Conference overemphasised FOBT.
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Australia↗
Biomedical subjects
A I Stern
Publications and source records attributed to A I Stern.
Distribution of colorectal adenomas: implications for bowel cancer screening.
OBJECTIVE: To determine the distribution of colorectal adenomas relative to the splenic flexure in an asymptomatic population undergoing colonoscopy, as an indicator of the number of patients with adenomas who would be missed by screening with flexible sigmoidoscopy. DESIGN: Retrospective survey of medical records. SETTING: Private endoscopy centres in Melbourne, Victoria. SUBJECTS: All 1131 asymptomatic individuals who underwent full colonoscopy between 1 January 1995 and 31 December 1997 after referral from a bowel cancer prevention program organised by the endoscopy centres. People referred were aged either 40 years or over with a first-degree relative with bowel cancer, or 50 years or over with marked anxiety about bowel cancer. MAIN OUTCOME MEASURES: Presence and distribution of colorectal adenomas. RESULTS: Polyps were found in 270 individuals (24%) and were confirmed to be adenomas in 138 (12%). These 138 comprised 106 men and 32 women, with mean age 54 years (range, 40-78 years). Most (86%) had a single adenoma. Position of adenomas in relation to the splenic flexure was: distal only in 85 of the 138 people (62%), proximal only in 34 (25%), and both distal and proximal in 19 (14%). CONCLUSIONS: In 25% of asymptomatic people found to have adenomas by this bowel cancer prevention program, the adenomas were found only in the proximal colon, well beyond the reach of the flexible sigmoidoscope. This distribution of adenomas suggests that screening programs cannot rely solely on flexible sigmoidoscopy.
Adenoma↗
Synthesis of 1-amino-6,7,8,8a-tetrahydroacenaphthene and its effect on the inhibition of the MAO-enzyme at the brain cortex and liver level.
(+/-)-1-Amino-6,7,8,8a-tetrahydroacenaphthene was synthesized and evaluated as a novel drug acting on the dopaminergic system. It was shown that the new compound displays activity as MAO inhibitor.
Acenaphthenes↗
Relationship between Electron Transport across the Plasmalemma and a pH Decrease in the Bulk Medium.
The hypothesis is tested that acidification of the bulk medium during transplasmalemma electron transport to ferricyanide is due solely to a requirement for charge balance. According to this hypothesis, reduction of the trivalent anion, ferricyanide, to the tetravalent anion, ferrocyanide, results in a charge difference that is balanced by protons. A coulometric device is used that rapidly and efficiently reoxidizes ferrocyanide to ferricyanide, thus maintaining a constant charge in the bulk medium. Oat (Avena sativa L. cv Garry) mesophyll protoplasts are chosen as experimental material to facilitate ferricyanide reduction and the concomitant ferrocyanide reoxidation by the coulometric device. The kinetics of ferricyanide reduction and proton excretion by protoplasts are similar to those of other cell types and tissues. Rates of net proton excretion are identical regardless of whether the ferrocyanide is simultaneously reoxidized. We conclude that acidification may occur during transplasmalemma electron transport when there is no change in negative charge of the bulk medium.
Journal Article↗
The role of plasma membrane redox activity in light effects in plants.
Stimulations by light of electron transport at the plasma membrane make it possible that redox activity is involved in light-induced signal transduction chains. This is especially true in cases where component(s) of the chain are also located at the plasma membrane. Photosynthetic reactions stimulate transplasma membrane redox activity of mesophyll cells. Activity is measured as a reduction of the nonpermeating redox probe, ferricyanide. The stimulation is due to production of a cytosolic electron donor from a substance(s) transported from the chloroplast. It is unknown whether the stimulation of redox activity is a requirement for other photosynthetically stimulated processes at the plasma membrane, but a reduced intermediate may regulate proton excretion by guard cells. Blue light induces an absorbance change (LIAC) at the plasma membrane whose difference spectrum resembles certain b-type cytochromes. This transport of electrons may be due to absorption of light by a flavoprotein. The LIAC has been implicated as an early step in certain blue light-mediated morphogenic events. Unrelated to photosynthesis, blue light also stimulates electron transport at the plasma membrane to ferricyanide. The relationship between LIAC and transmembrane electron flow has not yet been determined, but blue light-regulated proton excretion and/or growth may depend on this electron flow. No conclusions can be drawn regarding any role for phytochrome because of a paucity of information concerning the effects of red light on redox activity at the plasma membrane.
