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Western corn rootworm (WCR), or Diabrotica virgifera virgifera LeConte, became a very serious quarantine maize pest in Europe in the mid-1990s. Between 1995 and 2010, European countries were involved in international projects to share information and plan common research for integrated pest management (IPM) implementation. Since 2011, however, common efforts have declined, and an overview of WCR population spread, density, and research is in serious need of update. Therefore, we retained that it was necessary to (1) summarize the research activities carried out in the last 12 years in various countries and the research topics addressed, and analyze how these activities have contributed to IPM for WCR and (2) present the current distribution of WCR in the EU and analyze the current population levels in different European countries, focusing on different management strategies. A review of scientific papers published from 2008 to 2020, in addition to direct interviews with experts in charge of WCR management in a range of European countries, was conducted. Over the past 12 years, scientists in Europe have continued their research activities to investigate various aspects of WCR management by implementing several approaches to WCR control. A considerable amount of new knowledge has been produced, contributing to the development of pest management strategies applicable in EU farming systems. Among the 10 EU countries analyzed, there is no country reporting economic damage on a large scale. Thanks to intensive research leading to specific agricultural practices and the EU Common Agricultural Policy, there are crop-rotation-based solutions that can adequately control this pest avoiding insecticide use.

Lamin A, a main constituent of the nuclear lamina, is involved in mechanosignaling and cell migration through dynamic interactions with the LINC complex, formed by the nuclear envelope proteins SUN1, SUN2 and the nesprins. Here, we investigated lamin A role in Ewing Sarcoma (EWS), an aggressive bone tumor affecting children and young adults. In patients affected by EWS, we found a significant inverse correlation between LMNA gene expression and tumor aggressiveness. Accordingly, in experimental in vitro models, low lamin A expression correlated with enhanced cell migration and invasiveness and, in vivo, with an increased metastatic load. At the molecular level, this condition was linked to altered expression and anchorage of nuclear envelope proteins and increased nuclear retention of YAP/TAZ, a mechanosignaling effector. Conversely, overexpression of lamin A rescued LINC complex organization, thus reducing YAP/TAZ nuclear recruitment and preventing cell invasiveness. These effects were also obtained through modulation of lamin A maturation by a statin-based pharmacological treatment that further elicited a more differentiated phenotype in EWS cells. These results demonstrate that drugs inducing nuclear envelope remodeling could be exploited to improve therapeutic strategies for EWS.

Intensive agricultural practices are leading to loss of soil fertility and overexploitation of natural resources which cause nutrients imbalance and further impair ecosystem services. Organic farming (OF), also coupled with minimum tillage and crop rotations, represents one of the strategies to limit this process and maintain soil functions. In a two-year field trial, organic farming practices, including a set of fertilizations combined with crop rotations and association with nitrogen fixing cover crops, were compared. The aim of this research was to assess in the short-term the effects on soil organic carbon, aggregate stability, and soil enzymes activities of using a combination of promising management practices in the delta region of the Po river. Results did not show improvements in organic carbon content and soil aggregate stability. Conversely, enzymatic activities were always significantly higher in OF treatments than the conventional one. Crop rotation and associated legumes were effective in enhancing β-glucosidase and P fixation through phosphatases activities. The present work suggests that an effective choice of crop species coupled with legumes can enhance biological activity re-starting main mechanisms of microbial development even without a contemporary increase of organic matter.

Conservation Agriculture includes practices focused on the conservation and the restoration of main soil features, such as organic carbon content, structure, and biological diversity and activity. Our study was conducted in three farms in North-Eastern Italy in pairs of closely located fields to compare conservation agriculture (no tillage, cover cropping) with conventional agriculture. Differences in terms of soil enzymatic activity, such as FDA and β-glucosidase through spectrophotometric analyses, microbial biomass carbon and nitrogen contents, total organic carbon, and nitrogen contents with CNS Elemental Analyzer and soil arthropod community via the QBS-ar index were investigated. Enzymatic activities resulted to be readily and positively affected by conservation agriculture whereas total and microbial carbon, nitrogen contents, and microarthropod community seemed to be more dependent on the time factor. The responses to conservation agriculture differed between the three farms, pointing out that differences in soil features may drive the effectiveness of conservation management. N stock, maybe dependent on previous soil management, might be the key characteristic able to influence soil evolution in the studied conditions. The present results could be helpful to predict soil reaction to sustainable agriculture in short periods.

