Sustainable development and european banks: A non-financial disclosure analysis

none4noThis paper aims at contributing to the debate on the relationships between the European financial sector and sustainable development. Using a non-financial disclosure analysis of 262 European banks, the research sought, first, to investigate the "scope" of the contribution of European banks to the Sustainable Development Goals (SDGs) and, second, to explore the factors that seem to differentiate the SDGs approach among banks. The results show that country of origin, legal system, and adoption of an integrated report seem to differentiate banks in terms of contribution to the SDGs. The business model and stock exchange listing, conversely, do not seem to represent discriminatory factor in the contribution of banks toward the SDGs. The study can be useful for managers and decision makers to develop policies to support organizations in contributing to the SDGs.openCosma S.; Venturelli A.; Schwizer P.; Boscia V.Cosma, S.; Venturelli, A.; Schwizer, P.; Boscia, V

Identification of the agent of grapevine fleck disease

An antiserum against an Italian isolate of grapevine phloem-limited isometric virus (GPLIV) was used in an ELISA survey carried out for assessing the natural distribution of the virus and its association with fleck disease. A total of 591 vines of Vitis rupestris were checked for the presence of GPLIV. Of 150 plants with fleck symptoms, 138 (92 %) were ELISA-positive and 12 (8 %) negative. Of 441 symptomless V. rupestris, 435 (98,6 %) were ELISA-negative and 6 (1,4 %) positive for GPLIV. The virus was detected in about 30 % of 694 vines of different origin grown in Apulia (Southern Italy). The highest infection (53 %) was in a commercial vineyard of cv. Italia and the lowest (8 %) in a plot of certified and visually selected rootstocks. Fleck-infected, but not fleck-free V. rupestris contained virus particles and vesiculated inclusion bodies in phloem tissues. LN 33 plantlets derived from in vitro culture of meristem tips from ELISA-positive fleck-infected mother plants were found to be free from GPLIV, as ascertained by ELISA and thin-sectioning. These vines failed to induce fleck symptoms when grafted on V. rupestris. It is concluded that GPLIV is the agent of fleck and, therefore, it should be renamed grapevine fleck virus (GFKV)

Pseudococcus affinis MASK., new vector of grapevine trichoviruses A and B

Research Note Grapevine trichovirus A (GVA) and grapevine trichovirus B (GVB) were successfully transferred with bulk transmission trials under controlled conditions, from infected grapevines to herbaceous hosts by Pseudococcus affinis MASK., a pseudococcid mealybug that may attack grapevines. P. affinis is the fourth mealybug species capable of vectoring GVA and GVB, confirming that transmission by mealybugs of grapevine trichoviruses may not be species-specific

A non-mechanically transmissible isometric virus associated with asteroid mosaic of the grapevine

Research Not

First Report of 'Candidatus Phytoplasma phoenicium' on Almond in Southern Italy

In spring 2017, phytoplasma suspected symptoms were reported on 25% of 15-year-old almond plants, cultivars Filippo Ceo and Genco grafted onto GF677, in a commercial orchard (20 ha) located at Grottaglie, Apulia (southeast Italy). Among the symptoms, development of many axillary buds with small and yellowish leaves, and witches' brooms developing from the trunk, were the most frequent, followed by leaf rosetting, proliferation of slender shoots, tree decline, and dieback

Studies on ''corky rugose wood'' of grapevine and on the diagnosis of grapevine virus B

Vines affected by corky rugose wood (CRW), a field syndrome characterized by pronounced cork production by the scion of several grapevine varieties just above the graft union, contain a number of filamentous and isometric phloem-limited viruses, such as grapevine leafroll-associated virus 1, 2, and 3 (GLRaV-1, GLRaV-2, GLRaV-3), grapevine virus A and B (GVA and GVB), and grapevine fleck virus (GFkV). However, the same viruses, with the exception of GVB, are widely represented also in vines with rugose wood without excessive corkyness. Although GVB was found in all vines indexing positive in LN 33 for corky bark disease, iis occurrence in CRW-affected vines was not consistent enough to suggest that it may have a determining role in the induction of this syndrome. Monoclonal antibodies to GVB raised previously were characterized and their possible use for reliable detection of GVB in field-grown vines investigated in detail. A triple antibody sandwich ELISA protocol that under our experimental conditions afforded consistent and repeatable results, was based on the use of crude cortical scraping extracts from mature canes collected in autumn, antibodies from a polyclonal antiserum for plate coating (trapping) and a monoclonal antibody for antigen detection

