or without 10 mM NAC for 1 h then irradiated with LPLI (810 nm, 60 J/cm²). The treated cells were recovered for 6 h and 200 μM D-luciferin was added to monitor luciferase activity. (C) OECM-1 or Ca9-22 cells pretreated with (+) or without (-) 10 mM NAC were irradiated with LPLI (810 nm, 60 J/cm²) then recovered for 24 h. The recovered cells were harvested for immunoblotting to determine the protein levels of phosphorylated RelA, BECN1, and MAP1LC3-II. Protein levels for (D) phosphorylated RelA and (E) BECN1, and (F) the MAP1LC3-II/I ratio were quantified using ACTB as a normalization control. The data are expressed as the mean ± SEM from three independent experiments.</p

Autophagy inhibitors enhance LPLI-induced apoptosis in human oral cancer cells.

<p>OECM-1 or Ca9-22 cells were pretreated without (-) or with (+) 20 μM CQ for 1 h prior to irradiation with LPLI (810 nm, 60 J/cm²) and then recovered for 24 h. (A) The cell viability of the recovered cells was measured with CellTiter-Glo. The LPLI-treated (B) OECM-1 and (C) Ca9-22 cells were cultured for 14 days and stained with crystal violet to determine tumor colony formation. A representative sample of the results and the quantitative data are shown in the left and right panel, respectively. Scale bar: 100 μm. The recovered OECM-1 (D) and Ca9-22 (E) cells were fixed for staining with Hoechst 33342. The condensed nuclei of the cells were counted to quantify the number apoptotic cells. (F) The Ca9-22 and OECM-1 cells were pretreated with 20 μM CQ or 100 nM Baf A1 for 1 h prior to irradiation with LPLI and then recovered for 24 h. The recovered cells were harvested for PI/annexin V staining to verify the combined effects of LPLI and autophagy inhibitors on apoptosis in oral cancer cells. (G) The cells treated as panel F were lysed to measured caspase-3/7 activity with Caspase-Glo 3/7 luminescent assay. The results are expressed as the mean ± SEM from three independent experiments.</p

LPLI reduced tumor viability in spheroid culture.

<p>(A) OECM-1 or Ca9-22 cells were sphere cultured and then exposed to LPLI (810 nm, 60 J/cm²) in the presence or absence of CQ (20 μM) for 48 h. The spheres were lysed to measure ATP level for cell viability. (B) The viable and dead spheres as cultured and treated as (A) were imaged with LIVE (green)/DEAD (red) staining kit. Representative data are shown. Scale bar: 400 μm. (C) The green and (D) red fluorescence of the spheres as (B) was quantitated with a reader for the viable and dead cell population, respectively (n = 6). The quantified results are expressed as the mean ± SEM from 3 individual experiments. n.s., p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001.</p

LPLI-induced apoptosis is elevated in autophagy-deficient oral cancer cells.

<p>(A) OECM-1 cells stably harboring shRNA against ATG7 or SQSTM1 were treated without (-) or with (+) 20 μM CQ prior to harvest. The harvested cells were used for immunoblotting to determine the protein levels of ATG7, SQSTM1 and MAP1LC3-II. (B) The knockdown efficiency of ATG7 and SQSTM1 in the cells was quantified using ACTB as a normalization control (left panel). The net protein levels of MAP1LC3-II between cells treated with or without CQ were used to determine autophagic flux as quantitated results in the right panel. (C) The recovered cells were accessed for cell viability with CellTiter-Glo. (D) The LPLI-treated cells were irradiated with LPLI and cultured for 14 days. Colony formation was accessed by staining with crystal violet. (E) The irradiated cells were fixed and stained with Hoechst 33342 to determine the number of apoptotic cells. Scale bar: 100 μm. The number of apoptotic cells is shown in the right panel. (F) The cells treated as panel E were lysed to measured caspase-3/7 activity with Caspase-Glo 3/7 luminescent assay. The results are expressed as the mean ± SEM from three independent experiments.</p

LPLI induces autophagic flux in human oral cancer cells.

<p>(A) OECM-1 or Ca9-22 cells harboring GFP-MAP1LC3 plasmids were irradiated with LPLI (810 nm, 60 J/cm²) and then recovered after 24 h. The recovered cells were fixed to examine GFP-MAP1LC3 and SQSTM1 puncta under confocal microscopy. Cells were starved with EBSS for 4 h as controls for autophagy induction. Scale bar: 10 μm. (B) The GFP-MAP1LC3 puncta were counted. (C) The recovered cells were lysed to determine the accumulation of MAP1LC3-II by immunoblotting. (D) MAP1LC3 degradation in cells with or without CQ (20 μM) was quantified to determine autophagic flux using ACTB as a normalization control. The data are expressed as the mean ± SEM from three independent experiments.</p

RelA stimulates BECN1 expression and the induction of autophagy in LPLI-exposed oral cancer cells.

<p>OECM-1 or Ca9-22 cells stably harboring scramble shRNA or shRNA against RelA were irradiated with (+) or without (-) LPLI (810 nm, 60 J/cm²) and recovered for 24 h. (A) The recovered cells were harvested for immunoblotting to determine protein levels of RelA, BECN1, and MAP1LC3. The protein levels for (B) RelA and (C) BECN1, and (D) the MAP1LC3-II/I ratio were quantified using ACTB as a normalization control. The results are expressed as the mean ± SEM from three independent experiments.</p