Hymenoptera venom allergy is an epidemiologically underestimated condition representing an important cause of morbidity worldwide. Preventing future allergic reactions in patients who have developed a systemic reaction is based on the correct management of emergency followed by a correct diagnosis, prescription of adrenaline autoinjectors and, where indicated, specific venom immunotherapy (VIT). Some epidemiological studies highlight the poor knowledge of this disease and the frequent inadequacy of its management. Moreover, they emphasize the importance of such a life-saving treatment as specific immunotherapy. The availability of high quality Hymenoptera venom extracts for diagnostic and therapeutic use has dramatically improved the prognosis and the quality of life of allergic patients. The subcutaneous VIT represents the most effective form of immunotherapy with allergen presently available, with a carry-over effect lasting up to several years after its interruption. This report on the management of children and adults allergic to Hymenoptera venom was drawn up by a panel of Italian experts. The main objective of this consensus is to review the scientific evidences related to diagnosis, therapy and management of patients allergic to Hymenoptera venom and is aimed to improve the knowledge about this disease and promote good clinical practices. Practical suggestions for a correct diagnosis, prescription of emergency therapy and immunotherapy, as well as strategies for taking care of patients´ management are included.

Omalizumab is a humanized murine monoclonal antibody directed toward a portion of the IgE indicated in Europe for the treatment of severe persistent allergic asthma, inadequately controlled despite high-dose of ICS (mean BDP equivalent dose of inhaled corticosteroid 2224.68microg/die) in association with long-acting beta(2) agonists. Our aim was to describe the experience, efficacy and safety in a cohort of Italian patients treated with omalizumab in a real-life clinical setting. One hundred and forty two patients from 13 Italian Centers were observed and analysed. The dosage of omalizumab was established according to the labelling indication, with a median dose of IgE of 297.38IU/ml or kU/l. During the previous year, all patients experienced frequent exacerbations (mean=4.87), emergency visits (mean=4.45) and hospitalisation (mean=1.53). Following treatment with omalizumab, the annual rate of exacerbations, emergency visits and hospitalisation decreased by 79%, 88% and 95%, respectively. The proportion of patients without exacerbation, not needing emergency visits and hospitalization increased by 610%, 154% and 28%, respectively. The response to omalizumab measured with the GETE (global evaluation of treatment effectiveness) scale rated as good to excellent in 77% of patients. Overall, 9.6% (n=9) of the patients experienced one single adverse effect. Only one patient reported a serious adverse event (local reaction at the site of injection) leading to interruption of treatment. The observed reduction of asthma-related events in particularly poorly controlled patients in this Italian real-life setting is consistent with the results of other observational studies.

Fusarium subglutinans is an important pathogen of maize and other commodities worldwide. We examined MRC-115 and 71 other F. subglutinans strains from various geographic areas for their ability to synthesize fusaproliferin, a novel toxic sesterterpene recently isolated from F. proliferatum. Fusaproliferin production ranged from 30 to 1,500 g/g of dried ground substrate, with 33 strains producing more than 500 g/g. In particular, strain MRC-115 produced as much as 1,100 to 1,300 g/g. In toxicity studies of two invertebrate models, fusaproliferin was toxic to Artemia salina (50% lethal dose, 53.4 M) and to the lepidopteran cell line SF-9 (50% cytotoxic concentration, approximately 70 M, after a 48-h exposure). Fusaproliferin was also toxic to the human nonneoplastic B-lymphocyte cell line IARC/LCL 171 (50% cytotoxic concentration, approximately 55 M in culture in stationary phase after a 48-h exposure). Experiments performed with cells exposed at seeding suggested a possible cytostatic effect at subtoxic concentrations.

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Cyclooxygenase (COX), the key enzyme in prostaglandin cascade, is expressed in two isoforms: the constitutive COX-! and the inducible COX-2. Hyper-expression of COX-2 has been implicated in the pathogenesis of colon-rectal cancer in humans but it appears to play a significant role as a tumour progression factor also in other forms of human cancer, including oral cancer. The aim of this study was to analyze the expression of COX-2, at the protein level, in 45 cases of oral squamous cell carcinoma. Standard immunohistochemical streptavidin-biotin peroxidase analysis was carried out with a highly specific antibody against human COX-2 and cell specific markers, in 45 oral squamous cell carcinomas. Our study revealed a moderate to high COX-2 expression in 35 out of the 45 oral squamous cell carcinoma specimens (77.8 %). COX-2 expression appeared particularly abundant in the superficial ulcerated layers of relatively well differentiated carcinomas. However, we were unable to assess any statistically significant association between COX-2 hyper-expression and tumor site, tumor grading, tumor size, presence oflymph node metastases, tumor stage and age at onset, respectively. Interestingly, COX-2 expression was detected not only in areas of epithelial dysplasia adjacent to the primary layers (86 % of the cases) but also in normalappearing epithelium at the boundaries of squamous cell carcinomas (77% ), indicating a possible involvement in tumour progression by the apparently normal tissue surrounding the lesion. Moreover, intense COX-2 staining was observed in endothelial cells of intra-tumour vessels and extra-tumour vessels adjacent to the tumour nests, in a high proportion of cases (82 %). COX-2 positivity was associated with CD34 and VEGF positivity, indicating that these vessels were probably neo-formed. From this study, as well as from other works, it appears that COX-2 is over-expressed in this important human malignancy. However, further studies are necessary to understand the exact magnitude of this overexpression and, mostly, the possible role of COX-2 in the pathogenesis and progression of oral cancer.Several lines of evidence suggest that prostanoids may be involved in the pathobiology of human oral carcinogenesis (1-3). The enzyme cyclooxygenase (COX) catalyzes the first two steps of a cascade of biochemical reactions, leading to prostaglandin formation from arachidonic acid. COX is the rate-limiting enzyme in prostaglandin biosynthesis and is expressed in a constitutive (COX-I) and in an inducible (COX-2) isoform (4). Enhanced biosynthesis of prostaglandins, as a