All your sessions are belong to us: Investigating authenticator leakage through backup channels on Android

Security of authentication protocols heavily relies on the confidentiality of credentials (or authenticators) like passwords and session IDs. However, unlike browser-based web applications for which highly evolved browsers manage the authenticators, Android apps have to construct their own management. We find that most apps simply locate their authenticators into the persistent storage and entrust underlying Android OS for mediation. Consequently, these authenticators can be leaked through compromised backup channels. In this work, we conduct the first systematic investigation on this previously overlooked attack vector. We find that nearly all backup apps on Google Play inadvertently expose backup data to any app with internet and SD card permissions. With this exposure, the malicious apps can steal other apps' authenticators and obtain complete control over the authenticated sessions. We show that this can be stealthily and efficiently done by building a proof-of-concept app named AuthSniffer. We find that 80 (68.4%) out of the 117 tested top-ranked apps which have implemented authentication schemes are subject to this threat. Our study should raise the awareness of app developers and protocol analysts about this attack vector.No Full Tex

Phospholemman: a novel cardiac stress protein.

Phospholemman (PLM), a member of the FXYD family of regulators of ion transport, is a major sarcolemmal substrate for protein kinases A and C in cardiac and skeletal muscle. In the heart, PLM co-localizes and co-immunoprecipitates with Na(+)-K(+)-ATPase, Na(+)/Ca(2+) exchanger, and L-type Ca(2+) channel. Functionally, when phosphorylated at serine(68), PLM stimulates Na(+)-K(+)-ATPase but inhibits Na(+)/Ca(2+) exchanger in cardiac myocytes. In heterologous expression systems, PLM modulates the gating of cardiac L-type Ca(2+) channel. Therefore, PLM occupies a key modulatory role in intracellular Na(+) and Ca(2+) homeostasis and is intimately involved in regulation of excitation-contraction (EC) coupling. Genetic ablation of PLM results in a slight increase in baseline cardiac contractility and prolongation of action potential duration. When hearts are subjected to catecholamine stress, PLM minimizes the risks of arrhythmogenesis by reducing Na(+) overload and simultaneously preserves inotropy by inhibiting Na(+)/Ca(2+) exchanger. In heart failure, both expression and phosphorylation state of PLM are altered and may partly account for abnormalities in EC coupling. The unique role of PLM in regulation of Na(+)-K(+)-ATPase, Na(+)/Ca(2+) exchanger, and potentially L-type Ca(2+) channel in the heart, together with the changes in its expression and phosphorylation in heart failure, make PLM a rational and novel target for development of drugs in our armamentarium against heart failure. Clin Trans Sci 2010; Volume 3: 189-196

GSK-3alpha directly regulates beta-adrenergic signaling and the response of the heart to hemodynamic stress in mice.

The glycogen synthase kinase-3 (GSK-3) family of serine/threonine kinases consists of 2 highly related isoforms, alpha and beta. Although GSK-3beta has an important role in cardiac development, much remains unknown about the function of either GSK-3 isoform in the postnatal heart. Herein, we present what we believe to be the first studies defining the role of GSK-3alpha in the mouse heart using gene targeting. Gsk3a(-/-) mice over 2 months of age developed progressive cardiomyocyte and cardiac hypertrophy and contractile dysfunction. Following thoracic aortic constriction in young mice, we observed enhanced hypertrophy that rapidly transitioned to ventricular dilatation and contractile dysfunction. Surprisingly, markedly impaired beta-adrenergic responsiveness was found at both the organ and cellular level. This phenotype was reproduced by acute treatment of WT cardiomyocytes with a small molecule GSK-3 inhibitor, confirming that the response was not due to a chronic adaptation to LV dysfunction. Thus, GSK-3alpha appears to be the central regulator of a striking range of essential processes, including acute and direct positive regulation of beta-adrenergic responsiveness. In the absence of GSK-3alpha, the heart cannot respond effectively to hemodynamic stress and rapidly fails. Our findings identify what we believe to be a new paradigm of regulation of beta-adrenergic signaling and raise concerns given the rapid expansion of drug development targeting GSK-3

Three-Dimensional Curvy Electronics Enabled by Conformal Additive Stamp Printing

The dominant form of electronics, i.e. microelectronics, have been traditionally manufactured into planar layouts. Many electronics and devices, ranging from optoelectronics to wave electronics and to wearables, need to be configured into three dimensional (3D) curvy shapes to realize their functions. However, so far, there has been very limited success in realizing them, mainly due to the lack of effective&nbsp; manufacturing technology. Here, we reported conformal additive stamp (CAS) printing technology for reliably manufacturing 3D curvy&nbsp; electronics in a simple and effective way. CAS printing employs a pneumatically inflated elastomeric balloon as a conformal stamping&nbsp; medium to pick up the pre-fabricated electronic devices and print them onto curvy surfaces. Various devices in curvy shapes, including Si&nbsp; pellets, photodetector arrays, electrically small antennas, hemispherical solar cells, and smart contact lenses are demonstrated based on&nbsp; CAS printing. CAS printing is versatile as it can manufacture onto arbitrary 3D surfaces. Systematic investigations have revealed the key&nbsp; aspects, fidelity, and versatility of CAS printing. CAS printing opens doors towards the burgeoning 3D curvy electronics.</p