173 research outputs found
Inducible nitric oxide synthase expression in laryngeal neoplasia: correlation with angiogenesis
No full textHead Neck. 2002 Jan;24(1):16-23.
Inducible nitric oxide synthase expression in laryngeal neoplasia: correlation with angiogenesis.
Franchi A, Gallo O, Paglierani M, Sardi I, Magnelli L, Masini E, Santucci M.
Source
Department of Human Pathology and Oncology, University of Florence, Viale G. B. Morgagni 85, 50134 Florence, Italy. [email protected]
Abstract
BACKGROUND:
The nitric oxide (NO) pathway plays a relevant role in angiogenesis and tumor progression in squamous cell carcinoma (SCC) of the head and neck. The aim of this study was to assess whether the NO pathway may be correlated with angiogenesis in the transition from laryngeal dysplasia to invasive carcinoma.
METHODS:
We investigated the expression of the inducible NO synthase (iNOS) in 26 laryngeal precancerous lesions and 35 squamous cell carcinomas with respect to microvessel density. In addition, we determined iNOS activity and cGMP levels in specimens from SCCs.
RESULTS:
There was a significant increase of iNOS levels detected immunohistochemically passing from hyperplastic/mild dysplastic to moderate/severe dysplastic lesions to SCC (p =.04). Accordingly, Northern and Western analyses demonstrated higher iNOS mRNA and protein levels in SCCs than dysplastic mucosa. iNOS expression was significantly correlated with microvessel counts both in the group of preneoplastic lesions (p =.02) and in the group of SCCs (p =.01). In addition, iNOS activity was correlated with iNOS immunohistochemical expression (p =.1) and was significantly associated with increased vascularization (p =.03) in SCCs. Similarly, iNOS expression was significantly correlated with cGMP levels in SCC (p =.02) and increased tumor vascularization correlated with higher cGMP levels (rs =.4; p =.01).
CONCLUSIONS:
Our data indicate that the NO pathway may play a relevant role in the angiogenesis associated with the progression from laryngeal dysplasia to laryngeal SCC
Innovating cultural heritage museum service model through virtual reality and augmented reality: The effects on the overall visitor experience and satisfaction
No full textInducible nitric oxide synthase expression in benign and malignat cutaneous melanocytic lesions
No full textJ Pathol. 2001 Jun;194(2):194-200.
Inducible nitric oxide synthase expression in benign and malignant cutaneous melanocytic lesions.
Massi D, Franchi A, Sardi I, Magnelli L, Paglierani M, Borgognoni L, Maria Reali U, Santucci M.
Source
Dipartimento di Patologia Umana ed Oncologia, Università degli Studi di Firenze, Firenze, Italy.
Abstract
Nitric oxide (NO) is synthesized by nitric oxide synthases (NOS) and plays an important role in tumour growth. In this study, inducible NOS (iNOS) expression was evaluated by immunohistochemistry in 34 melanocytic naevi (13 common melanocytic naevi, six Spitz naevi, and 15 so-called 'dysplastic naevi'), ten cutaneous melanomas in situ, 50 stage I invasive melanomas, and eight subcutaneous metastases of melanoma. In addition, four samples of melanocytic naevi and four samples of invasive melanomas were collected in order to perform western blot and northern blot analysis. By immunohistochemistry, melanocytic naevi never expressed iNOS. Among cases of melanoma in situ, two were negative, seven displayed staining in less than 20% of melanoma cells, and positivity was observed in 21-50% of melanoma cells in only one case. iNOS expression was detected in 46 out of 50 invasive melanomas (92%). Among these cases, 18 showed positivity in less than 20% of melanoma cells, 18 showed positivity in 21-50% of melanoma cells, and ten showed iNOS expression in more than 50% of cells. Statistical analysis revealed a significant difference in iNOS expression between melanocytic naevi and cutaneous melanomas (p<0.001). In addition, iNOS expression was significantly higher in invasive melanomas than in melanomas in situ (p=0.01). Among primary cutaneous melanomas, no significant correlation was found between iNOS expression and histopathological parameters (histotype, level, thickness and presence of regression/inflammatory infiltrate) and disease-specific survival. In subcutaneous melanoma metastases, iNOS expression was diffuse in more than 50% of cells. Statistical analysis revealed that subcutaneous melanoma metastases showed greater iNOS immunoreactivity than invasive melanomas (p=0.02). Molecular analyses confirmed that iNOS mRNA and protein were highly expressed in melanoma samples. In conclusion, iNOS was constantly absent in melanocytic naevi, whereas it was frequently expressed in melanomas, with up-regulation of the enzyme paralleling tumour progression. These data suggest that iNOS may play a role in the malignant transformation of melanocytes and in tumour growth. In addition, iNOS may be useful as an immunohistochemical marker for malignant melanocytic lesions.
