Turbulent stress measurements downstream of three bileaflet heart valve designs in pigs

Objective: Mechanical heart valves can cause thromboembolic complications, possibly due to abnormal flow patterns that produce turbulence downstream of the valve. The objective of this study was to investigate whether three different bileaflet valve designs would exhibit clinically relevant differences in downstream turbulent stresses. Methods: Three bileaflet mechanical heart valves (Medtronic Advantage^®, CarboMedics© Orbis™ Universal and St. Jude Medical^® Standard) were implanted into 19 female 90 kg pigs. Blood velocity was measured during open chest conditions in the cross sectional area downstream of the valves with 10 MHz ultrasonic probes connected to a modified Alfred^® Pulsed Doppler equipment. As a measure of turbulence, Reynolds normal stress (RNS) was calculated at three different cardiac output ranges (3–4, 4.5–5.5, 6–7 L/min). Results: Data from 12 animals were obtained. RNS correlated with increasing cardiac outputs. The highest instantaneous RNS observed in these experiments was 47 N/m², and the mean RNS taken spatially over the cross sectional area of the aorta during systole was between 3 N/m² and 15 N/m². In none of the cardiac output ranges RNS values exceeded the lower critical limit for erythrocyte or thrombocyte damage for any of the valve designs. Conclusions: Reynolds normal stress values were below 100 N/m² for all three valve designs and the difference in design was not reflected in generation of turbulence. Hence, it is unlikely that any of the valve designs causes flow induced damage to platelets or erythrocytes.     

Participation of lipid peroxidation in the loss of hepatic drug-metabolizing activities in experimental fascioliasis in the rat

Fascioliasis causes a dramatic decrease in drug-metabolizing ability of the hepatic monooxygenase (MFO) and glucuronosyltransferase (GT) enzyme systems in the rat. The present study was undertaken to determine whether lipid peroxidation is involved in the enzymatic loss. Peroxidative damage of membrane lipids (as assessed by the tissue content of malonic dialdehyde, MDA, and the diene conjugation absorption in microsomal membranes) was found to occur over the entire course of the liver infection (concomitant to a decrease in glutathione levels), and to different degrees in relation to the various steps of the parasite cycle. The onset (MDA six times the controls; delta E 1% = 1.55 at the 20th day) coincides with the beginning of the loss of MFO (-30%) and GT (-20% at the 20th day), and peaks between the 30th and 40th day (MDA eight times the controls; delta E 1% = 1.96), when the loss in the enzyme activities is maximal (MFO - 60/70%; GT - 65/95%). There was a strict correlation at all the observation times between the extent of lipid peroxidation and the decrease in drug metabolizing ability: this supports the view that lipid peroxidation is the major agent in the impairment of MFO and GT enzyme activities, and very likely in the initiation of the pathological degeneration of the liver tissue. As evidenced by histological examination, the phagocytic response of the liver tissue to the parasite invasion and growth leads to oxidative stress, which is the causative agent in the initiation and development of lipid peroxidation.     

Dendritic competition: competition for what?

A lesion to the retina of a newborn rat results in the retrograde degeneration of ganglion cells in a sector of retina peripheral to the lesion. The dendritic tree of ganglion cells bordering the region depleted of ganglion cells have their dendrites preferentially directed into this area. We have examined the factors which play a role in this rearrangement of the dendritic tree. The results show that the lesion in neonates selects for or produces a population of cells with the axon directed away from the depleted area and primary dendrites directed towards the depleted area. The abnormal dendritic bias cannot be accounted for solely on the basis of a decrease in contact inhibition since a reduction in the density of all ganglion cells by 30% prior to making the retinal lesion does not attenuate the abnormal dendritic bias into the depleted area. The abnormal dendritic bias is present in animals operated on up to 15 days of age postnatally but not in more mature animals. The abnormal dendritic bias develops prior to the formation of a large number of synapses in the inner nuclear layer. Our results cannot be easily accounted for by competition for synaptic contacts or a loss of contact inhibition as previously suggested. We propose that chemotropic factors produced within the area depleted of ganglion cells induce the abnormal dendritic bias and the number of synaptic contacts may limit the size of the dendritic field.     

Blue Hue in the Dermoscopy Setting: Homogeneous Blue Pigmentation, Gray-Blue Area, and/or Whitish Blue Veil?

In dermoscopy, the correct recognition of the single parameters is fundamental to achieve great diagnostic accuracy, but the scarce morphologic expression of a parameter may lead to diagnostic errors. We report the case of a 27-year-old white man presenting a pigmented lesion of the back, which was present since puberty. Clinical examination revealed on the back the presence of a flat, gray-blue lesion and at the periphery a small dark-brown papule. An assessment of the lesion by means of dermoscopy was performed. The purpose of this report was to analyze the Blue Hue in dermoscopy with its histopathologic correlates, starting with the discussion of a clinical case.     

Carboxylic metabolites of tiadenol as "proximate" inducers of hepatic peroxisomal beta-oxidation activity

Chronic exposure of rats to the hypolipidemic agent tiadenol causes a dramatic dose-dependent increase of peroxisomal beta-oxidation activity. To elucidate which metabolite of the drug is the "proximate" inducer (tiadenol is eliminated completely in metabolized form after acute administration) we investigated the qualitative and quantitative metabolic profile of the drug at different doses (50, 150, 300 mg/Kg in two-weeks chronically treated rats, in parallel to that of a model compound, tiadenol-disulfoxide, a weak inducer of palmitoyl-CoA oxidation activity. No changes in the biodisposition of tiadenol (and tiadenol-disulfoxide) were found following chronic treatment for all the doses tested. For both the compounds a strict correlation was evidenced between the extent of formation of carboxylic metabolites and their inductive potencies on peroxisomal beta-oxidation activity. This indicates that tiadenol carboxylic metabolites act as the enzymatic effectors.