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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aluminum oxalate buffered with glycine to pH 0.5-2.5 has been proposed as a dentin pretreatment for the Gluma bonding system. In this experiment, the effects of 1-minute treatments of smear layers with these aluminum oxalates on the permeability of human dentin were determined in vitro. The aluminum oxalate solutions at pH 0.5-1.5 removed most of the original smear layer but occluded the tubules with crystalline deposits which decreased dentin permeability. Those solutions used at pH 2.0 and 2.5 increased dentin permeability. All dentin pretreatments increased dentin permeability when measured after a 24-hour storage period, especially the solutions at pH 2.0 and 2.5. The SEM correlates of these permeability changes indicated that these solutions remove the smear layer but reocclude the tubules with precipitates which are probably different forms of calcium oxalate, aluminum phosphate and calcium phosphates.
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PMID:Effects of aluminum oxalate/glycine pretreatment solutions on dentin permeability. 130 82

The effect of perfusate [Ca2+] on the function of cardiac sarcoplasmic reticulum (CSR) was assessed by the oxalate-supported Ca2+ uptake rate of ventricular homogenates of isolated rat hearts maintained in a modified Langendorff preparation. The total Ca2+ pumping activity of the CSR was determined by using 20 microM ruthenium red or 625 microM ryanodine to close the CSR Ca2+ release channel. The homogenate Ca2+ uptake rate in the absence of ruthenium red or ryanodine decreased progressively with increasing perfusate [Ca2+] (25.7 +/- 1.2, 21.4 +/- 1.5, 17.2 +/- 1.1, and 16.3 +/- 1.2 [mean +/- SEM] nmol Ca2+.min-1.mg-1 for hearts perfused for 5 minutes with 0.2, 1.4, 2.8, and 5.6 mM Ca2+, respectively; p = 0.0001; n = 8). This depression was not observed when Ca2+ uptake was assayed in the presence of ryanodine or ruthenium red. Since the Ca2+ uptake in the presence of ryanodine or ruthenium red is determined by the Ca(2+)-ATPase, this result suggests that perfusion with varying [Ca2+] did not affect the Ca(2+)-ATPase. The observed decrease in Ca2+ uptake in the absence of ryanodine or ruthenium red is caused by an increased efflux through the ryanodine-sensitive Ca2+ release channel. When hearts perfused for 5 minutes with 0.2 or 5.6 mM Ca2+ were reperfused for 10 minutes with 1.4 mM Ca2+, homogenate Ca2+ uptake rates were restored to near control levels. These effects of perfusate Ca2+ were not direct effects, because changes in the [Ca2+] of the homogenization medium did not alter the homogenate Ca2+ uptake activity in either the presence or absence of ryanodine. The homogenate Ca2+ uptake rates were unaffected by prior active loading of the CSR with Ca2+. These results suggest a regulatory role of perfusate Ca2+ in increasing the open state of the ryanodine-sensitive Ca2+ release channel that is distinct from the beat-to-beat regulation of Ca2+ release from the CSR by Ca2+ (Ca(2+)-induced Ca2+ release).
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PMID:Effect of perfusate [Ca2+] on cardiac sarcoplasmic reticulum Ca2+ release channel in isolated rat hearts. 138 83

The influences of nine dentin surface treatments were evaluated on the shear bond strength of a new light-cured glass-ionomer cement (GIC) and on the SEM morphology of the treated dentin surfaces. The following treatments were performed: saline solution (control), NaOCl, acidic glycine, EDTA, malic acid, malic acid plus glycine, polyacrylic acid, tannic acid, and neutral+acidic oxalate solutions. Buccal dentin surfaces were polished with #320-grit abrasive paper, treated with one of the chemicals, washed, and air-dried. Cylindrical GIC samples were then applied to the dentin surface, stored in 100% humidity, and tested after 24 h. SEM observations demonstrated no effect of saline or NaOCl treatment on the smear layer but its complete removal with exposure of collagen fibrils after malic or malic acid plus glycine treatment. Partial removal of the smear layer occurred following glycine treatment and with tannic or polyacrylic acids. Complete removal of the smear layer was seen after EDTA or pyruvic acid treatment. Oxalate treatment produced a layer of crystals, which completely covered the dentin surface. Shear bond strength of GIC was significantly increased only by treatment with the oxalate solutions.
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PMID:Effects of dentin surface treatments on the shear bond strength of Vitrabond. 152 80

Increasing the concentration of urate promotes the crystallization of calcium oxalate in human urine. In this study the possibility that this effect might be attributable to the attenuation of the inhibitory activity of urinary glycosaminoglycans (GAGs) was explored. Urine sample were collected from 20 men with no history of urolithiasis and the intact GAGs removed by 10 kDa ultrafiltration. Ten of these specimens, designated type A, spontaneously precipitated calcium oxalate crystals when the median urate concentration was increased from 3.13 to 7.33 mmol/liter by the addition of a saturated solution of sodium urate. In the remaining more dilute urines, which were designated type B, spontaneous calcium oxalate crystallization did not occur when the median urate concentration was raised from 2.20 to 6.40 mmol/liter. In these samples crystallization was induced by a standard load of oxalate above the empirically determined metastable limit. Addition of urate significantly reduced the median metastable limit from the control value of 125 to 46 mumol oxalate, and the volume of calcium oxalate deposited was increased fourfold from 25,000 to 104,000 microns 3/microliters. The median size of the precipitated particles was also increased in the presence of urate from 12.06 microns to 14.3 microns; this was confirmed by scanning electron microscopy, which demonstrated that the crystals precipitated in the presence of added urate, though individually smaller, were markedly more numerous and more highly aggregated than those deposited in the control. Re-ultrafiltration of the urines to which urate had been added did not alter the urate concentration, and SEM examination of the ultrafiltration membranes did not reveal the presence of any particulate material.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium oxalate crystallization in urine: role of urate and glycosaminoglycans. 159 51

