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961.
Targeted therapy of human glioblastoma via delivery of a toxin through a peptide directed to cell surface nucleolin
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Anne‐Chloé Dhez Elisabetta Benedetti Andrea Antonosante Gloria Panella Brigida Ranieri Tiziana M. Florio Loredana Cristiano Francesco Angelucci Francesco Giansanti Luana Di Leandro Michele d'Angelo Marina Melone Antonella De Cola Luca Federici Renato Galzio Ilaria Cascone Fabio Raineri Annamaria Cimini José Courty Antonio Giordano Rodolfo Ippoliti 《Journal of cellular physiology》2018,233(5):4091-4105
962.
Daniela Ghisi Alessandro Ricci Sandra Giannone Tiziana Greggi Stefano Bonarelli 《Scoliosis》2018,13(1):24
Background
Acute pancreatitis has been described as potential complication of both abdominal and non-abdominal surgeries. The pathogenetic mechanism underlying acute pancreatitis in spine surgery may include intraoperative hemodynamic instability causing prolonged splanchnic hypoperfusion, as well as mechanical compression of the pancreas due to scoliosis correction, with a higher risk in cases of more extended fusions, especially in young adults with lower body mass index (BMI).Case presentation
We report here a case of postoperative acute pancreatitis with benign evolution in a young female patient after the first and second surgery of a two-stage correction of right thoracic idiopathic scoliosis.In December 2017, the patient underwent first-stage T4-L3 posterior arthrodesis with T7-T12 osteotomies and temporary magnetic bar. Intraoperative blood loss required massive transfusion. In the immediate postoperative period, the patient started reporting nausea/vomiting, abdominal pain at pressure, moderate meteorism, abdominal distension, hypoactive bowel sounds, and fever. Laboratory tests indicated a progressive increase in aspartate aminotransferase, alanine aminotransferase, serum amylase, lipase, phospho-creatine kinase, and reactive C-protein. A CT scan showed free abundant abdominal fluid in the hepatic, renal, pancreatic, and pelvic regions. After the diagnosis, a hypolipidic diet was initiated, and good hydration per os was maintained. After gastroenterologic consultation, somatostatin, rifaximin, and ursodehoxycholic acid were initiated and maintained for 8 days. In the following days, laboratory tests showed a slow but consistent decrease in liver and pancreatic enzymes until normalization. In January 2018, the patient underwent second-stage surgery with removal of magnetic bar, definitive posterior fusion, and instrumentation T4-L3. Laboratory tests showed a second, even more significant, increase in the amylase and lipase level and a moderate increase in the reactive C-protein. Therapy was maintained until complete normalization of amylase and lipase levels.Conclusions
Early recognition of symptoms plays a key role in preventing severe morbidity after scoliosis surgery. When symptoms suggest abdominal complication, pancreatic and liver enzymes are to be evaluated for posing prompt diagnosis. Gastroenterologic consultation and eventual imaging are further steps in differential diagnosis and treatment of this rare complication.963.
Maria Pergola Amalia Gialdini Giuseppe Celano Marina Basile Donatella Caniani Mario Cozzi Tiziana Gentilesca Ignazio M. Mancini Vittoria Pastore Severino Romano Gennaro Ventura Francesco Ripullone 《The International Journal of Life Cycle Assessment》2018,23(8):1675-1684
Purpose
Wood pellet heating systems are considered as an essential component of European plans to reduce greenhouse gas (GHG) emissions. The goal of this analysis was to estimate and compare the environmental impacts and the costs of the production of packed wood pellets. Two pellet production systems, using roundwood logs (case 1) and mainly sawdust (case 2), have been analysed in 2015 in Basilicata region (Southern Italy).Methods
A life cycle assessment (LCA) analysis was applied to calculate the environmental impact indicators of each system, whilst a life cycle cost (LCC) analysis was implemented to evaluate the pellets’ cost production. Hence, the functional unit chosen was 1 t of produced pellets. The system boundaries considered for the purpose of the current investigation were from the tree felling to the pellet packaging. In particular, the following activities were considered: motor-manual felling and delimbing with a chainsaw, timber yarding with a tractor along the forest track, loading and transportation of the logs to the collection point, transportation of timber to the factories for a distance of 35 km, pellet production and pellet packaging in low-density polyethylene bags with a total weight of 15 kg bag?1.Results and discussion
The production of 1 t of pellets emitted about 83 kg of CO2eq in case 1 and 38 kg in case 2. In addition, 2.7 kg of SO2eq and 0.005 kg of PO3 4-eq were produced in case 1 and 1.4 kg of SO2eq and 0.002 kg of PO3 4-eq in case 2. Mineral extraction was equal to 0.9 MJ surplus energy in both cases. Case 1 led to higher environmental impacts (about 50% more), essentially for the operation of pelletisation, and in particular for the higher consumption of electricity that characterised it, whereas the production costs were 172 and 113 € t?1 in case 1 and case 2, respectively. In both study cases, consumption costs (costs for raw material, electricity consumption, fuel usage) were the most important cost items.Conclusions
Our studies highlight how, in both cases, the operations carried out in the forest produced the minor part of the environmental impact but, at the same time, were the most expensive operations. Further, our studies show how mixing lumbering by-products (sawdust) and forest management products (lumbers) can be an efficient solution to reduce both manufacturing costs and environmental impacts to produce wood pellets.964.
