Project description:Adhesion formation after flexor tendon repair remains a clinical problem. Early postoperative motion after tendon repair has been demonstrated to reduce adhesion formation while increasing tendon strength. It is hypothesized that during mobilization, tendon cells experience mechanical shear forces that alter their biology in a fashion that reduces scar formation but also activates key genes involved in tendon healing. To test this hypothesis, primary intrinsic tenocyte cultures were established from flexor tendons of 20 Sprague-Dawley rats and sheared at 50 rpm (0.41 Pa) using a cone viscometer for 6 and 12 hours. Total RNA was harvested and compared with time-matched unsheared controls using cDNA microarrays and Northern blot analysis. Microarray analysis demonstrated that mechanical shear stress induced an overall "antifibrotic" expression pattern with decreased transcription of collagen type I and collagen type III. Shear stress down-regulated profibrotic molecules in the platelet-derived growth factor, insulin-like growth factor, and fibroblast growth factor signaling pathways. In addition, shear stress induced an overall decrease in transforming growth factor (TGF)-beta signaling pathway molecules with down-regulation of TGF-beta2, TGF-beta3, TGF-RI, and TGF-RII expression. Moreover, sheared tendon cells increased expression of matrix metalloproteinases and decreased expression of tissue inhibitors of metalloproteinase, an expression pattern consistent with an antifibrotic increase in extracellular matrix degradation. However, up-regulation of genes implicated in tendon healing, specifically, vascular endothelial growth factor-A and several bone morphogenetic proteins. Interestingly, the known mechanoresponsive gene, TGF-beta1, also implicated in tendon healing, was differentially up-regulated by shear stress. Northern blot validation of our results for TGF-beta1, TGF-beta2, TGF-beta3, and collagen type I demonstrated direct correlation with microarray data. Groups of assays that are related as part of a time series. Keywords: time_series_design

Project description:BackgroundReduced gliding ability of the median nerve in the carpal tunnel has been observed in patients with carpal tunnel syndrome (CTS). The purpose of this study was to evaluate the gliding abilities of the median nerve and flexor tendon in patients with CTS and healthy participants in the neutral and 30° extended positions of the wrist and to compare the gliding between the finger flexion and extension phases.MethodsPatients with CTS and healthy participants were consecutively recruited in a community hospital. All the subjects received the Boston CTS questionnaire, physical examinations, nerve conduction study (NCS), and ultrasonography of the upper extremities. Duplex Doppler ultrasonography was performed to evaluate the gliding abilities of the median nerve and flexor tendon when the subjects continuously moved their index finger in the neutral and 30° extension positions of the wrist.ResultsForty-nine patients with CTS and 48 healthy volunteers were consecutively recruited. Significant differences in the Boston CTS questionnaire, physical examination and NCS results and the cross-sectional area of the median nerve were found between the patients and the healthy controls. The degree of median nerve gliding and the ratio of median nerve excursion to flexor tendon excursion in the CTS group were significantly lower than those in the healthy control group in both the neutral and 30° wrist extension positions. Significantly increased excursion of both the median nerve and flexor tendon from the neutral to the extended positions were found in the CTS group. The ratio of median nerve excursion to flexor tendon excursion was significantly higher in the finger flexion phase than in the extended phase in both groups, and this ratio had mild to moderate correlations with answers on the Boston CTS Questionnaire and with the NCS results.ConclusionsReduced excursion of the median nerve was found in the patients with CTS. The ratio of median nerve excursion to flexor tendon excursion was significantly lower in the patients with CTS than in the healthy volunteers. The median nerve excursion was increased while the wrist joint was extended to 30° in the patients with CTS. Wrist extension may be applied as part of the gliding exercise regimen for patients with CTS to improve median nerve mobilization.

Project description:Adhesion formation after flexor tendon repair remains a clinical problem. Early postoperative motion after tendon repair has been demonstrated to reduce adhesion formation while increasing tendon strength. It is hypothesized that during mobilization, tendon cells experience mechanical shear forces that alter their biology in a fashion that reduces scar formation but also activates key genes involved in tendon healing. To test this hypothesis, primary intrinsic tenocyte cultures were established from flexor tendons of 20 Sprague-Dawley rats and sheared at 50 rpm (0.41 Pa) using a cone viscometer for 6 and 12 hours. Total RNA was harvested and compared with time-matched unsheared controls using cDNA microarrays and Northern blot analysis. Microarray analysis demonstrated that mechanical shear stress induced an overall "antifibrotic" expression pattern with decreased transcription of collagen type I and collagen type III. Shear stress down-regulated profibrotic molecules in the platelet-derived growth factor, insulin-like growth factor, and fibroblast growth factor signaling pathways. In addition, shear stress induced an overall decrease in transforming growth factor (TGF)-beta signaling pathway molecules with down-regulation of TGF-beta2, TGF-beta3, TGF-RI, and TGF-RII expression. Moreover, sheared tendon cells increased expression of matrix metalloproteinases and decreased expression of tissue inhibitors of metalloproteinase, an expression pattern consistent with an antifibrotic increase in extracellular matrix degradation. However, up-regulation of genes implicated in tendon healing, specifically, vascular endothelial growth factor-A and several bone morphogenetic proteins. Interestingly, the known mechanoresponsive gene, TGF-beta1, also implicated in tendon healing, was differentially up-regulated by shear stress. Northern blot validation of our results for TGF-beta1, TGF-beta2, TGF-beta3, and collagen type I demonstrated direct correlation with microarray data. Groups of assays that are related as part of a time series. Computed

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Spontaneous flexor tendon rupture due to atraumatic chronic carpal instability.

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