The Na+/Ca2+ Exchanger 3 Is Functionally Coupled With the NaV1.6 Voltage-Gated Channel and Promotes an Endoplasmic Reticulum Ca2+ Refilling in a Transgenic Model of Alzheimer’s Disease

The remodelling of neuronal ionic homeostasis by altered channels and transporters is a critical feature of the Alzheimer’s disease (AD) pathogenesis. Different reports converge on the concept that the Na+/Ca2+ exchanger (NCX), as one of the main regulators of Na+ and Ca2+ concentrations and signalling, could exert a neuroprotective role in AD. The activity of NCX has been found to be increased in AD brains, where it seemed to correlate with an increased neuronal survival. Moreover, the enhancement of the NCX3 currents (INCX) in primary neurons treated with the neurotoxic amyloid β 1–42 (Aβ1–42) oligomers prevented the endoplasmic reticulum (ER) stress and neuronal death. The present study has been designed to investigate any possible modulation of the INCX, the functional interaction between NCX and the NaV1.6 channel, and their impact on the Ca2+ homeostasis in a transgenic in vitro model of AD, the primary hippocampal neurons from the Tg2576 mouse, which overproduce the Aβ1–42 peptide. Electrophysiological studies, carried in the presence of siRNA and the isoform-selective NCX inhibitor KB-R7943, showed that the activity of a specific NCX isoform, NCX3, was upregulated in its reverse, Ca2+ influx mode of operation in the Tg2576 neurons. The enhanced NCX activity contributed, in turn, to increase the ER Ca2+ content, without affecting the cytosolic Ca2+ concentrations of the Tg2576 neurons. Interestingly, our experiments have also uncovered a functional coupling between NCX3 and the voltage-gated NaV1.6 channels. In particular, the increased NaV1.6 currents appeared to be responsible for the upregulation of the reverse mode of NCX3, since both TTX and the Streptomyces griseolus antibiotic anisomycin, by reducing the NaV1.6 currents, counteracted the increase of the INCX in the Tg2576 neurons. In agreement, our immunofluorescence analyses revealed that the NCX3/NaV1.6 co-expression was increased in the Tg2576 hippocampal neurons in comparison with the WT neurons. Collectively, these findings indicate that NCX3 might intervene in the Ca2+ remodelling occurring in the Tg2576 primary neurons thus emerging as a molecular target with a neuroprotective potential, and provide a new outcome of the NaV1.6 upregulation related to the modulation of the intracellular Ca2+ concentrations in AD neurons

Na+/Ca2+ exchanger isoform 1 takes part to the Ca2+-related prosurvival pathway of SOD1 in primary motor neurons exposed to beta-methylamino-l-alanine

Background: The cycad neurotoxin beta-methylamino-l-alanine (L-BMAA), one of the environmental trigger factor for amyotrophic lateral sclerosis/Parkinson-dementia complex (ALS/PDC), may cause neurodegeneration by disrupting organellar Ca2+ homeostasis. Through the activation of Akt/ERK1/2 pathway, the Cu,Zn-superoxide dismutase (SOD1) and its non-metallated form, ApoSOD1, prevent endoplasmic reticulum (ER) stress-induced cell death in motor neurons exposed to L-BMAA. This occurs through the rapid increase of intracellular Ca2+ concentration ([Ca2+]i) in part flowing from the extracellular compartment and in part released from ER. However, the molecular components of this mechanism remain uncharacterized. Methods: By an integrated approach consisting on the use of siRNA strategy, Western blotting, confocal double- labeling immunofluorescence, patch-clamp electrophysiology, and Fura 2-/SBFI-single-cell imaging, we explored in rat motor neuron-enriched cultures the involvement of the plasma membrane proteins Na+/Ca2+ exchanger (NCX) and purinergic P2X7 receptor as well as that of the intracellular cADP-ribose (cADPR) pathway, in the neuroprotective mechanism of SOD1. Results: We showed that SOD1-induced [Ca2+]i rise was prevented neither by A430879, a P2X7 receptor specific antagonist or 8-bromo-cADPR, a cell permeant antagonist of cADP-ribose, but only by the pan inhibitor of NCX, CB-DMB. The same occurred for the ApoSOD1. Confocal double labeling immunofluorescence showed a huge expression of plasmalemmal NCX1 and intracellular NCX3 isoforms. Furthermore, we identified NCX1 reverse mode as the main mechanism responsible for the neuroprotective ER Ca2+ refilling elicited by SOD1 and ApoSOD1 through which they promoted translocation of active Akt in the nuclei of a subset of primary motor neurons. Finally, the activation of NCX1 by the specific agonist CN-PYB2 protected motor neurons from L-BMAA-induced cell death, mimicking the effect of SOD1. Conclusion: Collectively, our data indicate that SOD1 and ApoSOD1 exert their neuroprotective effect by modulating ER Ca2+ content through the activation of NCX1 reverse mode and Akt nuclear translocation in a subset of primary motor neurons. [MediaObject not available: see fulltext.

