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Xylella fastidiosa subsp. pauca is associated with the olive quick decline syndrome in Salento (Apulia region, Southern Italy). The first outbreak of the disease was noticed in the Gallipoli district, from where it subsequently reached nearby areas. To date, no specific study has verified if abnormal soil or leaf micronutrients is associated with the disease. Soil and leaf samples were taken from 23 olive farms showing symptoms of the syndrome located in Gallipoli and nearby areas. Each sample was analyzed for magnesium and micronutrients content using inductively coupled plasma atomic emission spectroscopy. Real-time PCR indicated that X. f. subsp. pauca was present in each sampled tree. There is a general lack of molybdenum in soil and low bioavailability of copper and molybdenum in tree leaves. Low content of manganese in soil was also found in some farms located in Gallipoli, Galatone and Trepuzzi. Olive trees grown in Gallipoli area also had low content of boron. Principal component analysis showed that soil and leaf samples from this area had lower micronutrient contents compared with other areas. General copper depletion in leaves was uncommon and has not been previously recorded in Italy in a large area. This could indicate that X. f. subsp. pauca infection causes a depletion of copper within olive leaves. Reduced copper content has been previously recorded in leaves infected with X. f. subsp. multiplex and for other bacterial pathogens. The role of copper in relation to X. fastidiosa infection is discussed.

In agreement with all authors of this paper the order of the authors and the contribution “Paola Lunetti[+], Alessandro Romano[+], Chiara Carrisi, Daniela Antonucci, Tiziano Verri, Giuseppe E. De Benedetto, Vincenza Dolce, Francesco P. Fanizzi, Michele Benedetti,* and Loredana Capobianco.* [+] These authors contributed equally to this paper. * Corresponding authors: Michele Benedetti and Loredana Capobianco, Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce.” is corrected to read the original order of the first submitted version of the paper: “Chiara Carrisi[+], Alessandro Romano[+], Paola Lunetti, Daniela Antonucci, Tiziano Verri, Giuseppe E. De Benedetto, Vincenza Dolce, Francesco P. Fanizzi, Michele Benedetti,* and Loredana Capobianco.* [+] These authors contributed equally to this paper. * Corresponding authors: Loredana Capobianco and Michele Benedetti, Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce.” For completeness the following individual contributions of the authors were added in the Supporting Information: “Author contributions: L.C., M.B., C.C., A.R. designed research; C.C., A.R., P.L. and D.A. performed research; L.C., M.B., C.C., A.R., V.D. and P.L. analysed data; F.P.F., A.R., L.C. and M.B. wrote the paper; L.C., M.B., T.V., G.D.B. and F.P.F. active discussion paper revision.”.

BACKGROUND AND PURPOSE It is thought that the mechanism of action of anticancer chemotherapeutic agents is mainly due to a direct inhibition of tumour cell proliferation. In tumour specimens, the endothelial cell proliferation rate increases, suggesting that the therapeutic effects of anticancer agents could also be attributed to inhibition of tumour angiogenesis. Hence, we investigated the potential effects of [Pt (O,O′-acac)(γ-acac)(DMS)] ([Pt(DMS)]), a new platinum drug for non-genomic targets, on human renal carcinoma and compared them with those of the well-established anticancer drug, cisplatin. EXPERIMENTAL APPROACH Tumour growth, tumour cell proliferation and microvessel density were investigated in a xenograft model of renal cell carcinoma, developed by injecting Caki-1 cells into BALB/c nude mice. The antiangiogenic potential of compounds was also investigated using HUVECs. KEY RESULTS Treatment of the Caki-1 cells with cisplatin or [Pt(DMS)] resulted in a dose-dependent inhibition of cell survival, but the cytotoxicity of [Pt(DMS)] was approximately fivefold greater than that of cisplatin. [Pt(DMS)] was much more effective than cisplatin at inhibiting tumour growth, proliferation and angiogenesis in vivo, as well as migration, tube formation and MMP1, MMP2 and MMP9 secretion of endothelial cells in vitro. Whereas, cisplatin exerted a greater cytotoxic effect on HUVECs, but did not affect tube formation or the migration of endothelial cells. In addition, treatment of the xenograft mice with [Pt(DMS)] decreased VEGF, MMP1 and MMP2 expressions in tumours. CONCLUSIONS AND IMPLICATIONS The antiangiogenic and antitumour activities of [Pt(DMS)] provide a solid starting point for its validation as a suitable candidate for further pharmacological testing.

Comparative studies on the effects of the platinum complexes in use or in clinical trials are carried out in order to discover differences in the neurotoxic potential and the reversibility of neurotoxicity. In this paper, we summarized the current literature on neurotoxicity and chemoresistance of cisplatin (cisPt) and discussed our recent efforts on the interference of cisPt and a new platinum compound [Pt(O,O′-acac)(γ-acac)(DMS)] (PtAcacDMS), with high specific reactivity with sulphur ligands instead of nucleobases as cisPt, on some crucial events of rat postnatal cerebellum development. The acute effects of drug treatments on cell proliferation and death in the external granular layer and granule cell migration and the late effects on the dendrite growth of Purkinje cells were evaluated. Together with the demonstrated antineoplastic effectiveness in vitro, compared with cisPt, data suggest a lower neurotoxicity of PtAcacDMS, in spite of its presence in the brain that involves considerations on the blood brain barrier permeability.