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71.
The paper is about some families of rewriting P systems, where the application of evolution rules is extended from the classical
sequential rewriting to the parallel one (as, for instance, in Lindenmayer systems). As a result, consistency problems for
the communication of strings may arise. Three variants of parallel rewriting P systems (already present in the literature)
are considered here, together with the strategies they use to face the communication problem, and some parallelism methods
for string rewriting are defined. We give a survey of all known results about each variant and we state some relations among
the three variants, thus establishing hierarchies of parallel rewriting P systems. Various open problems related to the subject
are also presented.
Danicla Besozzi: She is assistant professor at the University of Milano. She received her M.S. in Mathematics (2000) from the University
of Como and Ph.D. in Computer Science (2004) from the University of Milano. Her research interests cover topics in Formal
Language Theory, Molecular Computing, Systems Biology. She is member of EATCS (European Association for Theoretical Computer
Science) and EMCC (European Molecular Computing Consortium).
Giancarlo Mauri: He is full professor of Computer Science at the University of Milano-Bicocca. His research interests are mainly in the area
of theoretical computer science, and include: formal languages and automata, computational complexity, computational learning
theory, soft computing techniques, cellular automata, bioinformatics and molecular computing. On these subjects, he published
more than 150 scientific papers in international journals, contributed volumes and conference proceedings.
Claudio Zandron: He received Ph.D. in Computer Science at the University of Milan, Italy, in 2001. Since 2002 he is assistant professor at
the University of Milano-Bicocca, Italy. He is member of the EATCS (European Association for Theoretical Computer Science)
and of EMCC (European Molecular Computing Consortium). His research interests are Molecular Computing (DNA and Membrane Computing)
and Formal Languages. 相似文献
72.
Claudio Bonivento Author Vitae Author Vitae Lorenzo Marconi Author Vitae Andrea Paoli Author Vitae 《Automatica》2004,40(3):355-371
In this paper we propose an innovative way of dealing with the design of fault-tolerant control systems. We show how the nonlinear output regulation theory can be successfully adopted in order to design a regulator able to offset the effect of all possible faults which can occur and, in doing so, also to detect and isolate the occurred fault. The regulator is designed by embedding the (possible nonlinear) internal model of the fault. This idea is applied to the design of a fault-tolerant controller for induction motors in presence of both rotor and stator mechanical faults. 相似文献
73.
Teodolinda Di Risi Mariella Cuomo Roberta Vinciguerra Sara Ferraro Rosa Della Monica Davide Costabile Michela Buonaiuto Federica Trio Ettore Capoluongo Roberta Visconti Eleonora Riccio Antonio Pisani Lorenzo Chiariotti 《International journal of molecular sciences》2022,23(20)
Anderson–Fabry disease (FD) is an X-linked disease caused by a functional deficit of the α-galactosidase A enzyme. FD diagnosis relies on the clinical manifestations and research of GLA gene mutations. However, because of the lack of a clear genotype/phenotype correlation, FD diagnosis can be challenging. Recently, several studies have highlighted the importance of investigating DNA methylation patterns for confirming the correct diagnosis of different rare Mendelian diseases, but to date, no such studies have been reported for FD. Thus, in the present investigation, we analyzed for the first time the genome-wide methylation profile of a well-characterized cohort of patients with Fabry disease. We profiled the methylation status of about 850,000 CpG sites in 5 FD patients, all carrying the same mutation in the GLA gene (exon 6 c.901C>G) and presenting comparable low levels of α-Gal A activity. We found that, although the whole methylome profile did not discriminate the FD group from the unaffected one, several genes were significantly differentially methylated in Fabry patients. Thus, we provide here a proof of concept, to be tested in patients with different mutations and in a larger cohort, that the methylation state of specific genes can potentially identify Fabry patients and possibly predict organ involvement and disease evolution. 相似文献
74.
