Fault Attacks on Nonce-based Authenticated Encryption: Application to Keyak and Ketje

In the context of fault attacks on nonce-based authenticated encryption, an attacker faces two restrictions. The first is the uniqueness of the nonce for each new encryption that prevents the attacker from collecting pairs of correct and faulty outputs to perform, e.g., differential fault attacks. The second restriction concerns the verification/decryption, which releases only verified plaintext. While many recent works either exploit misuse scenarios (e.g. nonce-reuse, release of unverified plaintext), we turn the fact that the decryption/verification gives us information on the effect of a fault (whether a fault changed a value or not) against it. In particular, we extend the idea of statistical ineffective fault attacks (SIFA) to target the initialization performed in nonce-based authenticated encryption schemes. By targeting the initialization performed during decryption/verification, most nonce-based authenticated encryption schemes provide the attacker with an oracle whether a fault was ineffective or not. This information is all the attacker needs to mount statistical ineffective fault attacks. To demonstrate the practical threat of the attack, we target software implementations of the authenticated encryption schemes Keyak and Ketje. The presented fault attacks can be carried out without the need of sophisticated equipment. In our practical evaluation the inputs corresponding to 24 ineffective fault inductions were required to reveal large parts of the secret key in both scenarios

Thyroid dysfunctions secondary to cancer immunotherapy

International audienc

The multifaceted nature of diabetes mellitus induced by checkpoint inhibitors

Immune checkpoint inhibitors (CPI) are increasingly being used in oncology, and many autoimmune side effects have been described. Diabetes mellitus (DM) has been reported in approximately 1% of subjects treated with programmed cell death-1 and programmed death ligand 1 (PD-1/PD-L1) inhibitors, alone or in association with CTLA-4 inhibitors. In the present mini-review, we aimed to describe different clinical pictures and pathophysiology associated with these forms of diabetes. Data on CPI-related DM was gathered from the largest case series in the literature and from our centre dedicated to immunotherapy complications (ImmuCare-Hospices Civils de Lyon). Most cases are acute autoimmune insulin-dependent diabetes which are similar to fulminant diabetes (extremely acute onset with concomitant near-normal HbA1c levels). Other cases, however, have a phenotype close to type 2 diabetes or appear as a decompensation of previously known type 2 diabetes. The occurrence of diabetes can also be a complication of autoimmune pancreatitis induced by CPI use. Finally, two cases of diabetes in a context of autoimmune lipoatrophy have recently been described. Regarding the wide variety of CPI-induced diabetes, the discovery of a glucose disorder under CPI should motivate specialised care for aetiological diagnosis and appropriate treatment

Project of an architecture for the command of an electronic switching system

The peripheral devices and command modules communicate through a linking system using an entirely distributed allocation mechanism. This architecture is based upon a pool organisation of the command modules, series lines, etc. Modularity and safety-availability are the guidelines of the choices to be made. The aim is to study the problems arising in the design of a 50 dials/second, standard microprocessor-based, telephonic system

Diabetes mellitus induced by PD-1 and PD-L1 inhibitors: description of pancreatic endocrine and exocrine phenotype

AIMS: Programmed cell death-1 and programmed death ligand 1 (PD-1/PD-L1) inhibitors restore antitumor immunity, but many autoimmune side-effects have been described. Diabetes mellitus is a rare complication, and little data concerning its pathophysiology and phenotype have been published. This study aimed to describe both pancreatic endocrine and exocrine functions, immunological features and change in pancreas volume in subjects with diabetes mellitus induced by PD-1 and PD-L1 inhibitors. METHODS: We analyzed the data of six subjects treated with immunotherapy who presented acute diabetes. RESULTS: There were five men and one woman. Median age was 67 years (range 55-83). Three subjects were treated with nivolumab, two with pembrolizumab and one with durvalumab. Median time to diabetes onset after immunotherapy initiation was 4 months (range 2-13). Four patients presented fulminant diabetes (FD); none of these had type 1 diabetes (T1D)-related autoantibodies, none of them had T1D or FD-very high-risk HLA class II profiles. The bi-hormonal endocrine and exocrine pancreatic failure previously reported for one FD patient was not found in other FD subjects, but glucagon response was blunted in another FD patient. Pancreas volume was decreased at diabetes onset in 2 FD patients, and all patients presented a subsequent decrease of pancreas volume during follow-up. CONCLUSIONS: In the patients presented herein, immunotherapy-induced diabetes was not associated with T1D-related autoantibodies. The hormonal and morphological analysis of the pancreatic glands of these six cases contributes to the understanding of the underlying and probably heterogeneous mechanisms. There is a need to find biomarkers to identify patients at risk to develop these new forms of diabetes at early stages of the process to prevent ketoacidosis and to evaluate preventive strategies