Intraperitoneal reserpine (5 mg/kg every day for 5 days) produced solitary chronic ulceration of the rat stomach after 2 weeks. Gavage with 1 mL/day of 1% naftidrofuryl oxalate for 2 weeks protected 30% of rats against ulceration and this protection extended to 70% of cases with a 2% solution. Similar gavage with a 5% solution protected all rats against ulceration without significantly influencing the basal H+ output (14.8 +/- 0.6 versus 15.4 +/- 0.5 mumol, mean +/- SEM, n = 10); that is, cytoprotection was achieved.
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PMID:Naftidrofuryl protects the rat against chronic gastric ulceration. 194 62

Crystals of calcium oxalate monohydrate (COM), dihydrate (COD) and trihydrate (COT) were grown by slow diffusion of reacting ions from solutions using interfacially controlled crystallization. Phase transition of COT to COD and COM, and COD to COM were studied on single crystal by X-ray diffraction analysis of the same crystal before and after exposure to normal and stone formers' urine. Phase transition on the surface of single crystals has been demonstrated by SEM energy dispersive X-ray microanalysis using windowless detector, and scanning Auger electron microprobe. Data obtained in this study offer direct experimental evidence for phase transformation on the surface of the hydrated calcium oxalate single crystal. In presence of normal urine the surface of COT single crystal undergoes transformation into COD and in presence of recurrent calcium oxalate stone former's urine surface transformation to COM takes place.
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PMID:Surface phase transition of hydrated calcium oxalate crystal in the presence of normal and stone-formers' urine. 240 11

Plasma oxalate and erythrocyte glutamic oxaloacetate transaminase activity (EGOT) (an indicator of nutritional status with respect to pyridoxine) were measured in 21 patients maintained on regular continuous ambulatory peritoneal dialysis or haemodialysis before and after a 4-month period of supplementation with pyridoxine, 100 mg day-1. Prior to supplementation 10/21 patients showed subnormal EGOT activity, although the increment in activity on addition of pyridoxal-5-phosphate in vitro was within the normal range in all cases. Mean plasma oxalate was 31.5 mumol l-1 (SEM 2.9) prior to supplementation and did not change significantly with supplementation, despite normalization of EGOT activity in all but 2/21 patients. We conclude that pyridoxine deficiency does not contribute significantly to hyperoxalaemia in patients receiving dialysis and that 100 mg of pyridoxine daily is insufficient to reduce oxalate generation by a pharmacological action on glycine transamination.
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PMID:Effect of pyridoxine supplementation on plasma oxalate concentrations in patients receiving dialysis. 249 79

Whole blood ascorbate, plasma oxalate, serum cholesterol, and capillary fragility were measured at monthly intervals for 3 mth in 7 patients receiving continuous ambulatory peritoneal dialysis and 4 receiving haemodialysis, to whom ascorbate supplements had not been prescribed for at least 12 mth. Ascorbate supplements, 25 mg/day, were prescribed for the first month and 50 mg/day for the second month; in the final month patients received no supplements. Whole blood ascorbate was below normal in 6/11 patients at the start of the study but was normal in 10/11 patients when taking ascorbate 50 mg/day. No significant changes in plasma oxalate were observed with these doses of ascorbate, and correction of ascorbate deficiency had no effect on serum cholesterol, mean cell volume, or the results of capillary fragility tests. In a supplementary study, ascorbic acid 500 mg/day was administered for 3 wk to 11 patients. This resulted in a significant rise in mean plasma oxalate from 30.3 (SEM 3.5) to 48.4 (SEM 20.3) mumol/l.
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PMID:Correction of subclinical ascorbate deficiency in patients receiving dialysis: effects on plasma oxalate, serum cholesterol, and capillary fragility. 274 78

We wished to determine whether different types of dietary protein might have different effects on calcium metabolism and on the propensity for renal stone formation. Fifteen young normal subjects were studied during three 12-day dietary periods during which their diet contained vegetable protein, vegetable and egg protein, or animal protein. While these three diets were constant with respect to Na, K, Ca, P, Mg, and quantity of protein, they had progressively higher sulfur contents. As the fixed acid content of the diets increased, urinary calcium excretion increased from 103 +/- 15 ( +/- SEM) mg/day (2.6 +/- 0.4 mmol/day) on the vegetarian diet to 150 +/- 13 mg/day (3.7 +/- 0.3 mmol/day) on the animal protein diet (P less than 0.02). Despite the increased urinary calcium excretion, there was a modest reduction of urinary cAMP excretion and serum PTH and 1,25-dihydroxyvitamin D levels consistent with acid-induced bone dissolution. There was no change in fractional intestinal 47Ca absorption. The inability to compensate for the animal protein-induced calciuric response may be a risk factor for the development of osteoporosis. The animal protein-rich diet was associated with the highest excretion of undissociated uric acid due to the reduction in urinary pH. Moreover, citrate excretion was reduced because of the acid load. However, oxalate excretion was lower than during the vegetarian diet [26 +/- 1 mg/day (290 +/- 10 mumol/day) vs. 39 +/- 2 mg/day (430 +/- 20 mumol/day); P less than 0.02]. Urinary crystallization studies revealed that the animal protein diet, when its electrolyte composition and quantity of protein were kept the same as for the vegetarian diet, conferred an increased risk for uric acid stones, but, because of opposing factors, not for calcium oxalate or calcium phosphate stones.
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PMID:Relationship of animal protein-rich diet to kidney stone formation and calcium metabolism. 282 24

Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.
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PMID:Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. 297 Nov 39


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