The expression of dynamin 2 in tenocytes.

<p>Western blot analysis revealed that dynamin 2 was up-regulated by laser treatment. The tubulin (as internal control) and dynamin 2 were identified at 57 kDa and 100 kDa respectively. (A) Immnofluorescence staining revealed the significantly increased dynamin 2 expression in cytoplasm as indicated by fluorescent-green stain.</p

Real-time PCR revealed that the expression of dynamin 2 was up-regulated by laser (*indicates <i>p</i><0.05 between laser-treated and control tenocytes).

<p>Real-time PCR revealed that the expression of dynamin 2 was up-regulated by laser (*indicates <i>p</i><0.05 between laser-treated and control tenocytes).</p

Transwell filter migration assay revealed that laser stimulated tenocytes migration <i>in vitro</i> (*indicates <i>p</i><0.05 between laser-treated and control tenocytes).

<p>Transwell filter migration assay revealed that laser stimulated tenocytes migration <i>in vitro</i> (*indicates <i>p</i><0.05 between laser-treated and control tenocytes).</p

<i>In vitro</i> wound healing model revealed that few control cells (without laser treatment) migrated cross the wound border to enter the cell-free zone (A).

<p>Laser-treated group (B) revealed that more tenocytes migrated cross the wound border to enter the cell-free zone (200X).</p

Additional file 1: Figure S1. of Interplay of N-Cadherin and matrix metalloproteinase 9 enhances human nasopharyngeal carcinoma cell invasion

The expression of the precursor and active form of ADAM10 after PMA treatment. NPC cells were treated with PMA (100 nM) for the indicated times. Cell lysates underwent western blot analysis to detect levels of the precursor and active form of ADAM10. In response to PMA treatment, the expression of ADAM10 was not significantly changed in NPC cells. (TIF 645 kb

Dynasore inhibited the stimulation of tenocyte migration by low-level laser irradiation.

<p>Laser can not stimulate migration of tenocytes pre-treated with dynasore (“+”: with dynasore or laser treatment; “−”: without dynasore or laser treatment).</p

Additional file 1: Figure S1. of Interplay of N-Cadherin and matrix metalloproteinase 9 enhances human nasopharyngeal carcinoma cell invasion

The expression of the precursor and active form of ADAM10 after PMA treatment. NPC cells were treated with PMA (100 nM) for the indicated times. Cell lysates underwent western blot analysis to detect levels of the precursor and active form of ADAM10. In response to PMA treatment, the expression of ADAM10 was not significantly changed in NPC cells. (TIF 645 kb

Cerebral desaturation in heart failure: Potential prognostic value and physiologic basis

<div><p>Cerebral tissue oxygen saturation (SctO₂) reflects cerebral perfusion and tissue oxygen consumption, which decline in some patients with heart failure with reduced ejection fraction (HFrEF) or stroke, especially during exercise. Its physiologic basis and clinical significance remain unclear. We aimed to investigate the association of SctO₂ with oxygen transport physiology and known prognostic factors during both rest and exercise in patients with HFrEF or stroke. Thirty-four HFrEF patients, 26 stroke patients, and 17 healthy controls performed an incremental cardiopulmonary exercise test using a bicycle ergometer. Integrated near-infrared spectroscopy and automatic gas analysis were used to measure cerebral tissue oxygenation and cardiac and ventilatory parameters. We found that SctO₂ (rest; peak) were significantly lower in the HFrEF (66.3±13.3%; 63.4±13.8%,) than in the stroke (72.1±4.2%; 72.7±4.5%) and control (73.1±2.8%; 72±3.2%) groups. In the HFrEF group, SctO₂ at rest (SctO_2rest) and peak SctO₂ (SctO_2peak) were linearly correlated with brain natriuretic peptide (BNP), peak oxygen consumption (), and oxygen uptake efficiency slope (<i>r</i> between -0.561 and 0.677, <i>p</i> < 0.001). Stepwise linear regression showed that SctO_2rest was determined by partial pressure of end-tidal carbon dioxide at rest (P_ETCO_2rest), hemoglobin, and mean arterial pressure at rest (MAP_rest) (adjusted R = 0.681, <i>p</i> < 0.05), while SctO_2peak was mainly affected by peak carbon dioxide production () (adjusted R = 0.653, <i>p</i> < 0.05) in patients with HFrEF. In conclusion, the study delineates the relationship of cerebral saturation and parameters associated with oxygen delivery. Moreover, SctO_2peak and SctO_2rest are correlated with some well-recognized prognostic factors in HFrEF, suggesting its potential prognostic value.</p></div

Area under curve of hemodynamic variables during 1^st PLRT and VO_2VAT at 1st CPET.

<p>VAT: ventilatory anaerobic threshold; CD: change difference from HU to LR; CR: change ratio from HU to LR = CD/HU; HU: head-up; LR: leg raise; LR5: leg raise at the 5th minute; SR: supine rest; CO: cardiac output; CI: cardiac index; SV: stroke volume; SVCom: stroke volume compliance; SVIcom: stroke volume index compliance; TFC: thoracic fluid content; TPR: total peripheral resistance; TPRI: total peripheral resistance index</p><p>Area under curve of hemodynamic variables during 1^st PLRT and VO_2VAT at 1st CPET.</p

Area under curve of hemodynamic variables during 1^st PLRT and VO_2VAT at 1st CPET.

<p>VAT: ventilatory anaerobic threshold; CD: change difference from HU to LR; CR: change ratio from HU to LR = CD/HU; HU: head-up; LR: leg raise; LR5: leg raise at the 5th minute; SR: supine rest; CO: cardiac output; CI: cardiac index; SV: stroke volume; SVCom: stroke volume compliance; SVIcom: stroke volume index compliance; TFC: thoracic fluid content; TPR: total peripheral resistance; TPRI: total peripheral resistance index</p><p>Area under curve of hemodynamic variables during 1^st PLRT and VO_2VAT at 1st CPET.</p