Maria Infantino Aris Tsalouchos Edda Russo Selene Laudicina Valentina Grossi Barbara Lari Maurizio Benucci Lorenzo Stacchini Amedeo Amedei Patrizia Casprini Danilo Villalta Pietro Claudio Dattolo Mariangela Manfredi 《International journal of molecular sciences》2022,23(20)
The vulnerable population of kidney transplant recipients (KTRs) are low responders to COVID-19 vaccines, so specific immune surveillance is needed. The interferon-gamma (IFN-γ) release assay (IGRA) is effective in assessing T cell-mediated immunity. We assessed SARS-CoV-2-directed T cell responses in KTRs with absent antibody production after a third dose of the mRNA-1273 vaccine, using two different IGRAs. A cohort of 57 KTRs, who were actively followed up, received a third dose of the mRNA-1273 vaccine. After the evaluation of humoral immunity to SARS-CoV-2, 14 seronegative patients were tested with two commercial IGRAs (SD Biosensor and Euroimmun). Out of 14 patients, one and three samples were positive by IGRAs with Euroimmun and SD Biosensor, respectively. The overall agreement between the two assays was 85.7% (κ = 0.444). In addition, multivariate linear regression analysis showed no statistically significant association between the IFN-γ concentration, and the independent variables analyzed (age, gender, years since transplant, total lymphocytes cells/mcl, CD3+ cells/mcl, CD3+ CD4+ cells/mcl, CD3+ CD8+ cells/mcl, CD19+ cells/mcl, CD3-CD16+CD56+ cells/mcl) (p > 0.01). In a vulnerable setting, assessing cellular immune response to complement the humoral response may be advantageous. Since the two commercial IGRAs showed a good agreement on negative samples, the three discordant samples highlight the need for further investigations. 相似文献
75.
Claudio DAmore Christian Borgo Valentina Bosello Travain Mauro Salvi 《International journal of molecular sciences》2022,23(17)
Cystic fibrosis (CF) is caused by mutations in the gene encoding of the cystic fibrosis transmembrane conductance regulator (CFTR), an anion-selective plasma membrane channel that mainly regulates chloride transport in a variety of epithelia. More than 2000 mutations, most of which presumed to be disease-relevant, have been identified in the CFTR gene. The single CFTR mutation F508del (deletion of phenylalanine in position 508) is present in about 90% of global CF patients in at least one allele. F508del is responsible for the defective folding and processing of CFTR, failing to traffic to the plasma membrane and undergoing premature degradation via the ubiquitin–proteasome system. CFTR is subjected to different post-translational modifications (PTMs), and the possibility to modulate these PTMs has been suggested as a potential therapeutic strategy for the functional recovery of the disease-associated mutants. Recently, the PTM mapping of CFTR has identified some lysine residues that may undergo methylation or ubiquitination, suggesting a competition between these two PTMs. Our work hypothesis moves from the idea that favors methylation over ubiquitination, e.g., inhibiting demethylation could be a successful strategy for preventing the premature degradation of unstable CFTR mutants. Here, by using a siRNA library against all the human demethylases, we identified the enzymes whose downregulation increases F508del-CFTR stability and channel function. Our results show that KDM2A and KDM3B downregulation increases the stability of F508del-CFTR and boosts the functional rescue of the channel induced by CFTR correctors. 相似文献
76.
Caroline Barau Shirin Leick Claudio Caccia Lolita Portal Valerio Leoni Philippe Le Corvoisier Didier Morin Bijan Ghaleh Sandrine Pons 《International journal of molecular sciences》2022,23(18)
Exercise induces cardioprotection against myocardial infarction, despite obesity, by restoring pro-survival pathways and increasing resistance of mitochondrial permeability transition pore (mPTP) opening at reperfusion. Among the mechanisms involved in the inactivation of these pathways, oxysterols appear interesting. Thus, we investigated the influence of regular exercise on the reperfusion injury salvage kinase (RISK) pathway, oxysterols, and mitochondria, in the absence of ischemia-reperfusion. We also studied 7β-hydroxycholesterol (7βOH) concentration (mass spectrometry) in human lean and obese subjects. Wild-type (WT) and obese (ob/ob) mice were assigned to sedentary conditions or regular treadmill exercise. Exercise significantly increased Akt phosphorylation, whereas 7βOH concentration was reduced. Moreover, exercise induced the translocation of PKCε from the cytosol to mitochondria. However, exercise did not affect the calcium concentration required to open mPTP in the mitochondria, neither in WT nor in ob/ob animals. Finally, human plasma 7βOH concentration was consistent with observations made in mice. In conclusion, regular exercise enhanced the RISK pathway by increasing kinase phosphorylation and PKCε translocation and decreasing 7βOH concentration. This activation needs the combination with stress conditions, i.e., ischemia-reperfusion, in order to inhibit mPTP opening at the onset of reperfusion. The human findings suggest 7βOH as a candidate marker for evaluating cardiovascular risk factors in obesity. 相似文献
77.
