92 research outputs found
Comparison of in-situ delay monitors for use in Adaptive Voltage Scaling
In Adaptive Voltage Scaling (AVS) the supply voltage of digital circuits is
tuned according to the circuit's actual operating condition, which enables
dynamic compensation to PVTA variations. By exploiting the excessive safety
margins added in state-of-the-art worst-case designs considerable power
saving is achieved. In our approach, the operating condition of the circuit
is monitored by in-situ delay monitors. This paper presents different designs
to implement the in-situ delay monitors capable of detecting late but still
non-erroneous transitions, called Pre-Errors. The developed Pre-Error
monitors are integrated in a 16 bit multiplier test circuit and the
resulting Pre-Error AVS system is modeled by a Markov chain in order to
determine the power saving potential of each Pre-Error detection approach
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Human red blood cells at work: identification and visualization of erythrocytic eNOS activity in health and disease
A nitric oxide synthase (NOS)-like activity has been demonstrated in human red blood cells (RBCs), but doubts about its functional significance, isoform identity and disease relevance remain. Using flow cytometry in combination with the NO-imaging probe DAF-FM we find that all blood cells form NO intracellularly, with a rank order of monocytes > neutrophils > lymphocytes > RBCs > platelets. The observation of a NO-related fluorescence within RBCs was unexpected given the abundance of the NO-scavenger oxyhemoglobin. Constitutive normoxic NO formation was abolished by NOS inhibition and intracellular NO scavenging, confirmed by laser-scanning microscopy and unequivocally validated by detection of the DAF-FM reaction product with NO using HPLC and LC-MS/MS. Employing immunoprecipitation, ESI-MS/MS-based peptide sequencing and enzymatic assay we further demonstrate that human RBCs contain an endothelial NOS (eNOS) that converts L-3H-Arginine to L-3H-Citrulline in a Ca2+/Calmodulin-dependent fashion. Moreover, in patients with coronary artery disease, red cell eNOS expression and activity are both lower than in age-matched healthy individuals and correlate with the degree of endothelial dysfunction. Thus, human RBCs constitutively produce NO under normoxic conditions via an active eNOS isoform the activity of which is compromised in patients with coronary artery disease
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