Cell Membrane↗
Low-dose antacids and nonsteroidal anti-inflammatory drug-induced gastropathy in humans.
Gastroduodenal injury induced by nonsteroidal anti-inflammatory drugs (NSAIDs) is common. As yet, the ideal means to prevent NSAID-related mucosal injury remains controversial. Antacids are effective agents in treating gastric and duodenal ulcers unrelated to NSAIDs. The aim of this study was to assess the ability of a low-dose antacid to prevent NSAID injury in humans. Fifty healthy human volunteers were studied using a randomized, double-blind, placebo controlled, crossover design. After initial endoscopy, subjects were randomized to either Maalox TC (1 tablet q.i.d., acid neutralizing capacity of 104 mEq/day) or identical placebo while receiving 500 mg of naproxen b.i.d. for 21 days. After this period, a second endoscopy was performed to count antral and duodenal erosions and to evaluate symptoms and compliance with study medications. A 21-day washout period ensued, followed by a third endoscopy to insure a return to endoscopically normal mucosa. Subjects then crossed over into the alternate treatment arm for a further 21 days, followed by a fourth endoscopy to assess erosions. Forty subjects completed the study. Subjects receiving Maalox TC developed a significantly greater number of gastric erosions than did those on placebo. While this result was unforeseen, it is supported by statistical analysis and may have clinical relevance in regard to short-term NSAID therapy.
Adolescent↗
Lack of gastric mucosal protection by sucralfate during long-term aspirin ingestion in humans.
The ability of sucralfate to prevent gastric mucosal erosions caused by long-term aspirin ingestion was studied in 19 normal human subjects. A placebo-controlled, double-blind, crossover design was used to study the capacity of 4 g sucralfate daily to lessen the noxious effect on gastric mucosa of 3.6 g aspirin daily for 14 days. Gastric mucosal injury was assessed by endoscopic scoring of erosions. There was no significant difference in mean erosion scores or the degree of partial mucosal protection between the two groups. It was concluded that sucralfate lacks a mucosal protection capacity at the dosage studied in human subjects ingesting large doses of aspirin over a two-week period.
Adult↗
Regulation of transplasmalemma electron transport in oat mesophyll cells by sphingoid bases and blue light.
Long-chain sphingoid bases inhibit transplasmalemma electron transport in certain animal cells in part by inhibiting protein phosphorylation. As a first step in determining whether similar regulatory processes exist for cell surface redox activity in plants, peeled leaf segments of Avena sativa L. cv Garry were exposed to sphingoid bases and other long chain lipids. Sphingoid bases which are the most active inhibitors of protein kinase C in animal cells inhibit transplasmalemma electron transport by mesophyll cells in the dark as measured by reduction of exogenous ferricyanide. In white light, however, the same compounds markedly stimulate redox activity. The stimulation by sphingoid bases in the light is not eliminated by the inhibitor of photosynthesis, 3-(3,4-dichlorophenyl)-1,1 dimethylurea (DCMU). Redox activity remaining in the presence of DCMU and sphingoid bases can be observed in blue but not red light. A tentative hypothesis considering the involvement of two separate redox systems is presented in an attempt of explain the disparate action of sphingoid bases on electron transport across the plasmalemma.
Journal Article↗
Protective effect of sucralfate against aspirin-induced damage to the human gastric mucosa.
