Publications by authors named "Valeria Cavaliere"

Contrast associated acute kidney injury (CA-AKI) is a major complication of contrast media (CM) exposure following percutaneous coronary intervention (PCI), associated with high rates of morbidity and mortality in both early and late phases. During the past years, several CA-AKI prevention strategies based on CM sparing have been proposed, which differ significantly in terms of methodological features and efficacy. In this review, we propose a new classification of these techniques based on their dependency on operators' management.

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Article Synopsis
  • The study investigates the effectiveness of using a combination of urine flow rate-guided hydration (RenalGuard) and a device to reduce contrast media (DyeVert) to prevent contrast-associated acute kidney injury (CA-AKI) in patients undergoing coronary procedures.
  • A total of 55 high-risk patients were included; those using both RenalGuard and DyeVert had a lower contrast media dose and experienced significantly fewer cases of CA-AKI (9.1%) compared to those who only had RenalGuard (25.4%).
  • The findings suggest that combining device-based contrast reduction with hydration is more effective in preventing CA-AKI than relying solely on operator-driven methods with the same hydration strategy.*
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Article Synopsis
  • - The study aimed to determine the most effective intravenous volume expansion method to prevent contrast-associated acute kidney injury (CA-AKI) in patients with chronic kidney disease (CKD) undergoing cardiovascular procedures.
  • - Analyzed data from 1927 CKD patients revealed that CA-AKI occurred in 11% of cases, with those affected receiving less volume expansion and experiencing higher rates of acute pulmonary edema.
  • - Findings suggest that to prevent CA-AKI, an absolute volume expansion of at least 1430 mL and a volume-to-contrast media ratio of 17 or greater should be considered, warranting further testing in future trials.
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Biogenic amines are crucial signaling molecules that modulate various physiological life functions both in vertebrates and invertebrates. In humans, these neurotransmitters influence the innate and adaptive immunity systems. In this work, we analyzed whether the aminergic neurotransmission of dopamine, serotonin, and octopamine could have an impact on the humoral innate immune response of .

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Acetylcholine (ACh) is one the major neurotransmitters in insects, whose role in mediating synaptic interactions between neurons in the central nervous system is well characterized. It also plays largely unexplored regulatory functions in non-neuronal tissues. Here we demonstrate that ACh signaling is involved in the modulation of the innate immune response of Drosophila melanogaster.

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The transposon theory of aging hypothesizes the activation of transposable elements (TEs) in somatic tissues with age, leading to a shortening of the lifespan. It is thought that TE activation in aging produces an increase in DNA double-strand breaks, contributing to genome instability and promoting the activation of inflammatory responses. To investigate how TE regulation changes in somatic tissues during aging, we analyzed the expression of some TEs, as well as a source of small RNAs that specifically silence the analyzed TEs; the cluster named .

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Awd, the homologue of metastasis suppressors, plays key roles in many signaling pathways. Mosaic analysis of the null allele showed that loss of gene function blocks Notch signaling and the expression of its target genes including the Wingless (Wg/Wnt1) morphogen. We also showed that RNA interference (RNAi)-mediated silencing () in larval wing disc leads to chromosomal instability (CIN) and to Jun amino-terminal kinases (JNK)-mediated cell death.

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Transposable elements (TEs) are mobile genomic sequences that are normally repressed to avoid proliferation and genome instability. Gene silencing mechanisms repress TEs by RNA degradation or heterochromatin formation. Heterochromatin maintenance is therefore important to keep TEs silent.

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Eukaryotic genomes contain a large number of transposable elements, part of which are still active and able to transpose in the host genome. Mobile element activation is repressed to avoid deleterious effects, such as gene mutations or chromosome rearrangements. Control of transposable elements includes a variety of mechanisms comprising silencing pathways, which are based on the production of small non-coding RNAs.

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The () gene is the homolog of human and metastasis suppressor genes. These genes play a key role in tumor progression. Extensive studies revealed that intracellular NME1/2 protein levels could be related to either favorable or poor prognosis depending on tissue context.

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Polydnaviruses (PDV) are viral symbionts associated with ichneumonid and braconid wasps parasitizing moth larvae, which are able to disrupt the host immune response and development, as well as a number of other physiological pathways. The immunosuppressive role of PDV has been more intensely investigated, while very little is known about the PDV-encoded factors disrupting host development. Here we address this research issue by further expanding the functional analysis of ankyrin genes encoded by the bracovirus associated with Toxoneuron nigriceps (Hymenoptera, Braconidae).

