Magnesium oxide-pyridoxine therapy for recurrent urolithiasis.
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One way to improve the performance of scintillation dosimeters is to increase the light-collection efficiency at the coupling interfaces of the detector system. We performed a detailed study of surface preparation of scintillating fibers and their coupling with clear optical fibers to minimize light loss and increase the amount of light collected. We analyzed fiber-surface polishing with aluminum oxide sheets, coating fibers with magnesium oxide, and the use of eight different coupling agents (air, three optical gels, an optical curing agent, ultraviolet light, cyanoacrylate glue, and acetone). We prepared 10 scintillating fiber and clear optical fiber light guide samples to test different coupling methods. To test the coupling, we first cut both the scintillating fiber and the clear optical fiber. Then, we cleaned and polished both ends of both fibers. Finally, we coupled the scintillating fiber with the clear optical fiber in either a polyethylene jacket or a V-grooved support depending on the coupling agent used. To produce more light, we used an ultraviolet lamp to stimulate scintillation. A typical series of similar couplings showed a standard deviation in light-collection efficiency of 10%. This can be explained by differences in the surface preparation quality and alignment of the scintillating fiber with the clear optical fiber. Absence of surface polishing reduced the light collection by approximately 40%, and application of magnesium oxide on the proximal end of the scintillating fiber increased the amount of light collected from the optical fiber by approximately 39%. Of the coupling agents, we obtained the best results using one of the optical gels. Because a large amount of the light produced inside a scintillator is usually lost, better light-collection efficiency will result in improved sensitivity.
A large emphasis on precalving magnesium supplementation has substantially reduced the incidence of clinical hypocalaemia in pasture-based systems. Survey data in the major pasture-based systems suggest a 2 to 4% incidence of parturient paresis, although this can vary considerably between farms. Detailed blood measurements under research conditions suggests that approximately 5% of cows are clinically hypocalcaemic (blood calcium < 1.4 mmol/l) and between 30 and 40% of cows are subclinically hypocalcaemic (plasma calcium < 2.0 mmol/l). Systems of control have traditionally been based on preventing the paretic cow, with more emphasis of late being placed on preventing hypocalcaemia. Preventative measures vary, but largely involve either supplementation with magnesium oxide pre-calving, supplementation with calcium carbonate during the colostrum period or a combination of magnesium supplementation precalving and calcium supplementation post-calving. In New Zealand, the use of commercial products that bind calcium is increasing precalving, but is still only practiced by a small percentage of farmers. The dietary cation-anion difference (DCAD) of pasture is so high and so variable that changes in DCAD sufficient to change blood pH are not practical and very difficult to achieve with consistency. The use of magnesium chloride and magnesium sulphate in preference to magnesium oxide, as precalving magnesium supplements, is increasing.
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Magnesium oxide and bone meal were used as chemical defluoridating agents to reduce excessive amounts of fluoride from artificial water samples which had been prepared to simulate Kenyan water samples with a fluoride concentration ranging from 1 to 9.3 ppm. The water filtrate from bone meal was clear and palatable. The filtrate from magnesium oxide was slightly slimy and cloudy, but palatable. Either of these chemical agents may be used in simple defluoridation procedures in rural and suburban areas using borehole water to reduce the excess fluoride in the water to beneficial non-toxic levels. Both magnesium oxide and bone meal are inexpensive chemicals and readily available in Kenya.
Magnesium deficiency is seen with some frequency in the outpatient setting and requires oral repletion or maintenance therapy. The purpose of this study was to measure the bioavailability of four commercially-available preparations of magnesium, and to test the claim that organic salts are more easily absorbed. Bioavailability was measured as the increment of urinary maginesium excretion in normal volunteers given approximately 21 mEq/day of the test preparations. Results indicated relatively poor bioavailability of magnesium oxide (fractional absorption 4 per cent) but significantly higher and equivalent bioavailability of magnesium chloride, magnesium lactate and magnesium aspartate. We conclude that there is relatively poor bioavailability of magnesium oxide, but greater and equivalent bioavailability of magnesium chloride, lactate, and aspartate. Inorganic magnesium salts, depending on the preparation, may have bioavailability equivalent to organic magnesium salts.
