ABSTRACT
CONTEXT: Chronic plantarflexor (PF) stretching during ankle immobilization helps preserve calf girth, plantarflexion peak torque, and ankle dorsiflexion (DF) motion. Immobilization can lead to decreases in muscle peak torque, muscle size, and joint range of motion (ROM). Recurrent static stretching during a period of immobilization may reduce the extent of these losses. OBJECTIVE: To investigate the effects of chronic static stretching on PF peak torque, calf girth, and DF ROM after 2 weeks of ankle immobilization. DESIGN: Randomized controlled clinical trial. SETTING: Athletic training facility. PARTICIPANTS: A total of 36 healthy college-aged (19.81 [2.48]) females. INTERVENTIONS: Subjects were randomly assigned to one of 3 groups: control group, immobilized group (IM), and immobilized plus stretching (IM+S) group. Each group participated in a familiarization period, a pretest, and, 2 weeks later, a posttest. The IM group and IM+S group wore the Aircast Foam Pneumatic Walker for 2 weeks on the left leg. During this time, the IM+S group participated in a stretching program, which consisted of two 10-minute stretching procedures each day for the 14 days. MAIN OUTCOME MEASURES: One-way analysis of variance was used to determine differences in the change of ankle girth, PF peak torque, and DF ROM between groups with an α level of <.05. RESULTS: A significant difference was noted between groups in girth (F2,31 = 5.64, P = .01), DF ROM (F2,31 = 26.13, P < .001), and PF peak torque (F2,31 = 7.74, P = .002). Post hoc testing also showed a significance difference between change in calf girth of the control group compared with the IM group (P = .01) and a significant difference in change of peak torque in the IM+S group and the IM group (P = .001). Also, a significant difference was shown in DF ROM between the control group and IM+S group (P = .01), the control group and the IM group (P < .001), and the IM+S group and the IM group (P < .001). CONCLUSION: Chronic static stretching during 2 weeks of immobilization may decrease the loss of calf girth, ankle PF peak torque, and ankle DF ROM.
ABSTRACT
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a very common lethal monogenetic disease with significant morbidities and a high likelihood of progression to renal failure for which there is no proven disease-specific therapy currently available for clinical use. Human ADPKD cystic epithelia have proliferative abnormalities mediated by EGFR over-expression and mispolarization leading autocrine response to EGF family ligands. We now show that apical localization of EGFR complexes in normal fetal and ADPKD epithelia is associated with heterodimerization of EGFR(HER-1) with HER-2(neu/ErbB2), while basal membrane localization in normal adult renal epithelia is associated with EGFR(HER-1) homodimers. Since ADPKD epithelial cells have reduced migratory function, this was used as a bioassay to evaluate the ability of compounds to rescue the aberrant human ADPKD phenotype. General tyrosine kinase inhibition by herbimycin and specific inhibition of HER-2(neu/ErbB2) by AG825 or pretreatment with ErbB2 siRNA reversed the migration defect of ADPKD epithelia. Selective inhibition of EGFR(HER-1) showed partial rescue. Increased ADPKD cell migration after inhibition of p38MAP kinase but not of PI3-kinase implicated p38MAPK downstream of HER-2(neu/ErbB2) stimulation. Daily administration of AG825 to PKD1 null heterozygous mice significantly inhibited the development of renal cysts. These studies implicate HER2(neu/ErbB2) as an effector of apical EGFR complex mispolarization and that its inhibition should be considered a candidate for clinical therapy of ADPKD.
