In vitro stimulation with ASA + C5a leucocyte stimulation with other NSAIDs should be performed to achieve a higher sensitivity. This finding can be explained by the clinical observation of a high ratio of cross-reactivities between the mentioned NSAIDs.

Chip reliability becomes a great threat to the design of future microelectronic systems with the continuation of the progressive downscaling of CMOS technologies. Hence increasing the robustness of chip implementations in terms of error tolerance becomes an important issue. In this paper we present a case study in reliability-aware design tolerating transient errors. A state-of-the-art WiMAX channel decoder for LDPC codes is investigated on all design levels to increase its reliability for a given system performance with minimum hardware overhead. We show that an efficient exploitation of the algorithmic fault-tolerance yields a fairly small area overhead with nearly no degradation in communications performance even under high error injection rates.

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3GPP long term evolution (LTE) enhances the wireless communication standards UMTS and HSDPA towards higher throughput. A throughput of 150 Mbit/s is specified for LTE using 2×2 MIMO. For this, highly punctured Turbo codes with rates up to 0.95 are used for channel coding, which is a big challenge for decoder design. This paper investigates efficient decoder architectures for highly punctured LTE Turbo codes. We present a 150 Mbit/s 3GPP LTE Turbo code decoder, which is part of an industrial SDR multi-standard baseband processor chip.

Pituitary adenylate cyclase-activating polypeptide (PACAP, Adcyap1) activation of PAC1 receptors (Adcyap1r1) significantly increases excitability of guinea pig cardiac neurons. This modulation of excitability is mediated in part by plasma membrane G protein-dependent activation of adenylyl cyclase and downstream signaling cascades, as well as by endosomal signaling mechanisms. PACAP/PAC1 receptor-mediated activation of plasma membrane adenylyl cyclase (AC) and the resulting increase in cellular cAMP enhances a hyperpolarization-induced nonselective cationic current I, which contributes to the PACAP-induced increase in cardiac neuron excitability. Further, PACAP-mediated AC/cAMP/PKA downstream signaling also appears to enhance cardiac neuron I to facilitate the excitatory responses. PACAP activation of PAC1 receptors rapidly stimulates receptor internalization, and reducing ambient temperature or treatments with the clathrin inhibitor Pitstop2 or the dynamin I/II inhibitor dynasore to block endocytic events can suppress PACAP-enhanced neuronal excitability. Thus, endocytosis inhibitors essentially eliminate PACAP-enhanced excitability suggesting that endosomal platforms represent a primary signaling mechanism. Endosomal signaling is associated canonically with ERK activation and in accord, PACAP-enhanced cardiac neuron excitability is reduced by MEK inhibitor pretreatments. PACAP activation of MEK/ERK signaling can enhance currents through voltage-dependent Nav1.7 channels. Hence, PACAP-induced PAC1 receptor internalization/endosomal signaling, recruitment of MEK/ERK signaling, and modulation of Nav1.7 are implicated as key mechanisms contributing to the PACAP-enhanced neuronal excitability. PACAP/PAC1 receptor-mediated endosomal ERK signaling in central circuits can play key roles in development of chronic pain and anxiety-related responses; thus, PAC1 endosomal signaling likely participates in a variety of homeostatic responses within neuronal circuits in the CNS.