We presentthe results of a research work targeted to understanding thedomains and consequences of CASE tools usage in Nokia. We aimto evaluate the importance of the various CASE tools features,as rated by our developers, and how well such features are implementedin currently available CASE tools. A structured questionnairewas sent to our most experienced developers and CASE users. Fromthis survey, it emerged that CASE tools support is reputed mostuseful for the following functions: graphical drawing, automaticdocumentation generation and storage of diagrams. The resultshint to a mismatch between the features required by the developersand those offered by CASE products. Further research is neededbefore more definite conclusions can be drawn. 相似文献
78.
Claudio Rocchini Paolo Cignoni Fabio Ganovelli Claudio Montani Paolo Pingi Roberto Scopigno 《The Visual computer》2004,20(2-3):149-164
A new algorithm for the integration of partially overlapping range images into a triangular mesh is presented. The algorithm consists of three main steps: it locates the intersections between the range surfaces and a reference grid chosen by the user, then merges all nearly coincident and redundant intersections according to a proximity criterion, and, finally, reconstructs the merged surface(s) from the filtered intersection set.
Compared with previous methods, which adopt a volumetric approach, our algorithm shows lower computational costs and improves the accuracy of the surfaces produced. It takes into account the quality of the input measurements and is able to patch small holes corresponding to the parts of the 3D scanned object that were not observed by the acquisition device.
The algorithm has been tested on several datasets of range maps; graphical and numeric results are reported. 相似文献
79.
Camila Reyes Estefanía Nova-Lamperti Daniel Duran-Sandoval Daniela Rojas Jorge Gajardo Enrique Guzman-Gutierrez Camila Bustos-Ruiz Valeska Ormazbal Felipe A. Zúiga Carlos Escudero Claudio Aguayo 《International journal of molecular sciences》2022,23(13)
Oxidized low-density lipoprotein (ox-LDL) is the most harmful form of cholesterol associated with vascular atherosclerosis and hepatic injury, mainly due to inflammatory cell infiltration and subsequent severe tissue injury. Lox-1 is the central ox-LDL receptor expressed in endothelial and immune cells, its activation regulating inflammatory cytokines and chemotactic factor secretion. Recently, a Lox-1 truncated protein isoform lacking the ox-LDL binding domain named LOXIN has been described. We have previously shown that LOXIN overexpression blocked Lox-1-mediated ox-LDL internalization in human endothelial progenitor cells in vitro. However, the functional role of LOXIN in targeting inflammation or tissue injury in vivo remains unknown. In this study, we investigate whether LOXIN modulated the expression of Lox-1 and reduced the inflammatory response in a high-fat-diet mice model. Results indicate that human LOXIN blocks Lox-1 mediated uptake of ox-LDL in H4-II-E-C3 cells. Furthermore, in vivo experiments showed that overexpression of LOXIN reduced both fatty streak lesions in the aorta and inflammation and fibrosis in the liver. These findings were associated with the down-regulation of Lox-1 in endothelial cells. Then, LOXIN prevents hepatic and aortic tissue damage in vivo associated with reduced Lox-1 expression in endothelial cells. We encourage future research to understand better the underlying molecular mechanisms and potential therapeutic use of LOXIN. 相似文献
80.
Bibiana C. Mota Nathan Ashburner Laura Abelleira-Hervas Liyueyue Liu Robertas Aleksynas Lucio Claudio Rovati Gianfranco Caselli Magdalena Sastre 《International journal of molecular sciences》2022,23(13)
Recent evidence suggests that I2-imidazoline ligands have neuroprotective properties in animal models of neurodegeneration, such as Alzheimer’s disease (AD). We recently demonstrated that the I2-ligand BU224 reversed memory impairments in AD transgenic mice and this effect was not because of reductions in amyloid-β (Aβ) deposition. In this study, our aim was to determine the therapeutic potential of the powerful analgesic I2-imidazoline ligand CR4056 in the 5xFAD model of AD, since this ligand has been proven to be safely tolerated in humans. Sub-chronic oral administration of CR4056 (30 mg/kg for 10 days) led to an improvement in recognition memory in 6-month-old 5xFAD mice, but not in wild-type littermates, without affecting Aβ levels or deposition. Our results also revealed a change in the profile of microglia by CR4056, resulting in a suppression of pro-inflammatory activated microglia, but increased the density of astrocytes and the expression of ApoE, which is mainly produced by these glial cells. In addition, CR4056 restored fibrinogen extravasation, affecting the distribution of markers of astrocytic end feet in blood vessels. Therefore, these results suggest that CR4056 protects against Aβ-mediated neuroinflammation and vascular damage, and offers therapeutic potential at any stage of AD. 相似文献