Augmented PIN Authentication through Behavioral Biometrics

Personal Identification Numbers (PINs) are widely used today for user authentication on mobile devices. However, this authentication method can be subject to several attacks such as phishing, smudge, and side-channel. In this paper, we increase the security of PIN-based authentication by considering behavioral biometrics, specifically the smartphone movements typical of each user. To this end, we propose a method based on anomaly detection that is capable of recognizing whether the PIN is inserted by the smartphone owner or by an attacker. This decision is taken according to the smartphone movements, which are recorded during the PIN insertion through the built-in motion sensors. For each digit in the PIN, an anomaly score is computed using Machine Learning (ML) techniques. Subsequently, these scores are combined to obtain the final decision metric. Numerical results show that our authentication method can achieve an Equal Error Rate (EER) as low as 5% in the case of 4-digit PINs, and 4% in the case of 6-digit PINs. Considering a reduced training set, composed of solely 50 samples, the EER only slightly worsens, reaching 6%. The practicality of our approach is further confirmed by the low processing time required, on the order of fractions of milliseconds

Machine Learning for PIN Side-Channel Attacks Based on Smartphone Motion Sensors

Motion sensors are integrated into all mobile devices, providing information useful for several purposes. However, these sensor data can be read by any application and by websites accessed through a browser, without requiring security permissions. In this paper, we show that information about smartphone movements can lead to the identification of a Personal Identification Number (PIN) tapped by the user. To reduce the amount of sniffed data, we use an event-driven approach, where motion sensors are sampled only when a key is pressed. The acquired data are used to train a machine learning algorithm for the classification of the keystrokes in a supervised manner. We also consider that users insert the same PIN each time authentication is required, leading to further side-channel information available to the attacker. Numerical results show the feasibility of cyber-attacks based on motion sensors. For example, 4-digit PINs are correctly recognized at the first attempt with an accuracy of 37%, and in five attempts with an accuracy of 63%

In vitro effect of indomethacin and interferon-alpha on Th1 and Th2 cytokine synthesis in patients with chronic hepatitis C

Current evidences suggest that non-steroidal anti-inflammatory drugs could enhance the antiviral activity of interferon-\u3b1 in chronic HCV infection. In this study, we investigated the effect of indomethacin, a non-steroidal anti-inflammatory drug, and interferon-\u3b1 on cytokine production by peripheral blood mononuclear cells from 12 untreated patients with chronic hepatitis C. We evaluated the effect of incubation with indomethacin, interferon-\u3b1 or both on synthesis of Th1- (interleukin-2, interferon-\u3b3) and Th2-associated cytokines (interleukin-4, interleukin-10), and of the antiviral protein 2\u2032,5\u2032-oligoadenylate synthetase. Interferon-\u3b1 induced a significant increase in production of interleukin-2. Smaller increases were also seen in the presence of indomethacin, while incubation with both indomethacin and interferon-\u3b1 leads to a synergistic effect. Incubation with indomethacin decreased both interleukin-4 and interleukin-10, whereas interferon-\u3b1 increased these cytokines. The addition of indomethacin to interferon-\u3b1 significantly reversed this interferon-induced increase. Finally, both indomethacin and the association interferon-\u3b1 plus indomethacin determined a significant increase in 2\u2032,5\u2032-oligoadenylate synthetase production compared to both baseline and interferon-\u3b1 alone. In conclusion, indomethacin was able to enhance the antiviral activity of interferon-\u3b1 and to modulate the interferon-induced Th1 and Th2 cytokine response by increasing the Th1-response, fundamental for sustained clearance of HCV, and by decreasing the Th-2 type response, associated with HCV persistenc