Deficiency in the nuclear long noncoding RNA Charme causes myogenic defects and heart remodeling in mice 总被引:1,自引:0,他引:1
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965.
Maria Teresa Sciortino Tiziana Parisi Gabriel Siracusano Antonio Mastino Brunella Taddeo Bernard Roizman 《Journal of virology》2013,87(6):3271-3276
Earlier studies have shown that active MEK blocks the activation of protein kinase R (PKR), a component of antiviral innate immune responses. In this report we show that the herpes simplex virus 1 virion host shutoff (VHS) RNase protein and MEK (mitogen-activated protein kinase kinase) act cooperatively in blocking the activation of PKR. This conclusion is based on the following. (i) In contrast to viral gene expression in the parental cell line or a cell line expressing a constitutively active MEK, the replication of a VHS mutant is particularly impaired in cells expressing dominant negative MEK. In this cell line PKR is activated by phosphorylation, and the accumulation of several viral proteins is delayed. (ii) In transfected cells, wild-type VHS blocked the activation of PKR, whereas PKR was activated in cells transfected with a mutant VHS or with plasmids encoding the VHS RNase and VP16 and VP22, the two viral proteins that neutralize the RNase activity of VHS. The results suggest that early in infection the VHS RNase degrades RNAs that activate PKR. Coupled with published data, the results suggest that inhibition of activation of PKR or its effect on viral replication is staged early in infection by VHS, postsynthesis of VP16 and VP22 by the γ134.5 protein, and very late in infection by the US11 protein. 相似文献
966.
Tiziana DeAngelis Andrew Quong Andrea Morrione Renato Baserga 《Journal of cellular physiology》2013,228(7):1482-1486
The v‐src oncogene is one of only two oncogenes capable of transforming mouse embryo fibroblasts (MEFs) lacking the IGF‐IR gene (R‐cells). R‐/v‐src cells grow robustly in the absence of serum, suggesting the hypothesis that they may produce one or more growth factors that would sustain their ability to proliferate in serum‐free condition. Using proteomic approaches on serum‐free conditioned media derived from v‐src‐transformed cells, we have identified two growth promoting factors: ostepontin and proliferin. Subsequent experiments have indicated that osteopontin plays a prevalent role in promoting growth of v‐src‐transformed cells in serum‐deprived condition. J. Cell. Physiol. 228: 1482–1486, 2013. © 2012 Wiley Periodicals, Inc. 相似文献
967.
Angelika Falsone Veronica Wabitsch Elena Geretti Heide Potzinger Tanja Gerlza James Robinson Tiziana Adage Mauro?M. Teixeira Andreas?J. Kungl 《Bioscience reports》2013,33(5)
IL (interleukin)-8 [CXCL8 (CXC chemokine ligand 8)] exerts its role in inflammation by triggering neutrophils via its specific GPCRs (G-protein-coupled receptors), CXCR1 (CXC chemokine receptor 1) and CXCR2, for which additional binding to endothelial HS-GAGs (heparan sulphate-glycosaminoglycans) is required. We present here a novel approach for blocking the CXCL8-related inflammatory cascade by generating dominant-negative CXCL8 mutants with improved GAG-binding affinity and knocked-out CXCR1/CXCR2 activity. These non-signalling CXCL8 decoy proteins are able to displace WT (wild-type) CXCL8 and to prevent CXCR1/CXCR2 signalling thereby interfering with the inflammatory response. We have designed 14 CXCL8 mutants that we subdivided into three classes according to number and site of mutations. The decoys were characterized by IFTs (isothermal fluorescence titrations) and SPR (surface plasmon resonance) to determine GAG affinity. Protein stability and structural changes were evaluated by far-UV CD spectroscopy and knocked-out GPCR response was shown by Boyden chamber and Ca2+ release assays. From these experiments, CXCL8(Δ6F17KF21KE70KN71K) emerged with the most promising in vitro characteristics. This mutant was therefore further investigated in a murine model of mBSA (methylated BSA)-induced arthritis in mice where it showed strong anti-inflammatory activity. Based on these results, we propose that dominant-negative CXCL8 decoy proteins are a promising class of novel biopharmaceuticals with high therapeutic potential in inflammatory diseases. 相似文献
968.
