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L Vicentini

Publications and source records attributed to L Vicentini.

At least 19 recordsLinked to original sources
PubMed2006

Dust in the underground railway tunnels of an Italian town.

This article assesses hazards associated with exposure to dust in tunnels and platforms of the A and B lines of Rome's underground railway and provides an informed opinion on the risks to workers and the travelling public of exposure to tunnel dust. The study focused on the analysis and measurement of dust granulometric classes PM10, respirable fraction, respirable combustible dust, and the organic, metallic, siliceous, and fibrous components. Comparing the measurement values from the tunnels and platforms with those found at the entrances to the underground railway stations, it emerges that dust concentration in the tunnels and platforms is three times higher, with a maximum PM10 value of 479 microg/m3. Averaged over 24 hours, in relation to the above ground levels, drivers and station staff are exposed to an additional value of 11 microg/m3 and 10 microg/m3, respectively. If commuters were to remain in the trains or on the station platforms, the 24-hour average exposure would increase by 3 microg/m3. Iron and silica were the major components found in the dust. The use of silica sand in the emergency braking system of the carriages is capable of causing a dispersion of quartz in the air in percentages varying from 5% to 14%. Methods are suggested in this article for the reduction of dust dispersion.

Air Pollutants↗
PubMed2005

Risk factors associated to kidney stones in primary hyperparathyroidism.

Nephrolithiasis is the most important clinical manifestation of primary hyperparathyroidism (PHPT), although nowadays this disorder is often asymptomatic. Clinical or biochemical differences between PHPT patients with and without nephrolithiasis have not been clearly identified in most of the previous studies. The aim of the study was to investigate clinical and biochemical parameters in kidney stone former (SF) and non-stone former (NSF) patients with PHPT in order to identify potential risk factors. Serum and plasma samples from 55 consecutive patients (43 females, 12 males) with PHPT were collected after overnight fasting; 24-h urine collection and a fresh sample of urine for sediment analysis were obtained from all patients. Clinical data were recorded in all. Out of 55 patients, 22 had kidney stones, which were symptomatic in 73%. SFs showed circulating PTH, total and ionized calcium, 1,25 dihydroxyvitamin D3, urinary calcium excretion and 24-h urine oxalate levels significantly higher than NSFs. Hypercalciuria was often concomitant with massive quantities of calcium oxalate crystals in urine sediment. Hypercalciuria and relatively high oxaluria were associated with stone formation with an odds ratio (OR) of 4.0 and 7.0, respectively, which rose to 33.5 when they coexisted. Hypomagnesuria and hypocitraturia were common in at least one third of all PHPT patients, but they were not associated to an increased OR. As expected, they were positively correlated with urine calcium excretion, suggesting that calcium, magnesium and citrate are commonly regulated at renal level. In conclusion, hypercalciuria, higher oxalate excretion and severe PHPT are associated with kidney stones in PHPT.

Aged↗
PubMed2005

Ghrelin in human medullary thyroid carcinomas.

