Search

Conventional chemotherapy for acute myeloid leukemia regimens generally encompass an intensive induction phase, in order to achieve a morphological remission in terms of bone marrow blasts (&lt, 5%). The majority of cases are classified as Primary Induction Response (PIR), unfortunately, 15% of children do not achieve remission and are defined Primary Induction Failure (PIF). This study aims to characterize the gene expression profile of PIF in children with Acute Myeloid Leukemia (AML), in order to detect molecular pathways dysfunctions and identify potential biomarkers. Given that NUP98-rearrangements are enriched in PIF-AML patients, we investigated the association of NUP98-driven genes in primary chemoresistance. Therefore, 85 expression arrays, deposited on GEO database, and 358 RNAseq AML samples, from TARGET program, were analyzed for “Differentially Expressed Genes” (DEGs) between NUP98+ and NUP98-, identifying 110 highly confident NUP98/PIF-associated DEGs. We confirmed, by qRT-PCR, the overexpression of nine DEGs, selected on the bases of the diagnostic accuracy, in a local cohort of PIF patients: SPINK2, TMA7, SPCS2, CDCP1, CAPZA1, FGFR1OP2, MAN1A2, NT5C3A and SRP54. In conclusion, the integrated analysis of NUP98 mutational analysis and transcriptome profiles allowed the identification of novel putative biomarkers for the prediction of PIF in AML.

The proposed Time to Digital Converter architecture is based on a ring oscillator with an even number of delay units. The core system is able to convert time intervals ranging from 0.1 ns to 30 ns in a reduced silicon area of around 140×140 μm2 for 8 bit. The extension of the maximum time count can be performed by adding an higher-level counter. Moreover, each delay element of the converter can be evaluated by using a Built-In Self Test (BIST) procedure and calibrated in order to reduce process variability effects in each ring stage.

A model of a new class of total polymeric sensors known as ionic polymer–polymer composite $({\rm IP}^{2}{\rm C})$ has been developed. Starting from a previous model, new experimental investigations have been performed in order to increase the significance of the sensor model. The device uses Clevios P HC V4 electrodes and a conducting polymer, produced and distributed by Heraeus. The sensing behavior of ${\rm IP}^{2}{\rm Cs}$ has been modeled by applying a suitable set of deforming signals and using a data-driven identification procedure. The sensor model has been investigated in a suitable range of working frequencies by using an ad hoc realized setup. Also, Young's modulus of ${\rm IP}^{2}{\rm Cs}$ has been measured by means of the dynamic mechanical analysis and the results have been used in the identification of the ${\rm IP}^{2}{\rm Cs}$ sensor model. The model identification and validation have been performed by using a programmable mechanical vibration generator system, and experimental evidence of the suitability of the proposed model is given in this paper.

We have modeled the dependence on the gate voltage of the bulk contact resistance and interface contact resistance in staggered polycrystalline organic thin film transistors. In the specific, we have investigated how traps, at the grain boundaries of an organic semiconductor thin film layer placed between the metal electrode and the active layer, can contribute to the bulk contact resistance. In order to the take into account this contribution, within the frame of the grain boundary trapping model (GBTM), a model of the energy barrier EB, which emerges between the accumulation layer at the organic semiconductor/insulator interface and injecting contact, has been proposed. Moreover, the lowering of the energy barrier at the contacts interface region has been included by considering the influence of the electric field generated by the accumulation layer on the injection of carriers at the source and on the collection of charges from the accumulation layer to the drain contact. This work outlines both a Schottky barrier lowering, determined by the accumulation layer opposite the source electrode, as well as a Poole-Frenkel mechanism determined by the electric field of the accumulation layer active at the drain contact region. Finally it is provided and tested an analytical equation of our model for the contact resistance, summarizing the Poole-Frenkel and Schottky barrier lowering contribution with the grain boundary trapping model.