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The abnormal wing discs (awd) gene encodes the Drosophila homolog of NME1/NME2 metastasis suppressor genes. Awd acts in multiple tissues where its function is critical in establishing and maintaining epithelial integrity. Here, we analysed awd gene function in Drosophila epithelial cells using transgene-mediated RNA interference and genetic mosaic analysis.

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The Nm23/NME gene family has been under intensive study since Nm23H1/NME1 was identified as the first metastasis suppressor. Inverse correlation between the expression levels of NME1/2 and prognosis has indeed been demonstrated in different tumor cohorts. Interestingly, the presence of NME proteins in the extracellular environment in normal and tumoral conditions has also been noted.

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Dynamin GTPase (Dyn) plays a critical role in membrane-remodelling events underlying endocytosis. Studies in Drosophila identified a functional interaction between the Dyn homologue, encoded by the shibire (shi) gene, and Abnormal wing discs (Awd), a nucleoside diphosphate kinase (NDPK) that is the homologue of group I Nme human genes. These Drosophila studies showed that awd mutations enhance mutant shi phenotype and thus indicated the existence of a highly specific interaction between these genes.

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Maternal expression of the translational regulator 4EHP (eIF4E-Homologous Protein) has an established role in generating protein gradients essential for specifying the Drosophila embryonic pattern. We generated a null mutation of 4EHP, which revealed for the first time that it is essential for viability and for completion of development. In fact, 4EHP null larvae, and larvae ubiquitously expressing RNAi targeting 4EHP, are developmentally delayed, fail to grow and eventually die.

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Epithelial morphogenesis contributes greatly to the development and homeostasis of the organs and body parts. Here, we analysed the consequences of impaired ecdysone receptor (EcR) signalling in the Drosophila follicular epithelium. Besides governing cell growth, the three EcR isoforms act redundantly in controlling follicle cell positioning.

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Polydnaviruses are obligate symbionts integrated as proviruses in the genome of some ichneumonoid wasps that parasitize lepidopteran larvae. Polydnavirus free viral particles, which are injected into the host at oviposition, express virulence factors that impair immunity and development. To date, most studies have focused on the molecular mechanisms underpinning immunosuppression, whereas how viral genes disrupt the endocrine balance remains largely uninvestigated.

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Background: The Drosophila abnormal wing discs (awd) belongs to a highly conserved family of genes implicated in metastasis suppression, metabolic homeostasis and epithelial morphogenesis. The cellular function of the mammalian members of this family, the Nm23 proteins, has not yet been clearly defined. Previous awd genetic analyses unraveled its endocytic role that is required for proper internalization of receptors controlling different signaling pathways.

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Large-scale losses of honey bee colonies represent a poorly understood problem of global importance. Both biotic and abiotic factors are involved in this phenomenon that is often associated with high loads of parasites and pathogens. A stronger impact of pathogens in honey bees exposed to neonicotinoid insecticides has been reported, but the causal link between insecticide exposure and the possible immune alteration of honey bees remains elusive.

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Mutations in the human von Hippel-Lindau (VHL) genes are the cause of VHL disease, which displays multiple benign and malignant tumors. The VHL gene has been shown to regulate angiogenic potential and glycolic metabolism via its E3 ubiquitin ligase function against the alpha subunit of hypoxia-inducible factor (HIF). However, many other HIF-independent functions of VHL have been identified and recent evidence indicates that the canonical function cannot fully explain the VHL mutant cell phenotypes.

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SCO proteins are copper-donor chaperones involved in the assembly of mitochondrial cytochrome c oxidase (COX). Mutations in the two human SCO-encoding genes, SCO1 and SCO2, produce tissue-specific COX deficiencies associated with distinct clinical phenotypes. Here, we report the identification and characterization of scox, the single Drosophila melanogaster SCO-encoding gene.

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Polydnavirus-encoded IkappaB-like proteins are similar to insect and mammalian IkappaB, and an immunosuppressive function in the host cells has been inferred to these proteins. Here we show that the expression of one of these IkappaB-like viral genes, the TnBVank1, in the Drosophila germline affects the localization of gurken, bicoid, and oskar mRNAs whose gene products are relevant for proper embryonic patterning. The altered localization of these mRNAs is suggestive of general defects in the intracellular, microtubule-based, trafficking routes.

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The vasa gene, first identified in Drosophila, is a key determinant for germline formation in eukaryotes. Homologs of vasa have been identified and linked to germline development, in many invertebrates and vertebrates. Here, we analyze the distribution of Vasa in early germ cells (oogonia and oocytes) and previtellogenic ovarian follicles of the lizard Podarcis sicula.

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