Sucralfate, an agent that heals peptic ulcers in humans, has been shown to reduce aspirin-induced gastric mucosal damage in experimental animals. It has been suggested that the protective effect of sucralfate is due to stimulation of local prostaglandin production. The purpose of this study was to establish whether sucralfate was capable of reducing aspirin-induced gastric damage in humans. The effect of 1 g of sucralfate or identical placebo was studied in random order in eight healthy subjects. To determine if the effect of sucralfate was related to local prostaglandin synthesis, a second series of studies was performed in which prostaglandin production was inhibited with indomethacin 50 mg given orally eight hours before sucralfate. In each subject, all studies were performed at least one week apart. Following an overnight fast, upper gastrointestinal endoscopy was performed, with sucralfate or placebo given orally 30 minutes before ingestion of 1,200 mg of soluble aspirin in 50 ml of water. Both endoscopist and subject were unaware of the test agent. Ninety minutes after aspirin ingestion, endoscopy was again performed and gastric mucosal lesions were counted and graded to derive an erosion score. Results are expressed as mean +/- SEM. Aspirin produced endoscopic changes (score of 2.75 +/- 0.49) that were significantly (p less than 0.05) inhibited by sucralfate (score of 1.13 +/- 0.44). The protective effect of sucralfate was abolished by pretreatment with indomethacin (scores of 2.88 +/- 0.55 and 1.88 +/- 0.40, respectively). These results demonstrate that sucralfate significantly protects the human gastric mucosa against the acute damaging effects of aspirin. This effect is abolished by indomethacin, suggesting that the protective action of sucralfate on the gastric mucosa of humans may be related to stimulation of endogenous prostaglandins.
Aspirin↗
Relationship of Transplasmalemma Redox Activity to Proton and Solute Transport by Roots of Zea mays.
Transplasmalemma redox activity, monitored in the presence of exogenous ferricyanide stimulates net H(+) excretion and inhibits the uptake of K(+) and alpha-aminoisobutyric acid by freshly cut or washed, apical and subapical root segments of corn (Zea mays L. cv "Seneca Chief"). H(+) excretion is seen only following a lag of about 5 minutes after ferricyanide addition, even though the reduction of ferricyanide occurs before 5 minutes and continues linearly. Once detected, the enhanced rate of H(+) excretion is retarded by the ATPase inhibitors N,N'-dicyclohexylcarbodiimide, diethylstilbestrol, and vanadate. A model is presented in which plasmalemma redox activity in the presence of ferricyanide involves the transport only of electrons across the plasmalemma, resulting in a depolarization of the membrane potential and activation of an H(+)-ATPase. Such a model implies that this class of redox activity does not provide an additional and independent pathway for H(+) transport, but that the activity may be an important regulator of H(+) excretion. The 90% inhibition of K(+) ((86)Rb(+)) uptake within 2 minutes after ferricyanide addition can be contrasted with the 5 to 15% inhibition of uptake of alpha-aminoisobutyric acid. The possibility exists that a portion of the K(+) and most of the alpha-aminoisobutyric acid uptake inhibitions are related to the ferricyanide-induced depolarization of the membrane potential, but that the redox state of some component of the K(+) uptake system may also regulate K(+) fluxes.
Journal Article↗
Localization of a sulphate-activating system within Euglena mitochondria.
Intact mitochondria, obtained from Euglena gracilis Klebs var. bacillaris Cori mutant W10BSmL, which lacks plastids, and purified on Percoll density gradients, form adenosine 3'-phosphate 5'-phosphosulphate from sulphate. The optimal conditions include addition of 17 mM-Tricine/KOH, pH 7.6, 18 mM-MgCl2, 250 mM-sucrose, 5.66 mM-sodium ADP (or 0.94 mM-sodium ATP), 1 mM-K2SO4, carrier-free 35SO4(2-) (32.1 microCi) and 1.0 mg of mitochondrial protein in a total volume of 2.65 ml and incubation at 30 degrees C. Experiments with the inhibitor of adenylate kinase P1, P5-di(adenosine 5'-)pentaphosphate indicate that ATP is the preferred substrate for sulphate activation; ADP is utilized by conversion into ATP via adenylate kinase. ATP sulphurylase, adenylylsulphate kinase (APS kinase) and inorganic pyrophosphatase constitute the sulphate-activating system; ADP sulphurylase is undetectable. Fractionation of Euglena mitochondria with digitonin and centrifugation allowed the separation of outer-membrane vesicles and mitoplasts as judged by electron microscopy and selected enzymic markers. The detergent-labile association of the sulphate-activating system with the mitoplasts (similar to that of adenylate kinase), the fact that most of the adenosine 3'-phosphate 5'-phosphosulphate formed by intact mitochondria is found in the surrounding medium, and the ease with which nucleotide substrates reach the activating system in intact organelles, suggest that the enzymes of sulphate activation are located on the outer surface of the mitochondrial inner membrane.