The dynamics of intramolecular torsional motion of central phenylene ring in a series of phenylene ethynylene oligomer derivatives was investigated. On the basis of calculated hindered rotational potentials corresponding to this motion, the torsional energy levels were obtained by solving the torsional Schrodinger equation. Subsequently, the torsional correlation time and transition probability was computed within the Bloembergen–Purcell–Pound (BPP) formalism, considering both the classical and quantum mechanical tunneling contributions to the intramolecular rotation. The results were interpreted in the context of molecular conductivity switching behavior of the considered series of compounds. Also some other parameters relevant to molecular admittance were calculated, such as the HOMO–LUMO energy difference and the spatial extent of the frontier molecular orbitals. Classical electrostatic arguments were applied to understand the physical basis of the conformational stability differences in the studied compounds. It was found that halogenation of the central phenylene ring may be used for fine-tuning of molecular conduction behavior, in the sense of modulating the HOMO–LUMO energy difference, the spatial extent of frontier MOs, as well as the barrier height to torsional motion of the central phenylene ring. The time scale of the temperature induced stochastic conformational switching between the “on” and “off” states, along with the corresponding transition probability could be varied by an order of magnitude upon halogenation of the central phenylene ring. The tunneling contributions to the torsional correlation time were found to be of minor importance in this context, and this quantity may be quite correctly estimated with the classical BPP approach.

In this paper the locally active and the edge of chaos regions of the Hindmarsh–Rose (HR) model for neuron dynamics are studied. From these regions parameters are chosen to set emergent phenomena both in 2D and 3D grids of HR neurons.

Acute lymphoblastic leukemia (ALL) is the most common cancer in childhood, originating from a neoplastic deviation of B or T lymphocyte. Cytogenetic, cytofluorimetric, and genomic analyses clearly defined several subtypes of ALL. However, the leukemogenic process is characterized by different pathways' alteration which are still to be determined, in the attempt to identify specific targets to be druggable. In this review, we explore the main molecular pathways, which are commonly shared between different subtypes of pediatric ALL. These cell-signaling pathways affect many functions, including cell proliferation, apoptosis, migration, and differentiation. The PI3K/AKT/mTOR pathway is one of the most studied, with higher expected promises of being targetable. RAS pathway is also widely studied in all types of cancer. The Wnt/Beta catenin has been recently studied in ALL. Finally, CXCL12/CXCL4 axis has a crucial role in regulating hematopoietic stem cell and bone marrow niche. The complete characterization of these pathways will allow us to design a specific patient–disease profile associated with a tailored treatment, with the highest grade of efficacy and the lowest grade of toxicity.

In this paper, systems formed by networks of simple nonlinear cells are studied. Using lattice models, some of the fundamental features of complex systems such as self-organization and pattern formation are illustrated. In the first part of this work, a lattice of identical Chua's circuit is used to experimentally study its global spatiotemporal dynamics, according to the variation of some macroparameters, like the coupling coefficient or the neighboring dimension. The second part of the paper deals with the remarkable improvements regarding regularization and pattern formation, obtained in networks of nonlinear systems by introducing some spatial diversity, especially generated by deterministic, unpredictable dynamics. Simulation results show that synchronization and self-organization occur in networks with a few nonlocally connected cells, with irregular topology and small spatial diversity.

Background To identify the predictive factors for malignancies using basic clinical and laboratory information in children presenting with musculoskeletal pain and eventually diagnosed with juvenile idiopathic arthritis (JIA) or malignancy. Methods A retrospective case–control chart review research examining laboratory data from patients referred for musculoskeletal pain in 2001–2010 and diagnosed with malignancy or JIA was performed. The validity of each test for the diagnosis of neoplasia was assessed by calculating the sensitivity, specificity, positive predictive values (PPV), negative predictive values (NPV) and likelihood ratios. Results A total of 134 patients were enrolled. Statistically significant differences were found in neutrophil count, Hb, LDH, IgA and C4 values, ANA, anti-EA EBV IgG and anti-CMV IgG titres. High LDH value and anti-CMV IgG were the most predictive factors for neoplasia. High specificity factors for neoplasia were abnormal values of neutrophil count, Hb, IgA and C4, and the presence of anti-EA EBV and anti-CMV IgG. High PPV were recorded for abnormal neutrophil count, Hb value and anti-CMV titre. A low NPV was found only for anti-EA EBV and anti-CMV titres. Conclusions In this setting of patients, minimum changes in neutrophil count, particularly if associated with low Hb and high LDH levels, are to be thoroughly considered, because they appear as the most predictive factors for the diagnosis of tumour.

