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Biomedical subjects

A Del Maschio

Publications and source records attributed to A Del Maschio.

12 recordsLinked to original sources
PubMed1992

Magnetic resonance imaging of the kidney in type 1 (insulin-dependent) diabetes mellitus.

Reductions in the physiological cortical to medullary signal intensity ratio are found in magnetic resonance scans of the kidney in non-diabetic glomerular disease. Whether this abnormality can also characterise patients with Type 1 (insulin-dependent) diabetes mellitus and nephropathy is not known. We measured the cortical to medullary signal intensity ratio in magnetic resonance images of the kidney in 34 patients with Type 1 diabetes (ten with either clinical proteinuria or raised serum creatinine or both, nine with microalbuminuria, seven with normal urinary albumin excretion and long duration of diabetes and eight with Type 1 diabetes of short duration). The cortical to medullary signal intensity ratio showed a trend to cluster at lower values in the normoalbuminuric patients with normal serum creatinine rather than in the nine healthy individuals, independent of Type 1 diabetes duration (1.47 +/- 0.06 and 1.41 +/- 0.13 vs 1.63 +/- 0.16; five groups Scheffé F-test p = 0.05-0.1). Among the Type 1 diabetic patients, significant reductions in the cortical to medullary signal intensity ratio characterised overt nephropathy (1.19 +/- 0.15, p less than 0.05 vs all groups), but not microalbuminuria (1.47 +/- 0.13, p = NS), concomitantly with low glomerular filtration rate and elevated fractional excretion of uric acid, but independent of glycaemic control. The determinants of the renal cortical to medullary signal intensity ratio in Type 1 diabetes are uncertain. Reductions in the cortical to medullary signal intensity ratio may be a late finding in diabetic nephropathy, and parallel the accompanying impairment in kidney haemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Polymorphonuclear leukocyte adhesion to endothelial cells is inhibited by resting platelets.

The effect of human platelets on the adhesion of polymorphonuclear leukocytes (PMNs) to cultured endothelial cells was investigated. Resting platelets inhibited the adhesion of PMNs stimulated by N-formyl-methionyl-leucyl-phenylalanine (fMLP), leukotriene B4 (LTB4), and tumor necrosis factor-alpha (TNF-alpha). Platelets similarly inhibited PMN adhesion induced by endothelial cell activation with TNF-alpha. The inhibitory effect depended on platelet number, was not associated with detectable platelet activation, and was also exerted by paraformaldehyde-fixed platelets. Moreover, supernatants of U46619- or thrombin-stimulated platelets were ineffective, thus excluding a role for constituents released as a result of the platelet-release reaction. Strong inhibition of PMN adhesion was exerted by platelet lysates. The inhibitory activity associated with lysates was sedimentable, heat sensitive, and not dialyzable through a membrane with a molecular-weight cutoff of 8,000; it was directed toward PMNs and was not due to cytotoxic effects or a general inhibition of PMN responsiveness to stimulation, since enzymatic release from activated PMNs was unaffected by platelet lysates. Finally, the activity was not prevented by specific adenosine inhibitors and anti-P-selectin monoclonal antibody. These data suggest that resting platelets can exert an inhibitory effect on PMN adhesion to the vessel wall during inflammatory and thrombotic conditions.

Adenosine↗
PubMed1992

[Accuracy of magnetic resonance (0.5 T) in traumatic lesions of the knee. Controlled 87 cases].

In this study the authors investigated the diagnostic accuracy of Magnetic Resonance (MR) imaging as a method to recognise traumatic disorders of the knee; in particular its capability to identify meniscal and cruciate ligaments tears was examined. The results have been compared with those from arthroscopy and/or surgery, which were considered the gold standard of the study. Eighty-seven consecutive patients with suspected traumatic injury of the knee were prospectively studied. All patients underwent MR examination (0.5 Tesla magnet, gradient echo sequences, slices thickness = 5 mm) and, within 15 days/1 month, arthroscopy or surgery. The high diagnostic accuracy (internal meniscus = 87.5%; external meniscus = 88.5%; anterior cruciate ligament = 93.1%; posterior cruciate ligament = 96.5%) has confirmed the good diagnostic capabilities of MR in assessing traumatic lesions of the knee.

Arthroscopy↗
PubMed1991

Inactivation of endothelin by polymorphonuclear leukocyte-derived lytic enzymes.