Adenine Nucleotides↗
The gastric mucosal barrier.
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Anti-Inflammatory Agents↗
Redox activity at the surface of oat root cells.
Electron transport activity at the cell surface of intact oat seedlings (Avena sativa L. cv Garry) was examined by measuring the oxidation and/or reduction of agents in the medium bathing the roots. Oxidation of NADH with or without added electron acceptors and reduction of ferricyanide by an endogenous electron donor were detected. The activities appear to be due to electron transfer at, or across, the plasma membrane and not due to reagent uptake or leakage of oxidants or reductants. NADH-ferricyanide oxidoreductase activity was also detected in plasma membrane-enriched preparations from Avena roots. Based on redox responses to pH, various ions, and to a variety of electron donors and acceptors, the results indicate that more than one electron transport system is present at the plasma membrane.
Journal Article↗
A new method for quantitation of ion fluxes across in vivo human gastric mucosa: effect of aspirin, acetaminophen, ethanol, and hyperosmolar solutions.
A new, sensitive, and reproducible method for measuring hydrogen and sodium ion fluxes across the human gastric mucosa was developed and validated. By the use of a double-balloon tube that obstructed the pylorus, the stomach was converted into an in vivo Pavlov-type pouch. Duodenogastric reflux was prevented, and emptying of gastric contents into the duodenum was, on the average, 6%, thereby eliminating two important sources of error in quantitative gastric ion fluxes in humans. Transmucosal potential difference and endoscopic appearance of the gastric mucosa were also evaluated during each experiment. The mean percentage variation between duplicate tests for hydrogen ion was 3.2%, for sodium 17.5%, and the potential difference was 2.5%. Instillation of acetylsalicylic acid (36 mM, 1300 mg) in 200 ml of 100 mM hydrochloric acid for just 15 min resulted in a mean net hydrogen ion loss of 3.4 mmol/15 min, a net sodium ion gain of 1.9 mmol/15 min, a decrease in the potential difference of 23 mV, and marked gastric mucosal changes. Furthermore, exposure for 15 min to 20% ethanol (vol/vol, in 200 ml of 100 mM hydrochloric acid) and two separate hyperosmolar solutions (3600 mosmol/kg and 1800 mosmol/kg, both in 200 ml of 100 mM hydrochloric acid) also resulted in marked changes of net hydrogen ion loss (3.1, 4.8, 5.2 mmol/15 min, respectively), net sodium ion gain (2.4, 3.3, 2.4 mmol/15 min, respectively), decrease in potential difference (32, 30, 36 mV, respectively), and gross damage to the gastric mucosa. Each parameter was significantly different from the control test. Acetaminophen (86 mM, 2600 mg) or 10% ethanol (vol/vol) in 200 ml of 100 mM hydrochloric acid did not significantly alter ion fluxes or potential difference. Acetaminophen also did not significantly alter the endoscopic appearance of the gastric mucosa, whereas 10% ethanol had only a modest effect. In the control, aspirin, and acetaminophen experiments, maximal changes in the four parameters (i.e., hydrogen and sodium ion fluxes, potential difference, and endoscopic score) were significantly correlated with one another.
Acetaminophen↗
Effect of sodium taurocholate on the human gastric mucosa at acid and neutral pH's.