Background. Although the prognosis of acute lymphoblastic leukemia (ALL) has improved considerably in recent years, some cases still exhibit therapy-resistance and late relapse. CD9-CXCL12-CXCR4 pathway has been implicated in hematopoietic and leukemic stem cell homing, promoting cell adhesion and survival in bone marrow stromal niches and mediating cell dissemination to secondary lymphoid organs. We characterized the CD9-CXCL12-CXCR4 expression in specific biological subgroups of childhood ALL, comparing, in some cases, diagnosis vs relapse, in order to investigate the role of these genes, in the process of leukemia relapse and to preliminarily evaluate their impact as prognostic markers, even for those subtypes with well-established good outcome. Materials and Methods. We analyzed bone marrow (BM) samples from 68 children with ALL, 3 cases with chronic myeloid leukemia, as control for t(9;22) positive leukemia, and 4 healthy donors (HDs). Patients were enrolled and treated at our Center from 2000 to 2010. We reverse-transcribed 500 ng of patients' diagnostic RNA and performed a Real-time PCR using the SYBRTM Green PCR Master Mix (Applied Biosystems®), calculating the median fold-changes (MFCs) among different reactions and comparing with HDs. GUS gene mRNA was used as an internal positive control, showing no significant variation in our experiments. Each PCR experiment was carried out in duplicate. Sequences of oligonucleotides used for experiments, together with RQ-PCR protocol were previously published (Gandemer V. et al Leukemia Research 2010) Results. We analyzed for CD9, CXCL12 and CXCR4 expression 39 children with t(12;21) positive ALL, 12 cases with t(1;19) positive ALL, 8 cases with t(9;22) positive ALL, and 9 cases resulted negative for chromosomal translocation screening. Among the t(12;21) positive ALL we found that CD9 was overexpressed in 13 out of 39 patients (33%), CXCL12 in 14 out of 39 (35%) and CXCR4 in 9 out of 39 (23%), respectively. We noted that in 2 cases who presented a late relapse, one (CT13) showed a normal expression of the analyzed genes, conversely the other case (CT24), who suffered from a isolated extramedullary relapse, showed a high overexpression of CD9. In the t(1;19) subgroup we found only one case with overexpression of both CD9 and CXCR4 genes, respectively. Moreover we noted that comparing diagnosis vs relapse in one case, we observed a dramatic increased expression of CXCL12 (CT70 diagnosis 3,33 FCs vs relapse 38 FCs). In the subgroup of children with t(9;22) positive ALL, we observed an extremely high expression of the CD9-CXCL12-CXCR4 genes. In particular, we found an overexpression of CD9 in 4 out of 8 (50%) cases with this subtype of ALL; interestingly, all these case showed a BM relapse. One of these (CT56) showed an overexpression of all the three pathway's components. As negative counterpart, we also analyzed three cases with a t(9;22) positive CML, finding a normal expression of all genes. In order to determine this pathway's expression in children presenting an ALL without known chromosomal aberration, we analyzed other 9 cases. In only one (CT44) we found an overexpression of both CD9 and CXCL12. This patient suffered from an early relapse ( Conclusions. Our preliminary findings demonstrated that the CD9-CXCL12-CXCR4 pathway is mainly altered in children with t(12;21) and t(9;22) positive ALL. In the latter subgroup we found a linear correlation between overexpression and impending relapse, confirming that this pathway can be potentially used as prognostic marker. Among t(1;19) positive ALL, we found few cases with single gene aberration. More importantly, we found an overexpression of one or two pathway's components in diagnostic samples of those cases, who presented a subsequent relapse. These data need to be confirmed in a larger population and will pave the way to identify new prognostic marker and/or therapeutic target, since CXCR4 has already antagonist drugs in clinical use, showing very recent promising results (Randhawa S et al. British Journal of Hematology 2016). Disclosures No relevant conflicts of interest to declare.