Copyright 2001 John Wiley & Sons, Ltd.
PMID: 11400148 [PubMed - indexed for MEDLINE
Augmented and virtual reality in cultural heritage: enhancing the visitor experience and satisfaction at the ARA Pacis museum in Rome (Best Paper Award)
No full textCorrelation between nitric oxide synthase and cyclooxygenase-2 pathways in head and neck squamous cell carcinoma
No full textWe investigated the interactions between inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) pathways in head and neck squamous cell carcinomas (HNSCCs) and in two carcinoma cell lines. HNSCCs showed an up-regulation of both pathways which were strongly correlated with each other (p=0.02) and with tumor vascularization (p=0.0001 and p=0.008, respectively). In carcinoma cells, Escherichia coli lipopolysaccharide (LPS) and EGF treatment up-regulated both pathways. NOS inhibitor N(G)-monomethyl-L-arginine methyl ester (L-NAME) inhibited this up-regulation. LPS or EGF induced iNOS expression that was not altered by NOS or COX-2 inhibitors. Conversely, LPS or EGF promoted COX-2 expression that was decreased by L-NAME. The NO donor S-nitroso-acetyl-penicillamine (SNAP) up-regulated COX-2 pathway and this effect was reduced by the guanylate cyclase inhibitor methylene blue. Thus, in squamous carcinoma cells, NO increases the activity of COX-2 pathway and this effect is probably mediated by endocellular cGMP level, with potential implications on tumor growth, angiogenesis, and therapy
Down-regulation of nitric oxide synthase-2 and cyclooxygenase-2 pathways by p53 in squamous cell carcinoma
No full textThe goal of this study was to analyze the correlation between inducible nitric oxide synthase (iNOS) and COX-2 activities and p53 gene status in head and neck squamous cell carcinomas (HNSCCs) in vivo and in vitro. In a series of 43 HNSCCs we observed an up-regulation of both iNOS and COX-2 pathways in tumor tissues and both activities were correlated each other (rs = 0.612 and P = 0.0002). We also found that p53-mutated HNSCCs (25 cases, 58.1%) showed higher levels of iNOS activity and cGMP in comparison with wild-type p53 tumors (18 cases, 41.9%) (P = 0.0005 and P = 0.01), as well as higher iNOS immunohistochemical expression (P = 0.03). Analogously, higher PgE2 levels were documented in p53-mutated HNSCCs when compared with wild-type p53 tumors (P = 0.015) and COX-2 protein expression was higher in p53-mutated HNSCCs (P = 0.007). A431 cancer cells expressing a p53 temperature-sensitive mutant showed an 1.9- and 2.6-fold decrease in spontaneous NO2-/NO3- and PgE2 synthesis at permissive temperature, respectively, when compared with the same cells at nonpermissive temperature (P 0.001). Basal levels of iNOS and COX-2 proteins and mRNAs were markedly suppressed by restoration of p53 activity. Our results indicate that p53 gene mutation(s) may be responsible for iNOS and COX-2 up-regulation frequently observed in HNSCCs and suggest that restoration of wild-type p53 expression may interfere with tumor growth by inhibiting iNOS and COX-2 pathways
Non solo Prisco di Panion: Fritz Bornmann, la storiografia tardoantica e le raccolte bizantine
No full textL’articolo sviluppa il contributo della giornata di studi in memoria di Fritz Bornmann a venti anni dalla sua morte (Università di Firenze, 2017). Vi si riprendono e valorizzano i risultati dell’edizione di Prisco di Panion che Fritz Bornmann pubblicò nel 1979, per poi ripercorrere i passi e le metodologie che hanno portato l’autrice alla nuova edizione critica nel 2008. Infine si evidenziano le piste di ricerca aperte da Bornmann riguardo ai cosiddetti Excerpta Historica Constantiniana, che godono di un rinnovato interesse presso gli studiosi contemporanei (si vedano i contributi di Andras Neméth, Paolo Odorico, Dariya Rafiyenko, Emerance Delacenserie, Peter van Nuffelen, Paul Magdalino, Anthony Kaldellis, Francesco Monticini, Lorenzo Maria Ciolfi e molti altri).At the University of Florence in 2017 was held a memorial workshop for Fritz