The Internet of Hackable Things

The Internet of Things makes possible to connect each everyday object to the Internet, making computing pervasive like never before. From a security and privacy perspective, this tsunami of connectivity represents a disaster, which makes each object remotely hackable. We claim that, in order to tackle this issue, we need to address a new challenge in security: education

Deterministic and Stochastic Modeling of Human Papillomavirus Gene Regulatory Network

In this thesis a novel stochastic and deterministic mathematical model of Human papillomavirus (HPV) gene regulatory network was developed. The novelty of this project is both on methodological and biological /clinical site. The former is in line with the current challenge in recent years to have a holistic view of the basics regulatory mechanisms interconnected to form a complex machinery, where complex patterns can arise, only form the interconnection of basics modules. In fact, HPV offers a case of study of great interest in molecular systems biology. It involves a number of relevant regulatory mechanisms (e.g. transcription, translation, promoter modulation, polyadenylation regulation, splicing,…) connected together to form a complex network, albeit its genome is relatively simple, thus suitable for an accurate deterministic and even stochastic modeling. HPVs cause a series of diseases of the cutaneous and mucosal epithelium, ranging from minor lesions to precancerous cervical lesions and cervical cancer, which is considered one of the most common cancer in the women worldwide. Therefore, on the biological/clinical aspect the development of a mathematical model of HPV gene expression, is of great interest in order to dispose of an in silico simulator useful to achieve a better comprehension of the complex gene regulatory network, and capable to predict different scenarios from the first stages of viral infection up to a cervical cancer condition. As far as we know, there is no model of HPV gene regulation available in literature. A new synthesis of the HPV molecular biology with especial regard to gather/infer from literature the parameters useful for designing a dynamical model, and to shed light in what is still lacking in the biological literature, was preformed. The biological knowledge was translated into a stochastic model in terms of biochemical reactions. In particular, we modeled the HPV early and late promoters that account for the transcripts and proteins evolution during the entire viral life cycle. Even the post-transcriptional and post-translational modifications were modeled in order to properly capture the complex viral regulation known from literature. As far as we know, it is the first time a stochastic model accounts for the complex post-transcriptional control, modeling the splicing and polyadenylation sites regulation, and connect this latter to the transcriptional control layer, mediated by the promoters activities, in order to explore complex patterns that can arise only from the interconnection of different control layers. The Master Equation (ME) of the system was considered in order to predict and investigate its stochastic behavior. Because of the complex system structure it wasn't possible to solve the whole ME analytically, hence numerical exact simulations were performed by means of the Gillespie's algorithm. A quasi-equilibrium approximation of the ME was developed in order to get a deterministic approximation of the model. The model structure together with the fixed parameters we have gathered/inferred from literature was able to fit a dataset consistent of the early promoter activity and to qualitatively reproduce the main dynamical behavior of two of the most important regulatory transcripts during viral late phase. Different in silico experiments were designed to opportunely explore both the capability of the stochastic model to follows the deterministic predictions, when in fast fluctuations regimen, and to discover complex stochastic patterns, that can arise through the interconnection of the transcriptional and post-transcriptional control layers. In general, both the stochastic and deterministic formulation of the model showed the capability to reproduce the HPV gene expression dynamics, during the entire viral life cycle, in good agreement with the current biological knowledge

DDoS-Capable IoT Malwares: comparative analysis and Mirai Investigation

The Internet of Things (IoT) revolution has not only carried the astonishing promise to interconnect a whole generation of traditionally “dumb” devices, but also brought to the Internet the menace of billions of badly protected and easily hackable objects. Not surprisingly, this sudden flooding of fresh and insecure devices fueled older threats, such as Distributed Denial of Service (DDoS) attacks. In this paper, we first propose an updated and comprehensive taxonomy of DDoS attacks, together with a number of examples on how this classification maps to real-world attacks. Then, we outline the current situation of DDoS-enabled malwares in IoT networks, highlighting how recent data support our concerns about the growing in popularity of these malwares. Finally, we give a detailed analysis of the general framework and the operating principles of Mirai, the most disruptive DDoS-capable IoT malware seen so far

