The role of ATP signalling in response to mechanical stimulation studied in T24 cells using new microphysiological tools.

The capacity to store urine and initiate voiding is a valued characteristic of the human urinary bladder. To maintain this feature, it is necessary that the bladder can sense when it is full and when it is time to void. The bladder has a specialized epithelium called urothelium that is believed to be important for its sensory function. It has been suggested that autocrine ATP signalling contributes to this sensory function of the urothelium. There is well-established evidence that ATP is released via vesicular exocytosis as well as by pannexin hemichannels upon mechanical stimulation. However, there are still many details that need elucidation and therefore there is a need for the development of new tools to further explore this fascinating field. In this work, we use new microphysiological systems to study mechanostimulation at a cellular level: a mechanostimulation microchip and a silicone-based cell stretcher. Using these tools, we show that ATP is released upon cell stretching and that extracellular ATP contributes to a major part of Ca2+ signalling induced by stretching in T24 cells. These results contribute to the increasing body of evidence for ATP signalling as an important component for the sensory function of urothelial cells. This encourages the development of drugs targeting P2 receptors to relieve suffering from overactive bladder disorder and incontinence.

Glenoid bone loss: assessment with MR imaging.

PURPOSE: To investigate the agreement among magnetic resonance (MR) imaging, computed tomography (CT), and arthroscopy in the measurement of glenoid bone loss. MATERIALS AND METHODS: This study was approved by the institutional ethics committee. One hundred seventy-six patients (158 male and 18 female patients; mean age, 26.8 years ± 12.3) with anterior shoulder dislocation underwent both shoulder MR imaging and CT examination. Anterior straight line length, glenoid width, and best-fit bone loss were measured with MR imaging and CT. Sixty-five patients also underwent arthroscopy, which was used as the standard of reference. Assessment of glenoid bone loss at MR imaging was compared with that at CT and arthroscopy. Inter- and intrareader reproducibility of MR imaging-derived measurements of glenoid bone loss was evaluated. RESULTS: There was excellent correlation between CT and MR imaging with regard to anterior straight line length (r = 0.97, P < .0001), glenoid width (r = 0.95, P < .0001), and severity of glenoid bone loss-particularly with use of best-fit circle width (r = 0.83, P < .0001) rather than best-fit circle area (r = 0.82, P < .0001). In the assessment of glenoid bone loss, the correlation between CT and arthroscopy (r = 0.91, P < .0001) was marginally better than that between MR imaging and arthroscopy (r = 0.84, P < .0001). The inter- and intrareader correlations of MR imaging-derived measurements of glenoid bone loss were excellent (R = 0.90-0.95). CONCLUSION: MR imaging assessment of glenoid bone loss, particularly with use of glenoid width, is almost as accurate as CT assessment.