Multilacunarity as a spatial multiscale multi-mass morphometric of change in the meso-architecture of plant parenchyma tissue.

The lacunarity index (monolacunarity) averages the behavior of variable size structures in a binary image. The generalized lacunarity concept (multilacunarity) on the basis of generalized distribution moments is an appealing model that can account for differences in the mass content at different scales. The model was tested previously on natural images [J. Vernon-Carter et al., Physica A 388, 4305 (2009)]. Here, the computational aspects of multilacunarity are validated using synthetic binary images that consist of random maps, spatial stochastic patterns, patterns with circular or polygonal elements, and a plane fractal. Furthermore, monolacunarity and detrended fluctuation analysis were employed to quantify the mesostructural changes in the intercellular air spaces of frozen-thawed parenchymatous tissue of pome fruit [N. A. Valous et al., J. Appl. Phys. 115, 064901 (2014)]. Here, the aim is to further examine the coherence of the multilacunarity model for quantifying the mesostructural changes in the intercellular air spaces of parenchymatous tissue of pome and stone fruit, acquired with X-ray microcomputed tomography, after storage and ripening, respectively. The multilacunarity morphometric is a multiscale multi-mass fingerprint of spatial pattern composition, assisting the exploration of the effects of metabolic and physiological activity on the pore space of plant parenchyma tissue.

Nitric oxide reduces organ injury and enhances regeneration of reduced-size livers by increasing hepatic arterial flow.

BACKGROUND: Reduced-size livers suffer from portal hyperperfusion, diminished arterial blood flow and the risk of postoperative liver injury. The aim of this experimental study was to unravel the role of nitric oxide in this setting. METHODS: Rats underwent 85 per cent partial hepatectomy and either substitution of nitric oxide with molsidomine or inhibition of nitric oxide synthase (NOS) with N(G)-nitro-L-arginine methyl ester. Untreated hepatectomized animals served as controls and unresected animals as the sham group. RESULTS: Ultrasonic flowmetry following partial hepatectomy revealed a marked increase in portal venous inflow with a concomitant decrease in hepatic arterial inflow. Nitric oxide substitution counteracted the decline in hepatic arterial inflow and caused a significantly greater increase in cell proliferation after partial hepatectomy compared with control or NOS-inhibited animals. Hepatectomized animals further profited from nitric oxide substitution, as indicated by reduced aminotransferase release and improved liver function. CONCLUSION: Nitric oxide improves the postoperative course of rats with reduced-size livers by modulating hepatic macrohaemodynamics and mediating regeneration and cytoprotection, but not by reducing hepatic hyperperfusion and the accompanying sinusoidal shear stress.