Andreas Beckmann

Bio: Andreas Beckmann is an academic researcher from Forschungszentrum Jülich. The author has contributed to research in topics: Fast multipole method & Auxiliary memory. The author has an hindex of 6, co-authored 20 publications receiving 222 citations. Previous affiliations of Andreas Beckmann include Martin Luther University of Halle-Wittenberg & Goethe University Frankfurt.

Evidence for a melatonin receptor within pancreatic islets of neonate rats: functional, autoradiographic, and molecular investigations.

Abstract: In a recent perifusion investigation, we showed that the pineal secretory product melatonin reduces insulin secretion from isolated pancreatic islets of neonate rats stimulated with potassium chloride (KCl), glucose, and forskolin. This effect of melatonin was reproduced with doses ranging from 200 pmol/L to 5 micromol/L. Because it is generally accepted that melatonin exerts some of its biological effects through specific, high-affinity pertussis-toxin-sensitive G-protein-coupled receptors, we blocked the putative melatonin receptor of pancreatic islets using both the non-hydrolyzable guanosine triphosphate analog guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS, 30 micromol/L) and the melatonin antagonist luzindole (10 micromol/L). Both GTPgammaS and luzindole caused a near normalization of the melatonin-induced inhibition of the forskolin-stimulated insulin secretion. To localize putative melatonin receptors within the pancreatic islets autoradiographic studies were additionally carried out. These investigations showed specific binding of 2-[125I]iodomelatonin, which were in exact correspondence with the localization of the islets. In addition, gray-level analysis showed that unlabeled melatonin was able to reduce the binding of 2-[125I]iodomelatonin in a dose-dependent manner. Concentrations of unlabeled melatonin of 10(-9) mol/L produced a 50% reduction in specific binding, whereas concentrations of 10(-6) mol/L displaced the binding completely. Likewise, the results of molecular investigations showed that the rat pancreas contains a melatonin receptor, since reverse transcription polymerase chain reaction (RT-PCR) experiments, using specific primers for the rat melatonin receptor Mel1a, showed that mRNA for this melatonin receptor type is expressed in pancreatic tissue of newborn rats. In summary, it may be said that our functional. autoradiographic, and molecular results indicate that the Mel1a receptor is located on the pancreatic islets, possibly in the beta cells.

Building a parallel pipelined external memory algorithm library

Abstract: Large and fast hard disks for little money have enabled the processing of huge amounts of data on a single machine. For this purpose, the well-established STXXL library provides a framework for external memory algorithms with an easy-to-use interface. However, the clock speed of processors cannot keep up with the increasing bandwidth of parallel disks, making many algorithms actually compute-bound.

On Computational Models for Flash Memory Devices

Abstract: Flash memory-based solid-state disks are fast becoming the dominant form of end-user storage devices, partly even replacing the traditional hard-disks. Existing two-level memory hierarchy models fail to realize the full potential of flash-based storage devices. We propose two new computation models, the general flash model and the unit-cost model, for memory hierarchies involving these devices. Our models are simple enough for meaningful algorithm design and analysis. In particular, we show that a broad range of existing external-memory algorithms and data structures based on the merging paradigm can be adapted efficiently into the unit-cost model. Our experiments show that the theoretical analysis of algorithms on our models corresponds to the empirical behavior of algorithms when using solid-state disks as external memory.

Energy-efficient sorting using solid state disks

Abstract: We take sorting of large data sets as case study for making data-intensive applications more energy-efficient. Using a low-power processor, solid state disks, and efficient algorithms, we beat the current records in the JouleSort benchmark for 10GB to 1 TB of data by factors of up to 5.1. Since we also use parallel processing, this usually comes without a performance penalty.

Functional MT1 and MT2 melatonin receptors in mammals.

Abstract: Melatonin, dubbed the hormone of darkness, is known to regulate a wide variety of physiological processes in mammals. This review describes well-defined functional responses mediated through activation of high-affinity MT1 and MT2 proteinteoupled receptors viewed as potential targets for drug discovery. MT1 melatonin receptors modulate neuronal firing, arterial vasoconstriction, cell proliferation in cancer cells, and reproductive and metabolic functions. Ativation of MT2 melatonin receptors phase shift circadian rhythms of neuronal firing in the suprachiasmatic nucleus, inhibit dopamine release in retina, induce vasodilation and inhibition of leukocyte rolling in arterial beds, and enhance immune responses. The melatonin-mediated responses elicited by activation of MT1 and MT2 native melatonin receptors are dependent on circadian time, duration and mode of exposure to endogenous or exogenous melatonin, and functional receptor sensitivity. Together, these studies underscore the importance of carefully linking each melatonin receptor type to specific functional responses in target tissues to facilitate the design and development of novel therapeutic agent.

International Union of Basic and Clinical Pharmacology. LXXV. Nomenclature, Classification, and Pharmacology of G Protein-Coupled Melatonin Receptors

Abstract: The hormone melatonin (5-methoxy- N -acetyltryptamine) is synthesized primarily in the pineal gland and retina, and in several peripheral tissues and organs. In the circulation, the concentration of melatonin follows a circadian rhythm, with high levels at night providing timing cues to target tissues endowed with melatonin receptors. Melatonin receptors receive and translate melatonin's message to influence daily and seasonal rhythms of physiology and behavior. The melatonin message is translated through activation of two G protein-coupled receptors, MT1 and MT2, that are potential therapeutic targets in disorders ranging from insomnia and circadian sleep disorders to depression, cardiovascular diseases, and cancer. This review summarizes the steps taken since melatonin's discovery by Aaron Lerner in 1958 to functionally characterize, clone, and localize receptors in mammalian tissues. The pharmacological and molecular properties of the receptors are described as well as current efforts to discover and develop ligands for treatment of a number of illnesses, including sleep disorders, depression, and cancer.

Melatonin, energy metabolism, and obesity: a review.

Abstract: Melatonin is an old and ubiquitous molecule in nature showing multiple mechanisms of action and functions in practically every living organism. In mammals, pineal melatonin functions as a hormone and a chronobiotic, playing a major role in the regulation of the circadian temporal internal order. The anti-obesogen and the weight-reducing effects of melatonin depend on several mechanisms and actions. Experimental evidence demonstrates that melatonin is necessary for the proper synthesis, secretion, and action of insulin. Melatonin acts by regulating GLUT4 expression and/or triggering, via its G-protein-coupled membrane receptors, the phosphorylation of the insulin receptor and its intracellular substrates mobilizing the insulin-signaling pathway. Melatonin is a powerful chronobiotic being responsible, in part, by the daily distribution of metabolic processes so that the activity/feeding phase of the day is associated with high insulin sensitivity, and the rest/fasting is synchronized to the insulin-resistant metabolic phase of the day. Furthermore, melatonin is responsible for the establishment of an adequate energy balance mainly by regulating energy flow to and from the stores and directly regulating the energy expenditure through the activation of brown adipose tissue and participating in the browning process of white adipose tissue. The reduction in melatonin production, as during aging, shift-work or illuminated environments during the night, induces insulin resistance, glucose intolerance, sleep disturbance, and metabolic circadian disorganization characterizing a state of chronodisruption leading to obesity. The available evidence supports the suggestion that melatonin replacement therapy might contribute to restore a more healthy state of the organism.