Daria Sanna Piero Cossu Gian Luca Dedola Fabio Scarpa Ferruccio Maltagliati Alberto Castelli Piero Franzoi Tiziana Lai Benedetto Cristo Marco Curini-Galletti Paolo Francalacci Marco Casu 《PloS one》2013,8(6)
Pinna nobilis is the largest endemic Mediterranean marine bivalve. During past centuries, various human activities have promoted the regression of its populations. As a consequence of stringent standards of protection, demographic expansions are currently reported in many sites. The aim of this study was to provide the first large broad-scale insight into the genetic variability of P. nobilis in the area that encompasses the western Mediterranean, Ionian Sea, and Adriatic Sea marine ecoregions. To accomplish this objective twenty-five populations from this area were surveyed using two mitochondrial DNA markers (COI and 16S). Our dataset was then merged with those obtained in other studies for the Aegean and Tunisian populations (eastern Mediterranean), and statistical analyses (Bayesian model-based clustering, median-joining network, AMOVA, mismatch distribution, Tajima’s and Fu’s neutrality tests and Bayesian skyline plots) were performed. The results revealed genetic divergence among three distinguishable areas: (1) western Mediterranean and Ionian Sea; (2) Adriatic Sea; and (3) Aegean Sea and Tunisian coastal areas. From a conservational point of view, populations from the three genetically divergent groups found may be considered as different management units. 相似文献
969.
Luigi Laviola Maura Roberta Orlando Maria Angela Incalza Cristina Caccioppoli Mariangela Melchiorre Anna Leonardini Angelo Cignarelli Federica Tortosa Rossella Labarbuta Sabina Martemucci Consiglia Pacelli Tiziana Cocco Sebastio Perrini Annalisa Natalicchio Francesco Giorgino 《PloS one》2013,8(12)
Endothelial cells participate in inflammatory events leading to atherogenesis by regulating endothelial cell permeability via the expression of VE-Cadherin and β-catenin and leukocyte recruitment via the expression of E-Selectins and other adhesion molecules. The protein p66Shc acts as a sensor/inducer of oxidative stress and may promote vascular dysfunction. The objective of this study was to investigate the role of p66Shc in tumor necrosis factor TNFα-induced E-Selectin expression and function in human umbilical vein endothelial cells (HUVEC). Exposure of HUVEC to 50 ng/ml TNFα resulted in increased leukocyte transmigration through the endothelial monolayer and E-Selectin expression, in association with augmented phosphorylation of both p66Shc on Ser36 and the stress kinase c-Jun NH2-terminal protein kinase (JNK)-1/2, and higher intracellular reactive oxygen species (ROS) levels. Overexpression of p66Shc in HUVEC resulted in enhanced p66Shc phosphorylation on Ser36, increased ROS and E-Selectin levels, and amplified endothelial cell permeability and leukocyte transmigration through the HUVEC monolayer. Conversely, overexpression of a phosphorylation-defective p66Shc protein, in which Ser36 was replaced by Ala, did not augment ROS and E-Selectin levels, nor modify cell permeability or leukocyte transmigration beyond those found in wild-type cells. Moreover, siRNA-mediated silencing of p66Shc resulted in marked reduction of E-Selectin expression and leukocyte transmigration. In conclusion, p66Shc acts as a novel intermediate in the TNFα pathway mediating endothelial dysfunction, and its action requires JNK-dependent phosphorylation of p66Shc on Ser36. 相似文献
970.
The concept of “prion-like” has been proposed to explain the pathogenic mechanism of the principal neurodegenerative disorders associated with protein misfolding, including Alzheimer disease (AD). Other evidence relates prion protein with AD: the cellular prion protein (PrPC) binds β amyloid oligomers, allegedly responsible for the neurodegeneration in AD, mediating their toxic effects. We and others have confirmed the high-affinity binding between β amyloid oligomers and PrPC, but we were not able to assess the functional consequences of this interaction using behavioral investigations and in vitro tests. This discrepancy rather than being resolved with the classic explanations, differencies in methodological aspects, has been reinforced by new data from different sources. Here we present data obtained with PrP antibody that not interfere with the neurotoxic activity of β amyloid oligomers. Since the potential role of the PrPC in the neuronal dysfunction induced by β amyloid oligomers is an important issue, find reasonable explanation of the inconsistent results is needed. Even more important however is the relevance of this interaction in the context of the disease, so as to develop valid therapeutic strategies. 相似文献