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The antacid properties of seven antacids listed in the hospital formulary of a medical center were evaluated with in vitro tests. These included not only the preliminary antacid test and acid-neutralizing capacity test as described in the United States Pharmacopeia (USP XXIII), but also a buffering pH profile test. The preliminary antacid test measured the final pH of a 10-mL solution of 0.5 N HCl 10 minutes after addition of the minimum recommended dose of an antacid, while the neutralizing capacity test measured the amount (mEq) of HCl neutralized by the minimum recommended dose in 15 minutes. The buffering pH profile recorded the pH time course of dynamic simulated gastric fluid neutralization by a dose of an antacid. In the preliminary antacid test, magnesium oxide showed the highest pH (9.52 +/- 0.14, mean +/- standard deviation, n = 3); aluminum phosphate gel yielded a final pH of 2.51 +/- 0.01, thus failing to meet the criteria of an antacid (pH > 3.5). In the acid-neutralizing capacity test, hydrotalcite had the highest neutralizing capacity (28.26 +/- 0.3 mEq), while sodium bicarbonate had the lowest (7.40 +/- 0.12 mEq). In the buffering pH profile test, aluminum-magnesium hydroxide suspensions and hydrotalcite tablets maintained a steady optimum pH (3-5) for around 1.5 hours. One tablet of calcium carbonate, sodium bicarbonate or magnesium oxide could not raise the gastric pH to above 3, but two tablets increased the pH excessively (5.3 to 8.6). The higher dose (two tablets) of aluminum hydroxide hexitol complex could not raise the pH to the optimal level. These findings demonstrate that there is disparity in the antacid effectiveness estimated by the neutralizing capacity test and the buffering pH profile test and suggest that the efficacy of an antacid cannot be accurately predicted from its acid-neutralizing capacity. The dose of antacids greatly influences the neutralizing pH profiles. Aluminum-magnesium compounds appear to provide steadier buffering than carbonate compounds or magnesium oxide.
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An investigation of the rate of the 2,4-dinitrophenol absorption from the digestive tract into the blood with the use of an antidote and its components (activated charcoal, tannin, magnesium oxide), stach water and paraffin oil demonstrated the activated charcoal and magnesium oxide to be the best antidotes among the ones studied. The antidote exerts a somewhat less marked, but still quite a strong action.
Seven patients with severe neuromuscular symptoms due to hypomagnesaemia together with hypocalcaemia following extensive resection of the small bowel were treated orally with 1 alpha-hydroxylated metabolites of vitamin D and magnesium oxide. There was a rapid response in both plasma calcium and magnesium concentrations. The mean plasma magnesium rose from 0.24 to 0.45 mmol/l with the vitamin D metabolites alone and to 0.81 mmol/l when magnesium oxide was added. The plasma calcium rose from 1.78 to 2.21 mmol/l on vitamin D alone and then remained within the normal range. This was accompanied by a rapid resolution of the neuromuscular symptoms. Such oral treatment is both acceptable to the patient and effective both for acute symptoms and in the long term to maintain plasma magnesium concentrations.
This study examined the modifications of acid gastric secretion caused by magnesium oxide, peroxide, silicate and sulphate in 805 patients with duodenal ulcers; The calcium-magnesium antagonism on the one hand and the acetazolamide - magnesium synergia on the other, were also investigated. Our results show that administration of magnesium, either oral or parenteral, does not significantly modify gastric acid secretion, either basal or stimulated by maximal histamine. Administration of un infusion of calcium gluconate 15 mg/kg body weight, significantly increases gastric acid secretion as compared to basal secretion. Addition of a dose of magnesium sulphate to the infusion antagonises the effect of gastric acid secretion caused by calcium. Administration of 1.5 gr magnesium oxide along with 25 mg acetazolamide per kg/body weight, strengthens the inhibitory effect of acetazolamide upon gastric acid secretion, increasing the proportion of significant inhibitory effects up to 98% of the cases under investigation. Addition of magnesium to the classical therapy antagonises the noxious effects of calcium compounds; the presence of magnesium in the composition of antacid powders proves necessary.
This study examined the effects of widely used antacids (aluminum hydroxide, magnesium oxide, and calcium carbonate), ferrous sulfate, and ranitidine on the absorption of a fluorinated quinolone, (-)-(S)-9-fluoro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro- 7H- pyrido-[1,2,3,-de][1,4]benzoxazine-6-carboxylic acid hemihydrate (DR-3355), in healthy male volunteers enrolled in three separate randomized crossover studies. Study 1 used 100-mg doses of DR-3355 and concurrent doses of aluminum hydroxide (1 g) or magnesium oxide (500 mg), while study 2 used DR-3355 (100 mg) and concurrent ferrous sulfate (160 mg) or calcium carbonate (1 g). Study 3 used DR-3355 (100 mg) and concurrent ranitidine (150 mg). Each study included control doses of DR-3355 (100 mg) alone. When aluminum hydroxide, ferrous sulfate, and magnesium oxide were coadministered with DR-3355, the relative bioavailability of DR-3355 was decreased to 56, 81, and 78%, respectively, of that for DR-3355 (100 mg) alone. Urinary excretion of DR-3355 was also significantly decreased by coadministration of these drugs. Thus, the magnitude of the decrease in the area under the concentration-time curve for DR-3355 varied among antacids, and the ranking of their inhibitory effects correlated with previously reported rankings of stability constants for chelate formation. DR-3355 bioavailability was not influenced by the concurrent administration of calcium carbonate and ranitidine, indicating that changes in gastric pH do not affect DR-3355 absorption.
