Biomedical subjects
Publications and source records attributed to S Leoni.
The association of a human herpesvirus 6 primary infection with a fatal case of hemophagocytic syndrome in a 3 month old baby is described. The trigger mechanism of the virus for the clinical syndrome is discussed.
Glycerophosphoinositols are metabolites formed by a phosholipase A2 and a lysolipase specifically acting on membrane phosphoinositol lipids. High levels of these compounds characterize epithelial cells and fibroblasts transformed by ras and other cellular oncogenes. Here we have analyzed the glycerophosphoinositol levels in cells that are considered models of cell differentiation. Using rat hepatocytes at different stages of liver development we have shown that the glycerophosphoinositol basal levels of fetal cells were up to fourfold higher than in adult hepatocytes. No changes in glycerophosphoinositol were observed in regenerating rat liver, a model of differentiated cells proliferating in a synchronous manner, where only glycerophosphoinositol 4-phosphate increased by 80%. Similarly to fetal hepatocytes, a modest but significant increase (30%) in the levels of glycerophosphoinositols was observed in undifferentiated NG-108-15 cells as compared to the same cells induced to differentiate by cAMP. In a different neuronal cell line, PC12 cells, increased glycerophosphoinositol levels characterized the differentiated cells. Based on these observations we suggest that high glycerophosphoinositol levels characterize cellular phenomena associated with the activation of ras/mitogen-activated protein kinase pathways.
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We investigate the effect of EGF on IP3 production, PLC gamma phosphorylation, calcium transients in rat hepatocytes isolated in quiescent liver (G0 phase of cell cycle) and at 4 h (G1 phase of cell cycle) and 24 h (M phase of cell cycle) after partial hepatectomy. Our results show that EGF does not utilize IP3 and calcium as its signal transduction molecules when the hepatocytes are in vivo stimulated to entry in the cell cycle. In particular the growth factor does not phosphorylate PLC gamma and induces a decrease in IP3 content. These data suggest that EGF utilizes different signal transduction to send information from receptor to nucleus during PH with respect to the quiescent liver.
The modulation by epidermal growth factor (EGF) of the Na+/H+ antiport in fetal and adult rat hepatocytes was studied in nominally HCO3- free solution. EGF (10 nM) activated the antiport in adult rat hepatocytes by 0.22 +/- 0.03 (mean +/- SD;n=10) pH units over basal value, measured with the fluorescent pH-sensitive intracellular probe, 2',7'-bis(carboxyethyl)-5(6)- carboxyfluorescein (BCECF). The effect of EGF was inhibited by amiloride analogue 5-(N-ethyl-N-isopropyl) amiloride (EIPA), by ouabain, inhibitor of the Na+ pump, and by erbstatin analogue, an inhibitor of the tyrosine kinase activity of the EGF receptor. The effect of EGF on Na+/H+ antiport in adult rat hepatocytes appeared to be mediated by both protein kinase C (PKC) and G protein system. No effect of EGF and phorbol 12-myristate 13-acetate, an activator of PKC, on the Na+/H+ antiport was observed in fetal hepatocytes of 20 and 22 days. A different sensitivity of the antiport to high concentrations of amiloride and EIPA suggests that altered amount of the Na+/H+ antiport units or different isoforms could be expressed in fetal compared with adult cells.
Spiral or volumetric computed tomography (CT) is a new scanning technique which allows the scanning of body regions with a continuously rotating system based on the slip ring technology; the patient is also moved continuously, synchronously with data acquisition. The physical characteristics of spiral CT image acquisition were compared with those of conventional CT images. The modulation transfer function (MTF) has the same values for medium-resolution filters, but lower values for spiral CT for high-resolution and frequency-enhancement filters. The slice sensitivity profile (SSP) describes the longitudinal image resolution for multiplanar reconstructions and was measured in terms of FWHM of the SSP curve. We obtained, for 10-mm slice thickness, a FWHM = 10.4 mm (conventional CT), versus 10.7 mm (Spiral CT), while, for 5-mm slice thickness, the corresponding values were 5.2 mm (conventional CT) and 5.5 mm (spiral CT). Noise was evaluated simply by measuring the standard deviation of the CT numbers, in a region of interest, of a uniform image and with the power spectrum or Wiener spectrum of the same image. To assess overall image quality and yield, the noise equivalent quanta (NEQ) value was also calculated. The values were a little lower for the spiral technique, particularly with high-resolution and enhancement or convolution filters. Dosimetric evaluation of the computed tomography dose index (CTDI) and of the multiple scan average dose (MSAD) was done using an acquisition protocol for average lung dose, in an anthropomorphic phantom and with TL dosimeters. The MSAD was 6.17 +/- 0.20 cGy for conventional CT and 5.98 +/- 0.23 cGy for Spiral CT, while lung dose was 3.25 +/- 0.12 cGy and 3.01 +/- 0.16 cGy, respectively.
Stimulation of resident peritoneal macrophages with S-[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-C ysSerLys4 or S(-)[2,3-bis(pamitoyloxy)-(2R,2S)-propyl]-N-palmytoyl-(R)-++ +CysAlaLys4, two synthetic bacterial lipopeptides, promoted the expression of the inducible form of nitric oxide synthase, exhibiting a temporal pattern of nitric oxide release that was delayed with respect to the induction elicited by bacterial lipopolysaccharide. Treatment of macrophages with genistein blocked the nitric oxide synthesis triggered by the lipopeptides or lipopolysaccharide. Simultaneous incubation with lipopolysaccharide and lipopeptide resulted in an antagonistic effect on nitric oxide synthase mRNA levels and on nitrite plus nitrate release to the medium. Triggering with bacterial lipopeptides induced macrophage programmed cell death. In macrophages activated with lipopeptide, apoptosis was observed even in the absence of nitric oxide synthesis, therefore indicating the existence of alternative pathways in the control of programmed cell death in these cells.