Cultured bovine aortic endothelial cells (BAEC) released endothelin-1 (ET-1) in the culture medium in a time-dependent fashion. Coincubation of fMLP-activated human polymorphonuclear leukocytes (PMN) with BAEC caused a fast (maximal activity was reached within 15 minutes) and cell number-dependent disappearance of ET-1 from the medium. This effect was direct to ET-1, because it was also present when PMN were incubated with the synthetic peptide in the absence of BAEC. PMN-dependent disappearance of ET-1 was associated with loss of constrictor activity on isolated rabbit aorta. PMN-released products were responsible for ET-1 degrading activity, because supernatants of activated PMN were equally effective as the intact cells. Resting PMN, in the same time frame, were uneffective. Eglin C, a potent blocker of PMN-derived elastase and cathepsin G, reversed the ET-1 inhibitory activity of fMLP-stimulated PMN and of their supernatant. Direct addition of elastase and cathepsin G to synthetic ET-1 destroyed its immunoreactivity and this effect was blocked by eglin C. High-performance liquid chromatography (HPLC) analysis supported the hypothesis that ET-1 degradation by PMN was due to enzymatic proteolysis. These data provide evidence that activated PMN are able to degrade ET-1 through the release of proteases. Because physiologic concentrations of PMN can destroy high amounts (up to 100 nmol/L) of ET-1 within a few minutes, we propose that this mechanism of ET-1 inactivation has biologic relevance.

Animals↗
PubMed1991

Polymorphonuclear leukocyte-dependent modulation of platelet function: effect of cloricromene.

Cloricromene inhibits the activation of platelets and polymorphonuclear leukocytes (PMN) induced by specific stimuli. We report here that cloricromene caused a concentration-dependent reduction of platelet aggregation, beta-thromboglobulin (beta-TG) release and cytoplasmic Ca2+ movements induced by PMN stimulated with N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP), and enhanced the inhibitory action of unstimulated PMN on platelet responses to the stable endoperoxide analog U46619. These effects may be of pharmacological interest in view of the multiple interactions between platelets and leukocytes that occur in thrombotic and inflammatory diseases.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Adrenergic modulation of human polymorphonuclear leukocyte activation. Potentiating effect of adenosine.

The activation of polymorphonuclear leukocytes (PMN) is an important step in the development of tissue damage associated with inflammatory and ischemic conditions. Catecholamines have been reported to inhibit PMN functions, but the high concentrations required cast doubt on their actual relevance as a defense mechanism. We report here that adenosine, which is actively released in ischemic conditions, potentiates the effect of epinephrine and reduces the minimal active concentration required to inhibit PMN activation by at least two orders of magnitude. Epinephrine caused a dose-related reduction of chemiluminescence, superoxide anion generation, enzyme release (lysozyme and beta-glucuronidase), and adhesion to endothelial cell (EC) monolayers in human PMN activated by N-formyl-methionyl-leucyl-phenyl-alanine (fMLP). This effect was only apparent at 10(-7) to 10(-6) mol/L. As expected, adenosine caused dose-dependent reductions of superoxide anion production and PMN adhesion to EC. Adenosine and epinephrine combined had an additive effect on PMN superoxide production and adhesion to EC. The minimal effective concentration of epinephrine in combination with 10(-8) mol/L adenosine was in the range of 10(-10) to 10(-9) mol/L. In contrast, adenosine inhibited only slightly enzyme release and did not significantly enhance the inhibition by epinephrine on this parameter. Studies with adenosine analogs suggested that the potentiating effect of adenosine was mediated by A2 receptors. The mechanism of potentiation was not related to additive effect on intracellular cyclic adenosine monophosphate levels. Epinephrine's ability to modulate PMN activation and the potentiating effect of adenosine may constitute a form of physiologic protection against tissue injury in inflammatory and ischemic processes.

Adenosine↗
PubMed1979

[Anatomy of papilla and intra-renal reflux: microradiographic and histologic investigations (author's transl)].

After a group of autoptic kidneys, taken from new-born babies, had been injected via the ureter with micronised barium at various pressures, they were examined micro-radiographically and histologically in order to observe the appearance of intra-renal reflux and the anatomical structures involved. The radiological patterns, clinically observed during cysto-uretrography, were also considered. The intra-renal reflux is tubular, when injection is carried out at a low pressure, whereas at higher pressures one can observe the erosion of the fornices of the calyces and the following sino-lymphatic and/or venous drainage.

Histological Techniques↗
PubMedDate not supplied

Platelet-neutrophil interactions. Possible relevance in the pathogenesis of thrombosis and inflammation.

Evidence indicates that complex interactions occur between platelets and neutrophils. Mediators released by activated platelets may act as stimuli for neutrophils, but platelets may also limit neutrophil activation. Similarly, neutrophils, depending upon their degree of activation, may bring about both enhancement and inhibition of platelet responses. The elaborate cross-talk among platelets and neutrophils, cells involved in hemostatic and phlogistic reactions, may condition the development and the course of thrombotic and inflammatory diseases; therefore, modulation of platelet-neutrophil interactions may represent a therapeutic target in these conditions. In this review, the mediators involved in the platelet-dependent modulation of neutrophil activation and, conversely, the mechanisms whereby neutrophils modify platelet responses are described. Moreover, the possible relevance of these interactions in the pathogenesis of thrombosis and inflammation is discussed.

Arachidonic Acid↗