OBJECTIVE: Ghrelin is a novel gastrointestinal hormone involved in several metabolic functions. It has been identified previously in several normal and tumoral neuroendocrine tissues, including human medullary thyroid carcinomas (MTCs). The aim of the study was to evaluate ghrelin levels in patients with MTC and nontoxic goitre (NTG) with elevated calcitonin (CT) levels, as an additional marker of the disease. PATIENTS AND DESIGN: The study included 22 patients with MTC (four before and 18 after thyroidectomy), 12 patients with NTG with basal CT levels exceeding 10 ng/l and 15 healthy subjects matched for age, sex and body mass index (BMI). After thyroidectomy, MTC patients were considered cured when basal and pentagastrin-stimulated CT levels were < 0.2 and < 10 ng/l, respectively. A pentagastrin-induced CT peak over 50 ng/l was considered as an abnormal response while 100 ng/l was the cut-off accepted for the diagnosis of C-cell hyperplasia or tumour. Circulating ghrelin and CT levels were evaluated at baseline in patients and controls and at -10, 0, 1, 2, 5 and 15 min after pentagastrin injection (0.5 microg/kg body weight) in 12 patients with MTC and nine with NTG. Four surgically removed MTCs were tested for ghrelin expression. MEASUREMENTS: Total plasma ghrelin and CT levels were measured with a commercially available radioimmunoassay (RIA) and two-site chemiluminescence immunometric assays, respectively. In paraffin-embedded MTC samples ghrelin immunostaining was performed with a polyclonal antibody (1:1000) and the reaction visualized by an indirect immunoperoxidase system. RESULTS: Plasma ghrelin levels found in cured or not cured MTC and in NTG patients were similar to those of BMI-matched healthy controls. No correlation between ghrelin and CT levels, thyroid disease or previous thyroidectomy was observed. The administration of pentagastrin caused a 17% increase in ghrelin levels (basal ghrelin vs. peak: 162 +/- 62 pmol/l vs. 189 +/- 58 pmol/l, P < 0.05) that was particularly evident (33% increase) in patients with an abnormal CT response to the test (CT > 50 ng/l). Immunohistochemistry showed positivity for ghrelin in a small proportion of CT positive cells from the four MTCs removed. CONCLUSIONS: Patients with MTC, NTG and controls showed similar ghrelin levels, ruling out this parameter as a marker of MTC. The increase in ghrelin levels in patients with a positive CT response to pentagastrin, together with the immunopositivity for ghrelin in some MTC cells, suggests C cells as minor source of ghrelin production.

Adult↗
PubMed2005

Activity and function of the nuclear factor kappaB pathway in human parathyroid tumors.

Previous studies indicate that nuclear factor kappaB (NF-kappaB) transcription factor is deregulated and overexpressed in several human neoplasias. The aim of this study was to test the hypothesis that the NF-kappaB pathway may be involved in parathyroid tumorigenesis. For this purpose, we determined the level of NF-kappaB activity, evaluated as phosphorylation of the transcription subunit p65, its modulation by specific and non-specific agents and its impact on cyclin D1 expression. Phosphorylated p65 levels present in parathyroid neoplasias (n = 13) were significantly lower than those found in normal tissues (n = 3; mean optical density (OD) 0.19 +/- 0.1 vs 0.4 +/- 0.1, P = 0.007), but there was no significant difference between adenomas and secondary and multiple endocrine neoplasia type 1 (MEN1)-related hyperplasia. Conversely, MEN2A (Cys634Arg)-related parathyroid samples showed extremely high levels of phosphorylated p65 that exhibited a nuclear localization at immunohistochemistry (n = 3). Phosphorylated p65 levels negatively correlated with menin expression (r(2) = 0.42, P = 0.05). Tumor necrosis factor-alpha (TNFalpha) caused a significant increase in phosphorylated p65 levels (183 +/- 13.8% of basal) while calcium sensing receptor (CaR) agonists exerted a significant inhibition (19.2 +/- 3.3% of basal). Although TNFalpha was poorly effective in increasing cyclin D1 expression, NF-kappaB blockade by the specific inhibitor BAY11-7082 reduced FCS-stimulated cyclin D1 by about 60%. Finally, the inhibitory effects of CaR and BAY11-7082 on cyclin D1 expression were not additive - by blocking NF-kappaB CaR activation did not induce a further reduction in cyclin D1 levels. In conclusion, the study demonstrated that in parathyroid tumors: (1) p65 phosphorylation was dramatically increased by RET constitutive activation and was negatively correlated with menin expression, (2) p65 phosphorylation was increased and reduced by TNFalpha and CaR agonists respectively, and (3) blockade of the NF-kappaB pathway caused a significant decrease in cyclin D1 expression.

Cyclin D1↗
PubMed2004

Exhaled breath condensate eicosanoids and sputum eosinophils in asthmatic children: a pilot study.

