We first provide an overview of the state-of-the-art architectures for continuous availability, briefly covering such traditional concepts as high-availability (HA) clustering on distributed platforms and on the mainframe. We explain how HA can be achieved in environments based on Sun Microsystems J2EE™, which differ from classical clustering approaches, and we discuss how disaster recovery (DR) has become an extension of HA. The paper then presents aspects of service management, including the use and orchestration of process-based (ITIL®) systems management tasks within DR scenarios, where the key challenge is to ensure the right level of redundancy in the integration and service-oriented management of heterogeneous information technology landscapes.
This paper describes a set of function primitives which have been designed for support of expert systems and logic programs. The functions could be offered as part of the computer architecture by implementing them in microcode and partially in hardware. The functions are primarily (but not exclusively) oriented towards support of logic programming languages such as Prolog for implementing expert systems. Particular emphasis is given to supporting the parallel execution of expert system applications by multiple processors. The concepts described are based on the Concurrent Data Access Architecture (CDAA). It is shown that OR-parallelism, as well as AND-parallelism, can be supported.
Protein- and fat-rich test meals elicit a strong stimulatory effect on postprandial somatostatin (SLI) and pancreatic polypeptide (PP) release, whereas carbohydrate-rich meals rather attenuate the response of both hormones. Since there is evidence that intestinal hormones might contribute to the postprandial SLI and PP response, it was the aim of the present study to determine in dogs the effect of low-dose cholecystokinin octapeptide (CCK-8) on basal hormone levels and also during a background infusion of amino acids or glucose. In a group of six conscious dogs, sulfated CCK-8 was infused intravenously (i.v.) via a hindleg vein at stepwise increasing infusion rates of 10, 30, and 50 pmol X kg-1 X h. The infusion of CCK was applied during a background infusion of saline (2 ml/min), glucose (0.2 g/min), or an amino acid mixture (8.5%, 2 ml/min). CCK-8 had no effect on plasma insulin and glucagon levels under all experimental conditions. Plasma SLI levels were significantly stimulated by all doses of CCK. This stimulatory effect was similar during background infusions of either saline, glucose, or amino acids, respectively. Pancreatic polypeptide (PP) levels rose 200-300 pg/ml during CCK plus saline. This was slightly attenuated by glucose. During CCK plus amino acids, the PP response was augmented to 600-800 pg/ml. Since secretin is also released after the ingestion of a meal and intraduodenal acidification is a potent stimulus not only of secretin but also of gastric and pancreatic SLI release, the effect of secretin was examined additionally.(ABSTRACT TRUNCATED AT 250 WORDS)
A system structure supporting parallel processing in general and parallel logic programming and expert system applications in particular is described. It is not based on special hardware but has rather been designed as an evolutionary extension to most existing machine architectures. It is aimed at parallel processing support for e.g. PROLOG as well as for expert system (shells) implemented in a general purpose language. A layered structure consisting of an extended machine interface and a macro language is chosen to support a range of various applications.
Journal Article Endogenous opioids mediate motilin- and cholecystokinin-induced somatostatin release Get access R Schick, R Schick Abteilung Innere Medizin I, Universität Ulm Search for other works by this author on: Oxford Academic Google Scholar N Lenz, N Lenz Abteilung Innere Medizin I, Universität Ulm Search for other works by this author on: Oxford Academic Google Scholar V Schusdziarra V Schusdziarra Abteilung Innere Medizin I, Universität Ulm Search for other works by this author on: Oxford Academic Google Scholar Acta Endocrinologica (Norway), Volume 110, Issue 1_Supplement_a, Apr 1979, Page S65, https://doi.org/10.1530/acta.0.109S065 Published: 01 April 1985
Support of distributed data processing, especially in a local area network, requires major modifications and extensions of existing operating system structures to provide,for example, automatic data set exchange, remote spooling, and terminal passthrough. Most of these facilities can be considered under the common goal of achieving a single system image for a network of processors.
