Abstract. MD5 is one of the most widely used cryptographic hash functions nowadays. It was designed in 1992 as an improvement of MD4, and its security was widely studied since then by several authors. The best known result so far was a semi free-start collision, in which the initial value of the hash function is replaced by a non-standard value, which is the result of the attack. In this paper we present a new powerful attack on MD5 which allows us to find collisions efficiently. We used this attack to find collisions of MD5 in about 15 minutes up to an hour computation time. The attack is a differential attack, which unlike most differential attacks, does not use the exclusive-or as a measure of difference, but instead uses modular integer subtraction as the measure. We call this kind of differential a modular differential. An application of this attack to MD4 can find a collision in less than a fraction of a second. This attack is also applicable to other hash functions, such as RIPEMD and HAVAL.

Abstract. In this paper, we present new collision search attacks on the hash function SHA-1. We show that collisions of SHA-1 can be found with complexity less than 2 69 hash operations. This is the first attack on the full 80-step SHA-1 with complexity less than the 2 80 theoretical bound.

C‐Punkte zur Hand: Biokompatible lumineszierende Kohlenstoffnanopunkte mit geringer Toxizität und charakteristischer Photolumineszenz wurden synthetisiert. Diese „C‐Punkte“ könnten sich für vielfältige Anwendungen eignen, z. B. als Fälschungssicherung sowie zur Verschlüsselung oder Speicherung von Informationen.

Human sequence generated from three next-generation sequencing platforms reveals systematic variability in sequence coverage due to local sequence characteristics.

During development, neurotrophins help shape the nervous system by regulating neuronal survival and differentiation. Neurotrophin-3 (refs 1-5) is the most abundant neurotrophin during early development. Neurons responsive to neurotrophin-3 in vitro include primary sensory, sympathetic, motor, enteric, locus coeruleus, hippocampal and cerebellar neurons (ref. 9 for example). Here we report that mice lacking neurotrophin-3 have severe deficits in sensory and sympathetic populations. These mice lack muscle spindles and show abnormal limb positions. In contrast, motor neurons, the enteric nervous system, and the major anatomical regions of the central nervous system seem to develop normally. Comparisons with mutants deficient in other neurotrophins or their receptors indicate that some neurons require more than one neurotrophin during embryogenesis and suggest that neurotrophin-3 functions by binding receptors in addition to its primary receptor trkC (ref. 16). In particular, neurotrophin-3 is essential for survival of sympathetic and sensory neurons that later become dependent on nerve growth factor or brain-derived neurotrophic factor.

No abstract

C‐Punkte zur Hand: Biokompatible lumineszierende Kohlenstoffnanopunkte mit geringer Toxizität und charakteristischer Photolumineszenz wurden synthetisiert. Diese „C‐Punkte“ könnten sich für vielfältige Anwendungen eignen, z. B. als Fälschungssicherung sowie zur Verschlüsselung oder Speicherung von Informationen.

trkB encodes a receptor tyrosine kinase activated by three neurotrophins--brain-derived neurotrophic factor (BDNF), neurotrophin-3, and neurotrophin-4/5. In vivo, three isoforms of the receptor are generated by differential splicing--gp145trkB or the full-length trkB receptor, and trkB.T1 and trkB.T2, two cytoplasmically truncated receptors that lack kinases, but contain unique C termini. Although the truncated receptors appear to be precisely regulated during nervous system development and regeneration, their role in neurotrophin signaling has not been directly tested. In this paper, we studied the signaling properties and interactions of gp145trkB, trkB.T1, and trkB.T2 by expressing the receptors in a Xenopus oocyte microinjection assay. We found that oocytes expressing gp145trkB, but not trkB.T1 or trkB.T2, were capable of eliciting 45Ca efflux responses (a phospholipase C-gamma-mediated mechanism) after stimulation by BDNF. When trkB.T1 and trkB.T2 were coexpressed with gp145trkB, they acted as dominant negative receptors, inhibiting the BDNF signal by forming nonfunctional heterodimers with the full-length receptors. An ATP-binding mutant of gp145trkB had similar dominant inhibitory effects. Our data suggest that naturally occurring truncated trkB receptors function as inhibitory modulators of neurotrophin responsiveness. Furthermore, the homodimerization of gp145trkB appears to be an essential step in activation of the BDNF signaling cascade.