Cysteinyl leukotrienes (cys-LTs), LTB4 and 8-isoprostane are increased in the exhaled breath condensate (EBC) from asthmatic patients. The aim of this study was to investigate whether the measurement of cys-LTs, LTB4 and 8-isoprostane in EBC can reflect the level of airway inflammation assessed by induced sputum in asthmatic children sensitized to house dust mite (HDM) during natural avoidance of HDM allergens. Twelve children were evaluated at the time of admission (T0) and after 3 months of stay (T1) at the Istituto Pio XII (Misurina, Italian Dolomites 1756 m). Sputum eosinophil percentage and measurement of cys-LTs, LTB4 and 8-isoprostanes in the breath condensate at T0 and T1 were evaluated. Eosinophil percentage in induced sputum was 8.5 +/- 1.1% at T0 and 3.5 +/- 0.4% at T1 (p = 0.011). Neutrophil percentage in sputum was 1.1 +/- 0.5% at T0 and 1.5 +/- 1.0% at T1 (ns). Cys-LTs mean level was 14.24 +/- 4.53 pg/ml at T0 and 4.65 +/- 0.68 pg/ml at T1 (p = 0.0125). LTB4 level was 2.36 +/- 0.19 pg/ml at T0 and 2.41 +/- 0.23 pg/ml at T1 (ns). 8-Isoprostane level reduced from 17.47 +/- 3.18 pg/ml at T0 to 7.36 +/- 3.26 pg/ml at T1 (p = 0.003). This study show that exhaled cys-LTs and 8-isoprostane, as well as eosinophil percentage in induced sputum, are reduced after allergen avoidance in asthmatic children suggesting a potential application of EBC for the non-invasive evaluation of airway inflammation in asthma in allergic asthmatic children.

Adolescent↗
PubMed2003

Brown jaw tumors: today's unusual presentation of primary hyperparathyroidism.

Primary hyperparathyroidism (pHPT) has changed its clinical features in the last decade becoming a mild biochemical disease, in which the classical fibrous cystic osteitis is a rare complication. The more frequent bone involvement in primary hyperparathyroidism is observed at the distal 1/3 of the radius, where the cortical bone is primarily represented. However, lumbar and femoral osteopenia or osteoporosis prevalently affect hyperparathyroid post-menopausal women. We report two, otherwise healthy, young male patients, who presented a painful jaw swelling. In both patients standard radiographic imaging revealed a low-density well-defined lesion, which caused jaw bone destruction. High levels of serum calcium (14.1-16.6 mg/dl, n.v. 8.1-10.4) and PTH (1172-1928 pg/ml, n.v. 10-65) indicated the presence of pHPT associated with hypertension, asymptomatic renal involvement and osteoporosis with normal serum 25-hydroxyvitamin D levels in both patients. A single huge parathyroid adenoma was successfully removed and within 2 months jaw lesions were almost completely re-mineralized without any other therapeutic intervention in both patients. In conclusion, although brown jaw tumors are a rare complication of the hyperparathyroidism, they should be considered and identified in young patients with severe pHPT. Moreover, such a complication seems to be independent from vitamin D deficiency, suggesting the involvement of other pathogenetic factors.

Adult↗
PubMed2002

Mitogen-activated protein kinase cascade in human normal and tumoral parathyroid cells.