Background Although in recent years, the introduction of novel chemotherapy protocols has improved the outcome of T cell acute lymphoblastic leukemia (T-ALL) patients, refractory and/or relapsing disease remains a foremost concern. In this context, a major contribution was provided by the introduction of the nucleoside analog nelarabine, approved for salvage treatment of T-ALL patients with refractory/relapsed disease. However, nelarabine could induce a life-threatening, dose-dependent neurotoxicity. To improve nelarabine efficacy, we have analyzed its molecular targets, testing selective inhibitors of such targets in combination with nelarabine. Methods The effectiveness of nelarabine as single agent or in combination with PI3K, Bcl2, and MEK inhibitors was evaluated on human T-ALL cell lines and primary T-ALL refractory/relapsed lymphoblasts. The efficacy of signal modulators in terms of cytotoxicity, induction of apoptosis, and changes in gene and protein expression was assessed by flow cytometry, western blotting, and quantitative real-time PCR in T-ALL settings. Results Treatment with nelarabine as a single agent identified two groups of T-ALL cell lines, one sensitive and one resistant to the drug. Whereas sensitive T-ALL cells showed a significant increase of apoptosis and a strong down-modulation of PI3K signaling, resistant T-ALL cells showed a hyperactivation of AKT and MEK/ERK1/2 signaling pathways, not caused by differences in the expression of nelarabine transporters or metabolic activators. We then studied the combination of nelarabine with the PI3K inhibitors (both pan and dual γ/δ inhibitors), with the Bcl2 specific inhibitor ABT199, and with the MEK inhibitor trametinib on both T-ALL cell lines and patient samples at relapse, which displayed constitutive activation of PI3K signaling and resistance to nelarabine alone. The combination with the pan PI3K inhibitor ZSTK-474 was the most effective in inhibiting the growth of T-ALL cells and was synergistic in decreasing cell survival and inducing apoptosis in nelarabine-resistant T-ALL cells. The drug combination caused AKT dephosphorylation and a downregulation of Bcl2, while nelarabine alone induced an increase in p-AKT and Bcl2 signaling in the resistant T-ALL cells and relapsed patient samples. Conclusions These findings indicate that nelarabine in combination with PI3K inhibitors may be a promising therapeutic strategy for the treatment of T-ALL relapsed patients.

The identification of factors related to performance that can be improved during training is of primary interest for athletes. However, little is known about this issue among artistic gymnasts. The current pilot study aims to assess the association between training factors and anthropometric, body composition, and muscle strength (MS) variables in adolescent female artistic gymnastics. A total of 22 young female artistic gymnasts taking part in a professional team, who had a median age of 12.21 years and a median body mass index (BMI) of 18.72 kg/m2, were categorized into a competitive-level (8.00–17.00 h [h]/week) group (n = 16) and a pre-team-level (<4 h/week) one (n = 6). The training factors considered were (i) training hours per session, (ii) training hours per week, and (iii) training years. All the participants underwent complete anthropometric measurements, including body composition assessments by means of bioelectrical impedance vector analysis (BIVA), and an objective physical activity evaluation with a portable accelerometer SenseWear Armband (SWA). MS was assessed using a handgrip dynamometer. The correlation and partial correlation were evaluated to test the associations between variables. The competitive-level group had higher fat-free mass (FFM), body cell mass (BCM), and MS compared to the pre-team group. However, after adjusting for confounders, only the number of training hours per session was associated with MS (ρ = 0.445, p < 0.05) and BCM (ρ = 0.475, p < 0.05). In conclusion MS and BCM but not FFM are correlated with the number of training hours per session. Future studies are needed to test the effects of specific programs based on this training parameter on these variables, to determine whether they can impact athletic performance in young female artistic gymnasts.

