University of Naples Federico II

About: University of Naples Federico II is a education organization based out in Naples, Campania, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 29291 authors who have published 68803 publications receiving 1920149 citations. The organization is also known as: Università degli Studi di Napoli Federico II & Naples University.

Broad-spectrum bioactivities of silver nanoparticles: the emerging trends and future prospects

Abstract: There are alarming reports of growing microbial resistance to all classes of antimicrobial agents used against different infections. Also the existing classes of anticancer drugs used against different tumours warrant the urgent search for more effective alternative agents for treatment. Broad-spectrum bioactivities of silver nanoparticles indicate their potential to solve many microbial resistance problems up to a certain extent. The antibacterial, antifungal, antiviral, antiprotozoal, acaricidal, larvicidal, lousicidal and anticancer activities of silver nanoparticles have recently attracted the attention of scientists all over the world. The aim of the present review is to discuss broad-spectrum multifunctional activities of silver nanoparticles and stress their therapeutic potential as smart nanomedicine. Much emphasis has been dedicated to the antimicrobial and anticancer potential of silver nanoparticles showing their promising characteristics for treatment, prophylaxis and control of infections, as well as for diagnosis and treatment of different cancer types.

Enoxaparin versus unfractionated heparin in elective percutaneous coronary intervention.

Abstract: Enoxaparin at a dose of 0.5 mg per kilogram was associated with a significant reduction in the rate of non–CABG-related bleeding in the first 48 hours, as compared with unfractionated heparin (5.9% vs. 8.5%; absolute difference, –2.6; 95% confidence interval [CI], –4.7 to –0.6; P = 0.01), but the higher enoxaparin dose was not (6.5% vs. 8.5%; absolute difference, –2.0; 95% CI, –4.0 to 0.0; P = 0.051). The incidence of major bleeding was significantly reduced in both enoxaparin groups, as compared with the unfractionated heparin group. Target anticoagulation levels were reached in significantly more patients who received enoxaparin (0.5-mg-per-kilogram dose, 79%; 0.75-mgper-kilogram dose, 92%) than who received unfractionated heparin (20%, P<0.001). Conclusions In elective PCI, a single intravenous bolus of 0.5 mg of enoxaparin per kilogram is associated with reduced rates of bleeding, and a dose of 0.75 mg per kilogram yields rates similar to those for unfractionated heparin, with more predictable anticoagulation levels. The trial was not large enough to provide a definitive comparison of efficacy in the prevention of ischemic events. (ClinicalTrials.gov number, NCT00077844.)

Antitumor Activity of Sequential Treatment with Topotecan and Anti-Epidermal Growth Factor Receptor Monoclonal Antibody C225

Abstract: Epidermal growth factor (EGF)-related proteins such as transforming growth factor α (TGF-α) control cancer cell growth through autocrine and paracrine pathways. Overexpression of TGF-α and/or its receptor (EGFR) has been associated with a more aggressive disease and a poor prognosis. The blockade of EGFR activation has been proposed as a target for anticancer therapy. Monoclonal antibody (MAb) C225 is an anti-EGFR humanized chimeric mouse MAb that is presently in Phase II clinical trials in cancer patients. Previous studies have suggested the potentiation of the antitumor activity of certain cytotoxic drugs, such as cisplatin and doxorubicin, in human cancer cell lines by treatment with anti-EGFR antibodies. We have evaluated in human ovarian, breast, and colon cancer cell lines, which express functional EGFR, the antiproliferative activity of MAb C225 in combination with topotecan, a cytotoxic drug that specifically inhibits topoisomerase I and that has shown antitumor activity in these malignancies. A dose-dependent supraadditive increase of growth inhibition in vitro was observed when cancer cells were treated with topotecan and MAb C225 in a sequential schedule. In this respect, the cooperativity quotient, defined as the ratio between the actual growth inhibition obtained by treatment with topotecan followed by MAb C225 and the sum of the growth inhibition achieved by each agent, ranged from 1.2 to 3, depending on drug concentration and cancer cell line. Treatment with MAb C225 also markedly enhanced apoptotic cell death induced by topotecan. For example, in GEO colon cancer cells, 5 nm topotecan, followed by 0.5 μg/ml MAb C225, induced apoptosis in 45% cells as compared with untreated cells (6%) or to 5 nm topotecan-treated cells (22%). Treatment of mice bearing established human GEO colon cancer xenografts with topotecan or with MAb C225 determined a transient inhibition of tumor growth because GEO tumors resumed the growth rate of untreated tumors at the end of the treatment period. In contrast, an almost complete tumor regression was observed in all mice treated with the two agents in combination. This determined a prolonged life span of the mice that was significantly different as compared with controls ( P P P

Reelin gene alleles and haplotypes as a factor predisposing to autistic disorder

Abstract: Autistic disorder (MIM 209850) is currently viewed as a neurodevelopmental disease. Reelin plays a pivotal role in the development of laminar structures including the cerebral cortex, hippocampus, cerebellum and of several brainstem nuclei. Neuroanatomical evidence is consistent with Reelin involvement in autistic disorder. In this study, we describe several polymorphisms identified using RNA-SSCP and DNA sequencing. Association and linkage were assessed comparing 95 Italian patients to 186 ethnically-matched controls, and using the transmission/disequilibrium test and haplotype-based haplotype relative risk in 172 complete trios from 165 families collected in Italy and in the USA. Both case-control and family-based analyses yield a significant association between autistic disorder and a polymorphic GGC repeat located immediately 5' of the reelin gene (RELN) ATG initiator codon, as well as with specific haplotypes formed by this polymorphism with two single-base substitutions located in a splice junction in exon 6 and within exon 50. Triplet repeats located in 5' untranslated regions (5'UTRs) are indicative of strong transcriptional regulation. Our findings suggest that longer triplet repeats in the 5'UTR of the RELN gene confer vulnerability to autistic disorder.