The calcium-sensing receptor (CaR) activation has recently been shown to modulate the ERK1 and ERK2 cascade in different cell lines. The present study investigated this pathway in human normal and tumoral parathyroid cells. In cells from normal parathyroids and almost all hyperplasia increasing extracellular calcium concentrations (Ca(o)(2+)) induced a significant activation of ERK1 and -2, the percent stimulation over basal activity (at 0.5 mM Ca(o)(2+)) being 545 +/- 140 and 800 +/- 205 in normal cells and 290 +/- 71 and 350 +/- 73 in hyperplasia at 1 and 2 mM Ca(o)(2+), respectively. This effect was mediated by CaR because it was mimicked by the receptor agonist gadolinium and neomycin. Basal and Ca(o)(2+)-stimulated ERK1 and -2 activity was nearly abolished by the PKC inhibitor calphostin C, and PKA changes did not affect ERK1 and -2 activity. PI3K blockade by wortmannin, known to prevent G protein betagamma subunit effect on ERK1 and -2, induced a 30% reduction of the Ca(o)(2+)-stimulated ERK1 and -2 activity. Adenomatous cells showed high PKC-dependent ERK1 and -2 activity in resting conditions that was unresponsive to high Ca(o)(2+). A role of MAPK on PTH secretion was suggested by the finding that PD98059, a specific MEK inhibitor, abolished the inhibitory effect of 1.5 mM Ca(o)(2+) on PTH release from normal parathyroid cells. In conclusion, these data first demonstrate that CaR activation, through the PKC pathway and, to a lesser extent, PI3K, increases ERK1 and -2 activity in normal parathyroid cells and this cascade seems to be involved in the modulation of PTH secretion by Ca(o)(2+). Interestingly, this signaling pathway is disrupted in parathyroid tumors.

Adenoma↗
PubMed2001

In vitro release of activin A from human normal and pathological thyroid tissues.

Activin A is a dimeric glycoprotein belonging to the transforming growth factor beta (TGF-beta) superfamily characterized by the ability to affect FSH secretion. Activin A was originally indicated as a gonadal product but the expression of activin A has been successively identified in several different tissues, including the thyroid gland. The aim of this study was to evaluate the release of activin A from human normal and pathological thyroid tissues in culture. Activin A concentration was evaluated in media obtained from primary culture of perinodular normal tissues (no.=2), hyperplastic hyperfunctioning thyroid tissues due to Graves' disease (no.=3) and autonomous thyroid adenomas (no.=3). Detectable levels of activin A were found in the incubation media from all tissues, without significant differences between normal and pathological samples. We conclude that activin A is secreted by follicle thyroid cells in normal and pathological conditions.

Activins↗
PubMed2000

Exhaled nitric oxide is reduced after sputum induction in asthmatic children.

Exhaled nitric oxide (ENO) and eosinophil sputum markers are considered noninvasive markers of airway inflammation in asthma. The aim of this study was to evaluate whether the procedure of sputum induction can affect the level of ENO. We measured ENO before and after sputum induction by inhalation of hypertonic saline solution in 22 asthmatic children and 9 healthy controls. The ENO mean (+/- S. E.M.) value in the group of asthmatic children was reduced from a baseline value of 20.8 (+/- 3.0) ppb to 17.4 (+/- 2.4) ppb after sputum induction (P = 0.0012). In the healthy controls, the mean baseline value of ENO was 9.1 (+/- 2.1) ppb and it was reduced to 4. 8 (+/- 1.1) ppb after induction of sputum (P < 0.01). We suggest that measurements of ENO should be performed after the induction of sputum in asthmatic patients whenever both tests are done in sequence.

Adolescent↗
PubMed2000

Exhaled nitric oxide in asthmatic children exposed to relevant allergens: effect of flunisolide.

Inhaled corticosteroids are capable of reducing the level of exhaled nitric oxide (expiratory nitric oxide fraction (FE,NO)) in asthmatic patients in a dose-dependent fashion. The aim of this study was to evaluate whether or not treatment with an inhaled steroid can prevent changes in FE,NO after the exposure to relevant allergens, following avoidance, in asthmatic children allergic to house dust mite. Thirty-two house dust mite-allergy asthmatic children were randomly allocated to treatment with inhaled flunisolide (500 microg b.i.d) or placebo and evaluated before and 2 weeks after a period of natural exposure to mite antigens. Lung function and FE,NO were evaluated. FE,NO was increased in the placebo-treated group after antigen exposure. Treatment with inhaled flunisolide prevented such increase in FE,NO (p<0.001). No change was observed in lung function parameters. Inhaled flunisolide is effective in preventing the increase in airway inflammation observed in allergic asthmatic children re-exposed to allergens.