Bornmann, after 20 years since his death. The present article sheds light onto the critical edition with Italian translation of the Byzantine historian Priscus of Panion, which Fritz Bornmann published in 1979. Priscus wrote in 5th century AD and his fragmentary work is preserved mostly in the Byzantine collection of the so-called Excerpta Historica Constantiniana. After Bornmann’s edition, research was developed by the author up to the new critical edition in 2008 for the Bibliotheca Teubneriana. Bornmann had long indicated the need of such a publication, along with the methodology to achieve new results. His contribution from the 1970s deserves to be widely known to the scholarly community interested in the revival about the Excerpta Historica Constantiniana: Andras Neméth, Paolo Odorico, Dariya Rafiyenko, Emerance Delacenserie, Peter van Nuffelen, Paul Magdalino, Anthony Kaldellis, Francesco Monticini, Lorenzo Maria Ciolfi and many others)
Cyclooxygenase-2 Pathway Correlates with VEGF Expression in Head and Neck Cancer. Implications for Tumor Angiogenesis and Metastasis
No full textAbstractWe evaluated the role of COX-2 pathway in 35 head and neck cancers (HNCs) by analyzing COX-2 expression and prostaglandin E2 (PGE2) production in relation to tumor angiogenesis and lymph node metastasis. COX-2 activity was also correlated to vascular endothelial growth factor (VEGF) mRNA and protein expression. COX-2 mRNA and protein expression was higher in tumor samples than in normal mucosa. PGE2 levels were higher in the tumor front zone in comparison with tumor core and normal mucosa (P<0001). Specimens from patients with lymph node metastasis exhibited higher COX-2 protein expression (P=.0074), PGEZ levels (P=.0011) and microvessel density (P<.0001) than specimens from patients without metastasis. A significant correlation between COX-2 and tumor vascularization (rs=0.450, P=.007) as well as between COX-2 and microvessel density with VEGF expression in tumor tissues was found (rs=0.450, P=.007; rs=0.620, P=.0001, respectively). The induction of COX-2 mRNA and PGE2 synthesis by EGF and Escherichia coli lipopolysaccharide (LPS) in A-431 and SCC-9 cell lines, resulted in an increase in VEGF mRNA and protein production. Indomethacin and celecoxib reversed the EGF- and LPS-dependent COX-2, VEGF, and PGE2 increases. This study suggests a central role of COX-2 pathway in HNC angiogenesis by modulating VEGF production and indicates that COX-2 inhibitors may be useful in HNC treatment
Bigger than Expected: IRES-Dependent mRNA Translation Initiation Enlarges the Eukaryotic Proteome
No full textInteraction of urokinase with specific receptors stimulates mobilization of bovine adrenal capillary endothelial cells
No full textOn the basis of 125I-labeled plasminogen activator binding analysis we have found that bovine adrenal capillary endothelial cells have specific receptors for human urinary-type plasminogen activator on the cell membrane. Each cell exposes about 37,000 free receptors with a Kd of 0.8958 x 10(-9) M [corrected]. A monoclonal antibody against the 17,500 proteolytic fragment of the A chain of the plasminogen activator, not containing the catalytic site of the enzyme, impaired the specific binding, thus suggesting the involvement of a sequence present on the A chain in the interaction with the receptor, as previously shown in other cell model systems. Both the native molecule and the A chain are able to stimulate endothelial cell motility in the Boyden chamber, when used at nanomolar concentrations. The use of the same monoclonal antibody that can inhibit ligand-receptor interaction can impair the plasminogen activator and A-chain-induced endothelial cell motility, suggesting that under the conditions used in this in vitro model system, the motility of bovine adrenal capillary endothelial cells depends on the specific interaction of the ligand with free receptors on the surface of endothelial cells
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