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- Dias, Caroline Pieta, et al.
(author)
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Impaired mechanical properties of Achilles tendon in spastic stroke survivors : an observational study.
- 2019
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In: Topics in Stroke Rehabilitation. - : Taylor & Francis. - 1074-9357 .- 1945-5119. ; 26:4, s. 261-266
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Journal article (peer-reviewed)abstract
- BACKGROUND: The spasticity could lead to decreased functional capacity and changes in musculoskeletal tissue.OBJECTIVE: To compare the Achilles tendon properties between the affected and contralateral limbs of participants with spasticity due to stroke and the healthy subjects.METHODS: Fifteen individuals with ankle spasticity due to stroke and 15 healthy subjects were recruited. Maximal isometric ankle joint torque was obtained with an isokinetic dynamometer, and an ultrasound was used to determine tendon length, tendon cross-sectional area, and the medial gastrocnemius myotendinous junction displacement. The Achilles tendon strength, displacement, stress, strain, stiffness, and Young's modulus were obtained during a maximum voluntary isometric plantarflexion contraction.RESULTS: There were no differences between Achilles tendon length among participants. Both limbs of participants with stroke showed reduced tendon cross-sectional area (~18%) compared to healthy limb. The affected limb showed decreased tendon strength (686 ± 293.3 N), displacement (10.6 ± 1.7 mm), Young's modulus values (849 ± 235.6 MPa), and lower stiffness (196.6 ± 67.6 N/mm) compared to the contralateral limb (strength, 1357.1 ± 294.8 N; displacement, 15.2 ± 5.5 mm; Young's modulus, 1431.8 ± 301.9 MPa; stiffness, 337.5 ± 98.1 N/mm) and to the healthy limb. The contralateral limb also showed decreased tendon strength (~26.2%) and stiffness (~21.5%) compared to the healthy group.CONCLUSION: There is a decrement in Achilles tendon morphological and mechanical properties of the affected limb in individuals with spasticity due to stroke. The contralateral limb had a thinner tendon more compliant likely to physical activity reduction.
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| 2. |
- Niaudet, Colin, et al.
(author)
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Gpr116 Receptor Regulates Distinctive Functions in Pneumocytes and Vascular Endothelium
- 2015
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In: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 10:9
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Journal article (peer-reviewed)abstract
- Despite its known expression in both the vascular endothelium and the lung epithelium, until recently the physiological role of the adhesion receptor Gpr116/ADGRF5 has remained elusive. We generated a new mouse model of constitutive Gpr116 inactivation, with a large genetic deletion encompassing exon 4 to exon 21 of the Gpr116 gene. This model allowed us to confirm recent results defining Gpr116 as necessary regulator of surfactant homeostasis. The loss of Gpr116 provokes an early accumulation of surfactant in the lungs, followed by a massive infiltration of macrophages, and eventually progresses into an emphysemalike pathology. Further analysis of this knockout model revealed cerebral vascular leakage, beginning at around 1.5 months of age. Additionally, endothelial-specific deletion of Gpr116 resulted in a significant increase of the brain vascular leakage. Mice devoid of Gpr116 developed an anatomically normal and largely functional vascular network, surprisingly exhibited an attenuated pathological retinal vascular response in a model of oxygen-induced retinopathy. These data suggest that Gpr116 modulates endothelial properties, a previously unappreciated function despite the pan-vascular expression of this receptor. Our results support the key pulmonary function of Gpr116 and describe a new role in the central nervous system vasculature.
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