Administration, Inhalation↗
PubMed2000

Calcium-sensing receptor expression and signalling in human parathyroid adenomas and primary hyperplasia.

OBJECTIVE: Both in vivo and in vitro evidence indicates that primary hyperparathyroidism is characterized by a reduced sensitivity to extracellular calcium ([Ca2+]o). The existence of alterations in the expression and signalling of calcium sensing receptor (CaSR) in parathyroid neoplasia is still uncertain. In order to clarify the role of CaSR in the reduced [Ca2+]o sensing of parathyroid neoplasia we investigated PTH secretion and intracellular effectors triggered by CaSR activation as well as the levels of expression of CaSR and CaSR coupled G proteins (Gq/G11) in parathyroid adenomas and primary hyperplasia. MATERIALS AND METHODS: The study included 27 parathyroid adenomas, 4 cases of primary hyperplasia and pools of normal parathyroid biopsies. Tissues were either snap frozen in liquid nitrogen or placed in sterile medium for cell dispersion. The effects of increasing [Ca2+]o on in vitro PTH release, intracellular cAMP levels and intracellular calcium ([Ca2+]i) in cells loaded with the Ca2 + indicator fura-2 were evaluated. CaSR mRNA levels were assessed by semiquantitative RT-PCR analysis, using GAPDH as internal standard, while CaSR protein was detected by western blot analysis using a specific polyclonal antibody. Purified antisera selective for G11alpha and Gqalpha were used to detect this class of proteins. RESULTS: In basal conditions (at 0.5 mM [Ca2+]o) in vitro PTH released ranged from 29.4 to 1186 pg/well/60 minutes. Increasing [Ca2+]o from 0.5 to 1, 2.5 and 5 mM caused a variable effect. One group (n = 7) showed a significant but partial reduction of PTH release (of 17 to 60% of basal levels) that occurred at physiological [Ca2+]o concentrations (1 mM) while the remainder showed either inhibition detectable only at 2.5 mM (n = 15) or total (n = 9) resistance to [Ca2+]o. In the responsive cells, [Ca2+]o (1-5 mM) caused a pertussis toxin-insensitive [Ca2+]i rise (ranging from 10% to 260%), due to Ca2+ release from intracellular stores, and an inhibition of forskolin-stimulated cAMP levels. By RT-PCR almost all tumours tested showed a substantial reduction in CaSR mRNA levels when compared to the normal tissue (CaSR/GAPDH ratio: 3.1 +/- 0.5 vs. 15.5 +/- 3.1; P < 0.001), which was confirmed by immunoblotting analysis demonstrating low levels of CaSR protein in tumour tissues. Moreover, low amounts of G11alpha and Gqalpha, the G proteins involved in CaSR coupling, were observed in the majority of pathological tissues. CONCLUSIONS: The study shows that the activation of the calcium sensing receptors expressed in adenomatous parathyroid glands modulates intracellular effectors in a similar way to those operating in the normal parathyroid. Although a reduction of calcium sensing receptor expression is probably involved in the poor inhibition of PTH release induced by [Ca2+]o, this is not the only factor altering [Ca2+]o sensing in parathyroid adenomas, since tumours characterized by different in vitro sensitivity to [Ca2+]o showed similar CaSR levels. The low content of G proteins of the Gq subfamily might represent an additional alteration leading to a defective [Ca2+]o sensing.

Adenoma↗
PubMed1999

Very low density lipoprotein-mediated signal transduction and plasminogen activator inhibitor type 1 in cultured HepG2 cells.