Background. Acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood and a major cause of childhood cancer-related mortality. Although the cure rate now approaches 90%, certain pediatric ALL subgroups present subsequent relapse. For this reason, analyses of cell signaling pathways will help to identify new markers and/or targets for tailored therapy. PI3K/AKT/mTOR activation is frequently found in both B-ALL and T-ALL. Protein kinase Ck2 (CSNK2) activity in pediatric ALL was increased and its inhibition restored PTEN phosphatase activity with subsequent inactivation of AKT. Moreover, Ck2 may serve the activity of oncogenes such as BCR-ABL and c-MYC, control the activation of other critical signaling cascades (JAK-STAT), and sustain multiple cellular stress-elicited pathway such as the proteotoxic stress, unfolded protein and DNA-damage responses. Ck2 has also been shown to have an essential role in tuning signals derived from the stromal tumor microenvironment (Piazza F et al, Oncogene2016). Material and Methods. We analyzed cDNA collected from 46 patients with B-ALL [19 High Risk (HR) for Minimal Residual Disease (MRD) and 27 NON-HR] and 25 with T-ALL (8 HR and 17 NON-HR), respectively, diagnosed in our Center from 2000 to 2012. The latter subgroup was screened fro PTEN-Exon7 mutations and TXL3 rearrangements. We evaluated the gene expression of Ck2 and c-Myc genes using RQ-PCR with Sybr-Green and a relative quantification method (ΔΔCt method), comparing gene's expression from patients with samples from 6 healty donors (HDs). In order to demonstrate the correlation between genetic alteration and signaling transduction, specifically in HR patients , we analyzed some phosphoproteins by Phospho-flow approach. We profiled 5 proteins (STAT3, STAT5, CREB, PTEN and pS6) in 4 T-ALL cases (3 with PTEN-Exon 7 mutation). Results. We observed a significant difference of Ck2 expression in T-ALL NON-HR patients vs HDs (Mean Ck2 Fold-Changes 3.494 vs 1.17, p=0.0315) and in T-ALL HR patients (6.384 vs 1.17, p=0.0219) vs HDs (Fig 1A and B). Comparing NON-HR vs HR cases, we found a statistically significant difference (p Conclusions. Based on our preliminary findings, Ck2 could be considered as a marker and /or a potential candidate for targeted therapy, specifically in HR-ALL, as confirmed by the use of CK2 inhibitor (CX-4945) in ongoing clinical trials. c-Myc overexpression confirmed its association with HR features. The potential role as markers of both genes needs to be demonstrated in a larger population study. Combined application of genomic and phosphoproteomic strategies will lead us to better profile diagnostic samples of HR-ALL, addressing future tailored treatments. Disclosures No relevant conflicts of interest to declare.

Background. Aberrations in the DNA repair pathway among children with acute lymphoblastic leukemia (ALL) are largely unknown. Knowledge of such mutations may improve the understanding of tumorigenesis and direct patient care. Germline aberrations of the DNA-repair machinery are crucial for generating chromosomal instability and occurrence of acute leukemia. In order to better understand this mechanism, we addressed our research to NBS1 (Nijmegen Breakage Syndrome) gene and Fanconi Anemia/BRCA1 and BRCA2 pathway, in the attempt to identify mutations and aberrant expression, predisposing and/or cooperating with the leukemogenic process, among biological subgroups of childhood ALL. Materials and Methods. We analyzed 48 diagnostic samples from children with ALL treated at our institution from 2000 to 2010: 11 cases with chromosome Philadelphia positive (Ph+) leukemias (8 ALL and 3 CML), 15 with t(12;21), 11 with t(1;19) positive ALL, respectively and 10 samples with B-ALL without known translocations. We also analyzed three cases of relapse. In Ph+ subgroup, we analyzed remission samples in order to detect germline mutations. We performed RT-PCR and sequencing analyses to detect mutations in NBS1 gene (exons 3-6). The status of FANCD2 and PALB2 genes was studied by a multiplex ligation-dependent probe amplification (MLPA). Samples from healthy donors (HDs) were used as wild-type control. For data elaboration, we used Coffalyser.Net software for MLPA. We performed Sybr-Green Real-Time PCR amplification of BRCA1 (exons 14-15) and BRCA2 (exons 15-16) genes, respectively, calculating the expression in patients with method 2^-ΔΔC comparing with HDs. Results. Among the 15 cases with t(12;21) positive ALL, we found overexpression of BRCA1 and BRCA2 in 8 and 10 cases, respectively, showing a statically significant difference (pC;Glu185Gln; SNP-rs1805794) in NBS1 gene. Deletions or duplications for FANCD2 and PALB2 genes were not found. In the 8 cases with Ph+ B-ALL, we detected an overexpression of BRCA1 and BRCA2 in 4 and 7, respectively, showing a statistically significant difference (pC;Glu185Gln) in 2 cases (25%) with B-ALL and in 1 patients with CML, respectively. Analyses of FANCD2 showed deletions in 3 cases with B-ALL and 2 children with CML; PALB2 resulted deleted in 2 cases with B-ALL and 2 cases with CML. Interestingly, NBS1 mutations were detected in remission samples, showing a germline genomic aberration, as well. Surprisingly, deletions of FANCD2 and PALB2 were found only in leukemic samples. In 11 cases with t(1;19) positive ALL, we observed statically significant difference in BRCA1 (pC;Glu185Gln) in 4 patients (36%); in one case we detected an NBS1 exon 4 deletion. We found FANCD2 exon-1 duplication in 3 patients; in 4 cases we detected PALB2 genomic aberrations (3 duplication and one exon-1 deletion). Among 10 cases with B-ALL without known translocations, we observed statically significant difference in BRCA1 (pC;Glu185Gln) in NBS1. We also detected in 4 cases different mutations in FANCD2 and PALB2 genes (deletion in exons 9-30 and duplication in exons 1-2-29, respectively). Notably, the relapsed case within the latter subgroup, at diagnosis showed genomic aberrations in all the selected genes in association with BRCA1 and BRCA2 overexpression. Conclusion Our findings strongly suggest that the DNA repair machinery is frequently disrupted in childhood ALL. The significance of BRCA1 and BRCA2 overexpression in all subgroups is still unclear. NBS1 showed a missense mutation in a range from 25% to 45% of children with ALL. Interestingly, these mutations were found at germline level in cases with Ph+ leukemias, suggesting a predisposition profile. Aberrations of FANCD2 and PALB2 genes were mostly detected in the subgroup of children without known translocation. Finally the role in leukemic predisposition and the clinical impact of these genomic aberrations need to be more elucidated in a larger population. Disclosures No relevant conflicts of interest to declare.

