Diagnostic Utility of Heart Rate Recovery Following a Peak Exercise Stress Test in the Assessment of Diabetic Cardiac Autonomic Neuropathy

Human recognition has become an important topic as the need and investments for security applications grow continuously. Numerous biometric systems exist which utilize various human characteristics. Among all biometrics traits, face recognition is advantageous in terms of accessibility and reliability. In the thesis, two challenges in face recognition are analyzed. The first one is face spoofing. Spoofing in face recognition is explained together with the countermeasure techniques that are proposed for the protection of face recognition systems against spoofing attacks. For this purpose, both 2D photograph and 3D mask attacks are analyzed. The second challenge explored in the thesis is disguise variations, which are due to facial alterations, facial makeup and facial accessories (occlusions). The impact of these disguise variations on face recognition is explored, separately. Then, techniques which are robust against disguise variations are proposed.La Reconnaissance automatique des personnes est devenue un sujet de plus en plus important avec l'augmentation constante des besoins en sécurité. De nombreux systèmes biométriques existent. Ils utilisent différentes caractéristiques humaines. Parmi tous les traits biométriques, la reconnaissance faciale inclut des aspects positifs en termes d'accessibilité et de fiabilité. Dans cette thèse, deux défis en reconnaissance faciales sont étudiés. Le premier est le leurrage. Le leurrage en reconnaissance faciale est présenté. Des contre-mesures permettant d'améliorer les systèmes actuels sont proposés. A cet effet, les attaques basées sur des photographies 2D ou des masques 3D sont analysées. Le second défi exploré dans cette thèse est lié aux variations dues à des altérations du visage (i.e. chirurgie plastique), maquillage et accessoires pour le visage (e.g. occultations par la présence de lunettes). L'impact de ces variations en reconnaissance de visage est étudiée séparément. Ensuite, des techniques robustes contre les variations de camouflage sont proposées

Native T1 reference values for nonischemic cardiomyopathies and populations with increased cardiovascular risk: A systematic review and meta‐analysis

Background: Although cardiac MR and T1 mapping are increasingly used to diagnose diffuse fibrosis based cardiac diseases, studies reporting T1 values in healthy and diseased myocardium, particular in nonischemic cardiomyopathies (NICM) and populations with increased cardiovascular risk, seem contradictory. Purpose To determine the range of native myocardial T1 value ranges in patients with NICM and populations with increased cardiovascular risk. Study Type Systemic review and meta‐analysis. Population Patients with NICM, including hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM), and patients with myocarditis (MC), iron overload, amyloidosis, Fabry disease, and populations with hypertension (HT), diabetes mellitus (DM), and obesity. Field Strength/Sequence (Shortened) modified Look–Locker inversion‐recovery MR sequence at 1.5 or 3T. Assessment PubMed and Embase were searched following the PRISMA guidelines. Statistical Tests The summary of standard mean difference (SMD) between the diseased and a healthy control populations was generated using a random‐effects model in combination with meta‐regression analysis. Results: The SMD for HCM, DCM, and MC patients were significantly increased (1.41, 1.48, and 1.96, respectively, P < 0.01) compared with healthy controls. The SMD for HT patients with and without left‐ventricle hypertrophy (LVH) together was significantly increased (0.19, P = 0.04), while for HT patients without LVH the SMD was zero (0.03, P = 0.52). The number of studies on amyloidosis, iron overload, Fabry disease, and HT patients with LVH did not meet the requirement to perform a meta‐analysis. However, most studies reported a significantly increased T1 for amyloidosis and HT patients with LVH and a significant decreased T1 for iron overload and Fabry disease patients. Data Conclusions Native T1 mapping by using an (Sh)MOLLI sequence can potentially assess myocardial changes in HCM, DCM, MC, iron overload, amyloidosis, and Fabry disease compared to controls. In addition, it can help to diagnose left‐ventricular remodeling in HT patients. Level of Evidence: 2 Technical Efficacy: Stage 3 J. Magn. Reson. Imaging 2018;47:891–912

Interleukin-1β converting enzyme subfamily inhibitors prevent induction of CD86 molecules by butyrate through a CREB-dependent mechanism in HL60 cells

To investigate the underlying mechanism for induction of CD86 molecules, we analysed the ability of the histone deacetylase (HDAC) inhibitor, sodium butyrate (NaB), to induce CD86 at the transcriptional level in HL60 cells. Our studies showed that the expression of CD86 on the cell surface was increased by 24 hr of NaB treatment, and the enhancement of CD86 mRNA expression was observed by real-time polymerase chain reaction. When we measured NF-κB binding activity, significant activity was induced upon NaB stimulation, which was suppressed by the addition of pyrrolidine dithiocarbamate. Butyrate also induced phosphorylated cAMP response element-binding protein (CREB), which bound to cAMP-responsive elements. Dibutyryl (db) -cAMP induced active CREB and increased the levels of CD86 by 24 hr. These observations indicated that NF-κB and/or CREB are crucial for butyrate-dependent activation of CD86 gene expression. We examined the inhibitory effects of various caspase inhibitors on the expression of CD86 in cells treated with NaB, because NaB also induced apoptosis with slow kinetics. Intriguingly, our results demonstrated that inhibitors of the interleukin-1β converting enzyme subfamily (caspase-1, -4, -5 and -13) blocked the butyrate-induced increase in level of CD86. These inhibitors interfered with CD86 gene transcription in the presence of activated NF-κB, whereas phosphorylated CREB was down-regulated in the reactions where these inhibitors were added to inhibit CD86 gene expression. These results suggested that butyrate not only acetylates histones on the CD86 promoter through the suppression of HDAC activity, but that butyrate also regulates CREB-mediated transcription, possibly through the caspase activities triggered by NaB