In normal subjects and in patients with cardiovascular disease, plasma triglycerides are positively correlated with plasminogen activator inhibitor type 1 (PAI-1) levels. Moreover, in vitro studies indicate that VLDLs induce PAI-1 synthesis in cultured cells, ie, endothelial and HepG2 cells. However, the signaling pathways involved in the effect of VLDL on PAI-1 synthesis have not yet been investigated. We report that VLDLs induce a signaling cascade that leads to an enhanced secretion of PAI-1 by HepG2 cells. In myo-[(3)H]inositol-labeled HepG2 cells, VLDL (100 microg/mL) caused a time-dependent increase in [(3)H]inositol phosphates, the temporal sequence being tris>bis>monophosphate. VLDL brought about a time-dependent stimulation of membrane-associated protein kinase C (PKC) activity and arachidonate release. Finally, VLDL stimulated mitogen-activated protein (MAP) kinase, and this effect was reduced by 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7), which suggests that PKC plays a pivotal role in MAP kinase phosphorylation. VLDL-induced PAI-1 secretion was completely prevented by U73122, a specific inhibitor of phosphatidylinositol-specific phospholipase C, by H7 or by PKC downregulation, and by mepacrine (all P<0.01 versus VLDL-treated cells). 3,4,5-Trimethoxybenzoic acid 8-(diethylamino)-octyl ester, which prevents Ca2+ release from intracellular stores, inhibited VLDL-induced PAI-1 secretion by 60% (P<0.05), and the MAP kinase/extracellular signal-regulated kinase kinase (MEK) inhibitor PD98059 completely suppressed both basal and VLDL-induced PAI-1 secretion. These data demonstrate that VLDL-induced PAI-1 biosynthesis results from a principal signaling pathway involving PKC-mediated MAP kinase activation.

Antioxidants↗
PubMed1999

Cell-specific differences in the regulation of IL-6 expression by PMA.

We have studied the regulation of IL-6 expression in human blood monocytes and lymphocytes. LPS and IFN-gamma induced IL-6 gene expression with a similar qualitative profile in both cell types. Treatment of monocytes and lymphocytes with PMA resulted, instead, in different effects: monocytes accumulated IL-6 and its message, while lymphocytes were inhibited either in the absence or the presence of LPS and IFN-gamma. These results suggest that the signal transduction pathways triggered by LPS and IFN-gamma are similar in both cell types, while PMA may activate a tissue-specific pathway which leads to opposite responses.

Cells, Cultured↗
PubMed1999

Gene expression and production of the monokine induced by IFN-gamma (MIG), IFN-inducible T cell alpha chemoattractant (I-TAC), and IFN-gamma-inducible protein-10 (IP-10) chemokines by human neutrophils.

Monokine induced by IFN-gamma (MIG), IFN-inducible T cell alpha chemoattractant (I-TAC), and IFN-gamma-inducible protein of 10 kDa (IP-10) are related members of the CXC chemokine subfamily that bind to a common receptor, CXCR3, and that are produced by different cell types in response to IFN-gamma. We have recently reported that human polymorphonuclear neutrophils (PMN) have the capacity to release IP-10. Herein, we show that PMN also have the ability to produce MIG and to express I-TAC mRNA in response to IFN-gamma in combination with either TNF-alpha or LPS. While IFN-gamma, alone or in association with agonists such as fMLP, IL-8, granulocyte (G)-CSF and granulocyte-macrophage (GM)-CSF, failed to influence MIG, IP-10, and I-TAC gene expression, IFN-alpha, in combination with TNF-alpha, LPS, or IL-1beta, resulted in a considerable induction of IP-10 release by neutrophils. Furthermore, IL-10 and IL-4 significantly suppressed the expression of MIG, IP-10, and I-TAC mRNA and the extracellular production of MIG and IP-10 in neutrophils stimulated with IFN-gamma plus either LPS or TNF-alpha. Finally, supernatants harvested from stimulated PMN induced migration and rapid integrin-dependent adhesion of CXCR3-expressing lymphocytes; these activities were significantly reduced by neutralizing anti-MIG and anti-IP-10 Abs, suggesting that they were mediated by MIG and IP-10 present in the supernatants. Since MIG, IP-10, and I-TAC are potent chemoattractants for NK cells and Th1 lymphocytes, the ability of neutrophils to produce these chemokines might contribute not only to the progression and evolution of the inflammatory response, but also to the regulation of the immune response.

Apoptosis↗