Serum creatine kinase (CK) activity, calcium (Ca) and magnesium (Mg) contents of skeletal muscle and isolated mitochondria, as well as oxidative phosphorylation of X-linked muscular dystrophic (mdx) mice were compared with normal control animals at ages 5, 10, and 23 weeks. Serum CK is elevated in mdx mice at all ages, with highest activities at 5 weeks. The Ca content of dystrophic skeletal muscle is increased at all ages, whereas no clearly abnormal trend in muscle Mg levels was observed. Noncollagen protein (NCP), which was used as a reference base, is significantly diminished in muscle from 10- and 23-week-old mdx animals. Isolated mitochondria from mdx mice have elevated calcium content and decreased respiratory control ratios with NAD-linked substrates pyruvate/malate. The findings are distinct from those in dystrophic mice, strain 129/ReJ, but similar to observations in dystrophic hamsters and Duchenne muscular dystrophy and reflect the occurrence of overt muscle cell necrosis.
It has been reported that 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin (CPT-11) and its active metabolite, 7-ethyl-10-hydroxy-camptothecin (SN-38), have absorption characteristics of weakly basic drugs, suggesting that alkalization of the intestinal lumen might reduce reabsorption and its attendant side effects. Furthermore, stasis of stools containing these compounds is thought to induce damage to the intestinal mucosa. The prevention of CPT-11-induced side effects by oral alkalization (OA) combined with control of defecation (CD) was estimated in a case-control study of lung cancer patients. Coinciding with day 1 of CPT-11 infusion and for 4 days thereafter, OA and CD were practiced utilizing orally administered sodium bicarbonate, magnesium oxide, basic water and ursodeoxycholic acid. OA involved the daily use of all four therapeutics, and CD required doses of up to 4.0 g/day of magnesium oxide and 2 L/day of excess basic water. From three ongoing prospective phase I/II studies, we selected 37 consecutive patients who were treated with CPT-11 in combination with cisplatin in the presence of OA and CD (group B). Thirty-two control subjects who were matched to the background characteristics of the case patients were treated with the same regimen in the absence of OA and CD (group A). Toxicities induced by the CPT-11/cisplatin combination were evaluated and analyzed in group A and group B in a case-control format. The use of OA and CD resulted in significantly higher stool pH (p < 0.0001), while reducing the incidence of delayed diarrhea (> or = grade 2: group A 32.3% versus group B 9.4%; p = 0.005), nausea (p = 0.0001), vomiting (p = 0.001) and myelotoxicity, especially granulocytopenia (p = 0.03) and lymphocytopenia (p = 0.034). In addition, dose intensification was well tolerated in patients receiving OA and CD, allowing dose escalation from 35.6 +/- 6.0 to 39.9 +/- 5.6 mg/m(2)/week (p < 0.001). Tumor response rates for non-small cell lung cancer were 59.3% (16/27 patients) in group B compared with 38.5% (10/26 patients) in group A. Multivariate analysis revealed that the risk of CPT-11-induced delayed diarrhea greater than grade 2 was associated with OA and CD (odds ratio for delayed diarrhea, 0.14 with use of OA and CD; 95% confidence interval, 0.05 to 0.4; p = 0.0002) and age (odds ratio, 1.08 per increase in age; 95% confidence interval, 1.02 to 1.15; p = 0.009). OA and CD appear to be useful in preventing the dose-limiting side effects of CPT-11 noted in clinical practice, mainly nausea, vomiting, granulocytopenia and especially delayed diarrhea. Risk factors statistically associated with delayed diarrhea include advanced age and the use of CPT-11 without OA and CD.
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Ceramic implants are manufactured from aluminium oxide ceramics (Al2O3) doped with magnesium oxide (MgO). The yellow or brown discoloration following gamma-sterilization does not constitute a material defect, but rather a property of the material. This chromic effect is explained in the following article.
Rana esculenta tadpoles that are fed spinach develop an oxalic calculogenesis. The addition of cholestyramine, orthophosphate, citrate, allopurinol and tungstate to the tank water prevented calculi formation while succinimide, magnesium oxide, hydrochlorothiazide and tetracycline were ineffective. Methylene blue proved lethal to tadpoles, and its anti-lithogenic activity could not be assessed. These findings, except for the non-effectiveness of magnesium oxide, are in agreement with both the theoretical expectations and the results obtained in other experimental models. Experimental frog calculogenesis seems to be a simple and valid method for evaluating anti-lithogenic activity.