AntibIoTic: Protecting IoT Devices Against DDoS Attacks

The 2016 is remembered as the year that showed to the world how dangerous Distributed Denial of Service attacks can be. Gauge of the disruptiveness of DDoS attacks is the number of bots involved: the bigger the botnet, the more powerful the attack. This character, along with the increasing availability of connected and insecure IoT devices, makes DDoS and IoT the perfect pair for the malware industry. In this paper we present the main idea behind AntibIoTic, a palliative solution to prevent DDoS attacks perpetrated through IoT devices

Modelli stocastici della regolazione trascrizionale

La Systems Biology è una disciplina che mira a studiare i circuiti regolativi, a livello cellulare ed intra-cellulare, delle funzioni biologiche. L’attività di tesi ha riguardato lo studio di un semplice modello di trascrizione del DNA descrivendolo stocasticamente in termini di Chemical Master Equation da cui è stata ricavata la descrizione di potenza (convalidata anche con simulazioni di Gillespie). Inoltre è stata dimostrata la stazionarietà a regime del sistema. Nel contesto di dinamica veloce del fattore di trascrizione è stata ricavata la descrizione di Fokker-Planck potendo delineare un comportamento di tipo passa-basso del primo ordine. Inoltre è stata valutata la densità di probabilità e la proprietà di ergodicità. Infine dalla descrizione di Fokker – Planck è stata ricavata la descrizione in termini di Equazione Differenziale Stocastica convalidandone la validità descrittiva del modello consideratoopenEmbargo per motivi di segretezza e di proprietà dei risultati e informazioni sensibil

Joining Jolie to Docker Orchestration of Microservices on a Containers-as-a-Service Layer

Cloud computing is steadily growing and, as IaaS vendors have started to offer pay-as-you-go billing policies, it is fundamental to achieve as much elasticity as possible, avoiding over-provisioning that would imply higher costs. In this paper, we briefly analyse the orchestration characteristics of PaaSSOA, a proposed architecture already implemented for Jolie microservices, and Kubernetes, one of the various orchestration plugins for Docker; then, we outline similarities and differences of the two approaches, with respect to their own domain of application. Furthermore, we investigate some ideas to achieve a federation of the two technologies, proposing an architectural composition of Jolie microservices on Docker Container-as-a-Service layer.Comment: 9 pages, 3 figure

Role of E6 in Maintaining the Basal Cell Reservoir during Productive Papillomavirus Infection.

Papillomaviruses exclusively infect stratified epithelial tissues and cause chronic infections. To achieve this, infected cells must remain in the epithelial basal layer alongside their uninfected neighbors for years or even decades. To examine how papillomaviruses achieve this, we used the in vivo MmuPV1 (Mus musculus papillomavirus 1) model of lesion formation and persistence. During early lesion formation, an increased cell density in the basal layer, as well as a delay in the infected cells' commitment to differentiation, was apparent in cells expressing MmuPV1 E6/E7 RNA. Using cell culture models, keratinocytes exogenously expressing MmuPV1 E6, but not E7, recapitulated this delay in differentiation postconfluence and also grew to a significantly higher density. Cell competition assays further showed that MmuPV1 E6 expression led to a preferential persistence of the cell in the first layer, with control cells accumulating almost exclusively in the second layer. Interestingly, the disruption of MmuPV1 E6 binding to MAML1 protein abrogated these phenotypes. This suggests that the interaction between MAML1 and E6 is necessary for the lower (basal)-layer persistence of MmuPV1 E6-expressing cells. Our results indicate a role for E6 in lesion establishment by facilitating the persistence of infected cells in the epithelial basal layer, a mechanism that is most likely shared by other papillomavirus types. Interruption of this interaction is predicted to impede persistent papillomavirus infection and consequently provides a novel treatment target. IMPORTANCE Persistent infection with high-risk HPV types can lead to development of HPV-associated cancers, and persistent low-risk HPV infection causes problematic diseases, such as recurrent respiratory papillomatosis. The management and treatment of these conditions pose a considerable economic burden. Maintaining a reservoir of infected cells in the basal layer of the epithelium is critical for the persistence of infection in the host, and our studies using the mouse papillomavirus model suggest that E6 gene expression leads to the preferential persistence of epithelial cells in the lower layers during stratification. The E6 interaction with MAML1, a component of the Notch pathway, is required for this phenotype and is linked to E6 effects on cell density and differentiation. These observations are likely to reflect a common E6 role that is preserved among papillomaviruses and provide us with a novel therapeutic target for the treatment of recalcitrant lesions