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We report a case of a man who died after ingestion of cantharidin as aphrodisiac. After evaluating the toxicology, we examined the development and therapeutic possibilities of handling the poisoning including charcoal hemoperfusion.
This report takes into consideration the complications due to "body packers" cocaine absorption. In particular we report a clinical case in which severe dysrhythmias occurred. We think an early insertion of a pacemaker able to rid ectopic focus by overdriving is essential by comparison with an effective anti-dysrhythmic therapy. We also examine the cocaine metabolites values in the patient's serum and urine.
Diabetes mellitus is one of the main endocrinological disease complicating the course of thalassemia major. This study aimed evaluate beta-cell secretion in 24 patients with thalassemia major attending the hematological Day Hospital at the Pediatric Clinic in Modena where transfusion therapy is performed in all thalassemic patients so as to maintain minimum hemoglobin levels above 10.5 g/dl, together with intensive ferrochelating therapy (desferrioxamine 50-60 mg/kg/die s.c. 6 days a week). A C peptide challenge with glucagon was performed in three patients already receiving insulin therapy for diabetes mellitus; this unexpectedly revealed a slight residual beta-cell secretion. An intravenous glucose tolerance test (IVGTT) was performed in the remaining 21 non-diabetic patients, with widely varying findings regarding insulin secretion: from below 50 microUl/ml in 5 patients to above 200 microUl/ml in 5 patients, and between 50 and 150 microUl/ml in the remaining 11 patients. This study therefore confirmed that insulin secretion frequently alters in thalassemic patients. Moreover, insulin secretion is not correlated to ferritinemia or influenced by familiar diabetes or patient age.
[1-14C]-2-aminoisobutyric acid (AIB) uptake and signal transduction pattern after epidermal growth factor (EGF) stimulation were examined in freshly isolated hepatocytes from 20-day-old fetuses and 3-month-old rats. EGF induced a transient increase of AIB transport after 10 min only in adult animals; the observed unresponsiveness of fetal liver is not dependent on a lack of EGF receptors which are present though to a lesser extent on the plasma membrane in this period. As far as the production of the second messengers, inositol trisphosphate (IP3) and calcium, is concerned, substantial differences were found: EGF increased IP3 production in adult hepatocytes, whereas it had no effect in fetal ones. Moreover, the addition of EGF induced a calcium transient in hepatocytes from adult animals, while there was no increase in fetal cells. The lack of EGF effect on amino acid transport in fetal cells could be due to its inability to produce both IP3 and calcium transients, suggesting that this transduction pathway is not activated during fetal life.
The changes in intracellular calcium concentration and IP3 production after the addition of epinephrine were analysed in adult, fetal (20th-22nd day of intrauterine life), and regenerating rat hepatocytes (4 h-24 h after partial hepatectomy) to determine whether the signal transduction is the same in quiescent proliferating and differentiating cells. The epinephrine treatment causes a significative cytosolic calcium transient in hepatocytes isolated in the last day of fetal life (22-day old) and in the early stage of regeneration (4 h). This effect is not significant in the previous stage of fetal life (20-day old) and at the onset of M phase of cell cycle after partial hepatectomy (24 h). [3H]myo inositol incorporation into IP3 and IP4 is higher in 20 day fetal and regenerating hepatocytes with respect to the control. In these cells the epinephrine does not affect basal level of IP3 and IP4, while it causes a substantial increase of these inositol phosphates in adult hepatocytes. [3H]myo inositol incorporation into PIP2 is very low at the 20th day of fetal life. Epinephrine has no effect on this parameter in fetal and regenerating hepatocytes. Our results show that the epinephrine signal is mediated differently in proliferating and in quiescent hepatocytes.
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The relationship between cell proliferation and inositol lipid turnover has been studied by comparing the steady state of inositol derivative metabolism in quiescent and regenerating rat hepatocytes isolated at 4 h (G1 phase of first cell cycle) and 24 h (onset of M phase) after partial hepatectomy. The effect of two hormones able to regulate hepatic regeneration, insulin and vasopressin, has been considered, and the results can be summarized as follows: (i) at 4 h after partial hepatectomy, the precursor incorporation into inositol polyphosphates and the particulate phospholipase C activity increase with respect to quiescent hepatocytes, whereas the content of 11, 4, 5P3 does not change, suggesting an increased turnover of this molecule in this step of cell cycle priming; (ii) 24 h after partial hepatectomy, the radioactivity linked to IP3 and IP4, as well as soluble and particulate phospholipase C activity, and IP3 content increase, suggesting the presence, at the onset of M phase, of second messenger accumulation; (iii) only 24 h after partial hepatectomy, the inositol derivative metabolism is affected by vasopressin; and (iv) insulin exerts a modulatory role on inositol polyphosphate production without involving membrane-bound PLC activity or phosphoinositide hydrolysis. These data suggest that inositol-derived signal molecules are associated with hepatic regeneration; moreover, the metabolic pathway of such compounds seems to be regulated so that only specific inositol phosphates are present in each step of the cell cycle.