This study was conducted to determine whether taurocholate alters human gastric function and structure at a neutral pH, when ionized, and to contrast this with its effect at an acid intraluminal pH, when pronated. Five fasted healthy subjects were studied on 4 days in random order. Net ion fluxes, mucosal damage (as quantitated endoscopically), and potential difference were measured. The control solution instilled into the stomach in the first, third, and fourth 15-min periods contained 200 ml of 100 mM HCl, 54 mM mannitol, and [14C]polyethylene glycol. Taurocholate (10 mM) was added to the control solution (pH 1.1) or citrate buffer (pH 7.0) during the second 15-min period. The effect of citrate buffer alone or control solution alone was also tested. Because hydrogen and sodium fluxes could not be quantitated at pH 7 in the presence of citrate buffer, the net ion fluxes during the 15 min immediately after exposure to the test agent were measured. At both pH 1.1 and 7.0 taurocholate produced similar and significant increases in net hydrogen ion flux (-1.7 +/- 0.4 and -1.8 +/- 0.3 mmol/15 min, respectively), net sodium ion flux (1.8 +/- 0.4 and 1.7 +/- 0.2 mmol/15 min, respectively), decreases in potential difference, and mucosal erosions. The net hydrogen ion fluxes were significantly greater than occurred after citrate buffer alone or the HCl control. The net sodium fluxes after taurocholate in citrate were significantly greater than the pH 1.1 acid control, but not citrate buffer alone. These findings indicate that pronated (pH 1.1) or ionized (pH 7.0) taurocholate significantly damaged the in vivo human gastric mucosa. Taurocholate at pH 7 could in part be responsible for the gastric mucosal injury that occurs in patients with bile reflux gastritis.
Adult↗
Protective effect of acetaminophen against aspirin- and ethanol-induced damage to the human gastric mucosa.
Aspirin and ethanol damage the gastric mucosa in humans, whereas acetaminophen does not. Acetaminophen increases prostacyclin activity in animals and thus may increase endogenous prostaglandin synthesis. The effect of acetaminophen was examined in five healthy subjects after intragastric aspirin or ethanol. Hydrogen and sodium ion fluxes were measured in the pylorus-occluded stomach that prevents duodenogastric reflux and gastric fluid losses. Studies were in random order and on 8 separate days. Potential difference was measured throughout and mucosal erosions were endoscopically quantitated (endoscopist masked, no premedication). The isoosmolar test solution (200 ml, 100 mM HC1, 54 mM mannitol, [14C]polyethylene glycol) was instilled into the stomach and removed 15 min later for four 15-min periods. Either aspirin (1300 mg) or ethanol (20% vol/vol) was added to the test solution only during the second 15 min. Acetaminophen (2600 mg) was given orally 1 h before aspirin or ethanol administration. To determine if the effect of acetaminophen was related to prostaglandin synthesis, prostaglandin production was inhibited with indomethacin (50 mg orally 12 h and 1 h before acetaminophen). Aspirin and ethanol alone each produced significant changes in net hydrogen and sodium fluxes, potential difference, and endoscopic changes. Acetaminophen significantly inhibited hydrogen ion flux, change in potential difference, and endoscopic damage; however, it did not totally abolish these changes. The protective effect of acetaminophen was abolished by pretreatment with indomethacin, suggesting that the effect of acetaminophen is likely to be prostaglandin-mediated. Indomethacin alone was without effect. These results demonstrate that oral acetaminophen protects the human gastric mucosa against the damaging effects of aspirin and ethanol.
Acetaminophen↗
Comparison of the serial dilution indicator and intragastric titration methods for measurement of meal-stimulated gastric acid secretion in man.
Two in vivo methods that permit quantitation of gastric acid secretion immediately after the meal are currently in use: intragastric titration and the serial dilution indicator method. During intragastric titration, intragastric pH is artificially maintained at 5.5 to 7 by the continuous addition of alkali to the gastric contents, while during serial dilution the intragastric pH is permitted to seek its natural pH. This study compared gastric acid secretion and serum gastrin in response to a liquid protein meal measured by both techniques in 10 subjects. Mean (+/- SE) 3-hr acid outputs were almost identical (53.6 +/- 6.0 mmol/3 hr with intragastric titration and 52.0 +/- 8.5 mmol/3 hr with serial dilution indicator). Furthermore, 30 min secretory responses in individual subjects were highly correlated (r = 0.98 +/- 0.01, P less than 0.001). Also, in spite of intragastric pH being less than 1.5 by 90 min after the meal during the serial dilution method, total integrated serum gastrin concentrations after the meal were similar (intragastric titration = 20.6 +/- 7.3 ng min/ml versus serial dilution indicator = 23.5 +/- 9.8 ng min/ml) and individual 30-min gastrins during the two separate tests were highly correlated (r = 0.80 +/- 0.06, P less than 0.01). It is concluded that both meal-stimulated gastric acid secretion and serum gastrin concentrations as measured by intragastric titration and by the serial dilution indicator method produced similar results.
Dietary Proteins↗