Glycogen synthase kinase-3 (GSK-3) is an evolutionarily conserved, ubiquitously expressed, multifunctional serine/threonine protein kinase involved in the regulation of a variety of physiological processes. GSK-3 comprises two isoforms (α and β) which were originally discovered in 1980 as enzymes involved in glucose metabolism via inhibitory phosphorylation of glycogen synthase. Differently from other proteins kinases, GSK-3 isoforms are constitutively active in resting cells, and their modulation mainly involves inhibition through upstream regulatory networks. In the early 1990s, GSK-3 isoforms were implicated as key players in cancer cell pathobiology. Active GSK-3 facilitates the destruction of multiple oncogenic proteins which include β-catenin and Master regulator of cell cycle entry and proliferative metabolism (c-Myc). Therefore, GSK-3 was initially considered to be a tumor suppressor. Consistently, GSK-3 is often inactivated in cancer cells through dysregulated upstream signaling pathways. However, over the past 10–15 years, a growing number of studies highlighted that in some cancer settings GSK-3 isoforms inhibit tumor suppressing pathways and therefore act as tumor promoters. In this article, we will discuss the multiple and often enigmatic roles played by GSK-3 isoforms in some chronic hematological malignancies (chronic myelogenous leukemia, chronic lymphocytic leukemia, multiple myeloma, and B-cell non-Hodgkin’s lymphomas) which are among the most common blood cancer cell types. We will also summarize possible novel strategies targeting GSK-3 for innovative therapies of these disorders.

The discovery of the expression of opioid receptors in the skin and their role in orchestrating the process of tissue repair gave rise to questions regarding the potential effects of clinical morphine treatment in wound healing. Although short term treatment was reported to improve tissue regeneration, in vivo chronic administration was associated to an impairment of the physiological healing process and systemic fibrosis. Human mesenchymal stem cells (hMSCs) play a fundamental role in tissue regeneration. In this regard, acute morphine exposition was recently reported to impact negatively on the functional characteristics of hMSCs, but little is currently known about its long-term effects. To determine how a prolonged treatment could impair their functional characteristics, we exposed hMSCs to increasing morphine concentrations respectively for nine and eighteen days, evaluating in particular the fibrogenic potential exerted by the long-term exposition. Our results showed a time dependent cell viability decline, and conditions compatible with a cellular senescent state. Ultrastructural and protein expression analysis were indicative of increased autophagy, suggesting a relation to a detoxification activity. In addition, the enhanced transcription observed for the genes involved in the synthesis and regulation of type I collagen suggested the possibility that a prolonged morphine treatment might exert its fibrotic potential risk, even involving the hMSCs.

Lipid signaling pathways are involved in cell growth, differentiation, and apoptosis, and could have a role in the progression of myelodysplastic syndromes (MDS) into acute myeloid leukemia (AML). Indeed, recent studies showed that phosphoinositide-phospholipase (PI-PL)Cbeta1 mono-allelic deletion correlates with a higher risk of AML evolution. Also, a single patient treated with azacitidine, a DNA methyltransferase inhibitor currently used in MDS, displayed a direct correlation between PI-PLCbeta1 gene expression and drug responsiveness. Consequently, we hypothesized that PI-PLCbeta1 could be a target for demethylating therapy. First, we analyzed the structure of PI-PLCbeta1 gene promoter, then quantified the degree of PI-PLCbeta1 promoter methylation and gene expression in MDS patients at baseline and during azacitidine administration. Indeed, PI-PLCbeta1 mRNA increased in responder patients, along with a reduction of PI-PLCbeta1 promoter methylation. Also, the molecular response correlated to and anticipated the clinical outcome, thus suggesting that PI-PLCbeta1 gene reactivation could predict azacitidine responsiveness. Our results demonstrate not only that PI-PLCbeta1 promoter is hypermethylated in high-risk MDS patients, but also that the amount of PI-PLCbeta1 mRNA could predict the clinical response to azacitidine, therefore indicating a promising new therapeutic approach.

This study presents new data on biogenic and terrigenous particle fluxes collected by an oceanographic mooring (Mooring A) deployed in the south-western Ross Sea (Antarctica) in the frame of the Italian Long-Term Ecological Research network (LTER-Italy). Results from the years 2005 and 2008 document high mass fluxes during the summer and early autumn seasons, not coincident with the algal bloom. Downward particle fluxes exhibit a high inter-annual variability of both particulate fluxes and composition that seem related to the different factors as the phytoplankton increases, occurring between the beginning of February and the end of March, to the variations in the sea ice extent and to the resuspension and/or lateral advection processes. The flux variability may have been influenced by Iceberg B-15 that resided in the investigated area between 2000 and 2005. The decoupling of biogenic silica and organic carbon cycles is documented by differences in the rates of their respective key processes: biogenic silica dissolution and organic carbon degradation.