Background. Aberrations in the DNA repair pathway among children with leukemia are largely unknown. Knowledge of such mutations may improve the understanding of tumorigenesis, direct patient care, and enable genetic counseling of patients and families. Germline aberrations of the DNA-repair machinery are crucial for generating chromosomal instability and occurrence of acute leukemia in children. In order to better understand this mechanism, we studied a specific subgroup of childhood leukemia, e.g. t(9;22) or chromosome Philadelphia positive (Ph+) acute lymphoblastic and chronic myeloid leukemias. We addressed our research to specific genes (Nijmegen Breakage Syndrome (NBS1) and Fanconi Anemia) involved in the DNA repair pathway, in the attempt to identify mutations and aberrant expressions, predisposing and/or cooperating with the leukemogenic process. Materials and Methods. We analyzed diagnostic and remission samples of 12 children: 8 with a Ph+ acute lymphoblastic leukemia (ALL) and 4 with a chronic myeloid leukemia (CML) diagnosed and treated at our institution from 1999 to 2013. We performed RT-PCR analyses to detect mutations in exons 3-6 of the NBS1 gene, followed by a direct sequencing analysis (BMR - Padova - Italy). The status of FANCD2 and PALB2 genes was studied by a multiplex ligation-dependent probe amplification (MLPA) using the Salsa MLPA P057-025R FANCD2-PALB2 Probemix and SALSA MLPA EK1 kit (MRC-Holland, Amsterdam, the Netherlands). Samples from five healthy donors (HDs) were used as wild-type controls. For data elaboration, we used Coffalyser.Net software for MLPA. Moreover we performed a real-time PCR amplification of BRCA1 (exons 14-15) and BRCA2 (exons 15-16) genes, respectively, calculating the median fold-changes (MFC) in patients comparing with HDs. Results. We detected the NBS1 E185Q polymorphism (c533G>C, rs1805794) in both diagnostic and remission samples in 3 out of 12 children with a Ph positive acute leukemia (2 ALL, 1 CML). We also found two pairs of deletions in FANCD2 (Δ32-35; Δ35-38) and PALB2 (Δ2; Δ2-6) in 4 out of 12 Ph positive cases (2 ALL and 2 CML). These aberrations were mutually exclusive. Thus a total of 7 cases (58%) showed an aberrant pathway. Moreover we determined that the MFC of BRCA1 expression among children with Ph positive ALL and CML was slightly higher than HDs (1,388 vs 0,433 and 1,625 vs 0,451, respectively). Surprisingly the MFC of BRCA2 expression was strongly higher than HDs in both children with Ph positive ALL (5,924 vs 0,002) and CML (54,504 vs 0,256). Conclusion. Our preliminary findings strongly suggest that germline mutations or deletions in association with aberrant expression of specific genes that regulate the DNA repair machinery may contribute to the chromosomal instability in children with Ph positive leukemias. These data will be confirmed in a larger population of different subtypes of pediatric leukemia. Citation Format: Nellina Andriano, Paola Bonaccorso, Valeria Iachelli, Manuela La Rosa, Emanuela Cannata, Luca Lo Nigro. Genetic aberrations in the DNA repair pathway among children with Philadelphia chromosome positive leukemias. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2428.