Occurrence of grapevine virus A (GVA) and other closteroviruses in Tunisian grapevines affected by leafroll disease

Vorkommen von Grapevine-Virus A (GVA) und anderen Closteroviren in blattrollkranken tunesischen RebenReben, die aus den Hauptweinbaugebieten Tunesiens stammten, wurden auf die Anwesenheit von Closteroviren hin überprüft. Während in keiner der symptomfreien Reben Viruspartikel entdeckt wurden, enthielten alle Reben mit Blattrollsymptomen - außer zweien - Closteroviruspartikel, die durch IEM (immune electron microscopy) in konzentrierten Blattextrakten oder unmittelbar in Rohsaft durch ISEM (immunosorbent electron microscopy) identifiziert wurden. Alle vier derzeit bekannten Closteroviren (GClV-1, GClV-2, GClV-3 und GVA) waren, meistens im Gemisch, in Reben mit Blattrollsymptomen vorhanden. GClV-3 und GVA wurden in 77 bzw. 50 % der geprüften Reben entdeckt. Ein tunesisches Isolat von GVA, das durch Planococcus citri auf krautige Testpflanzen übertragen wurde, unterschied sich in biologischer Hinsicht, aber nicht in den charakteristischen physikalisch-chemischen und serologischen Eigenschaften von zwei italienischen Isolaten desselben Virus

Rebound effects of NCX3 pharmacological inhibition: A novel strategy to accelerate myelin formation in oligodendrocytes

The Na+/Ca2+ exchanger NCX3 is an important regulator of sodium and calcium homeostasis in oligodendrocyte lineage. To date, no information is available on the effects resulting from prolonged exposure to NCX3 blockers and subsequent drug washout in oligodendroglia. Here, we investigated, by means of biochemical, morphological and functional analyses, the pharmacological effects of the NCX3 inhibitor, the 5–amino-N-butyl-2–(4–ethoxyphenoxy)-benzamide hydrochloride (BED), on NCXs expression and activity, as well as intracellular [Na+]i and [Ca2+]i levels, during treatment and following drug washout both in human MO3.13 oligodendrocytes and rat primary oligodendrocyte precursor cells (OPCs). BED exposure antagonized NCX activity, induced OPCs proliferation and [Na+]i accumulation. By contrast, 2 days of BED washout after 4 days of treatment significantly upregulated low molecular weight NCX3 proteins, reversed NCX activity, and increased intracellular [Ca2+]i. This BED-free effect was accompanied by an upregulation of NCX3 expression in oligodendrocyte processes and accelerated expression of myelin markers in rat primary oligodendrocytes. Collectively, our findings show that the pharmacological inhibition of the NCX3 exchanger with BED blocker maybe followed by a rebound increase in NCX3 expression and reversal activity that accelerate myelin sheet formation in oligodendrocytes. In addition, they indicate that a particular attention should be paid to the use of NCX inhibitors for possible rebound effects, and suggest that further studies will be necessary to investigate whether selective pharmacological modulation of NCX3 exchanger may be exploited to benefit demyelination and remyelination in demyelinating diseases