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A novel strategy for constructing the tangent graph, which employs binary search, logarithmic approximation, and half-plane computation methods, is presented. The strategy lends itself well to Very Large Scale Integration (VLSI) implementation, which facilitates high-performance computation.

Design studies have been completed to investigate the impact of improvements in fast energy storage systems on the designs of: larger future simulators (such as a 15-MA plasma radiation source (PRS) simulator), simulator upgrades of operational machines (such as Double-EAGLE), and for very compact, smaller simulators. The fast energy storage system that has been investigated and is presently under development is a fast Marx generator (FMG) with inductance capacitance (LC) 1/2 = 200 ns and LC 1/2 = 300 ns, depending on the capacitance per stage. This new fast Marx energy storage system uses newly developed, low-inductance rail switches and low-inductance capacitors. These components are configured in a low-inductance FMG stage and then stacked in series to form a unit for the voltage required and a number of units in parallel for the required system inductance and stored energy. A four-stage fast Marx prototype has been demonstrated with a total of 60-kJ energy stored and an output voltage of 680 kV. This new FMG technology will provide the capability to build X-ray machines in a significantly more compact configuration. The new FMG technology minimizes or eliminates the need for storing the energy in a large water transfer capacitor. A design sketch of a 15-MA PRS machine driven by a fast Marx will be presented. This generator would consist of 48 eight-stage FMG units and would drive the PRS directly without further pulse compression. We will also present the concept of a high voltage (2-3 MV), compact X-ray machine that uses a nine-stage fast Marx module to directly charge a vacuum inductive store. A plasma opening switch (POS) is used to switch the inductive store and deliver the electron beam to the load. Index Terms--Capacitors, fast Marx generator, inductance, marx stage, plasma opening switch, plasma radiation source, plasma radiation source machine, rail gap switch, simulator, transfer capacitor.

Background and aim: The role of Helicobacter pylori ond aspirin in peptic ulcer formation and recurrence remains an important clinical topic. The interaction between aspirin and H pylon in vitro [...]

Background: The use of proton pump inhibitors for the treatment of functional dyspepsia is controversial and the role of Helicobacter pylori infection in functional dyspepsia is uncertain. Aim: To evaluate [...]

Research describing the use of a high temperature, superconducting quantum interference device gradiometer for geophysical exploration is presented. The device is successfully tested against a Cs-vapour gradiometer under field conditions.

Research has been conducted on the DNA motifs at informative loci in Helicobacter pylori strains from five continents. The study of these motifs via PCR and sequencing in investigating this gastric pathogen's evolution is presented.

Antral gastritis is an inflammatory condition of the portion of the stomach near the opening into the duodenum. This condition occurs in virtually all patients with duodenal ulcers. High levels of gastric acid, which are known to be important in the development of duodenal ulcer, play an unknown role in antral gastritis. Infestation with the bacteria Helicobacter pylori is known to be important in the development of antral gastritis, but its importance in duodenal ulcer is poorly understood. To evaluate the effects of the drug omeprazole on H. pylori levels and the severity of antral gastritis, a study was carried out with 270 patients with active duodenal ulcers. Omeprazole is used in the treatment of duodenal ulcer because of its potency in suppressing gastric acid secretion. Patients were given either low doses of omeprazole, high doses of omeprazole, or a standard dose of the histamine H2 receptor blocker ranitidine (also commonly used in the treatment of duodenal ulcer). All drugs were administered for four consecutive weeks. The sex, age, and pretreatment gastric acid output levels were similar in all three groups of patients. The two dosages of omeprazole resulted in almost identical rates of improvement in clinical symptoms of gastritis (maximum of 53 percent of the patients showed improvement in the final week); ranitidine-treated patients showed a significantly less dramatic rate of improvement (maximum of 33 percent of the patients showed improvement in the final week). Microscopic evaluation of biopsy specimens to determine inflammatory activity yielded very similar results in the omeprazole groups. In addition, patients receiving either high-dose or low-dose omeprazole treatment showed a reduction in H. pylori levels; this did not occur in ranitidine-treated patients. Among patients receiving omeprazole, those showing a reduction in H. pylori infection enjoyed a greater reduction in gastritis symptoms. These findings suggest that the level of acidity and H. pylori infection may both play a role in the development of antral gastritis. (Consumer Summary produced by Reliance Medical Information, Inc.)

There is extensive evidence linking cigarette smoking to peptic (gastric and duodenal) ulcer disease, but the exact mechanisms underlying this association remain unknown. Nicotine, an important component of cigarette smoke, has been shown to potentiate (increase) the gastric damage resulting from ethanol (alcohol) ingestion, but does not appear to cause ulceration in and of itself. The effect of nicotine on the microscopic structure of the gastric mucosa is not known; subthreshold damage may require the actions of an additional irritant, such as ethanol, for the pathology to become apparent. To evaluate the effects of nicotine on gastrointestinal microscopic anatomy, and to investigate the effects of sucralfate (a protective agent) and feeding on nicotine-induced changes in gastric morphology, an animal study was carried out with anesthetized male rats who had been either food-deprived for 24 hours or fed as they desired prior to the experiment. The stomach was exposed to nicotine, sucralfate, ethanol, or a combination of these drugs, and the rat stomachs were removed and subjected to microscopic analysis. Both nicotine and ethanol induced microscopically detectable injury, and the two drugs acted synergistically to produce a greater degree of damage than the sum of each individually. Sucralfate pretreatment reduced the amount of damage done by both nicotine and ethanol. By the same token, prior feeding reduced the amount of injury induced by both nicotine and ethanol. (Consumer Summary produced by Reliance Medical Information, Inc.)

Nicotine, the principal pharmacological agent in tobacco, has been associated with increased incidence of gastric and duodenal ulcers. Alcohol consumption has also been linked to nicotine in the etiology of gastric and duodenal ulcer, but conflicting reports do not allow any conclusions to be drawn. A study was carried out in rats, in which several doses of nicotine were administered orally either chronically (10 days) or acutely (15 minutes prior to alcohol exposure). The animals' stomachs and duodenums were surgically exposed and immersed in a dilute alcohol solution. Gastric mucosal blood flow (GMBF), gastric acidity, total gastric secretion, and extent of mucosal damage were quantified. Alcohol treatment alone caused a decrease in gastric acid secretion and GMBF, which was accompanied by an increase in mucosal damage. Acute nicotine treatment increased gastric acid secretion and prevented the decrease in GMBF and the mucosal damage. Chronic nicotine administration had different effects, depending on the dose given. Both high and low doses prevented the inhibitory action of alcohol on gastric acid secretion; the high dose potentiated alcohol's effects on GMBF and mucosal damage, while the low dose had just the opposite effect (increased GMBF and less mucosal damage). It is concluded that acute nicotine administration has a protective effect on the stomach and intestines against the effects of alcohol, while chronic administration has differential effects, perhaps as a result of the differential effects on GMBF. Additionally, the acid secretory state of the stomach appears unrelated to the severity of ulceration caused by alcohol, at least in this model. (Consumer Summary produced by Reliance Medical Information, Inc.)