Low amplitude rhythmic contraction frequency in human detrusor strips correlates with phasic intravesical pressure waves.

PURPOSE: Low amplitude rhythmic contractions (LARC) occur in detrusor smooth muscle and may play a role in storage disorders such as overactive bladder and detrusor overactivity. The purpose of this study was to determine whether LARC frequencies identified in vitro from strips of human urinary bladder tissue correlate with in vivo LARC frequencies, visualized as phasic intravesical pressure (p ves) waves during urodynamics (UD). METHODS: After IRB approval, fresh strips of human urinary bladder were obtained from patients. LARC was recorded with tissue strips at low tension (<2 g) and analyzed by fast Fourier transform (FFT) to identify LARC signal frequencies. Blinded UD tracings were retrospectively reviewed for signs of LARC on the p ves tracing during filling and were analyzed via FFT. RESULTS: Distinct LARC frequencies were identified in 100% of tissue strips (n = 9) obtained with a mean frequency of 1.97 ± 0.47 cycles/min (33 ± 8 mHz). Out of 100 consecutive UD studies reviewed, 35 visually displayed phasic p ves waves. In 12/35 (34%), real p ves signals were present that were independent of abdominal activity. Average UD LARC frequency was 2.34 ± 0.36 cycles/min (39 ± 6 mHz) which was similar to tissue LARC frequencies (p = 0.50). A majority (83%) of the UD cohort with LARC signals also demonstrated detrusor overactivity. CONCLUSIONS: During UD, a subset of patients displayed phasic p ves waves with a distinct rhythmic frequency similar to the in vitro LARC frequency quantified in human urinary bladder tissue strips. Further refinements of this technique may help identify subsets of individuals with LARC-mediated storage disorders.

Repair of the dura mater with processed collagen devices.

BACKGROUND: We evaluated in a canine duraplasty model how specific differences in device physicomechanical properties, porosity, and crosslinking influenced the biological performance of three processed collagen dural substitutes. METHODS: Three collagen dural substitutes were studied: Dura-Guard, DuraGen, and Durepair. The initial strength, stiffness, and suture retention force were measured using standard mechanical test methods. The relative pore sizes of each device were assessed with a scanning electron microscope. Differential scanning calorimetry was used to measure their respective collagen denaturation temperatures. The biologic response and performance of the materials were evaluated via an acute (1 month) and long-term (3 and 6 months) canine bilateral duraplasty study. RESULTS: The mechanical properties of Dura-Guard and Durepair were similar to native dura. We could not quantify the mechanical properties of DuraGen because of its fragile nature. The denaturation temperature of DuraGen and Dura-Guard differed significantly from that reported for native collagens. The denaturation temperature of Durepair was comparable with the values reported for native collagens. All three materials were tolerated well by the animals. DuraGen did not maintain its structural integrity beyond 1 month. Dura-Guard and Durepair persisted for 6 months. Durepair was populated by fibroblasts and blood vessels, whereas Dura-Guard was not. CONCLUSIONS: The three dural substitutes tested were found to be safe and effective in healing surgically created defects in the dura mater. Although each of these dura substitutes are composed of collagen, differences in the collagen source and processing influenced device physicomechanical properties, porosity, and the nativity of the collagen polymer. These measured differences influenced device intraoperative handling and installation as well as the post-operative biological response, where differences in device resorption, cell penetration, vascularization, and collagen remodeling were observed.

The specificity of phenotypic induction of mouse and human stem cells by signaling complexes.

Controlling the specific differentiation of stem cells (SCs) is a goal sought by many because of the benefits it would yield for repair or replacement of damaged tissues and organs. We report the discovery of signaling complexes and describe their use in predictably guiding the differentiation of mouse and human SCs. The signaling complexes (Signal-plexes [S-ps]) induce mouse and human SCs to express specific phenotypes. The S-ps have been used to identify a new source of human SCs (Hu abba-1) and have been shown to induce differentiation of multiple tissue-specific phenotypes selectively in mouse pluripotent embryonic cells as well as in Hu abba-1 cells. Endocrine and exocrine pancreas, liver, lung, kidney, heart, cartilage, bone, and other cell types have been induced in SCs by S-ps, as shown by morphology, immunostaining, enzyme-linked immunosorbent assay, and reverse transcriptase-polymerase chain reaction analysis.