Musculoskeletal pain is a common symptom in childhood and in a few cases is the initial sign of a severe disease such a chronic inflammatory disease or a malignancy.

In this work the design and realization of an artificial vestibular system demonstrator is presented. The whole system is biologically inspired to the human vestibular apparatus. The mototransduction capabilities of ionomeric polymer-metal composite (IPMC) have been used in order to develop the prototype [1]. The reported results are the starting point to the future design and development of a miniaturized artificial vestibular system, integrating biocompatible materials and all-organic electronic devices [2].

This work aims at being a contribution for the characterization of a new class of complex systems built as arrays of coupled fuzzy logic based chaotic oscillators and an investigation on their collective dynamical features. Different experiments were carried out varying the parameters related to the single-unit dynamics, as Lyapunov exponent, and to the macrosystem structure, as the number of connections. Four types of global behaviors have been identified and characterized distinguishing their patterns as follows: the spatiotemporal chaos, the regular synchronized behavior, the transition phase, and the chaotic synchronized behavior. These collective behaviors and the synchronization capability have been highlighted by defining a mathematical indicator which weights the slight difference among a wide number of spatiotemporal patterns. To investigate the effects due to the network architecture on the synchronization characteristics, complex fuzzy systems have been reproduced using fuzzy chaotic cells connected through different topologies: regular, “small worlds,” and random.

The concept of stochastic resonance introduced the idea that the presence of noise in nonlinear systems may have benefic effects. In this paper different regular topologies of populations of FitzHugh-Nagumo neurons have been investigated with respect to the presence of noise in the network. Each neuron is subjected to an independent source of noise. In these conditions the behavior of the population depend on the connection among the elements. In population of uncoupled neurons the so-called stochastic resonance without tuning was observed. Moreover, we show that globally coupled neurons have increasing response-to-stimulus coherence for increasing values of the coupling strength. In locally coupled neurons the performance depend on the neighborhood radius and in general are higher than in the case of uncoupled neurons.

In this work neuron information exchanges have been investigated by modeling nonlinear lattices by connecting Hindmarsh-Rose neurons. In the first phase, regular network models have been characterized by varying the coupling strength in bidimensional arrays of neurons. In the second one, dynamical behavior of 2-D small world configurations, with long term connections, has been considered. Several experiments have been characterized by quantifying a synchronization index. A trade off between network architecture complexity and information exchange performances has been discussed.

Ionic polymer–polymer composites (IP2Cs) are a novel class of all-organic electroactive polymers that can operate both as electromechanical actuators and as sensors. They are an evolution of ionic polymer–metal composites (IPMCs), since the metallic layers, used to realize the electrodes, are substituted by using organic conductors based on PEDOT:PSS. For the IPMC based actuators it is generally reported that solvents different from water can be used to avoid the dehydration phenomenon. Here the possibility to use ethylene glycol and an ionic liquid, 1-ethyl-3-methylimidazolium trifluoromethanesulfonate, as diluents for the IP2C is investigated. Moreover, different materials have been used for the manufacture of the device electrodes and the performances of different organic transducers have been observed and compared. Reported results show that the use of both ethylene glycol and EmI-Tf as the solvent can have beneficial effects both on the working time duration of IP2C and on the corresponding transduction behaviors.

In this paper different topologies of populations of FitzHugh-Nagumo neurons have been introduced in order to investigate the role played by the noise in the network. Each neuron is subjected to an independent source of noise. In these conditions the behavior of the population depends on the connection among the elements. By analyzing several kinds of topology (ranging from regular to random) different behaviors have been observed. Several topologies behave in an optimal way with respect to the range of noise level leading to an improvement in the stimulus response coherence, while others with respect to the maximum values of the performance index. However, the best results in terms of both the suitable noise level and high stimulus response coherence have been obtained when a diversity in neuron characteristic parameters has been introduced and the neurons have been connected in a small-world topology.