Finite-time Lyapunov exponent-based analysis for compressible flows.

The finite-time Lyapunov exponent (FTLE) technique has shown substantial success in analyzing incompressible flows by capturing the dynamics of coherent structures. Recent applications include river and ocean flow patterns, respiratory tract dynamics, and bio-inspired propulsors. In the present work, we extend FTLE to the compressible flow regime so that coherent structures, which travel at convective speeds, can be associated with waves traveling at acoustic speeds. This is particularly helpful in the study of jet acoustics. We first show that with a suitable choice of integration time interval, FTLE can extract wave dynamics from the velocity field. The integration time thus acts as a pseudo-filter separating coherent structures from waves. Results are confirmed by examining forward and backward FTLE coefficients for several simple, well-known acoustic fields. Next, we use this analysis to identify events associated with intermittency in jet noise pressure probe data. Although intermittent events are known to be dominant causes of jet noise, their direct source in the turbulent jet flow has remained unexplained. To this end, a Large-Eddy Simulation of a Mach 0.9 jet is subjected to FTLE to simultaneously examine, and thus expose, the causal relationship between coherent structures and the corresponding acoustic waves. Results show that intermittent events are associated with entrainment in the initial roll up region and emissive events downstream of the potential-core collapse. Instantaneous acoustic disturbances are observed to be primarily induced near the collapse of the potential core and continue propagating towards the far-field at the experimentally observed, approximately 30° angle relative to the jet axis.

In vivo assessment of microvascular nitric oxide production and its relation with blood flow.

To assess the hypothesis that microvascular nitric oxide (NO) is critical to maintain blood flow and solute exchange, we quantified NO production in the hamster cheek pouch in vivo, correlating it with vascular dynamics. Hamsters (100-120 g) were anesthetized and prepared for measurement of microvessel diameters by intravital microscopy, of plasma flow by isotopic sodium clearance, and of NO production by chemiluminescence. Analysis of endothelial NO synthase (eNOS) location by immunocytochemistry and subcellular fractionation revealed that eNOS was present in arterioles and venules and was 67 +/- 7% membrane bound. Basal NO release was 60.1 +/- 5.1 pM/min (n = 35), and plasma flow was 2.95 +/- 0.27 microl/min (n = 29). Local NO synthase inhibition with 30 microM N(omega)-nitro-L-arginine reduced NO production to 8.6 +/- 2.6 pmol/min (-83 +/- 5%, n = 9) and plasma flow to 1.95 +/- 0.15 microl/min (-28 +/- 12%, n = 17) within 30-45 min, in parallel with constriction of arterioles (9-14%) and venules (19-25%). The effects of N(omega)-nitro-L-arginine (10-30 microM) were proportional to basal microvascular conductance (r = 0.7, P < 0.05) and fully prevented by 1 mM L-arginine. We conclude that in this tissue, NO production contributes to 35-50% of resting microvascular conductance and plasma-tissue exchange.

Follow-up of a case of retroperitoneal fibroses treated sequencially via right side autotransplant and left uterolysis with wrapper of posterior preperitoneal fat.

We present a case of retroperitoneal fibrosis treated with a renal autotransplantation in a patient inicially treated with endourologic measures and corticotherapy without success. The extense ureteral affectation was the indication to carry out an autotransplant. The follow-up is of nine years, with the function of the renal unity still preserved. We checked the literature for the therapeutic possibilities, medical as much as surgical, of the retroperitoneal fibrosis with special attention to the usage of the refractory IRF to other treatments.

Stimulation of NO production and of eNOS phosphorylation in the microcirculation in vivo.

The role of nitric oxide (NO) in microvascular permeability is controversial, in part because the regulation of its endothelial constitutive synthase, eNOS, has been studied in vitro but not in vivo. Our study was designed to detect the morphologic and functional presence of eNOS and to test whether eNOS could be phosphorylated by platelet-activating factor (PAF), an agent that induces hyperpermeability. Immunocytochemistry was applied using human anti-eNOS antibodies in the hamster cheek pouch (hcp). The hcp microvessels demonstrated positive reaction products in the endothelium. The functional presence of eNOS in hcp was investigated by topical application of 10(-7) M PAF to the hcp and by measuring NO production by chemiluminescence. The mean baseline value of NO release was 63.3 +/- 6.9 pmol/ml (mean +/- SE). Application of PAF led to an increase in mean NO release to 120.8 +/- 31.2 pmol/ml (P < 0.05). In another series of experiments, 10(-7) M PAF was applied topically to hcp preincubated with [(32)P]orthophosphoric acid. Immunoprecipitation and Western blots detected (32)P-labeled bands that migrated with the mobility of positive eNOS indicating phosphorylated eNOS protein. The intensity of the radioactive bands was evaluated by computer-assisted image analysis. Comparison of the net band intensities yielded a mean PAF-treated/control ratio of 1.6 +/- 0.1. Our data demonstrate the morphologic and functional presence of eNOS in the microcirculation. The data also provide evidence that the function of microvascular eNOS is subject to regulation by phosphorylation.

Atropine- and tetrodotoxin-resistant motor activity, responsive to 4-aminopyridine, present in isolated rabbit jejunum.

The effects of 4-aminopyridine on the spontaneous contractile activity of rabbit jejunum segments were studied. Apart from its effects on the cholinergic component of the spontaneous activity, the drug was found to be effective to increase an atropine-, tetrodotoxin-resistant activity of the preparation, suggesting either a direct effect on intestinal smooth muscle cells or an indirect effect through an unidentified excitatory innervation.