Journal Article Effect of cholecystokinin (CCK) on insulin release is modulated by endogenous opiates Get access N Lenz, N Lenz Abteilung für Innere Medizin I, Universität Ulm Search for other works by this author on: Oxford Academic Google Scholar B Rewes B Rewes Abteilung für Innere Medizin I, Universität Ulm Search for other works by this author on: Oxford Academic Google Scholar Acta Endocrinologica (Norway), Volume 104, Issue 4_Supplement_b, Dec 1984, Page S18, https://doi.org/10.1530/acta.0.107S018 Published: 01 December 1984
Recently we have demonstrated in dogs and man that endogenous opioids participate in the regulation of pancreatic endocrine function following the ingestion of a meal. Since intestinal hormones such as cholecystokinin (CCK) are also released by the presence of nutrients in the gastrointestinal tract and participate in the postprandial stimulation of pancreatic endocrine function, an interaction between CCK and endogenous opioids seems possible. The present study was designed to examine this further. In a group of 8 conscious dogs the octapeptide of CCK was infused intravenously in its sulfated (CCK-8S) or nonsulfated (CCK-8NS) form and in addition the tetrapeptide of CCK (CCK-4) was given at increasing infusion rates of 50, 200 and 500 pmol/kg . h, respectively. The experiments were performed during a background infusion of saline to assess the effect on basal insulin and during a background infusion of glucose (0.2 g/min) to determine the effects on stimulated insulin release. The effect of endogenous opioids was examined by addition of the opiate-receptor antagonist naloxone. The studies demonstrate that in the basal state CCK-8S has no stimulatory effect on insulin secretion unless naloxone is added indicating that endogenous opioids help to prevent insulin secretion in the absence of elevated glucose levels. During i.v. glucose naloxone reduced the stimulatory effect of CCK-8S at 50 and 200 pmol/kg . h and that of CCK-4 at 50 pmol/kg . h. Infusion of CCK-8S and CCK-4 at 500 pmol/kg . h had no effect on glucose-stimulated insulin levels, however, the addition of naloxone elicited a significant stimulatory effect. These data demonstrate stimulatory as well as inhibitory effects of endogenous opioids depending on the dose of CCK-8 and -4. CCK-8NS reduced glucose-stimulated insulin release already at the lowest dose of 50 pmol/kg . h. This was reversed to a stimulatory effect with the addition of naloxone. These data demonstrate that the interaction between CCK-8 and -4 and endogenous opioids on prestimulated insulin secretion is much more dependent on the dose of CCK - low doses induce stimulatory and high doses inhibitory mechanisms via endogenous opioids. In view of previous in vitro and in vivo studies with exogenously infused opiate-active compounds it might be speculated that increasing doses of CCK elicit a parellel increase in the release of endogenous opioids which might be responsible for some but certainly not all of the effects observed recently for the action of naloxone in the post-prandial state.
Previously, we have demonstrated the effects of exogenously administered opiates on somatostatin release in dogs and therefore the present study was designed to determine the effect of endogenous opiates via naloxone-induced opiate receptor blockade on somatostatin release. Additionally, plasma insulin and pancreatic polypeptide (PP) levels were determined in response to intragastrically instilled protein, carbohydrate and fat test meals in a group of eight conscious dogs. To all test meals either naloxone (4 mg) or saline was added. The rise of plasma somatostatin levels in response to liver extract, sucrose and fat was attenuated significantly by naloxone. Naloxone had no effect on the rise of postprandial plasma insulin and PP levels. The present data demonstrate that endogenous opiates have a stimulatory effect on postprandial somatostatin release in dogs which indicates a tight interaction that might be of relevance for nutrient homeostasis.
The present study was designed to determine the role of carbohydrates during naloxone-induced opiate receptor blockade upon the postprandial rise of plasma somatostatin (SLI), insulin and pancreatic polypeptide (PP) levels in response to protein and fat test meals in conscious dogs. Test meals consisting of 50 g liver extract + 50 g sucrose or 50 g corn oil + 50 g sucrose dissolved in 300 ml water were instilled intragastrically, respectively. Additionally, liver extract and fat meals were given with a concomitant intravenous infusion of glucose. To all test meals either naloxone (4 mg) or saline was added. The addition of sucrose to liver extract or the infusion of i.v. glucose during the liver meal abolished the inhibitory effect of naloxone on the rise of postprandial somatostatin levels which has been described recently. The addition of carbohydrate either orally or intravenously to the fat meal resulted in an even stimulatory effect of naloxone upon the rise of postprandial somatostatin levels. Insulin levels were not changed during liver extract + sucrose or i.v. glucose, respectively. When sucrose or i.v. glucose was administered together with the fat meal the addition of naloxone augmented postprandial insulin secretion. Pancreatic polypeptide (PP) release was augmented during the combination of sucrose or i.v. glucose with the fat and liver meal when naloxone was present in the meals. The present data demonstrate that the addition of carbohydrates either orally or intravenously to fat and protein meals modulates the effect of endogenous opiates in the regulation of postprandial somatostatin, insulin and pancreatic polypeptide release in dogs in a way that carbohydrates induce inhibitory mechanisms that are mediated via endogenous opiate receptors.